Ijmrhs Vol 2 Issue 4

DOI: 10.5958/j.2319-5886.2.4.
115
International Journal of Medical Research

&
Health Sciences
www.ijmrhs.com
Volume 2 Issue 4 Oct-Dec
Coden: IJMRHS
th
Received: 10 July 2013
Revised: 8th Aug 2013
Copyright @2013
ISSN: 2319-5886
Accepted: 15th Aug 2013
Research article
COMPARATIVE STUDY ON EFFICACY & SAFETY OF INTRAVENOUS IRON SUCROSE
VERSUS INTRAMUSCULAR IRON SORBITOL THERAPY IN ANEMIA DURING
PREGNANCY
*Lomte DB1, Bhosale RS2, Jambdade V3, Gore PR4
1
Asso. Prof, Dept. of Pharmacology, Dr. V.P.M.C. Nashik, Maharashtra, India

Civil Hospital Nashik, 3Head of Dept., OBGY, Civil Hospital Nashik, Maharashtra, India
2,4
*Corresponding author email: rahulbraje@gmail.com, vasantjamdhade@gmail.com

ABSTRACT
Aims and Objectives: To compare the efficacy, safety, and rate of response of intravenous iron sucrose
and intramuscular iron Sorbitol therapy for anemia during pregnancy. Material and Methods: 100
antenatal cases of gestational age 16-32 weeks were included in this prospective study. Cases were
randomly divided into two groups. Group A, having 50 cases received intravenous iron sucrose, and
50cases in group B received intramuscular iron sorbitol. Response to therapy in both groups was studied
and compared. Results: The mean pretherapy hemoglobin in group A was 6.49 g/dl and in group B was
6.48 g/dl. The rise in hemoglobin after 4 weeks of starting therapy was 3.52 g/dl in group A and 2.33
g/dl in group B The difference was Statistically significant (P<0.01) The mean time taken to achieve
target hemoglobin (>11 g/dl) was 6.37 weeks in group A and 9.04 weeks in group B. In group A, 8%
(four) cases had grade I adverse effects. In group B, 24% (12) cases had grade I adverse effects. The
difference was statistically significant (P=0.027). In both the groups no case discontinued the therapy.
Conclusion: Intravenous iron sucrose is safe, convenient, more effective, and faster acting therapy than
intramuscular iron sorbitol therapy for treating moderate to severe anemia during pregnancy.
Keywords: Iron sucrose, Iron sorbitol, Pregnancy, Iron deficiency.
INTRODUCTION
Anemia is associated with higher perinatal

mortality and morbidity1. Anemia is the most
common hematologic abnormality diagnosed
during pregnancy. It is most often caused by iron
deficiency & occasionally by more complex
conditions involving deficient production of or
accelerated destruction of erythrocytes.1
In
developing countries nearly two third of the
pregnant women suffering from anemia out of
which 95% of cases are having iron deficiency

anemia.2
Over the past years, various routine methods like
oral iron therapy, intramuscular iron therapy, and
blood transfusion were used to treat anemia
during pregnancy3,4. These methods are not
without deficiencies, and also there are
conditions in which these conventional iron
therapies are not helpful, like inadequate
719
Lomte DB et al.
Int J Med Res Health Sci. 2013;2(4):719-723
gastrointestinal absorption, late pregnancy, and

intolerance to required oral iron, requirement of
emergency supplement, and severe anemia with
contraindications to blood transfusion5. So, to
treat these conditions, we require a relatively
new mode of iron therapy with better efficacy,
less side effects, fast action and better
compliance. Intravenous iron sucrose therapy
seems to be a safe convenient and more effective
treatment for anemia during pregnancy
MATERIALS AND METHODS
After the approval of

Institutional Ethics
committee of Dr VPMC, Nashik, total 100
antenatal women between 16 and 32 weeks of
gestation with hemoglobin level of 8 g/dl or less,
attending the outpatient department & antenatal
ward at Civil Hospital Nashik, were included in
the present study.
Inclusion Criteria: 1. Pregnant women aged
18, gestational week between 16 to 32, at
baseline with normal antenatal screening test
results, Pregnant women willing to give conform
consent form for the study 2. Iron deficiency
anemia defined as Hb concentration 8g/dl,
serum iron less than 60 micro g/dl, and total ironbinding capacity more than 400 micro g/dl
Excusing Criteria: 1. The cases having
hemoglobin level >8 g/dl 2. Gestational age <16
or >32 weeks
3. History of allergic reaction to previous iron
therapy 4. Anemia due to causes other than iron
deficiency.
All the 100 cases enrolled in the study were
assigned into two groups. Group A: 50 cases
received intravenous iron sucrose, Group B: 50

cases received intramuscular iron sorbitol
therapy. Iron was given after proper sensitivity
testing in both the groups. All the selected cases
were subjected to a thorough history taking,
general, systemic and obstetrical examination.
The dose of iron required in both the groups was
calculated by the formula
Total iron required =Body weight (kg) X Hb
deficit X 0.3 + (Body Wt.(kg) X10)
[Hb deficit=target Hb- patient`s Hb (Target
Hb=11g/dl)]
In group A iron sucrose was given as 150 mg (3
ampoules, each of 2.5ml) in 100 ml of 0.9%
normal saline infusion over 1 hr every third day
up to the total calculated dose. In group B, iron
sorbitol complex was given as a daily
intramuscular injection of 1.5 ml till the total
calculated dose, by means of Z technique. All
the cases were monitored for adverse effects.
Adverse effects were graded as grade I and grade
II. Grade I reactions were mild to moderate and
settled with an antiallergic drug but not requiring
discontinuation of drug. Grade II reaction was
severe in nature threatening the life of patients
and requiring discontinuation of therapy.
Statistical analysis:
Statistical analysis was carried out by using
pairedt test for comparing effects of
intravenous iron sucrose & intramuscular iron
sorbitol before and after therapy. For
comparisons between intravenous iron sucrose &
intramuscular iron sorbitol unpaired t test was
applied.
RESULTS
Table 1: Demographic distribution of cases
Mean age (years)

Mean period of gestation
Parity >2 (% of cases)
Socioeconomic status class
IV or lower (%of cases)
Group A
(n=50)
26.46
24.48
68
76
Group B
(n=50)
26.62
23.94
56
80
720
Lomte DB et al.
Table 2: Hemoglobin level before starting therapy

Hemoglobin level
Group A
(g/dl)
No.
<4
6
4.1-6
8
6.1-8
36
Mean
6.49
P value
Group B
%
12
16
72
No.
3
12
35
6.48
%
6
24
70
>0.05
Table 3: Hemoglobin level 2 and 4 weeks after starting therapy

Hemoglobin After 2 weeks of therapy
level (g/dl)
Group A
Group B
No.
%
No.
%
5-7
7
14
12
24
7.1-9
16
32
33
66
9.1-11
27
52
5
10
>11
Mean
8.79
7.74
P value
< 0.01
After 4 weeks of therapy

Group A
No.
%
9
18
39
78
2
4
10.01
<0.01
Group B
No.
5
21
24
8.81
%
10
42
48
-
Table 4: Time period taken to achieve target hemoglobin level (>11g/dl)
Time period
(weeks)
Group A
2-4
>4-8
>8-12
>12
No.
3
42
5
-
Mean
P value
6.37
<0.01
Group B
%
6
84
10
-
No.
17
28
5
%
34
56
10
9.4
Table 5: Adverse effects in both the groups
Adverse effects (all grade I)
Group A
Group B
No.
No.
Local phlebitis
Shivering and weakness
Moderate abdominal pain
Local pain
2
1
1
-
4
2
2
-
12
Skin staining
12
Headache
Total
12
24
721
Lomte DB et al.
The mean pre therapy hemoglobin level in group

A was 6.49 g/dl and in group B was 6.48 g/dl
(Table 2). In group A, the mean hemoglobin
level after 2 weeks of staring therapy was 8.79
g/dl with a rise of 2.33 g/dl. In group B, the mean
hemoglobin level after 2 weeks of starting
therapy was 7.74 g/dl with a rise of 1.26
g/dl(Table 3) the difference was statistically
significant (P<0.01).
After 4 weeks of starting therapy, the mean
hemoglobin level in group A was 10.01 g/dl with
a rise of 3.52 g/dl and I group B mean
hemoglobin was 8.81 g/dl with a total rise of
2.23g/dl from the pre therapy level (Table 3).
The difference was statistically significant
(P<0.01). In group A, 90% (45) cases achieved
target hemoglobin level after 8 weeks of starting
therapy, while in group B only 34% (17) cases
achieved target hemoglobin levels after 8 weeks
of therapy. The difference was statistically highly
significant (P< 0.001).
The mean time period taken to achieve target
hemoglobin level was 6.37 g/dl in group A and
9.04 weeks in group B (Table4). The difference
was found to be statistically significant (P<0.01).
In group A, 8% (four) cases had grade I adverse
effects: while in group B, 24% (12) cases had
grade I adverse effects (Table5). The adverse
effects
were
minimal
and
managed
symptomatically. On statistically analyzing the
results, the difference was found significant (P=
0.027).
In group A, 60% (30) cases were completely
relieved of their clinical symptoms at 4 weeks
after therapy: while in group B, only 20% (10)
cases were completely relieved of their
symptoms. The difference was statistically
highly significant.
DISCUSSION
The current study was undertaken to evaluate the

efficacy and safety of intravenous iron sucrose
therapy for treating anemia during pregnancy and
compare it with intramuscular iron sorbitol
therapy. The rise in hemoglobin level in cases,
which were given intravenous iron sucrose

therapy, was 2.3 g/dl after 2 weeks and 3.52 g/dl
after 4 weeks (table 3). It was significantly
higher when compared to rise after intramuscular
iron sorbitol therapy. The rise in hemoglobin
level was 2.6 g/dl in intravenous group and 1.2
g/dl in intramuscular group after 3 weeks of
therapy in the study by Hashmi et al.5 In the
study conducted by wali et al.6 the rise in
hemoglobin level was 2.8 g/dl after 3 weeks of
intravenous iron sucrose therapy.
90% (45) cases achieved the target hemoglobin
level of >11g/dl after 8 weeks of intravenous iron
sucrose therapy, while only 34% (17) cases
achieved target hemoglobin level after 8 weeks
of intramuscular iron sorbitol therapy. The
difference was statistically significant (p< 0.001).
In the study by Hashmi et al.6, 80% cases
achieved target hemoglobin in intravenous iron
group and only 20% cases achieved target
hemoglobin level in intramuscular iron group
after 6 weeks of therapy.
In our study, the mean time period taken to
achieve the target hemoglobin level was 6.37
weeks in intravenous iron sucrose group and 9.04
weeks in intramuscular iron sorbitol group
(Table 4) this difference was statistically
significant (P<0.01). In the study by Raja et al.8
the mean time period to achieve target
hemoglobin level was 5 weeks in the intravenous
iron sucrose group.
Only 8 % (four) cases had adverse effects which
were of grade I type with intravenous iron
sucrose therapy, while 24% (12)9-12 cases had
grade I adverse effect with intramuscular iron
sorbitol therapy (Table 5). The difference was
statistically significant (P= 0.027). There were no
grade II adverse effects in either of the groups. In
the study conducted by Wali et al.7, 12% cases
had grade I adverse effects, with intravenous iron
sucrose therapy, while 50% cases had grade I
adverse effects with intramuscular iron sorbitol
therapy. In group A, 60% (30) cases were
completely relieved of their symptoms: while in
group B, only 20% (10) cases were completely
722
Lomte DB et al.
relieved of their symptoms. The difference was

statistically significant (P<0.001). The results of
our study shown that the mean hemoglobin level
achieved in intravenous iron sucrose group was
significantly higher and the rate of increase in
hemoglobin level
was also higher in
intravenous group. The number of cases
achieving target hemoglobin was significantly
higher in intravenous group and also the target
hemoglobin was achieved in a shorter time
period in intravenous group. The incidence of
adverse effects was also significantly lower in
intravenous group.
CONCLUSION
Intravenous iron sucrose therapy is safe,

convenient, more effective, and faster acting than
intramuscular iron sorbitol therapy for the
treatment of moderate to severe anemia during
pregnancy.
REFERENCES
1. Fernando Arias, Shirish ND. Anemia in

pregnancy. Text book of Obstetrics. 2010,
466-469
2. Allen LH. Pregnancy and iron deficiency:
Unresolved Issues. Nutr Rev. 1997; 55; 91101.
3. Bayoumeu F, Subiran-Buisset C, Baka NE.
Iron therapy in iron deficiency anemia in
pregnancy: intravenous route versus oral
route. Am J Obstet Gyneco. 2002; 186; 51822.
4. Kanani SJ, Poojara RH. Supplementation
with iron & folic acid enhances growth. Jr
Nutrition 2000; 130:452S-455S
5. Perewusny KG, Huck R, Huck A. Parenteral
iron-sucrose complex. Br. J Nutr. 2002;88;310
6. Hashimi Z, Bashir G, Azzem P. Effectiveness
of intra-venous iron sucrose complex versus
intra-muscular iron sorbitol in iron deficiency
anemia. Ann Pak Inst Med Sci. 2006;2;18891.

7. Waili A, Mushtaq A. Comparative Studyefficacy. Safety and compliance of
intravenous iron sucrose and intramuscular
iron sorbitol in iron deficiency anemia of
pregnancy. J Pak Med Assoc. 2002; 52; 39295.
8. Raja KS, Janjua NB, Khokhar N. Intravenous
iron Sucrose complex therapy in iron
deficiency anemia in the pregnant women.
Rawal Med J. 2003; 28; 40-3.
9. Sharma JB, Vibha Fatedar. Iron deficiency
anemia in pregnancy. Obs & Gynae Today.
2006;9(3);147-148.
10. Pollitt E, Soemangri AG, Yunis F, cognitive
effects of Iron deficiency anemia. Lancet
1985; 1:158.
11. Lazoff B, Jimenez E, Walf AW long term
developmental out come of infants with iron
deficiency. New Eng I J Med 1991;
325(10):687-95.
12. Abel R, Raja ratnamJ, Sapatkumar V.
Anemia in pregnancy impact of iron, IEC,
RUSHA Depatt Tamilnadu: CMC Vellore
1999.
723
Lomte DB et al.
DOI: 10.5958/j.2319-5886.2.4.116

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
IMMEDIATE EFFECT OF SURYANADI PRANAYAMA ON PULMONARY FUNCTION

(VENTILATORY VOLUMES AND CAPACITIES) IN HEALTHY VOLUNTEERS
Shravya Keerthi G1, Hari Krishna Bandi2, Suresh M3, *Mallikarjuna Reddy N4
1
Dept of Physiology, Narayana Medical College, Nellore Currently affiliated with JIPMER, Puducherry,
India.
2
Department of Physiology, JIPMER, Puducherry, India
3
Dept of Physiology, Meenakshi Medical College Hospital & Research Institute, Kancheepuram,
Tamilnadu, India
4
Department of Physiology, Narayana Medical College, Nellore, Andhra Pradesh, India
*Corresponding author email: res.publications@gmail.com
ABSTRACT
Objectives: we found only effects of at least a short term practice extended over a period of a few days
to weeks of pranayama (alternate nostril breathing) rather than acute effects of unilateral right nostril
breathing (suryanadi pranayama). Keeping this in mind the present study was designed to test the
hypothesis that 10 min. of right nostril breathing have any immediate effect on ventilatory volumes and
capacities in healthy volunteers. Methodology: Forced vital capacity (FVC), Forced expiratory volume
in the first second (FEV1), Forced expiratory volume percent (FEV1/FVC%), Peak expiratory flow rate
(PEFR), Forced expiratory flow25-75% (FEF25-75%), Maximum voluntary ventilation (MVV), Slow vital
capacity (SVC), Expiratory reserve volume (ERV), Inspiratory reserve volume (IRV) and Tidal volume
(TV) were recorded before and after Surya Nadi Pranayama. Results & Conclusion: There was a
significant increase in FVC (p<0.0001), FEV1 (p<0.0007), PEFR (p<0.0001), FEF25-75% (p<0.0001),
MVV (p<0.0001), SVC (p<0.0001), ERV (0.0006), IRV (p<0.0001) and TV (0.0055) after suryanadi
pranayama. The immediate effect of suryanadi pranayama practice showed alleviation of ventilatory
capacities and volumes. Any practice that increases PEFR and FEF2575% is expected to retard the
development of COPDs. The increase in PEFR, vital capacities and flow rates by suryanadi pranayama
practice obviously offers an increment in respiratory efficiency and it can be advocated to the patients of
early bronchitis and as a preventive measure for COPD.
Keywords: Pulmonary function, Suryanadi pranayama, immediate effect, ventilatory volumes and
capacities
INTRODUCTION
Yoga is the best lifestyle, which aims to attain

the unity of mind, body and spirit through asanas
(exercise),
pranayama
(breathing),
and
1.
meditation Pranayama, the fourth step of astang
724
Shravya etal.,
Int J Med Res Helath Sci. 2013;2(4):724-729
yoga is an important component of yoga

training2. Pranayama and Asanas are considered
as important part which is prescribed by modern
medicine too. Many physicians now recommend
yoga to the patients at risk for heart diseases, as
well as those with back pain, arthritis, depression
and other chronic diseases3.The beneficial effects
of Pranayama are well reported and have a sound
scientific basis. It was reported different types of
Pranayama produce different physiological
responses in healthy young volunteers2,4.
Pranayama is a method of breathing and chest
expansion exercise which has been reported to
improve cardio respiratory function in health and
disease5,6. The practice of pranayama has been
known to modulate cardiac autonomic status
with an improvement in Cardio respiratory
functions5, 7. Autonomic nervous system consists
of two branches i.e; sympathetic nervous system
and parasympathetic nervous system. Although
individual asana and pranayama practices can
selectively affect sympathetic or parasympathetic
nervous system, the overall effect of yoga
practice is to bring a state of parasympathetic
dominance2,8,9. The practice of breathing exercise
increases parasympathetic activity and decreases
sympathetic activity, improves cardiorespiratory
functions by affecting oxygen consumption,
metabolism and skin resistance9-11.
Humans breathe preferably through one nostril at
a time. Kayser defined nasal cycle as a
phenomenon
of
alternating
congestion,
decongestion response of erectile tissues of nasal
turbinate and septum of two nostrils, which
effectively altered the unilateral nasal resistance
and was existent on account of prevailing
sympathetic and parasympathetic tone12.The
preferred nostril alternates in a simultaneous
congestion-decongestion cycle. The nostril
congestion-decongestion cycle is believed to
reflect the dynamic lateralization of the
autonomic nervous system10,13. Prolonged
unilateral nostril breathing as a result of complete
or partial nasal obstruction is correlated with a
number of chronic disorders such as unilateral
migraine, peptic ulcer, dysmenorrhoea, lack of

libido,
cardiac
symptoms,
fever,
hyperthyroidism, asthma, inadequate oral intake
and electrolyte imbalance14. It is believed that
there is an activation of the contra lateral cerebral
cortex with unilateral nostril breathing as evident
from the rise in EEG amplitude10, 14. The right
hemisphere is believed to play a major role in
parasympathetic
activity than
the
left
13
hemisphere . Left nostril breathing increases
intraocular pressure (IOP) by 4.5% while right
nostril breathing decreases IOP significantly13,14 .
Pranayama breathing through right nostril
increases sympathetic activity, left nostril
breathing reduces it.
Breathing exercises have been recommended in
physiotherapy to improve respiratory and bowel
function, in occupational therapy to facilitate
spiritual emergence5,6,13. It has been assumed
single nostril breathing can be used to
therapeutically influence autonomic function and
may significantly affect other hemispherespecific functions6,13. Yoga practices can also be
used as psycho-physiological stimuli to increase
the secretion of melatonin which might be
responsible for perceived well-being and has a
calming effect on the mind, helps an individual
to de-stress. These yoga practices might be
interacting with various somatic and neuroendocrine
mechanisms
bringing
about
9,15
therapeutic effects . This calming effect may
also exert profound physiological effects on
pulmonary, cardiovascular, and mental functions
of the brain7,11.
The literature search through PUBMED central
and other search engines, showed very scanty
data on immediate effects of suryanadi
pranayama on pulmonary functions. In our
literature search, we found only effects of at least
a short term practice extended over a period of a
few days to weeks of pranayama (alternate
nostril breathing) rather than acute effects of
unilateral right nostril breathing (suryanadi
pranayama). Keeping this in mind the present
study was designed to test the hypothesis that 10
Shravya etal.,
725
min. of right nostril breathing have any

immediate effect on ventilatory volumes and
capacities in healthy volunteers.
Subject selection: This is a cross-sectional study

carried out in the Pulmonary Function Testing
Laboratory, Department of Physiology, Narayana
medical college (NMC), Nellore (A.P), India.
After obtaining approval of Institutional Ethics
Committee (IEC), pulmonary function tests were
conducted in 30 healthy volunteers in the age
group of 18 to 40 years; age, BMI matched
students and residents of NMC. The subjects of
both genders were included. Subjects with a past
history of smoking, hypertension, respiratory
diseases, chest wall injuries, congestive cardiac
failure, kyphoscoliosis and who are already
trained in yoga and exercise were excluded from
the study.
Study protocol: The volunteers were properly
explained about the objectives, methodology,
expected outcome and implications of the study
and written informed consents were obtained
from them. They were instructed to report to PFT
lab of Physiology department at about 9 A.M.
Their age, height, weight, was recorded and BMI
calculated. Volunteers are trained to right nostril
breathing (Suryanadi pranayama) by experienced
yoga teacher from Narayana Yoga and
Naturopathy College, and volunteers also get
familiarized with our research lab and procedure
of pulmonary function testing.
Methodology: Volunteers were asked to sit in a
calm, quiet airy place in an easy and steady
posture with the head, neck and trunk erect and
in a straight line in order to keep the body still.
Asked them to bring the right hand up to the
nose, fold the index and middle finger in a way
so that the right thumb closed the right nostril
and the ring finger closed the left nostril (Vishnu
Mudra)12. The volunteer was asked to close the
left nostril by the ring finger and slowly breathe
in up to a maximum, through the right nostril by
counting 1to 6 over a period of 6 seconds and

then and exhale slowly up to maximum over a
period of 6 seconds. Recordings for pulmonary
function parameters were taken before and after
practicing suryanadi pranayama.
Pulmonary functions were assessed by
computerized spirometer (Spirowin Version 2.0
of Genesis Medical systems pvt Ltd) which gives
ERS-93 predicted values at BTPS conditions.
After preliminary trials, a baseline reading was
taken. Volunteers followed the instructions given
by qualified and experienced yoga teacher for
Suryanadi pranayama of 6 cycles/min for 10
mins. After practicing Suryanadi pranayama (6
cycles/min) for 10 min, the test was performed
three times and the best reading was considered.
During the procedure, the subjects inhaled deeply
and then exhaled with maximum effort as much
as possible into the mouthpiece for FVC test. The
subjects inhaled deeply and exhaled slowly and
completely as much as possible, this was
repeated for 3-4 times followed by normal
respiration for SVC test. The following
parameters were recorded: Forced vital capacity
(FVC), Forced expiratory volume in the first
second (FEV1), Forced expiratory volume
percent (FEV1/FVC%), Peak expiratory flow rate
(PEFR), Forced expiratory flow 25-75% (FEF2575%), Maximum voluntary ventilation (MVV),
Slow vital capacity (SVC), Expiratory reserve
volume (ERV), Inspiratory reserve volume (IRV)
and Tidal volume (TV).
RESULTS
The data were expressed as mean SD, were

analyzed using the GraphPad Instat Version3.0
for Windows, GraphPad Software, La Jolla
California USA, www.graphpad.com. The
Gaussian distribution of the data was determined.
Normally distributed data were tested by the
paired t-Test. Non-normally distributed data
were tested with the Wilcoxon signed rank test.
A value of P<0.05 was considered as significant.
Table 1 shows the anthropometric parameters of
the subjects. Table 2 shows the respiratory
726
Shravya etal.,
variables like ventilatory capacities, volumes and

flow rates before and after suryanadi pranayama.
There was significant increase in FVC
(p<0.0001), FEV1 (p<0.0007), PEFR (p<0.0001),
FEF25-75% (p<0.0001), MVV (p<0.0001), SVC

(p<0.0001), ERV (0.0006), IRV (p<0.0001) and
TV (0.0055) after suryanadi pranayama.
Table 1. Anthropometric parameters
S.no
1.
Parameter
Age (Yrs)
Mean SD
21.03 4.43
2.
Weight (Kgs)
54.911.56
3.
Height (m)
1.62 0.09
4.
BMI (kg/m2)
20.72 3.28
5.
BSA ( m2)
1.57 0.18
Table 2. Comparison of respiratory variables before and after suryanadi pranayama
S.no
Parameter
Mean SD
P value
Before
After
1.
FVC(L)
2.45 0.49
2.75 0.59
0.0001*
2.
FEV1(L)
2.09 0.49
2.30 0.55
0.0007*
3.
FEV1/FVC%
83.82 10.59
84.29 9.38
0.79
4.
PEFR(L/S)
4.14 1.32
4.32 1.06
0.0001*
5.
FEF25-75%(L/S)
2.62 0.79
2.67 0.62
0.0001*
6.
SVC(L)
3.61 1.93
4.47 2.81
0.0001*
7.
ERV(L)
1.22 1.18
1.70 1.54
0.0006*
8.
IRV(L)
2.09 1.85
2.87 2.62
0.0001*
9.
TV(L)
0.92 0.49
1.07 0.43
0.0055*
10.
MVV(L)
69.39 17.10
77.98 19.65
0.0001*
FVC: Forced Vital capacity, FEV1: Forced Expiratory Volume in 1 sec, PEFR: Peak Expiratory Flow
rate, FEF25-75%: Forced Expiratory Volume, SVC: Slow vital capacity, ERV: Expiratory Reserve
Volume, IRV: Inspiratory Reserve Volume, TV: Tidal Volume and MVV: Maximal Voluntary
Ventilation. * signifies p< 0.001 which shows values are statistically significant.
DISCUSSION
Yoga is the ancient science which makes use of

voluntary regulation of breathing to make
respiration rhythmic, calm the mind to reach the
ultimate goal3,4. A person practicing Pranayama
will try to keep his attention on the act of
breathing, leading to concentration which
removes his attention from day to day worries
and de-stress the individual3,4.
Each cycle of suryanadi pranayama is a complex

voluntary act, which includes two distinct
phases, Puraka, and Rechaka i.e., inspiration &
expiration. The technique of pranayama includes
specific rules regarding the method of breathing,
in terms of force of breathing, the duration of
each phase of breathing, the number of rounds of
pranayama and attention on breathing16. The
various physiological changes occur during
different phases of pranayama16. During
pranayama, deep inhalation (puraka) stimulates
Shravya etal.,
727
the respiratory system and fills the lungs with

fresh air, retention of air (kumbhaka) raises the
internal temperature and increase the absorption
of oxygen, slow exhalation (rechaka) causes the
diaphragm to return to original position, air full
of toxins and impurities is forced out by
contractions of intercostals muscles4,16. These are
the main components of pranayama which
massage the abdominal muscles and tone up the
working of respiratory organs of body4. This
deep inspiration, retention of air and slow
expiration increases the overall capacity of the
lungs and gradually improves the ventilatory
functioning of lungs4. Due to the proper working
of these organs, vital energy flows to maintain
the normal homeostasis of the body and thus it
helps in prevention, control and rehabilitation of
many respiratory diseases4, 16. These results are
in line with the findings of Krogh and Lindhard,
which might be the result of impulses from
cerebral cortex influencing the respiratory
centre4.
From the results (table 2) it is evident that
immediate effect of suryanadi pranayama
showed significant improvement in FVC, FEV1,
PEFR, FEF25-75%, MVV, SVC, ERV, IRV and
TV. FEV1 is the volume of air that is exhaled in
the first second during FVC manoeuvre. It is
useful to detect generalized airway obstruction.
FEV1/FVC% is the volume of air expired in the
first second, expressed as percentage of FVC. It
is a more sensitive indicator of airway
obstruction, than FVC or FEV1 alone. FEF25-75%
is the average flow rate during middle 50% of
FVC. It indicates patency of the small airways.
FEF25-75% depends on non-bronchopulmonary
factors like, neuromuscular factors and
mechanical equipment factors of inertial
distortion of lungs. PEFR and FEF2575% are the
first parameters to decline on many respiratory
diseases. Healthy persons expire 7090% of FVC
in the first second of the test which means that
they take about 5 second to expire the last 10
30% of the FVC12. Any practice that increases
PEFR and FEF2575% is expected to retard the
development of COPDs. Our results show the
positive impact of suryanadi pranayama on

PEFR and FEF2575%.
These findings are similar to the study
conducted by Nidhi Jain et al., Baljinder Singh
Bal, Upadhyay et al. and Puja et al, showed a
significant increment in Peak expiratory flow
rate (PEFR) and FEF 25-75%12,14,15. The increased
PEFR might be a consequence of small airway
opening in lungs. The number of minute alveoli
in the lungs goes on increasing up to 8 yrs of age.
After this the alveoli increases only in size and
this is the ideal age to introduce pranayama16.
The work of Yadav and Das attributed the
increase in PEFR by yogic exercise due to
following changes in respiratory dynamics i.e.,
Increased respiratory muscle strength, cleansing
of airway secretions and efficient use of
diaphragmatic and abdominal muscles, thereby
emptying and filling the respiratory apparatus
more efficiently and completely3.
Previous studies also showed the effect of
Pranayama on alleviation of the respiratory
muscle efficiency and lung compliance by
reducing elastic and viscous resistance of lung
present during inspiration. Pranayama acts as
physiological stimuli for release of lung
surfactant and prostaglandins into alveolar spaces
which increase the lung compliances. Our
findings were consistent with the results of
sivapriya etal., immediate increase in PEFR and
increase in FVC, MVV, TV, Expiratory
capacities etc16.
Shravya etal.,
CONCLUSION
The immediate effect of suryanadi pranayama

practice showed alleviation of ventilatory
capacities and volumes. The increase in PEFR,
vital capacities and flow rates by suryanadi
pranayama practice obviously offers an
increment in respiratory efficiency and it can be
advocated to the patients of early bronchitis and
as a preventive measure for COPD.
Future Directions: Further research is required
to determine whether forced nostril breathing has
greater effects than relaxed single nostril
728
breathing, and whether the effects are greater if

applied when a nostril is in its non-dominant
phase of the nasal cycle.
ACKNOWLEDGEMENT
We kindly acknowledge Mr. Sukumar BV,

Technical Supervisor, Pulmonary Function
Testing Laboratory, Naryana Medical College
(NMC) for his technical support, students and
residents of NMC, who have participated in the
study and led to complete the study successfully.
REFERENCES
1. Roopa
BA, Anita
Herur, Shailaja
Patil, Shashikala GV, Surekharani Chinagudi.
Effect of Short-Term Pranayama and
Meditation on Cardiovascular Functions in
Healthy
Individuals.
Heart
Views.
2011;12(2): 5862.
2. Madanmohan. Effect of slow and fast
pranayamas
on
reaction
time
and
cardiorespiratory variables. Indian J Physiol
Pharmacol 2005; 49(3): 313-18.
3. Upadhyay Dhungel K, Malhotra V, Sarkar
D, Prajapati R. Effect of alternate nostril
breathing exercise on cardiorespiratory
functions. Nepal Med Coll J 2008; 10(1): 2527.
4. Shivraj P. Manaspure, Ameet Fadia,
Damodara Gowda KM. Effect of selected
breathing techniques on respiratory rate and
breath holding time in healthy adults.
IJABPT.2011; 2(3): 225-29.
5. Sukhdev Singh. Effects of a 6-week nadishodhan
pranayama
training
on
cardiopulmonary parameters. Journal of
Physical Education and Sports Management.
2011; 2(4): 44-47.
6. Chanavirut R. Yoga exercise increases chest
wall expansion and lung volumes in young
healthy thais. Thai journal of Physiological
sciences 2008; 19(1): 1-7.
7. Subbalakshmi NK, Saxena SK, Urmimala,
Urban JA, DSouza. Immediate effect of
Nadi-Shodhana pranayama on some selected
parameters of cardiovascular, pulmonary, and
higher
functions
of
brain.
TJPS.
2005;18(2):10-16.
8. Madanmohan. Effect of six week yoga
training on weight loss following step test,
respiratory pressures, handgrip strength and
handgrip endurance in young healthy
subjects. Indian J Physiol Pharmacol 2008;
52 (2): 164-70.
9. Pal GK, Velkumary S, Madanmohan. Effect
of short-term practice of breathing exercises
on autonomic functions in normal human
volunteers. Indian J Med Res.2004;120:115121.
10. Ravinder Jerath, John WE, Vernon AB,
Vandna Jerath. Physiology of long
pranayamic breathing: Neural respiratory
elements may provide a mechanism that
explains how slow deep breathing shifts the
autonomic nervous system.Med Hypotheses.
2006;67(3):566-71.
11. Shankarappa V, Prasanth P, Nachal

Annamalai,Varunmalhotra. The short term
effect of pranayama on the lung parameters.
JCDR, 2012; 6(1):27-30.
12. Puja Dullo, Neeraj Vedi, Usha Gupta.
Improvement in respiratory functions after
alternate nostril breathing in healthy young
adults. Pak J Physiol 2008;4(2):15-16.
13. Venthan JM. Single-nostril breathing to
influence cognitive and autonomic Functions.
Indian Journal of Physiotherapy and
Occupational Therapy. 2008; 2(4):41-46.
14. Nidhi Jain, Srivastava RD, Anil Singhal. The
effects of right and left nostril breathing on
cardiorespiratory and autonomic parameters.
IJPP 2005;49(4):469-74.
15. Baljinder Singh Bal. Effect of anulom vilom
and bhastrika pranayama on the vital capacity
and maximal ventilatory volume. J. Phys.
Educ. Sport Manag. 2010;1(1):11-15.
16. Sivapriya DV, Suba Malani S, Shyamala
Thirumeni. Effect of Nadi-Shodhana
pranayama on respiratory parameters in
school students. Rec. Res. Sci. Tech.
2010;2: 32-39
729
Shravya etal.,
DOI: 10.5958/j.2319-5886.2.4.117

&
Health Sciences
www.ijmrhs.com Volume 2 Issue 3 July - Sep Coden: IJMRHS
Received: 14th July 2013
Research article
Copyright @2013 ISSN: 2319-5886

RELATIONSHIP BETWEEN THE RETINAL NERVE FIBRE LAYER (RNFL) PARAMETERS

AND VISUAL FIELD LOSS IN ESTABLISHED GLAUCOMA PATIENTS IN SOUTH INDIAN
POPULATION
*Elangovan Suma1, Puri K Sanjeev2
1,2
Assistant Professor of Ophthalmology, Meenakshi Medical College and Research Institute, Enathur,
Kanchipuram, Tamilnadu, India
*Corresponding author email: elangovansuma@hotmail.com
ABSTRACT
Purpose: Optical coherence tomography (OCT) and Scanning LASER polarimetry (GDX-VCC) are
newer techniques to analyse retinal nerve fibre loss in glaucoma. This study aims to evaluate the
relationship between the Retinal Nerve Fibre Layer(RNFL) parameters measured using Stratus-OCT and
GDx-VCC and visual field loss by Octopus interzeag perimetry in established glaucoma patients in South
Indian Population. Materials and methods: Prospectively planned cross sectional study of 67 eyes of 34
established glaucoma patients on medical management. The mean age of patients was 46.911 years
(SD+13.531). A complete ophthalmic examination, automated perimetry with octopus interzeag 1-2-3
perimeter, retinal nerve fibre analysis with GDx VCC and Stratus OCT was done. The differences
between the mean RNFL parameters in the presence or absence of field defects were evaluated. Results:
The data analysed were mean deviation, loss variance, OCT total average nerve fibre thickness, GDX
VCC- TSNIT average and Nerve fibre indicator (NFI).The data were split into two subgroups on the basis
of presence or absence of visual field defect and analysed. The difference between the mean value of NFI
between the subgroups was highly significant with a p value < 0.01.The OCT parameter Total average
nerve fiber layer thickness differed significantly between the two subgroups (p value <0.05). The mean
GDx TSNIT average did not differ significantly between the two subgroups. Conclusion: The total
average nerve fibre thickness by OCT correlated better with visual field loss than the GDX TSNIT
average .Among the GDx parameters, the NFI was found to be a better indicator of visual field damage
than the average thickness.
Key words: Retinal nerve fibre analysis, OCT, GDX-VCC
INTRODUCTION
Glaucoma is a disease which is associated with

progressive damage to the optic nerve and retinal
nerve fibre layer 1. Visual field loss in glaucoma
is due to structural damage and it is documented
by automated perimetry . However, the results of

perimetry are variable as the test is subjective2.
Up to 40 percent of the RNFL may be lost before
a defect is apparent on the visual fields 3,4.
730
Suma etal.,
Various studies have shown that structural

changes of the optic nerve head5-7 and nerve fibre
layer4,8-11 appear before the visual field changes.
The optic nerve head and RNFL changes over
time were studied by stereoscopic photographic
images. Though they provide objective
information for comparisons, the interpretation of
photographs remains subjective, and variations in
assessment among even experienced observers are
well documented11-13.
Furthermore,
qualitative
assessment
of
photographs may not be sensitive to small
changes over time, and it is difficult to pick up
diffuse damage on these photographs. Newer
technologies such as confocal scanning laser
ophthalmoscopy (HRT), retinal thickness analyser
(RTA), scanning laser polarimetry with fixed and
variable corneal compensator (GDxVCC), optical
coherence tomography (OCT) have become
available that provide quantitative reproducible,
and objective measurements of RNFL thickness.
As visual field assessment has been considered as
the gold standard for glaucoma diagnosis, all
structure based investigatory modalities need to
compare with automated perimetry. The purpose
of this study is to evaluate the relationship
between structural changes evaluated by OCT and
GDX VCC and visual field defects in established
glaucomatous eyes.
This was a cross sectional study, prospectively

planned. 67 eyes of 34 glaucoma patients
attending glaucoma clinic were included in this
study after ethical committee clearance. Informed
consent was obtained from all the patients.
Inclusion criteria:
1. Established primary open angle glaucoma
patients (open angles>2 by Shaffers grading
on gonioscopy) on medical treatment and
routine follow up were chosen for the study.
The patients were diagnosed as glaucomatous
by the following criteria: at least three or more
occasions of elevated intra ocular pressure
>21 mm Hg now on medical control and

significant optic nerve head changes with or
without visual field defects.
2. Refractive errors : Hyperopia < +2.50D ,
Myopia < -3.00 D , Astigmatism<+2.00 D
3. Best corrected visual acuity 6/ 12 or better
4. Pupil size 3.0-5.0 mm
5. Relative intelligence to understand the test and
patients co-operative for visual field analysis.
Exclusion criteria:
1. Closed angles /narrow angles by gonioscopy
2. All patients who had secondary glaucomas,
juvenile and congenital glaucomas, media
opacities, retinal and neurological pathologies.
3. Primary open angle glaucoma patients who
undergone surgical or laser therapy for
glaucoma
All subjects underwent a
complete
ophthalmologic
examination
including
refraction, Slit lamp biomicroscopy for anterior
segment evaluation and fundus examination with
+90 D lens, gonioscopy, Intra ocular pressure
measurement using Goldmann applanation
tonometry and also direct ophthalmoscopy.
Glaucomatous appearance of the Optic disc was
defined as an increased C: D ratio, asymmetry of
the C: D ratio of >0.2 between the two eyes,
Neuro retinal rim thinning disc haemorrhage,
notching and excavation.
Visual field analysis was performed with Octopus
Interzeag1-2-3 perimeter. The tendency oriented
perimetry strategy was used
An abnormal
visual field was defined as: Field plotting with
mean deviation > 4, Loss variance > 6 , a local
dip in the Bebies curve outside 2 SD normal
limits, Points of depressed sensitivity especially
in the arcuate areas, paracentral areas , nasal step
region or advanced tubular fields. All fields were
reliable with false positive and false negative
catch trials < 15%.
RNFL analysis was performed by OCT and GDX
VCC. All scans were performed by trained
technicians who were unaware of the patients
diagnosis.
731
Suma etal.,
RNFL analysis with Optical coherence

tomography: Retinal nerve fibre layer
measurements were obtained with Stratus OCT
(Zeiss) version 4.0.1. All scans were performed
by well trained technicians who were masked to
the patient diagnosis and characteristics. For each
patient three 3.4 mm diameter circular scans were
obtained, judged to be of acceptable quality and
averaged by trained technicians to provide mean
measurements of RNFL thickness.
RNFL analysis with GDX VCC: The GDX
VCC (Version 5.2.3) is a scanning laser
polarimeter that measures RNFL thickness using
polarized light. The placement of the ellipse on
the disc margin for the scan was done by the same
technician.
All scans were performed by the same well
trained technician. The disc margin on the image
was established with an ellipse whose parameters
were adjusted by the experienced technician who
was masked to the patient diagnosis and
characteristics. All these investigating modalities
were carried out within a period of 3 weeks to
obtain the best cross sectional comparison and to
nullify the effect of any temporal lag.
Statistical analysis: statistical analysis carried out

using SPSS software. Students t test was used
to derive the significance of the difference
between the means.
RESULTS
67 eyes of 34 established Primary open angle

glaucoma patients were analysed in this study.
The mean age of the patients in this study was
46.911 years (SD+13. 531) .The ages of these
patients ranged from 26 to 70 years. Out of the 34
patients, 10 patients were females accounting for
about 29.41%. The global visual field indices
obtained from octopus perimetry were mean
defect (MD) and loss variance (LV). The mean
MD for our group of patients was 5.1405.853
and the mean LV was 22.551 20.79.
The
Retinal nerve fibre layer thickness was analysed
by Optical coherence tomography .The parameter
which was studied was the Total average nerve
fibre layer thickness (OCT T Avg).
The GDX
VCC RNFL analysis parameters studied were the
TSNIT average (TSNIT Avg) and the nerve fibre
indicator (GDX NFI). (Table:1)
Table: 1. Analysis of the visual field indices obtained from octopus perimetry ( mean defect (MD) and loss
variance (LV)and OCT and GDX VCC parameters in the 67 study eyes:
Parameter
MD
LV
OCT Total average thickness(microns)
GDX-VCC TSNIT average thickness
(microns)
GDX-VCC Nerve fibre indicator
Primary open angle glaucoma (N=67)

Mean SD
5.140 5.85
22.55120.79
Min
-1.4
1.8
Max
24.9
88.4
87.7422.21
20
129
48.216 9.02
24.160
64.710
32.463 25.36
98
732
Suma etal.,
Table 2: Analysis of the RNFL parameters on the basis of presence or absence of visual field loss:
Parameter
Group
Normal fields
Abnormal fields
MD
Mean SD
-0.100.90
MeanSD
6.285.85
Significance of
difference between the
means (Students t Test) P
value
0.000**
LV
3.481.32
26.71 20.73
0.000**
85.75 23.48
47.579.59
34.9527.13
0.023*
0.075***
0.003**
OCTT Avg (microns) 96.9211.95

GDXTSNIT(microns) 51.185.10
NFI
21.088.63
r = Pearsons correlation coefficient; p =p value , *p<0.05 (0.01 to 0.05) significant at 5% level

** p< 0.01- significant at 1% level, *** p> 0.05 not significant at 5% level
Fig 1: Bar chart showing the difference between the mean values among the two subgroups
Analysis on the basis of presence or absence of

visual field loss: (Table:2, Figure1): The data
was split on the basis of presence or absence of
visual field loss and analysed. Out of the 67 eyes,
12 eyes did not show any field defect whereas the
rest had a significant visual field loss.
Statistically significant difference (p <0.05 (0.01
to 0.05) significant at 5% level) was obtained for
the OCT Total average thickness (96.92 um
11.95 in the normal field group and
85.75
um23.48 in the group with abnormal field)
When the GDX parameter, TSNIT average was
analysed, no significant difference was
appreciated between the two subgroups
(51.18+5.10 in the normal field subgroup and
47.579.59 in the other subgroup; p value= 0.075
( p > 0.05 not significant at 5% level ).
Significant difference was obtained (p< 0.01)

between the two subgroups for the GDx
parameter, NFI (21.08 +8.63 in the normal field
subgroup and 34.9527.13 in the subgroup with
field changes; the p value obtained was 0.003).
DISCUSSION
This study was designed with the objective to

determine the relationship between the results
obtained by these two methods( OCT and GDX
VCC) for quantitatively assessing the RNFL and
visual field defects by autoperimetry
in
established glaucomatous eyes in south Indian
population.
The primary strength of this study is that the
instruments were compared in a single population.
The advantage of examining the performance of
733
Suma etal.,
these instruments in a single population is that

population characteristic based variables are
eliminated, thus allowing direct comparison of the
results obtained with the different instruments.
Limitations of this study include a small number
of subjects. Another limitation, inherent in any
comparable study is that different diagnostic
techniques evaluated in this study are currently at
different stages of development. In general,
established technologies benefit from robust
normative databases and more sophisticated
analysis strategies. Also, different techniques may
identify different characteristics of glaucomatous
damage.
Various studies have demonstrated good
diagnostic accuracy with different modalities of
imaging in glaucoma14-19. Good comparability of
OCT and GDX has been demonstrated by many
studies in various stages of glaucoma20-24
The data were split into two subgroups on the
basis of presence or absence of visual field defect
and analysed (table: 4). A gross difference was
observed between the mean values of MD, LV,
OCT T Avg , TSNIT Avg, and NFI in the two
subgroups. The difference between the mean
values of M D and LV and NFI were highly
significant with a p value < 0.01- significant at
1% level. Also, the OCT parameter, Total average
nerve fiber layer thickness differed significantly
between the two subgroups (p value <0.05
significant at 5% level).
The mean GDx TSNIT average did not differ
significantly between the two subgroups. These
data could suggest that while using the GDx the
NFI is a higher predictor of visual field damage,
than the GDX TSNIT average thickness. Also,
among the Total average nerve fibre layer
thickness measured by OCT and GDx (TSNIT
average), the OCT parameter seems to correlate
better with visual field damage than the GDx
parameter.
Studies by Kanamori et al have shown that visual
field defect has a strong correlation with OCT
total average thickness25.
Reus et al 26 reported that GDx-VCC correlated

well with mild to moderate visual field loss in
glaucoma patients.
Our data demonstrated that patients with
advanced field defects have a greater RNFL loss.
Also, for a specific value of visual field index
there was a large range of RNFL values. Two
explanations can be reasoned out for this: one is
the variability of the RNFL values among the
normal population and the other reason may be
the amount of RNFL damage required for the
field loss may vary among different patients. This
problem has been mentioned by other studies
also27. The influence of variability among patients
can be overcome by conducting a longitudinal
analysis.
This is a Pilot study carried out in an attempt to
establish the relationship between the Visual field
indices and RNFL parameters in glaucoma
patients in our south Indian population. This study
brings out statistically significant correlations in
spite of the above limitations. This finding
validates both techniques as indicators of
glaucomatous damage. A similar study, if
undertaken, with a larger sample with inclusion of
the normal population as age matched controls
and carried out longitudinally would possibly
make the results much more specific. Also,
inclusion of glaucoma suspects, ocular
hypertensives and early glaucoma patients in
subsequent trials would serve to establish the
utility of these newer diagnostic technologies in
glaucoma management and research.
Outcomes of the study:
1. The total average nerve fibre thickness by
OCT correlated better with visual field loss
than The GDX TSNIT average.
2. Among the GDx parameters, the NFI was
found to be a better indicator of visual field
damage than the average thickness.
CONCLUSION
Though visual field testing is subjective, at

present it cannot be replaced by imaging
734
Suma etal.,
modalities. The new instruments are valuable

tools that have become available to provide
quantitative
reproducible
and
objective
measurements of RNFL thickness.
Structural information provided by the OCT and
GDx and functional information provided by the
field analysis are both important and
complementary to each other
ACKNOWLEDGEMENT
The authors wish to express their gratitude to
Prof.V.Velayutham for his guidance and support
in carrying out this study.
REFERENCES
1. Lan YW, Henson DB, Kwartz AJ. The

correlation between optic nerve head
topographic measurements, peripapillary
nerve fibre layer thickness, and visual field
indices
in
glaucoma,
Br.
J.
Ophthalmol.2003;87: 1135
2. Guedes, V. Schuman JS, Hertzmark. Optical
coherence tomography measurement of
macular & nerve fibre layer thickness in
normal
and
glaucomatous
eyes.
Ophthalmology. 2003;110 (1): 177-178.
3. Son P, Sibota R, Tewari HK, Venkatesh P,
Singh R. Quantification of the RNFL
thickness in normal Indian eyes with OCT,
Indian J. Ophthalmology2004;52: 303-09
4. Quigley HA, Addicks EM, Green WR. Optic
nerve damage in human glaucoma ischemic
neuropathy,
papilledema
and
toxic
neuropathy, Arch Ophthalmol.1982;100:13546
5. Sommer A, Pollackk I, Maumenee AE. Optic
disc parameters and onset of glaucomatous
field loss I methods and progressive changes
in disc morphology. Arch Ophthalmol. 1979;
97 (8): 1444-8.
6. Pederson J. Anderson D. The mode of
progressive
disc
cupping in
ocular
hypertension and glaucoma. Arch Ophthalmol
1980; 98: 490-5.
Suma etal.,
7. Quigley HA, Katz J. Derick RJ. An evaluation

of optic disc and nerve fibre layer examination
in monitoring progressive of early glaucoma
damage. Ophthalmology 1992: 99 (1): 19-28.
8. Sommer A. Miller NR. Pollack I. The nerve
fiber layer in the diagnosis of glaucoma Arch
Ophthalmol 1977; 95 (12): 2149-56.
9. Summer A, Quigley HA, Robix AL.
Evaluation of nerve fibre layer assessment .
Arch Ophthalmol 1984; 102 (12): 1766-71.
10. Sommer A., Katz J, Quigley HA. Clinically
detectable nerve fibre atrophy procedure the
onset of glaucomatous field loss. Arch
Ophthalmol 1991; 109 (1): 77-83.
11. Lichter PR. Variability of expert observes in
evaluating the optic disc .Trans AM
ophthalmol Soc 1976, 74: 532-72.
12. Tielsch JM, Katz J, Quigley HA, Miller NR,
Sommer A. Intraobserver and inter observer
agreement in measurement of optic disc
characteristics. Ophthalmology 1988; 95: 3506.
13. Varma R, Steinmann WC, Scott IU. Expert
agreement in evaluating the optic disc for
glaucoma. Ophthalmology 1992; 99: 215-21.
14. Medeiros FA, Zangwill LM, Bowd C.
Comparison of the GDx VCC scanning laser
polarimeter, HRT II confocal scanning laser
ophthalmoscope, and Stratus OCT optical
coherence tomography for the detection of
glaucoma. Arch Ophthalmol.2004;122:827--837.
15. Bowd C, Weinreb RN, Wiliam JM. The
retinal nerve fiber layer thickness in ocular
hypertensive, normal and glaucomatous eyes
with optical coherence tomography. Arch
Ophthalmol. 2000;118:22-26.
16. Zangwill LM, Bowd C, Berry CC.
Discriminating
betweennormal
and
glaucomatous eyes using Heildelberg Retina
Tomograph,GDx Nerve FiberAnalyzer, and
Optical
Coherence
tomograph.
Arch
Ophthalmol. 2001;119:985-93.
17. Greaney MJ, Hoffman DC, Garway-Heath
DF. Comparisonof optic nerve imaging
735
methods to distinguish normaleyes from those

with glaucoma. Invest Ophthalmol Vis
Sci.2002;43:140-45.
18. Chen HY, Huang ML. Discrimination
between normal and glaucomatouseyes using
Stratus optical coherence tomography in
Taiwan Chinese subjects. Graefes Arch Clin
Exp Ophthalmol. 2005;243:894-902.
19. Chen HY, Huang ML, Tsai YY. Comparing
glaucomatousoptic neuropathy in primary
open angle and primary angleclosure
glaucoma eyes by scanning laser polarimetryvariablecorneal compensation. J Glaucoma.
2008;17:105-110.
20. Bagga. H, Greenfield DS, Feuer.W, Knighton
RW. Scanning Laser polarimetry with variable
corneal compensation and optical coherence
tomography in normal and glaucomatous eyes.
Am J Ophthalmol 2003; 135:4:521-29.
21. Halkiadakis I, Kipioti A, Emfietzoglou I.
Comparison of optical coherence tomography
and scanning laser polarimetry in glaucoma,
ocular hypertension, and suspected glaucoma.
Ophthalmic
Surg
Lasers
Imaging.
2008;39:125-32.
22. Brusini P, Salvetat ML, Zeppieri M.
Comparison between GDx VCC scanning
laser polarimetry and Stratus optical
coherence tomography in the diagnosis of
chronic glaucoma. Acta Ophthalmol Scand.
2006;84:650-55
23. Medeiros FA, Vizzeri G, Zangwill LM.
Comparison of retinal nerve fiber layer and
optic disc imaging for diagnosing glaucoma in
patients suspected of having the disease.
Ophthalmology. 2008;115:1340-46
24. Chen, Hsin-Yi, Huang, Mei-Ling, Wang, IJong, Chen, Wen-Chi. Correlation between
Stratus OCT and
GDX VCC in early
glaucoma, ocular hypertension and glaucoma
suspect eyes. J Optom. 2012;05:24-30.
25. Kanamori A, Nakamura M, Escano MFT.
Evaluation of the Glaucomatous Damage on
Retinal nerve fiber layer thickness measured
by Optical Coherence Tomography. AmJ

Ophthalmol. 2003;135:513-20.
26. Reus NJ, Lemij HG. The relationship between
standard automated perimetry and GDx VCC
measurements. Invest Ophthalmol Vis. Sci.
2004;45:3:840-45.
27. Kwon YH, Hong S, Honkanen RA.
Correlation of automated visual field
parameters and peripapillary nerve fiber layer
thickness as measured by scanning laser
polarimetry. J Glaucoma 2000;9:281-8
736
Suma etal.,
DOI: 10.5958/j.2319-5886.2.4.118

&
Health Sciences
www.ijmrhs.com Volume 2 Issue 4 Oct-Dec
Coden: IJMRHS
Copyright @2013
ISSN: 2319-5886
th
th
Revised: 12 Aug 2013
Research article
GENDER DIFFERENCES IN AUTONOMIC FUNCTIONAL STATUS IN RESPONSE TO
STRESS
Sahera Shabnam S1, Gopathy Sridevi2, *Prema Sembulingam3
1
Student, final year, 2Lecturer in the Department of Physiology, Sathyabama University Dental College
and Hospital, Jeppiar Nagar, Rajiv Gandhi Salai, Chennai, Tamilnadu, India
3
Professor of Physiology, Madha Medical College and Research Institute, Kuntrathur Main Road, Kovur,
Thandalam near Porur, Chennai, Tamilnadu, India
* Corresponding author email: prema_sembu@yahoo.com
ABSTRACT
Introduction: Men and women are similar in their cognitive appraisal of a stress. But their behavior is
different when exposed to stress. As stress responses and cognitive abilities are closely associated with
autonomic nervous system, an attempt had been made to evaluate the behavioral pattern of autonomic
functional status in males and females under stressed conditions. Methodology: 30 normal young male
and female students (15 each) participated in this study. Systolic blood pressure (SBP), diastolic blood
pressure (DBP), heart rate (HR) and heart rate variation (HRV) were recorded before and after postural
change, Valsalva maneuver and cold exposure. Results: SBP and DBP decreased and HR increased
after standing from lying posture (p < 0.000) in both the genders. But the changes were less in males
than in females (SBP and HR non significant, DBP p < 0.008,) 30:15 ratio was higher in males (p <
0.001) upon standing. After Valsalva maneuver, SBP decreased (p < 0.05) and DBP increased (p <
0.000) with a higher Valsalva ratio (p < 0.002) in females than in males. After exposure to cold, males
showed more decrease in SBP and DBP and less increase in HR (non-significant) than females.
Discussion: Results reveal more sympathetic activity in males than in females when exposed to stress.
This may be because of the altered baroreceptor mechanism, male-female type of fat distribution,
difference in vascular bed resistance, influence of cortisol and hypothalamus-pituitary-adrenal axis.
Conclusion: The fact that females have less tolerance to stress may help us in understanding the sex
linked pathophysiology of cardiovascular diseases and developing a different approach in treating the
similar cardiovascular disease in men and women.
Key words: Blood pressure, Heart rate, Heart rate variation, Postural change, Valsalva
maneuver, Cold pressor test
INTRODUCTION
The World Health Organization (WHO) defines

health as A state of physical, mental and social
wellbeing and not necessarily the absence of
Sahera etal.,
disease and infirmity. The conventional

definition of health normally fails to take care of
tension or stress, the two universally
737
recognized phenomena which are more

prevailing in the developed countries, but by no
means, absent elsewhere.
Stress of any kind induces physical and mental
disturbances in an individual mainly because of
its role in creating an imbalance between the
demands of an environment and the capability of
the individual to meet these demands. Sometimes
it may end up with an anxiety-like state with the
exaggerated response. The cognition of the stress
and the physiological responses associated with
stress are all believed to be integrated and
interpreted in the autonomic nervous system
(ANS)1. Among the two divisions of ANS, viz.,
Sympathetic division and the parasympathetic
division, sympathetic division are concerned
with flight and fight reactions which help an
organism to cope up with emergency reactions
with the expenditure of unusual bodily sources
and parasympathetic division is concerned with
the conservation of bodily sources.
Normally, the reciprocal inhibition between these
two systems is responsible for the normal
behavioral homeostasis in an individual1
However, when exposed to a stressed situation,
depending upon the type and intensity of the
stress, a series of responses occur which are
expressed in a slightly exaggerated pattern both
physically and emotionally. It is generally
believed and noticed that in a similar stress
situation, the females react in a more pronounced
manner, creating an anxiety-like state than the
males.
Though But most of the studies were
disproportionately based more on the males than
on females. As a result, the processes involved in
stress responses in females are less well
understood. And, until the late 1990s, there was
no scientific proof to show the sex differences in
the autonomic functional status during stress.
However, in the last decade, an avalanche of
studies has come up to demonstrate such
differences.
Leonard Sax had shown that exposure to stress
modulates the autonomic functions in both males
Sahera etal.,
and females and parasympathetic nervous system

(PNS) played a major role in females and
sympathetic nervous system (SNS) played a
major role in males in controlling autonomic
responses 2. According to Aimee Midei, females
were capable of confronting the stress in a better
way than males; he noticed that nonhuman
female primates showed more substantial female
preference under stress compared to males and
their coping style is more emotion-focused than
that of males3 due to more involvement of SNS.
Yet another report contradicted these statements
with the suggestion that men and women
responded identically to achievement-related
stressor4.
As the reported evidences reflect a lot of
controversies, it is worthwhile to reinvade the
field and re-search for the gender differences in
autonomic functions in response to stress.
Objective: 1. To evaluate the autonomic
functional status in normal subjects by using the
cardiovascular parameters viz, BP, HR and HRV
2. To find out whether these parameters reflect
any gender differences under various stressed
situations
30 normal young healthy students of both

genders (15 in each gender) in the age group of
17 to 20 years participated in this study from
Sathyabama Dental College and Hospital,
Jeppiaar Nagar, Rajiv Gandhi Road, Chennai. All
participants were non-exercisers, non-athletics
and non-smokers. Those who were on
medication for some reason or other and obese
persons were excluded from this study. In
females, recording was done in their preovulatory period. The Institutional Ethical
Committee had cleared the project. Written
informed consent was obtained from all the
participants after explaining the experimental
procedure and making them fully aware of their
role in the project. Simple bedside tests of
autonomic functions based on the cardiovascular
reflexes, postulated by Ewing and Clarke5 and
738
adapted by Prema Sembulingam et al6 were

chosen for the present study.
The cardiovascular parameters recorded in the
present study were blood pressure (BP) as
systolic blood pressure (SBP) and diastolic blood
pressure (DBP) to assess the sympathetic activity
and heart rate (HR) and heart rate variation
(HRV) to assess the parasympathetic activity.
HRV was assessed in the form of 30:15 ratio and
Valsalva ratio. These parameters were recorded
under basal conditions and after various stressed
conditions namely lying to standing posture, cold
pressor test (CPT) and Valsalva maneuver (VM).
BP and HR were recorded by using fully
automated BP apparatus (OMRON). HRV was
assessed from Lead II Electrocardiogram (ECG)
recorded in three channels Student Physiograph
as 30:15 ratio in postural change and as a
Valsalva ratio (VR) in Valsalva maneuver.
Procedure
1. Postural change: The subject was made to lie
down in supine position. After five minutes of
mental and physical rest, the basal BP and HR
were recorded. Then, the subject was instructed
to get up briskly and stand erect without any
support and the three parameters were measured
immediately after standing. Simultaneously,
ECG was recorded continuously in lead II in the
lying posture (10 waves), while getting up and
after standing (60 waves). 30:15 ratios was
calculated from the ECG as the longest R-R
interval at around 30th beat divided by the
shortest R-R interval at around 15th beat after
standing.
2. Valsalva maneuver: After measuring the
basal BP and HR in sitting posture, the subject
was
instructed
to
blow
into
the
sphygmomanometer to raise the mercury column
to about 40 mmHg5, 6 and retain it at that level
for 15 Sec. BP and HR were recorded
immediately after 15 seconds strain and an ECG
was recorded continuously before (10 waves),
during and after the strain (60 waves).
Valsalva ratio was calculated from the ECG as
the ratio of the longest R-R interval after the
Sahera etal.,
maneuver to the shortest R-R interval during the

maneuver.
3. Cold pressor test: CPT was performed as
described by Hines and Brown7 with a slight
modification; ie., in the present study the test was
performed in sitting posture whereas in the
previous study, it was performed in supine posture.
After recording the basal BP and HR, the subject
was instructed to immerse the dominant hand up to
the wrist joint in cold water with the temperature
of 50 C for one minute. At the end of one minute,
BP and HR were recorded from the other hand.
Statistical analysis: The data were analyzed in
the computer by using Studentt test in SPSS
Software (17th version). Values were expressed
as mean SD and Significance was fixed at the
level of p < 0.05.
RESULTS
Anthropometric parameters: There was no
significant difference in the age and BMI
between the males and females. But expectedly,
the height and weight of the males were
significantly more than those of females (p <
0.002, 0.001) (Table 1)
Effect of postural change on BP and HR in
males and females:
There was a highly
significant decrease in SBP upon standing from
lying posture (p < 0.000%) in both males and
females and the decrease was less in males (17.00 11.15) than in females (-20.87 11.29)
though it was not statistically significant (p <
0.168) (Table 2)
DBP also showed highly significant decrease
after standing from supine posture (p < 0.000) in
both the groups (Table 2). Between the groups,
the level of decrease was significantly less in
males than in females (p < 0.008) (Table 2)
HR increased significantly after standing from a
lying posture in both the groups (p < 0.000%)
and the increase was less in males (16.87 8.95)
than in females (19.73 8.21) but not
significantly (p < 0.354) (Table 2).
739
Effect of Valsalva maneuver on BP and HR in

males and females: SBP showed highly
significant decrease (p < 0.000) after VM in
males and females and the level of decrease was
less in males than in females (p = < 0.052) (Table
3)
DBP showed different behaviour in both the
groups. In males DBP decreased significantly (p
< 0.000) and in females it increased significantly
(p < 0.000). Between the groups, the level of
increase in females was more than the level of
decrease in males (p < 0.002). HR increased
slightly in males without significance but in
females HR showed highly significant decrease

after VM (p < 0.002) (Table 3)
Effect of cold pressor test on BP and HR in
males and females: SBP, DBP and HR showed
highly significant decrease after CPT in both
males and females (p < 0.000, 0.007 and 0.000
respectively) and there was no significant
difference in the level of decrease (Table 4)
30:15 ratios: 30:15 ratio was more in males than
in females and the difference was highly
significant (p < 0.001) (Table 5).
Valsalva ratio: VR was more in females than in
males and the difference was highly significant
(p < 0.002) (Table 5).
Table 1: Comparison of anthropometric parameters between males and females
variables
Gender
Mean SD
Mean difference
P value
Age (years)
Male
18.73 0.70
0.40 0.91
0.111
Female
18.33 0.62
Male
176.00 7.72 10.17 10.12
Female
165.83 8.44
Male
69.07 8.44
Female
57.73 5.15
Male
22.37 3.09
Female
20.98 1.43
Height (cm)
Weight (kg)
BMI
0.002*
11.33 10.11
0.001*
1.39 3.31
0.127
Table 2: Effect and the difference in the effect of postural change on BP and HR in males and females
Posture
Parameters
SBP
(mm HG)
DBP
(mm HG
HR
(beats/min)
Sahera etal.,
Gender
Lying
Standing
P value
Male
Female
Male
109.60 10.21
92.27 9.39
72.53 5.24
92.60 7.60
71.40 6.28
60.60 5.15
0.000*
0.000*
0.000*
Mean difference:
Lying to standing
- 17.00 11.15
- 20.87 11.29
- 10.27 5.08
Female
65.27 6.76
48.40 6.27
0.000*
- 16.87 7.09
Male
Female
76.80 7.10
69.60 10.25
93.67 6.16
89.33 9.08
0.000*
0.000*
16.87 8.95
19.73 8.21
P Vlaue
0.168
0.008*
0.354
740
Table 3: Effect and the difference in the effect of Valsalva maneuver on BP and HR in males &
females
VM
Gender
Parameters
SBP
(mm HG)
DBP
(mm HG
p
value
Mean
difference
Before VM
After VM
109.53 8.65
91.40 7.89
0.000* - 18.13 14.67
71.93 8.81
0.000* - 31.07 15.32
69.47 7.11
51.07 8.01
0.000*
- 10.27 5.08
Female 55.87 5.10
78.07 7.36
0.000*
- 16.87 7.09
87.47 9.24
0.319
3.40 11.09
63.27 5.54
0.000*
11.13 14.28
Male
Female 103.00 14.41

Male
p value
0.05*
0.000*
Male 84.60 10.43

HR
(beats/min) Female 78.00 8.41
0.002*
VM - Valsalva maneuver
Table 4: Effect and the differences in the effect of cold pressor test on BP and HR in males and females
CPT
Parameters
SBP
(mm HG)
DBP
(mm HG
HR
(beats/min)
Gender
Before CPT
Male
Female
Male
Female
Male
110.13 10.21
96.53 8.54
64.87 6.63
61.87 8.24
76.87 7.96
94.27 12.04
Female
CPT Cold pressor test
After CPT
82.80 8.82
69.80 6.38
50.53 5.36
51.33 7.06
54.73 8.11
69.87 5.91
p
value
0.000*
0.000*
0.000*
0.007*
0.000*
Mean
difference
after CPT
- 27.33 12.92
- 26.73 15.32
- 14.33 8.56
- 10.53 13.01
- 22.13 10.63
0.000* - 24.49 13.58
p
value
0.878
0.389
0.640
Table 5: 30:15 ratio and Valsalva ratio in males and females
Parameter
30:15 ratio
Valsalva ratio
Male
1.52 0.24
2.06 0.51
Female
1.26 0.16
2.35 0.44
Sig
0.001*
0.002*
DISCUSSION
The results of the present study confirm the

existence of gender difference in the functional
status of ANS under basal conditions as well as
stressed conditions. Males were found to have
higher sympathetic activity than females which
was revealed by the behavioral pattern of SBP,
DBP, HR and 30:15 ratios in postural change and
Valsalva maneuver (Table 2, 3, 4, 5). All these
indicate that females have less tolerance to stress
than the males. This correlates with the results of
Sahera etal.,
previous studies showing that women were

significantly less capable of meeting the
orthostatic challenges in maintaining BP than
males8, 9.
Various mechanisms were postulated for this
gender difference in response to stress. Greater
orthostatic intolerance in women was associated
with less responsiveness of specific mechanisms
of blood pressure regulation. Normally, BP is
regulated by baroreflex mechanism and renin741
angiotensin mechanism through sympathetic

nervous system (SNS)10-12. Immediately after
standing from a lying position, blood pools in the
legs, decreasing the venous return and cardiac
output drastically. This leads to transient
decrease in BP and increase in HR. These
changes are attributed to cardiac vagal
withdrawal leading to increased sympathetic
activity13. The present study also shows that
females demonstrated greater elevation in HR
(non-significant) than the males (Table 2) upon
standing from a lying position. Lack of statistical
significance may be attributed to less number of
subjects. Similar results were observed in other
studies also14, 15. Leading to the hypothesis that
vagal withdrawal may the more important
mechanism than sympathetic activity in the
regulation of BP in women 16, 17. The results of
the present study confirm those of previous
investigations18, 19 that women have significantly
lower capacity to regulate blood pressure and
maintain orthostatic function compared with
men.
The greater 30:15 ratio in males in the present
study also depicts a higher sympathetic activity
in males (Table 5). According to Convertio, in
males, the sympathetic discharge is more in
lower limbs whereas in females it is more in
upper limbs17. This may be the reason for greater
30:15 ratio in males than in females. Another
school of thoughts postulates that these malefemale differences in sympathetic activity are
related to body fat distribution17, 19. Elevated
sympathetic activity was found to be more
common in male type fat distribution than the
female type fat distribution 11. Frey and Hoffler
found that in most of the vascular beds, males
showed greater sympathetically mediated
vasoconstriction than the females16.
There are controversial statements regarding the
effect of VM on BP and HR in the literature 13- 15.
Basically, VM initially creates a low intra-aortic
pressure which stimulates the sympathetic
nervous system. Following the release of the
breath, a vagal response is triggered to decrease
Sahera etal.,
the heart rate. In the present study females

showed highly significant decrease in DBP and
HR and less significant decrease in SBP
compared to that of males (Table 3) depicting a
reduced sensitivity to baroreceptors during a
VM16. This is further substantiated by the
increased VR in females in our study.
When exposed to cold stress, SBP and DBP
decreased both in males and females and the
decrease was more in males than in females in
the present study (non-significant) (Table 4).
This result correlates with the results of the other
studies20,21. The response to cold may be due to
the stimulation of thermoreceptors leading to
increased sympathetic activity and this is more
pronounced in males than in females20, 21. The
lack of statistical significance in our present
study may be may be because of less number of
subjects.
Rick Nauert further confirms the gender
difference in the stress response. When exposed
to stress, men develop fight and flight attitude
through the hypothalamus-pituitary-adrenal
(HPA) axis with elevated cortisol level and
women adopts tender and befriend nature
through activation of the limbic system-the
higher center for emotions22.
Vasan et al says that men and women differ in
the size of the heart and blood vessels - men
having larger size than the women of the same
age and race. It comes as a surprise to know that
men and women differ not only in the
physiological aspects of stress management but
also in their anatomical setup of organ sizes23.
Admittedly, a number of subjects are less in the
present study which may be the reason for lack
of significance in a few places. But our results
are substantiated by the previous documentations
in the literature which encourages us to develop
the study further in a different angle and prosper.
The results may help us in designing sex-based
diagnostic tools, understanding the sex linked
pathophysiology of cardiovascular diseases and
developing a different approach in treating the
742
similar cardiovascular disease in men and

women.
CONCLUSION
This study enlightens the growing evidence of

the gender differences in the response to stress
with the implication that females have less
tolerance to stress than males. Understanding the
differences in the physiological and emotional
reactions to stress between boys and girls may
help the parents and teachers to handle them
more carefully and help them to develop positive
coping strategies in life and challenge the
stressors psychologically and psychosomatically
and avoid unpleasant and unwanted incidents of
suicides. Knowing the cause is the first step in
preventing the consequences.
ACKNOWLEDGEMENT
This project is the Students research project

scheme of ICMR in the Year 2011, Ref.No:
2011-02610. We are thankful to ICMR for
sponsoring our undergraduate project. Our
thanks are due to Sathyabama University Dental
College for permitting us to apply for the scheme
and encouraging us to complete it successfully.
Our thanks are due to our lab technician, Ms.
Sunitha, for her valuable technical assistance.
REFERENCES
1. Martin B. Anxiety and neurotic disorders.

John Wiley and Sons, Inc. New York. 1971;
21-34
2. Leonard Sax. Six Degrees of Separation.
What Teachers Need to Know about the
Emerging Science of Sex Differences?
Educational Horizons Spring. 2006; 190-200
3. Aimee Midei. Gender Differences in
Behavioral Responses to Stress. Fight or
Flight vs Tend and Befriend. Molecular
Psychiatry 2003;310-206-9
4. Ptacek JT, Dodge KL. Gender differences in
coping with stress: when stressor and
Sahera etal.,
appraisals do not differ. Pers Soc Psychol B.

1994; 20: 42130.
5. Ewing DJ and Clarke BF; Diagnosis and
management
of
diabetic
autonomic
neuropathy.Br Med Journal. 1982; 285: 91618
6. Prema
Sembulingam,
Sembulingam,
Namasivayam.. Evaluation of autonomic
status in generalized anxiety disorder
patients. Biomedicine 2000; 20(2):109-121
7. Hines EA and Brown GE. The cold pressor
test for measuring the reactibility of the blood
pressure; Deta concerning 571 normal and
hypertensive subjects. The American Heart
Journal. 1936; 11 (1): 1-9
8. Frey MAB, and GW Hoffler. Association of
sex and age with responses to lower-body
negative pressure. J. Appl. Physiol. 1988; 65:
175256
9. Frey MAB, Mathes KL, Hoffler GW.
Cardiovascular responses of women to lower
body negative pressure. Aviat. Space
Environ. Med. 1986;7: 53138
10. Guyton and Hall. Text Book of Medical
Physiology 12th Ed. Saunders ELSEVIER.
Page 201
11. Ganongs Review of Medical Physiology, a
LANGE medical book, 23rd Ed. Tata
McGraw Hill Education Private Limited,
Page 558
12. Sembulingam K, Prema Sembulingam.
Essentials of Medical Physiology, 6th Ed,
JAYPEE Brothers Medical Publishers (P)
LTD. 2013; Chapter 103, Page 607-609
13. Ewing DJ, Hume I, Campbell I W, Murray
A, Neilson JMM and Clarke BF. Autonomic
mechanism in the initial heart response to
standing. J Appl Physiol. 1980. 49: 809-814
14. Montgomery LD, PJ Kirk, PA Payne, RL
Gerber, SD Newton, and BA Williams.
Cardiovascular responses of men and women
to lower body negative pressure. Aviat. Space
Environ. Med. 1977;48: 13845
15. White DD, Gotshall RW, and A Tucker.
Women have lower tolerance to lower body
743
negative pressure than men. J. Appl. Physiol.

1996;80: 113843
16. Frey MAB, Hoffler GW. Association of sex
and age with responses to lower-body
negative pressure. J. Appl. Physiol.
1988;65:175256
17. Convertio VA. Gender differences in
autonomic functions associated with blood
pressure regulation. American Journal of
Physiology: 1909;20:8
18. Hogan TR, Cubitt M, Ecken MK, and Davis
JE. Effect of gender on orthostatic tolerance
(Abstract). Med. Sci. Sports Exerc. 1995;27:
S188
19. Jones PP, Snitker S, Skinner JS, Ravussin E.
Gender differences in muscle sympathetic
nerve activity: effect of body fat distribution.
American Journal of Physiology.1996; 270 :
363-66.
20. Bartelink ML, de Wit A,Wollersheim
H,Theeuwes A and Thien T. Skin vascular
reactivity in healthy subjects: influence of
hormonal status. Journal of Applied
Physiology. 1993;74(2): 727-32
21. Bartelink ML, Wollersheim H, Leesmans E,
de Boo T, Thien TA standardized finger
cooling test for Reynauds phenomenon:
diagnostic value and sex differences.
European Heart Journal. 1993;14:614-62.
22. Rick Nauert. Response to stress is gender
specific. http://psychcentral.com/news/ 2007/
11/20/respose-tstressis gender specific/ 1559.
Source: University of Pennsylvania School of
Medicine
23. Vasan RS, Larson MG, Levy D, Evans JC,
Benjamin EJ. Distribution and categorization
of echocardiographic measurements in
relation to reference limits: The Framingham
Heart Study. Formulation of a height- and
sex-specific classification and its prospective
validation. Circulation 1997;96: 186373
Sahera etal.,
744
DOI: 10.5958/j.2319-5886.2.4.119

&
Health Sciences
Coden: IJMRHS
Copyright @2013
ISSN: 2319-5886
th
th
Research article
EFFECT OF TELMISARTAN ON SERUM LIPID PROFILE IN PATIENTS WITH
HYPERTENSION AND DYSLIPIDEMIA
*Vanitha M1, Vijayal K2
1
2
Department of Pharmacology, Osmania Medical College, Hyderabad

Department of Pharmacology, Dr VRK Womens Medical College & Research Institute, Hyderabad
*Corresponding author email: hayavanitha@yahoo.in

ABSTRACT
Background and Objectives: Hypertension and dyslipidemia are two major risk factors for
cardiovascular disease and they commonly occur together. Management of dyslipidemia in a
hypertensive patient significantly reduces the total cardiovascular risk .Telmisartan is an Angiotensin
receptor blocker with a partial agonistic action on PPAR-. In the present study, the effect of
Telmisartan on serum Lipid Profile was evaluated in hypertensive patients who also have associated
Dyslipidemia and also the efficacy of Telmisartan in reducing systolic and diastolic BP was assessed in
these patients. Materials and Methods: A total of 50 outpatients from the medical outpatient
department of Gandhi Hospital, Secunderabad, were enrolled into the study. These patients had grade
essential Hypertension and mild dyslipidemia. After the study period of 24 weeks, the efficacy of
Telmisartan in reducing serum lipid profile was evaluated apart from its effect on reducing systolic and
diastolic BP. Results: Telmisartan was very effective in reducing serum triglycerides (27 %, P<0.01),
VLDL-C (27 %, P<0.01), LDL-C (22%, P<0.01). It also decreased serum cholesterol by 16%
(P<0.01). HDL-C increased by 14% (P<0.05). Telmisartan in a dose of 40-80 mg/day, significantly
reduced both systolic BP by 18 %( P<0.01) and diastolic BP by 12 %( P<0.01) Conclusion: In our
study, Telmisartan proved to be effective not only in controlling BP, but had a favorable effect on lipid
profile also So, in conclusion, all the patients with uncomplicated Hypertension and mild dyslipidemia
can be effectively treated with Telmisartan.
Key words: Telmisartan, Hypertension, Dyslipidemia, Serum lipid profile
INTRODUCTION
Coronary heart disease continues to be the

leading cause of morbidity and mortality in the
world1. Several factors increase the risk of CHD
such
as
hypertension,
advancing
age,
dyslipidemia, type 2 diabetes mellitus, family
history of coronary artery disease, cigarette
Vanitha et al.,
smoking, obesity etc,.

Hypertension and
dyslipidemia are the most common risk factors
for cardiovascular disease. It is found that
hypertensive patients have lower levels of HDLcholesterol and higher levels of triglycerides
compared to normal individuals. In patients with
745
hypertension,
dyslipidemia
substantially
increases the cardiovascular risk. So, there is a
need for disciplined diet plan and appropriate
pharmacological therapy in these patients. The
exact pathophysiology by which dyslipidemia
may be involved in the development of
hypertension is not well established. Lipid
disorders cause endothelial dysfunction and this
may become manifest as hypertension
edication therapy for hypertension and
dyslipidemia is becoming more complicated, as
over two-thirds of patients require two or more
anti-hypertensive agents and at least one lipid
lowering agent. The mechanism of action of
majority of anti-hypertensive drugs in use today
is to primarily target the factors which contribute
to development of increased blood pressure.
They do not in any way modify the
pathophysiological
mechanisms
causing
dyslipidemia. Angiotensin II receptor blockers
(ARB) are efficient anti hypertensive agents that
act through inhibition of AT1 receptors. In
experimental models, as well as in some clinical
trials, ARBs have been found to significantly
affect lipid metabolism .More precisely; ARBs
improved the overproduction and accumulation
of TGL in the liver, in experimental models,
through mechanisms independent of their
hypotensive action2. Furthermore, there are
preclinical studies showing that telmisartan
exerts a favourable effect on lipid abnormalities,
due to its partial activation of peroxisome
proliferator-activated receptor-gamma (PPAR-).
The finding that Telmisartan acts as both an
ARB and a partial agonist of PPAR- has
important implications in the prevention of
atherosclerosis and cardiovascular disease.
Moreover, it has been shown that activation of
PPAR-, downregulates the expression of
angiotensin II type I receptor and modifies the
effects of angiotensin II on intracellular signaling
pathways3.Telmisartan
is
a
potent,
insurmountable and highly selective antagonist
of AT1 receptors, with a long terminal
elimination half-life, Telmisartan is capable of
Vanitha et al.,
activating the nuclear peroxisome proliferatoractivated receptor (PPAR) - also, in addition to

blocking the angiotensin II type I receptor.
PPAR- is a nuclear transcription factor that
exists in the form of a heterodimer complex with
the retinoid X receptor-4. Activation of PPAR-
causes the receptor complex to affect the
expression of key target genes that mediate
beneficial effects on glucose and lipid
metabolism. Evidence for the importance of
PPAR- in regulating key features of the
metabolic syndrome comes from the studies of
individuals with mutated forms of the receptor.
Such individuals exhibit multiple features of the
metabolic syndrome, including severe insulin
resistance,
hypertriglyceridemia,
elevated
concentrations of non esterified fatty acids, low
concentrations of HDL cholesterol and
hypertension. Infact PPAR- is an important
target for drugs used in the treatment of insulin
resistance, diabetes mellitus and the metabolic
syndrome4. Thiazolidinedione PPAR- activators,
pioglitazone and rosiglitazone are currently
available, and these agents have been shown to
increase the insulin sensitivity and decrease FA
and triglyceride concentrations in patients with
type 2 diabetes5.
In contrast to other ARBs, relatively low
concentrations of telmisartan were also found to
increase the expression of phosphoenol-pyruvate
carboxykinase (PEPCK) gene in human visceral
adipocytes. PEPCK is a key target gene that
contributes to the ability of PPAR- activators to
reduce the FA levels. Further evidence that
telmisartan activates PPAR- comes from the
findings that telmisartan induces adipocyte
differentiation in vitro and is more effective than
other ARBs in reducing serum concentrations of
glucose, insulin and triglyceride in rats
maintained on a diet rich in fats carbohydrates. In
contrast to glitazones, telmisartan is a selective
PPAR- modulator that activates only a subset of
genes targeted by the full PPAR- agonists and
thats why it has fewer adverse effects compared
746
to full PPAR- agonists. Telmisartan is highly

lipophilic, and has a high mean volume of
distribution of 460-510 L. This high apparent
volume of distribution and the lipophilic nature
of telmisartan suggest that it may have greater
capacity to enter intracellular compartments and
gain better access to PPAR- than other ARBs
The present study was conducted in the
Departments of Pharmacology and Medicine,
Gandhi Medical College and Gandhi Hospital,
Secunderabad. 50 newly diagnosed cases of
essential hypertension, having dyslipidemia were
included in the study. The patients were enrolled
from the medical OPD and the study was
conducted in the period from October 2010 to
May 2011. After getting approval from the
Institutional Ethics Committee, newly diagnosed
cases of grade I essential hypertension were first
screened for dyslipidemia by doing serum lipid
profile after overnight fasting for about 10 hrs.
Those patients having both hypertension and
dyslipidemia were included in the study.
Exclusion criteria:
Patients with Diabetes
mellitus, secondary causes for hypertension,
Hepatic or renal insufficiency, coronary artery
disease or cerebrovascular diseases were
excluded from the study. The age of the patients
ranged from 38-65 years with a mean of 52 1.2
years and consisted of 31 males (62%) and 19
females (38%). In each case after the informed
consent was obtained, a detailed clinical history
was taken. All the patients underwent complete
clinical examination including recording of
pulse, B.P, detailed clinical examination of
respiratory system, cardiovascular system and
central nervous system. The biochemical
investigations including Blood sugar, serum
creatinine and serum lipid profile were done.
LFT, TSH, X-ray chest and resting 12 leads
electrocardiogram were done in all the patients.
Serum lipid profile was repeated at the end of 24
weeks. All the patients were started on
Vanitha et al.,
Telmisartan 40 mg orally once daily. They were

followed up with BP recording once in 15 days
and the dose of telmisartan titrated according to
the response.
RESULTS
Initial lipid profile: The initial total serum
cholesterol in the patients ranged between 171281 mg/dl with a mean of 218.86 3.91. The
initial serum triglycerides ranged between 93275 mg/dl with a mean of 170.8 5.25. The
initial LDL-C, ranged between 107-197 mg/dl
with a mean of 144.08 3.65. The initial HDLC, ranged between 32-58 mg/dl with a mean of
40.62 0.76. The initial VLDL-C, ranged
between 19-55 mg/dl with a mean of 34.16
1.04.
All the parameters including total
Cholesterol, LDL-C, Serum Triglycerides, HDLC and VLDL-C, were marginally higher in
female patients, when compared with male
patients.
Lipid profile after 24 weeks: (Table1): After
24 weeks of study period, the mean Total
Cholesterol decreased significantly from 218.86
mg/dl to 185.06 mg/dl (15%,P<0.01). The mean
Serum Triglycerides decreased significantly from
170.8 mg/dl to 123.86 mg/dl (27%, P<0.01).
The mean LDL-C decreased significantly from
144.08 mg/dl to 112.5 mg/dl (22%, P<0.01).
The mean HDL-C increased from 40.62 mg/dl to
47.5 mg/dl (14%, P<0.05). The mean VLDL-C
decreased from 34.16 mg/dl to 25.06 mg/dl
(27%, P<0.01).
Blood Pressure initial Vs after 24 weeks:
(Table2) The initial systolic BP ranged from 140160 mm Hg with a mean of 149.96 1.0 mm Hg
and the initial diastolic BP ranged from 80-99
mm Hg with a mean of 92.88 0.52 mm Hg.
After 24 weeks of treatment with Telmisartan,
the mean systolic BP in the patients decreased
significantly from 149.96 mm Hg to 122.72 mm
Hg (18%, P<0.01) Similarly, the mean DBP
also decreased from 92.88 mm Hg to 81.92 mm
Hg (12%, P<0.01).
747
Table.1: Lipid profile initial vs after 24 weeks
Lipid parameters (mean Initial

values mg/dl)
Total cholesterol
218.86 3.91
Serum Triglycerides
170.85.25
LDL Cholesterol
144.08 3.65
HDL Cholesterol
40.62 0.76
VLDL Cholesterol
34.16 1.04
After 24 weeks
% of
P value
185.065.29
123.860.52
112.56.11
47.53.12
25.061.42
15%
27%
22%
- 14%
27%
< 0.01
< 0.01
< 0.01
< 0.05
< 0.01
Table.2: Blood pressure initial vs after 24 weeks
Parameters
Initial
Mean Systolic BP (mm Hg)

Mean Diastolic BP (mm Hg)
149.96 1.0
92.88 0.52
After
24 % of
weeks
122.723.4 18%
81.922.33 12%
P value
< 0.01
< 0.01
DISCUSSION
Hypertension is not the only determinant of

cardiovascular damage and the propensity of a
subject to develop atherosclerotic vascular
disease is markedly affected by the presence of
other risk factors such as age, gender, obesity,
smoking, diabetes and dyslipidemia.
There is no doubt that the management of lipid
disorders in hypertensive patients ameliorates
their total cardiovascular risk. Clinical trials
suggest that some antihypertensive agents may
have a beneficial effect on lipid metabolism
through
various
possible
mechanisms.
Telmisartan is an unique angiotensin receptor
blocker (ARB) with an additional PPAR-
modulating action6.
It is possible that the lipid lowering effect of
Telmisartan is due to numerous mechanisms. The
ARBs activate PPAR- which regulates lipid
metabolism; thereby reduce triglyceride and
LDL-C
levels.
Furthermore,
there
is
experimental evidence suggesting an interaction
between angiotensin system and lipid
metabolism. The ARBs reduce the AT-II
mediated
endothelial
injury and
lipid
7
peroxidation by blocking the AT1 receptor .
Telmisartan is commonly prescribed for grade I
essential hypertension in the medical outpatient
Vanitha et al.,
department. In the present study, the effect of

long term administration of Telmisartan on
serum lipid profile was evaluated. .The patients
who were enrolled into the study had both
hypertension and dyslipidemia. Also, the efficacy
of Telmisartan in reducing both systolic and
diastolic BP was evaluated in this study. In the
present study, there was significant effect on
serum lipid profile in the patients, who were
given Telmisartan 40-80 mg/day, for 6 months.
The total serum cholesterol decreased by 16 %(
P<0.01), LDL-C by 22% (P<0.01), serum
triglycerides decreased by 27 %( P<0.01) and
VLDL-C decreased by 27 %( P<0.01). The
HDL-C increased by 14 %( P<0.05)
This favourable effect on serum lipid profile was
in addition to the proved effect of Telmisartan as
an antihypertensive drug. Telmisartan in a dose
of 40-80 mg/day, significantly reduced both
systolic BP by 18 %( P<0.01) and diastolic BP
by 12 %( P<0.01). In our study, Telmisartan was
well tolerated, except for some minor and
transient side effects like headache, dizziness and
fatigue in a few patients.
The significant effect of Telmisartan on serum
lipid profile in the present study is supported by
preclinical studies conducted on rabbits and also
748
by STAR trial, (Saga Telmisartan Aggressive

Research Study), a single arm, prospective,
multicentric clinical trial conducted in Japan on
197 patients with hypertension and dyslipidemia.
CONCLUSION
In our study, Telmisartan proved to be effective

not only in controlling BP, but had a favorable
effect on lipid profile also. Telmisartan treatment
results in amelioration of cardiovascular risk
factors, not only through arterial pressure
regulation but also through reduction of serum
lipid profile. So, in conclusion, all the patients
with
uncomplicated
hypertension
and
dyslipidemia without other associated risk factors
can be effectively treated with Telmisartan.
5. Diamant M Heine RJ. TZD in type 2

diabetes mellitus (Current clinical evidence).
Drugs.2003; 63:1373 05
6. Schupp M, Janke J, Clasen R. Angiotensin
type 1 receptor blockers induce peroxisome
proliferatoractivated
receptor
activity.
Circulation, 2004;109: 205457.
7. Keidar S, Kaplan M, Hoffman A.
Angiotensin II stimulates macrophagemediated oxidation of low density
lipoproteins. Atherosclerosis 1995; 115: 20115.
ACKNOWLEDGEMENT
The authors are thankful to Management and

staff of Medical Out Patient Department ,Gandhi
Hospital, Secunderabad, Andhra Pradesh , for
providing necessary facilities to carryout the
research work .
REFERENCES
1. American Heart Association. Heart disease

and stroke statistics, 2007 update AHA,
Dallas, Texas,2007
2. Ran J, Hirano T, Adachi M. Angiotensin II
type I receptor blocker ameliorates
overproduction
and
accumulation
of
triglycerides in the liver of Zucker fatty rats.
Am J physiol. Endocrinol. Metab. 2004; 2:
227-32.
3. Takeda K, Ichiki T, Tokanar T. Peroxisome
proliferator-activated
receptor
gamma
activators down regulate angiotensin II type I
receptor in vascular smooth muscle cells
circulation 2000; 102: 1834-39
4. Pershad Singh HA. Peroxisome proliferatoractivated receptor: therapeutic target for
diseases beyond diabetes. Expert opine invest
Drugs. 2004;13:215- 28
Vanitha et al.,
749
DOI: 10.5958/j.2319-5886.2.4.120

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
A STUDY OF AUTONOMIC FUNCTION TESTS IN OBESE PEOPLE

*Rinku Garg1, Varun Malhotra2, Neera Goel3, Usha Dhar2, Yogesh Tripathi2
1
Assistant Professor, 2Professor, 3Assistant Professor, Department of Physiology, Santosh Medical

College, Ghaziabad, India
*Corresponding author email: rgrinkigarg6@gmail.com
ABSTRACT
Background: Obesity is one of the common significant health hazards and is associated with autonomic
dysfunction. Aims and objectives: The present study was designed to assess the underlying autonomic
neuropathy in obese subjects and to compare it with age-matched controls. Material and Methods:
Thirty obese subjects in the age group of 21-40 years were recruited for the study. Six non-invasive
autonomic function tests were performed out of which four were based mainly on parasympathetic
control (Heart rate response to standing (30:15 ratio), The S:L (standing to lying) ratio, The Valsalva
ratio, Heart rate response to deep breathing ) and the other two were mainly sympathetic (Isometric
Handgrip Exercise Test and Cold Pressor Test). Statistical Analysis: Results were analysed by ANOVA
with SPSS version 17.0 using unpairedt test. Results: Results showed that Heart rate response to
standing(30:15 ratio), The S:L (standing to lying) ratio, The Valsalva ratio, Heart rate response to deep
breathing, Isometric Handgrip Exercise Test and Cold Pressor Test were significantly lower (p <0.05)
in obese subjects as compared to control subjects. Conclusions: Latent autonomic neuropathy may be
present in otherwise healthy obese individuals. Early and regular screening of obese individuals is
necessary to prevent any future complications.
Keywords: Obesity, Autonomic nervous system, Cold pressor test
INTRODUCTION
Obesity is a condition in which excess body fat

accumulates to the extent that it may have an
adverse effect on health1. Obesity is a common
and significant health hazard2. At an individual
level, an excess of energy intake and an
inadequacy of energy expenditure is thought to
explain most cases of obesity3,4. A complex
interaction among different factors like
endocrine, nervous, metabolic factors maintains
Garg et al.,
constant energy storage5. Obesity is considered

to be a risk factor for a variety of cardiovascular
conditions like hypertension, ischemic heart
disease and stroke3 and is characterized by
hemodynamic and metabolic alterations6.
Autonomic nervous system is a centre for the
coordination of different body system7. Since the
ANS is involved in energy metabolism and in the
regulation of the cardiovascular system8-10, it is
750
conceivable that one or more subgroups of

persons with idiopathic obesity have an alteration
in their autonomic nervous system that may
account for several clinical consequences of
obesity7. Laitinen et al11 showed that total body
fat and central body adiposity are associated with
altered autonomic activity.
MATERIAL & METHODS
The present study was a cross-sectional study,

conducted in Santosh Medical College;
Ghaziabad, and the study was approved by the
Institutional Ethics Committee.
Thirty obese subjects with BMI >30 were
selected for the study. The results were compared
with thirty age-matched non-obese controls with
BMI between18.5-24.9.Informed consent was
taken from all the subjects. Subjects with age
above 40years, h/o any chronic illness, on any
medication, and smokers were excluded from the
study.
Height was measured using a standard
stadiometer with the subject standing in an erect
posture. The readings were taken to the nearest
0.1cm. Weight was recorded in kgs using a
calibrated weighing machine (Avery) scale with
a capacity of 120 kg and a sensitivity of 0.05 kg.
The BMI was calculated as the weight in
kilograms divided by the square of the height in
meters [weight (kg) /height (m2)] 12
Subjects were divided into 2 groups as per WHO
classification on BMI.
Group I-Control group with BMI 18.5-24.9kg/m2
Group II-Study group with BMI >30kg/m2
For Assessing Parasympathetic Activity

1. Resting heart rate was calculated from ECG
by using standard limb leads14.
2. Heart rate response to standing (30:15
ratio) was calculated as the ratio between the
R-R interval at beats 30 and 15 of the ECG
recorded immediately upon standing. 15
3. The S:L (standing to lying) ratio was taken
as the ratio of the longest R-R interval during
the 5 beats before lying down to the shortest
R-R interval during the 10 beats in the ECG
after lying down16.
4. The Valsalva ratio. Subjects were instructed
to exhale into a mouthpiece connected to a
mercury manometer and to maintain the
expiratory pressure of 40 mmHg for 15 Sec.
ECG was recorded during the manoeuvre and
45 sec after the manoeuvre. The ratio was
calculated between the maximum R-R
interval ( after release of strain) and the
minimum R-R interval (during strain)17
5. Heart rate response to deep breathing:
Heart rate was recorded first during normal.
Breathing (at rest), and then during deep
breathing (6/min). ECG 3rd & 6th respiration,
minimum R-R intervals and corresponding
heart rate were calculated18.
The following autonomic function tests were

performed:
For Assessing Sympathetic Activity:

Isometric Hand Grip Exercise Test: Before the
exercise, subjects were allowed to rest for 10
minutes in a quiet room to reduce the anxiety.
Resting blood pressure of all the subjects was
measured by the auscultatory method with the
help of a mercury sphygmomanometer
(DIAMOND). First Kortk off sound indicated
systolic blood pressure (SBP) and fifth Kortkoff
sound indicated diastolic blood pressure (DBP).
Isometric handgrip exercise test was done in both
the study group and control groups. After
recording basal blood pressure, subjects were
asked to perform isometric handgrip exercise.
Subjects were told to hold the handgrip spring
dynamometer in the right (or dominant hand) to
have a full grip on it. Handles of the
Garg et al.,
Table 1: WHO Classification of BMI13
BMI
<18.5
18.5-24.9
25-29.9
30-39.9
>40
Category
Underweight
Healthy
Overweight
Obese
Morbid obese
751
dynamometer were compressed by the subject

with maximum effort for few seconds. This
whole procedure was repeated thrice with rest in
between to prevent fatigue. Mean of the three
readings was referred as maximal isometric
tension (T max). Then, the subjects were asked
to perform isometric handgrip exercise at 30% of
T max for 2 minutes. During the test, blood
pressure was recorded from the non-exercising
arm. Blood pressure was again recorded 5
minutes after completion of the exercise19.
Cold Pressor Test: After recording basal blood

pressure, subjects were asked to dip left arm in
the cold water (temp at 2-40 C) for 2 minutes and
blood pressure was recorded from the right arm.
Blood pressure was once again recorded 5
minutes after hand was taken out from the cold
water20.Statistical Analysis: Results were
analysed by ANOVA with SPSS version 17.0
using an unpairedt test
RESULTS
Table.2: Anthropometric variables

Variables
Age(yrs)
Height(mts)
Weight(kgs)
BMI(kg/m2)
Group I(Controls)
33.084.8
1.620.42
58.114.3
22.111.04
Group II(Obese)
32.125.4
1.510.56
81.134.9
35.132.08
Table 3: Parasympathetic function tests in Group I and Group II

Variables
Group I
(BMI 18.5-24.9)
Heart rate response to standing(30:15 ratio)
S:L (standing to lying)ratio
Valsalva ratio
Heart rate response to deep breathing(HRDB)
* p<0.05 versus group I
1.14 0.11
1.20.03
1.650.28
23.464.31
Group II
(BMI >30)
P value
1.060.02
1.110.02
1.450.11
16.462.11
<0.05
<0.05
<0.05
<0.05
Table 4: Statistical analysis of sympathetic function tests in Group I and Group II

Variables
Group I(BMI Group
P
18.5-24.9)
II(BMI >30) value
IHG SBP
IHG DBP
CPT SBP
CPT DBP
12.21.2
12.11.4
12.21.6
13.11.8
8.31.3
8.11.2
8.21.4
9.11.4
<0.05
<0.05
<0.05
<0.05
Data presented in Table 3 shows that there was

significant decrease in the Heart rate response to
standing(30:15 ratio), Valsalva ratio & Heart rate
response to deep breathing (HRDB) in Group II
individuals as compared to Group I(p<0.05).S:L
ratio also decreased, and the decrease was
statistically significant(p<0.05).
Data presented in Table 4 shows that there was

significant decrease in the systolic and diastolic
blood pressure in obese subjects (group II) as
compared to controls (group I)during the
application of isometric handgrip exercise and
cold pressor tests (p<0.05) and the decrease was
statistically significant (p<0.05).
Garg et al.,
752
DISCUSSION
The results of the present study show that the

valsalva ratio, heart rate response to deep
breathing and heart rate response to standing
(30:15) in obese subjects were significantly
lower as compared to the control group, it
indicates decrease in parasympathetic nerve
function and baroreflex sensitivity in obese
subjects. Baroreceptors resetting may occur in
obese individuals due to atherosclerosis that
hardens the carotid sinus walls. This decreases
compliance. Obese group is less responsive to
blood pressure changes to posture. Similar results
were shown by some other investigators21-,23.
There was less increase of
blood pressure
response to cold pressor test in the obese people
in contrast to the control group. The afferent
fibres for this response are the pain fibres which
are stimulated by placing the hand in cold water
and the efferent fibres are the sympathetic fibres.
A lesser increase in the blood pressure after the
cold
water
immersion
points
towards
sympathetic insufficiency in obese subjects20.
Obesity impairs autonomic control of heart rate
and blood pressure. Obese subjects exhibit lower
sympathetic response on exposure to cold. Our
study results were in accordance with reported
study of Monterio et al24.There was also
decreased in blood pressure response to isometric
handgrip exercise test in the obese people in
contrast to the control group. It shows the
decreased activity of the sympathetic nervous
system25 or to a lower increase in peripheral
resistance to manoeuvres activating sympathetic
system26. Baek et al27 stated that in normal
conditions sympathetic activity increases during
isometric handgrip exercise and cold pressor test.
This reduced sympathetic reactivity in
established obesity may be responsible for the
maintenance of obese state.
Valensi et al22 have demonstrated sympathetic
insufficiency in obese people. It was shown that
glucose induced inhibition of the lipid oxidation
rate in obese people is greater in the patients with
autonomic dysfunction which could be due to

decrease in parasympathetic activity.
Decrease in the sympathetic activity may result
in a disordered homeostatic mechanism thus
promoting excessive storage of energy as
suggested by Peterson9.
It has been shown that increased sympathetic
activity induced by cold water stress causes
norepinephrine release and elevation of blood
pressure more in obese subjects. This greater
increase in blood pressure might be contributed
by more release of endothelins, prostaglandins
and angiotensin II29, 30 in obese. Various
investigators have shown that parasympathetic
damage or decreased vagal tone may occur due
to hyperinsulinaemia or insulin resistance or
there may be decreased in baroreflex activity28.
Garg et al.,
CONCLUSIONS
Obesity is associated with both sympathetic and

parasympathetic nervous system dysfunction
which may result in various cardiovascular
complications. So, if this dysfunction is
diagnosed early by doing various autonomic
function tests, it will be of great help in
identification of those which are prone to weight
gain and at risk of various cardiovascular
complications.
ACKNOWLEDGMENT
The authors are thankful to Dr. R K Arya,

Professor & HOD, Department of Community
Medicine, for his help in statistics. We are also
thankful to subjects and all the technical staff for
their contribution in the completion of the
project.
Conflict of Interest: Nil
REFERENCES
1. Haslam DW, James WP. Obesity. Lancet

2005;366(9492):1197-209.
753
2. Simran G, Vidushi G. Effect of obesity on

autonomic nervous system. Int J Cur Bio
Med Sci 2011;1(12):15-18.
3. Esler M, Straznicky N, Eikelis N, Masuo K,
Lambert G. Mechanism of sympathetic
activity in obesity-related hypertension.
Hypertension.2006;48:787
4. Lau DC, Douketis JD, Morrison KM,
Hramaik IM, Sharma AM, Ur E.2006
Canadian clinical practice guidelines on the
management and prevention of obesity in
adults and children summary. CMAJ
2007;176(8):S1-13.
5. Valensi P, Thi BN, Lormeau B, Paries J,
Attali JR. Cardiac autonomic dysfunction in
obese patients. Int J Obes Relat Metab Disord
1995;19(2): 113-18.
6. Colak R, Donder E, Karaoglu A, Ayhan O,
Yalniz A. Obesity and the activity of
autonomic nervous system. Turk J Med Sci
2000;30:173-76.
7. Bray GA. Autonomic and endocrine balance
in the regulation of energy balance. Fed Proc
1986;45:1404-10.
8. Landsberg L, Young JB. The role of the
sympathoadrenal system in modulating
energy expenditure. Clin Endocrinol Metab
1984; 13:475-99.
9. Bray GA. Integration of energy intake and
expenditure in animals and man: the
autonomic and adrenal hypothesis. Clin
Endocrinol Metab 1984; 13: 521-46.
10. Peterson HR, Rothschild M, Weinberg CR,
Fell RD, McLeish KR, Pfeifer MA. Body fat
and the activity of the autonomic nervous
system. N Engl J Med 1988; 28: 1077-83.
11. Laitinen T. Cardiovascular autonomic
dysfunction is associated with central obesity
in persons with impaired glucose tolerance.
Diabet Med 2011;28(6) 699-704.
12. Harrison. Biology of obesity. In: Harrison
Principles of Internal Medicine. 17th ed.
McGraw Hill;2008.P.462-67.
13. Hilsted J, Jenson SB. A simple test for

autonomic neuropathy in juvenile diabetes.
Acta Med Scand 1979;205:385-87.
14. WHO. Obesity: Preventing and managing the
global epidemic:
Report of the WHO
consultation of obesity. Geneva:World
Health Organisation 1998.
15. Page MM, Watkins PJ. The heart in
diabetes:autonomic
neuropathy
and
cardiomyopathy. Clin Endocrinol Metabol
1977;6:377-88.
16. Rodrigues EA, Ewing DJ. Immediate heart
rate response to lying down: simple test for
cardiac
parasympathetic
damage
in
diabetes.Br Med J 1983;800:287-9.
17. Levin AB. A simple test of cardiac function
based upon the heart rate changes induced by
the valsalva maneuver.Am J Cardiol
1966;1:90-99.
18. Mathias CJ and Bannister R. Autonomic
failure. A Textbook of Clinical Disorders of
the Autonomic Nervous System.3rd ed.
Newyork: Oxford University Press;1992.
19. Ewing DJ, Irwing JB, Kerr F, Wildsmith
JAW, Clarke RF, Cardiovascular response to
sustained handgrip in normal subjects and in
patients with diabetes mellitus: a test of
autonomic function. Clin Sci Mol Med
1974;46:295-306.
20. LeBlanc J, Dulac S, Cote J, Girard B.
Autonomic nervous system and adaption to
cold in man. J App Physiol 1975;39(2):1816.
21. Emdin M, Gastaldelli A, Muscelli E,
Macerata A, Natali A, Camastra S and
Ferrannini
E.
Hyperinsulinemia
and
autonomic nervous system dysfunction in
obesity:
Effect
of
weight
loss.Circulation.2001;103:513-19.
22. Valensi P, Lormeau B, Dabbech M, Miossec
P, Paries J, Dauchy F. Glucose induced
thermogenesis, inhibition of lipid oxidation
rate and autonomic dysfunction in nondiabetic
obese
women.
Int
J
Obes.1998;22:494-499.
Garg et al.,
754
23. Borne PVD, Hausberg M, Hoffman RP,

Mark
AL
and
Anderson
EA.
Hyperinsulinaemia produces cardiac vagal
withdrawl and nonuniform sympathetic
activation in normal subjects. Am J Physiol
Regul Integr Comp Physiol 1999;276:178183.
24. Monteiro G, Chathoth V,K Kishan. Cardiac
autonomic response during a cold pressor test
in
normal
and
overweight
adults.
International Journal of Biomedical and
Advance Research 2012;3(6):514-516.
25. Nageshwari K, Rajeev S and Divyanshoo
RK. Assessment of respiratory and
sympathetic cardiovascular parameters in
obese school children. Ind J Physiol
Pharmaco 2007;51(3):235-43.
26. Valensi P, Bich Ngoc PT, Idriss S, Paries J,
Cazes P, Lormeauet B et al. Haemodynamic
response to an isometric exercise test in
obese patients. Influence of autonomic
dysfunction. Int J of Obesity 1999;23:543-49.
27. Baeks MA Van. The peripheral sympathetic
nervous system in human obesity. J
Endocrinol 2000;164:59-66.
28. Akhter S, Begum N, Ferdousi S, Khan SM.
Autonomoc neuropathy in obesity. J
Bangladesh Soc Physiol 2011;6(1):5-9.
29. Velasco M, Gomez J, Blanco M, Rodriguez I.
The cold pressor test: pharmacological and
therapeutic aspects. American Journal of
Therapeutics 1997;4(1):34-38.
30. Rinku Garg, Yogesh Tripathi, Varun
Malhotra. Sympathetic Reactivity to Cold
Pressor Test in Medical Students of
Hypertensive and Normotensive Parents.
International Journal of current research and
review 2012;4(18):89-94.
Garg et al.,
755
DOI: 10.5958/j.2319-5886.2.4.121

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Coden: IJMRHS
nd
Research article
Copyright @2013
ISSN: 2319-5886
PULMONARY FUNCTION TESTS IN TYPE II DIABETICS IN CORRELATION WITH

FASTING BLOOD GLUCOSE
* Srikanth Sajja1, Pragathi BH2
1
Professor, Department of Physiology, Dr PSIMS& RF, Chinnavutapalli, Andhrapradesh, India,

Tutor, Department of Physiology, St.Joseph Dental College, Eluru, Andhrapradesh, India.
* Corresponding author email: minni_shp@yahoo.com

ABSTRACT
Background & Objectives: Diabetes mellitus (DM) is a significant public health problem worldwide
which is associated with hormonal, metabolic and micro vascular abnormalities. The angiopathic
complications affect eyes, kidneys, nervous, cardiovascular and respiratory system, which are primarily
due to biochemical alterations in connective tissue. Materials & Methods: In this study, we included
100 subjects, 50 Diabetic (25 Male and 25 Female) and 50 (25 Male and 25 Female) healthy
individuals aged 30-55 years. The pulmonary function tests were performed by the computerized
spirometer in the Clinical Physiology Lab, Department of Physiology, Dr. PSIMS & RF,
Chinnavutapalli. Results: The results of our study showed a statistically significant reduction in
FEF50%, FEF75% & FEV1 /FVC ratio in diabetic male subjects when compared with control male
subjects (p< 0.0001) and diabetic female subjects showed a reduction in FEV1/FVC which is not
statistically significant (p = 0.0004) but we observed a statistically significant reduction in FEF50% &
FEF75% in diabetic female subjects when compared with control female subjects (p< 0.0001). On
spirometry, Diabetic subjects showed a significant reduction in FEV1/ FVC ratio, FEF 50%, FEF 75%
relative to non diabetic controls. Conclusion: We conclude from our study that diabetic subjects
showed impairment in lung function. We found a decrease in FEV1/FVC ratio, FEF50% and FEF75%
in diabetic subjects as compared to control subjects.
Keywords: Diabetes, Forced Vital capacity, Forced expiratory Volume, Forced Expiratory Flow
INTRODUCTION
Diabetes is a systemic disease that produces

changes in the structure and function of several
tissues.
The
pathogenesis
of
diabetic
complications involves both microangiopathic
process and non-enzymatic glycosylation of
tissue proteins. This process results in
Srikanth et al.,
biochemical alterations in connective tissue

constituents leading to impaired collagen and
elastin cross-linked with a reduction in strength
and elasticity of connective tissue, also, due to a
non-enzymatic glycosylation of proteins 1.
Presence of an abundant connective tissue in the
756
lung and an extensive microvascular circulation

can be the possible cause of lung to be a target
organ in diabetic patients2. Due to increase in
the incidence and prevalence of DM particularly
in Asian Indians, it is essential to study
pulmonary function in patients having type2 DM
and
examine
their
correlation
with
microangiopathic complications. Several clinical
studies 3, 4,5 have suggested a possible association
between pulmonary function abnormalities and
diabetic renal microangiopathy and retinopathy.
Changes in pulmonary diffusing capacity for
carbon monoxide (DLCO) as a manifestation of
pulmonary microangiopathy have been reported6.
Defective pulmonary function in asymptomatic
diabetic patients is more prevalent than generally
recognized involving 60% of adult cases.
Autopsy findings in human diabetic subjects and
experiments in rats with diabetes, have included
thickening of the alveolar epithelia, pulmonary
capillary basal lamina, centrilobular emphysema,
and
pulmonary
microangiopathy7.These
anatomical changes may be due to the
biochemical alteration of connective tissue
constituents caused by a non-enzymatic
glycosylation of proteins and peptides induced
by chronic high circulating glucose 8.Tests of
lung mechanical function include measurement
of lung elasticity , airflow resistance, and forced
spirometric pulmonary function tests. Diabetes
has been inconsistently associated with
spirometric abnormalities in a number of small
retrospective cross-sectional studies, involving
even fewer than 50 subjects. Alterations such as
hyperglycaemia, oxidative stress from autooxidation of glucose, non-enzymatic protein
glycosylation, and alterations of nitric oxide
(NO) metabolism have been reported as
metabolic markers of the diabetic state. The
source of free radicals in diabetes is not fully
understood, but glycation of proteins can lead to
oxidative stress by direct release of O2 and H2O2
and activation of phagocytes through a
specialized receptor for advanced glycation end
products. Oxidants include reactive oxygen
Srikanth et al.,
species (ROS), reactive nitrogen species (RNS),

sulfur centered radicals and others. Phagocytic
cells generate large amounts of NO and other
ROS. Peroxynitrite (ONOO) is formed when
NO reacts with superoxide (O). This reaction
occurs rapidly and promotes the nitration of
biomolecules including protein tyrosine residues.
Peroxynitrite anion and peroxynitrous acid
(ONOOH) can freely pass through lipid
membranes and can mediate oxidation, nitration,
or nitrosation reactions. Peroxynitrite is more
than two orders of magnitude more potent than
H2O2 in catalyzing lipid oxidation in vivo.
During diabetes, there are also disturbances in
antioxidant defense systems evidenced by
alterations in antioxidant enzymes9, impaired
glutathione metabolism 10,11 and decreased
ascorbic acid levels 11,12 .
The pathophysiologic connection between
diabetes and lung function was explained by a
possible
pro-inflammatory
stimulus
of
hyperglycemia causing impaired lung function
through increased intrapulmonary inflammation
and apoptosis. Another possible cause of
impaired lung function could be increased
sclerosis of bronchial arteries as a consequence
of generalized arteriosclerosis in diabetes.
Diaphragm elevation with increased closing
volume and decreased FVC in absence of
detectable bronchial obstruction is another
possible cause of impaired lung function.
MATERIALS & METHODS
In this study, we included 100 subjects, 50

Diabetic (25 Male and 25 Female) and 50
healthy individuals (25 Male and 25 Female)
aged 30-55 years, after obtaining their consent.
An approval was obtained from Institutional
Ethical committee. Individuals were classified as
having diabetes (as per the criteria Adapted from
American Diabetes Association Criteria 1997), if
any of the following criteria were met: fasting
glucose level of at least 7.0mmol/lit (126mg/dl);
non fasting blood glucose level at least 11.1
757
mmol/lit (200mg/dl); current use of anti diabetic

medication.
Inclusion criteria: The persons who had never
smoked and without any self reported respiratory
complaints or any history of respiratory diseases.
Exclusion criteria: Individuals with heavy
smoking, Alcohol intake, Anemia, Malnutrition,
productive cough, Exertional dyspnoea, and
cardiovascular diseases, Individuals with chronic
lung diseases (like pulmonary TB, Bronchial
asthma, Chronic Bronchitis, etc), Individuals
who had undergone Abdominal & Chest surgery,
Kypho scoliosis, Pectus carinatum, Pectus
excavatum,
Occupational
diseases
like
Pneumoconiosis.
Procedure: The pulmonary function tests were
performed by Computerized Spirometer model
RMS Helios 401 in the Clinical Physiology Lab,
Department of Physiology, Dr. PSIMS& RF,
Chinnavutapalli. First FVC was recorded using

the Helios spirometer as per the instructions.
For SVC test same procedure is followed but the
subject is instructed to take a deep breath
followed by deep exhalation. Both inhalation and
exhalation should be performed to the maximum
extent but slowly. After this patient was
instructed to take few gentle and normal breaths.
For MVV test patient was asked to breathe
deeply and quickly through the mouthpiece for
12-15 sec. The maneuver should imitate rapid
breathing during exercise. Fasting blood glucose
levels are estimated by using NIPRO Diagnosis
Blood Glucose Monitoring System.
Statistical analysis: The statistical analysis was
performed using Graph Pad Prism 5.0 Version.
As the analysis is done between the groups,
UNPAIRED T TEST was used.
RESULTS
Table: 1. Comparison of Mean Values of FEV1/FVC, FEF50% and FEF75% in Male, female subjects
PARAMETER
FEV1/ FVC
FEF50%
(L/sec)
FEF75%
(L/sec)
Male
Fe male
CONTROL
DIABETIC
P-value
CONTROL
DIABETIC
P-value
82.4 1.63
79.5 1.87
0.0001
80.4 1.35
78.9 1.40
0.0004
3.8 0.31
3.0 0.50
0.0001*
3.8 1.24
2.60.33
0.0001*
1.26 0.13
1.02 0.20
0.0001*
1.2 0.12
0.9 0.11
0.0001*
When compared with Control male subjects, the

Diabetic male subjects showed a reduction of
mean FEV1/ FVC ratio by 3.51 % ( i.e.,2.9 ) , a
reduction of mean FEF50% by 21.05 % (i.e., 0.8
L/s) and a reduction in the mean FEF 75% by
19.04 % ( i.e., 0.24 L/s ). When compared with
Control female subjects , the Diabetic female
subjects showed a reduction of mean FEV1/
FVC ratio by 3.48 % ( i.e.,1.8 ) , a reduction of
mean FEF50% by 31.57% (i.e., 1.2 L/s) and a
reduction in the mean FEF 75 by 25% ( i.e., 0.3
L/s ).
Srikanth et al.,
On spirometry, the Diabetic subjects showed a

significant reduction in FEV1/ FVC ratio, FEF
50%, FEF 75% relative to non diabetic controls.
The results of our study showed a reduction in
FEV1 /FVC ratio in diabetic male subjects when
compared with control male subjects which is
statistically significant (p< 0.0001 ) and also,
diabetic female subjects showed a reduction in
FEV1/FVC which is not statistically significant
(p = 0.0004). The results of our study showed a
statistically significant reduction in FEF50% in
diabetic male subjects when compared with
control male subjects ( p< 0.0001 ) and also ,
758
diabetic female subjects showed a statistically

significant reduction in FEF50% ( p value <
0.0001 ). The results of our study showed a
statistically significant reduction in FEF75% in
diabetic male subjects when compared with
control male subjects (p< 0.0001) and the
diabetic female subjects also showed a reduction
in FEF75% (p< 0.0001) which is statistically
significant.(Table-1)
DISCUSSION
A lot of studies dealing with the problem of lung

dysfunction in diabetes mellitus are crosssectional, with the inclusion of a small number of
patients suffering either from insulin-dependent
diabetes mellitus (type I) or type II diabetes
mellitus.
Diabetes mellitus has an impact on the
mechanical and microvascular function of the
lung and influences ventilatory control.
Numerous studies of lung function in diabetic
subjects have shown slightly decreased indices of
forced expiration and lung volumes in both type I
and type II diabetes mellitus. Lange P , Groth S,
Kastrup J et al.,13conducted study to find the
relation between diabetes mellitus, forced vital
capacity and forced expiratory volume in one
second. They observed that diabetic subjects in
all age groups showed an impairment of lung
function. The forced vital capacity (FVC), forced
expiratory volume in one second (FEV1) and
forced mid-expiratory flow are reduced by 8
20% with a moderately restrictive defect without
airway obstruction 14,15,16. Other studies failed to
show significant differences between patients
with diabetes and normal controls in spirometric
lung function tests17, 18. The Cardiovascular
Health Study19 in determining reference
standards for a healthy population, found
diabetes to be significantly associated with a
decreased FEV1. In the Framingham Heart
Study20, diagnosis of DM was associated with a
greater reduction in FVC than FEV1, suggesting
a restrictive pathology. On the contrary, when
Srikanth et al.,
those with diabetes on therapy were excluded,

higher levels of fasting blood glucose were
associated with larger reduction in FEV1 than
FVC. The resulting progressive decrement in
residual FEV1/ FVC ratio with increasing level
of blood sugar suggests that higher fasting blood
sugar was associated with more obstructive
physiology. In the Fremantle Diabetes Study 21
reduced spirometric lung function was observed
in patients with type 2 diabetes.
Goya wannamethee S, Gerald Sharper A, Ann
Rumley et al 22 prospectively studied the
relationship between lung function, risk of type-2
diabetes. They opined that inflammation may be
the cause for these associations. They concluded
that Restrictive rather than obstructive
impairment of lung function is associated with
incident type 2 diabetes. Ali M.O, Begum S,
Begum N et al.,23 conducted studies to observe
the relation between different lung function
parameters in type 2 diabetic patients. They
concluded that the ventilatory function of lung
may be reduced in type 2 diabetes which may be
related to the duration of the disease. Mohhamed
Irfan, Abdul jabbar, Ahmed Suleman Haque et al
24
studied about the pulmonary function in
Diabetics. They observed impaired lung function,
independent of Smoking in diabetics. The results
of our study were in accordance with this study.
The decline of FEV1 and FVC in diabetic
individuals is similar to that observed in nondiabetic subjects in certain longitudinal studies25.
Few studies have been conducted for
investigating respiratory muscle function in
diabetes mellitus.
DLCO was used to study pulmonary vascular
changes. Even though some studies showed no
defects in diabetes mellitus26, the majority of
studies reported reduced diffusing capacity
among diabetic patients27. Carmela Maiolo,
Ehab I Mohamed, Angela Andreoli 28conducted
studies to assess the relation between Body Fat
Distribution & reduced pulmonary function in
obese Type 2 Diabetic adult women. They
concluded that the DLCO and respiratory muscle
759
function explain the relationship between

pulmonary dysfunction and body composition.
A potential mechanism that explains the finding
of decreased lung function was decreased muscle
strength in diabetic subjects because of defective
muscle metabolism 29 or it may be due to
inflammatory origin.
CONCLUSION
The cause for the decline in lung function in

diabetes remains unclear. Taking into
consideration of increased prevalence of
lifestyle-related chronic diseases like diabetes,
the complications for patients with diabetes, with
overt pulmonary diseases claim special attention.
To study the possible pathophysiological
mechanisms further research is needed. Our
study has several limitations. First, there were
less number of subjects. So we cannot generalize
the result in different groups i.e., diabetic and
control groups. Secondly, we did not measure
DLCO in our subjects. Several studies showed a
reduction in DLCO in diabetic subjects, also in
subjects with normal spirometric values. Lung
function should be monitored regularly to know
the degree of impairment in diabetic or pre diabetic subjects.
ACKNOWLEDGEMENT
We acknowledge the subjects who participated in

the study.
Conflicts of Interest: None
Source of Funding: Nil
REFERENCES
1 Innocenti F, Fabbri A, Anichini R, Tuci S,
Pettina G, Vannucci F et al. Indications of
reduced pulmonary function in type 1
(insulin-dependent)
diabetes
mellitus.
Diabetes Res Clin Pract 1994; 25:161168.
2 Sandler M. Is the lung a target organ in
diabetes mellitus. Arch Intern Med. 1990;
150:138588.
Srikanth et al.,
3 Ljubic S, Metelko Z, Car N. Reduction of

diffusion capacity for carbon monoxide in
diabetic patients. Chest 1998; 114:103335.
4 Sinha S, Guleria R, Misra A, Pandey RM,
Yadav R, Tiwari S. Pulmonary functions in
patients with type 2 diabetes mellitus and
correlation
with
anthropometry
and
microvascular complications. Indian J Med
Res 2004; 119: 66-71.
5. Marvisi M, Bartolini L, del Borrello P.
Pulmonary function in non-insulin-dependent
diabetes mellitus. Respiration 2001; 68:268
72.
6. Isotani H, Nakamura Y, Kameoka K, Tanaka
K, Furukawa K, Kitaoka H. Pulmonary
diffusion capacity, serum angiotensin
converting enzyme activity and the
angiotensin- converting enzyme gene in
Japanese noninsulin dependent diabetes
mellitus patients. Diabetes Res Clin Pract
1999; 43:17377.
7. Vracko R, Thorning D, Huang TW. Basal
lamina of alveolar epithelial and capillaries.
Quantitative changes with
aging and
diabetes mellitus. Am Rev Respir Dis 1979;
120:97383.
8. Brownlee M, Vlassara H, Cerami A. Nonenzymatic glycosylation and the pathogenesis
of diabetic complications. Ann Intern Med
1984; 101: 527537.
9. Strain JJ. Disturbances of micronutrient and
antioxidant status in diabetes. Proc Nutr Soc
1991; 50: 591604.
10. McLennan SV, Hefferen S, Wright L, Rae C,
Fisher E, Yue DK et al. Changes in hepatic
glutathione metabolism in diabetes. Diabetes
1991; 40: 344348.
11. Gumieniczek A, Hopkala H, Wojtowicz Z,
Wysocka M. Changes in antioxidant status of
lung tissue in experimental diabetes in
rabbits. Clin Biochem 2002; 35: 14749.
12. Young IS, Torney JJ, Trimble ER: The effect
of ascorbate supplementation on oxidative
760
stress in the streptozotocin diabetic rat. Free

Radic Biol Med 1992; 13: 4146.
13. Lange P, Groth S, Mortensen J. Diabetes
mellitus and ventilatory capacity: a five year
follow up study. Eur Respir J 1990; 3: 288
92.
14. Engstrom GM, Janzon L. Risk of developing
diabetes is inversely related to lung function:
a
population-based cohort study. Diabet
Med 2002; 19:167-70.
15. Fuso L, Cotroneo P, Basso S. Postural
variations of pulmonary diffusion capacity in
insulin dependent diabetes mellitus. Chest
1996; 110:100913.
16. Primhak RA, Whincup G, Tsanakas JN,
Milner RD.
Reduced vital capacity in
insulin-dependent diabetes. Diabetes 1987;
36: 32426.
17. Mori H, Okubo M, Okamura M, Yamane K,
Kado S, Egusa G et al. Abnormalities of
pulmonary function in patients with noninsulin- dependent diabetes mellitus. Intern
Med.1992;31:189 93
18. Benbassat CA, Stern E, Krammer M ,
Lebzelter J, Blum I, Fink G. Pulmonary
function in patients with diabetes mellitus.
Am J Med Sci 2001; 322: 12732.
19. Enright P, Kronmal R, Higgins M, Schenker
M, Haponik E. Spirometry reference values
for women and men 65 to 85 years of age.
Am Rev Respir Dis 1993; 147:12533.
20. Walter RE, Beiser A, Givelber RJ, OConnor
GT, Gottlieb DJ.
Association between
glycemic state and lung function: the
Framingham Heart Study. Am J Respir Crit
Care Med 2003; 167:91116.
21. Davis T, Knuiman M, Kendall P, Vu H,
Davis WA. Reduced pulmonary function and
its associations in type 2 diabetes: the
Fremantle Diabetes Study.
Diabetes Res
Clin Pract 2000; 50: 15359.
22. Wannamethee SG, Gerald shaper A, Rumley
A. Lung functions and risk of Type 2
Diabetes and fatal and nonfatal major
coronary heart disease events: possible
Srikanth et al.,
associations with Inflammation. Diabetes

Care. 2010;33:199096
23. Ali MO, Begum S, Begum N, Ali T, Ferdousi
S, Begum A: FVC, FEV1 and FEV1/FVC%
in Type 2 Diabetes and Their Relationships
with Duration of the Disease. J Bangladesh
Soc Physiol. 2009;4(2): 81-87
24. Irfan M, Abdul jabbar, Suleman Haque A,
Safia Awan: Pulmonary functions in patients
with diabetes mellitus. Lung India.
2011;28(2):89-92
25. Lange P, Parner J, Schnohr P, Jensen G.
Copenhagen City Heart Study; longitudinal
analysis of ventilatory capacity in diabetic
and nondiabetic adults. Eur Respir J 2002;
20: 140612.
26. Schernthaner G, Haber P, Kummer F,
Ludwig H. Lung elasticity in juvenile-onset
diabetes mellitus. Am Rev Respir Dis 1977;
116: 54446.
27. Strojek K, Ziora D, Sroczynski J. Pulmonary
complications of type 1 diabetic patients.
Diabetologia 1992, 35:117376.
28. Maiolo C, Mohamed EI, Andreoli A,
Candeloro N, Rossi P, De Lorenzo A. Is
altered body fat distribution responsible for
reduced pulmonary function in obese type 2
diabetic adult women. Diabetes Care 2001;
24: 96162.
29. Lazarus R, Sparrow D, Weiss ST. Handgrip
strength and insulin levels: cross-sectional
and prospective associations in the
Normative Aging study. Metabolism 1997:
46: 126669.
761
DOI: 10.5958/j.2319-5886.2.4.122

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
Accepted: 22nd Aug 2013
EVALUATION OF ANTIULCER ACTIVITY OF ETHANOLIC EXTRACT OF MOMORDICA

DIOICA ON PYLORUS LIGATURE INDUCED AND IBUPROFEN INDUCED ULCER IN
ALBINO RATS
Raveendra Kumar N1, Siva Kumar N2, Yakaiah Vangoori3
1
Associate Professor, 2Assistant Professor of Pharmacology, Alluri Sitaramaraju Academy of Medical

Sciences (ASRAM), Eluru, Andhra Pradesh, India
3
Assistant Professor of Pharmacology, Santhiram Medical College, Nandyal, Andhra Pradesh, India
*Corresponding author email: raveendrapharma@gmail.com
ABSTRACT
Objective: The aim of the present study is to evaluate the anti-ulcer activity of Ethanolic extract of
Momordica Dioica in pylorus ligation and ibuprofen induced gastric ulcers in rats. Methods: Gastric
ulcer was induced by giving ibuprofen (200mg/Kg) and by pylorus ligation method. The animals used
for the experiment were divided into 4 groups for each model, 6 rats in each group. In pylorus ligation
model, all groups of rats were pre-treated with test drugs, Group-I (control) received 2%gum acacia2ml/100g, Group-II (standard) received Ranitidine (60mg/kg.) and group-III, IV were treated with
Ethanolic extracts 150mg/kg, 300mg/kg. respectively orally 30mins prior to pylorus ligation. The
Antiulcer activity of Momordica Dioica was assessed by determining and comparing gastric volume,
free acidity, total acidity, pH, percentage of ulcer protection, ulcer index. In ibuprofen induced ulcer
model, all groups of rats were treated with test drugs for 7 days prior to ibuprofen induced ulcer.
Animals were divided into 4 groups and treated with drugs as in above model. After 7 days of treatment,
animals were fasted for 24 hrs. Ulcers were produced by giving ibuprofen (200mg/Kg) on the day of
sacrifice. The animals were sacrificed 4 hours later and stomachs were open along the greater curvature
and ulcers were graded. Percentage of ulcer protection, ulcer index were observed and calculated.
Results: The extract of Momordica Dioica in pylorus ligation model, it decreased the ulcer index (1.66)
and there was a decrease in total gastric acid and free acid (p<0.0001), and increases the pH value
(p<0.0001) and also reduces the total gastric volume (p<0.0003), increases the percentage of ulcer
protection (61.66%). In ibuprofen induced ulcer model, it decreases the ulcer index (10.66) and
increases the ulcer protection (72.09%). Conclusion: The Ethanolic extract of Momordica Dioica was
clearly shows a protective effect against total acid, free acid, gastric volume and ulcer index and also
increases pH and percentage of protection against ulcers in both models.
Key words: Momordica Dioica, Gastric protection, Ibuprofen, Ulcer Index
762
Raveendra et al.,
Int J Med Res Health Sci. 2013;2(4): 762-767
INTRODUCTION
Peptic ulcer remains a prevalent condition

affecting up to 10% of the population and is
responsible for considerable morbidity and loss
of work time.1 the high incidence and chronicity
of the suffering and decreased ability to work
associated with it, has made peptic ulcer an
important health problem. An ulcer is thought to
develop when the equilibrium is disturbed either
by enhanced aggressiveness or by lessened
mucosal resistance2 Drugs that affect acid and
enhance defensive mechanisms are available. Of
late, the concept is now changing from chemical
pH to microbial Hp (pH= acidity, Hp= H.pylori)3
Flood gates of research on Helicobacter pylori
actually opened up when Marshall and Warren in
1984 demonstrated the association between this
organism with active chronic gastritis and peptic
ulcer4Long term use of NSAIDs can also cause
gastric ulcer. Treatment cost is estimated more
than 2-4$ billion per year, so most of the ulcers
heal by using synthetic drugs. After 6-8 weeks
there is a problem of recurrence of side effects.
Therefore people prefer natural product drugs for
disease treatment. Over 3 quarters of the world
population relieved by plants and plant extracts
for health care. More than 30% of the entire plant
species at one time or other has been used for
medicinal purpose 5 Momordica Dioica is an
important medicinal plant with potent antiinflammatory activity. It contains the various
chemical classes such as alkaloids, tannins,
flavonoids, carbohydrates. Momordica Dioica
commonly known as teasel gourd and used as
vegetable.15 Momordica dioica Roxb belongs to
the family Cucurbitaceae6 and under the genus
Momordica, a genus of annual or perennial
climbers that contains about 80 species.
Momordica dioica climber plant commonly
known as Teasle Gourd, Kakrol, Kankro, Kartoli,
Kantoli, Kantola, Kantroli, Ban karola or Small
bitter-gourd is a relatively small oval to ovoid
vegetable. It is also called as janglee karela. It is
often cultivated for its fruits, which are used as
vegetable. The Fruits are reported to show antiinflammatory, anti-ulcer, anti-oxidant, and
hepatoprotective6. Traditionally this fruit was
used in ulcer but scientifically not proved. Hence
the present study was aimed to investigate the
anti ulcer effect of Momordica Dioca in
experimental animal models
Experimental animals: Swiss albino rats

weighing 150-200g of either sex were used for
this experiment, supplied by authentic animal
suppliers Sainath Agencies, Hyderabad, AP, and
India. They were randomly distributed into
groups and housed in cages (6/cage) and kept
under standard conditions at 262 C and relative
humidity 44-56% and 10 hours light: 14 hrs dark
cycles each day for 1 week before and during the
experiments. All animals were fed the standard
rodent pellet diet and ad libitum. This study was
cleared by the institutional animal ethics
committee according to CPCSEA guidelines.
Plant material: Fresh green fruits of Momordica
Dioica popularly known as spine gourd were
obtained in sufficient quantity from local forest
in Eluru, A.P in March 2013.They were carefully
washed to remove dust particles and other
foreign materials and cut into small pieces dried
in shaded areas. The dried pieces of fruit make a
fine powder with grinder.
Preparation of alcohol extract: The dried fine
powder of the Momordica Dioica powder was
weighed on balance 30g. and taken into the sac
like cloth material and placed in the Soxhlet
basket. 300 ml of ethyl alcohol was taken as
solvent into the Soxhlet flask. Cold tap water
must flow through the inlet and outlet of the
condenser. The Soxhlet apparatus kept running
for 24hours for proper extraction. The extract
laden solvent falling from the Soxhlet basket is
dark in color and it becomes clearer, that
indicates the extraction process is finished. At
the end of the extraction process the solvent is
763
Raveendra et al.,
then evaporated7, total yields was 5gm,

percentage yield was16.6% as mg per gm dried
powder. The extract 600mg was suspended in
2ml of 2% Gum acacia and administered
according to dose mentioned as bellow by oral
route.
Experimental design: The animals used for the
experiment were divided into 4 groups for each
model, 6 rats in each group.
In Pylorus ligation model: All groups of rats
were pre-treated with test drugs, Group-I
(control) received 2% gum acacia-2ml/100g,
Group-II
(standard)
received
Ranitidine
8
(60mg/kg) and group-III, IV were treated with
Ethanolic
extracts
150mg/kg,
300mg/kg
respectively orally 30mins prior to pylorus
ligation. After giving drugs all groups of animals
were anesthetized with ether and lower
abdominal wall was opened and pyloric end was
ligated. Then abdominal wall was closed with
interrupted sutures. During this procedure strict
aseptic conditions were maintained to prevent
infections. After 4 hours of pylorus ligation,
animals were sacrificed and stomach was opened
along with the greater curvature and total gastric
contents were collected and centrifuged. The
Antiulcer activity of Momordica Dioica was
assessed by determining and comparing gastric
volume, free acidity, total acidity, pH, percentage
of ulcer protection, ulcer index.
In the Ibuprofen induced ulcer model, all
groups of rats were treated with test drugs for 7
days prior to ibuprofen induced ulcer. Animals
were divided into 4 groups and treated with
drugs as in above model. After 7 days of
treatment, animals were fasted for 24 hrs. Ulcers
were produced by administration of ibuprofen
(200mg/Kg)9. The animals were sacrificed after 4
hours administration of ibuprofen and stomachs
were open along the greater curvature and ulcers
were graded. Percentage of ulcer protection ulcer
index were observed and calculated.10
Gastric juice collection: gastric juice was
collected and filtered through glass wool in a
measuring cylinder. The gastric contents were

centrifuged at 3000rpm for 5 min, and the
supernatant was used for the estimation of total
acidity (pH). The volume of gastric juice was
expressed as ml/100g of body weight.11
Estimation of total acidity: 1 ml of supernatant
was diluted to 10 ml of distilled water. The
solution was titrated against the 0.05 ml/L NaOH
using phenolphthalein as an indicator. Titration
was continued until the color changed to light
pink. The volume of NaOH required was noted
and was taken as corresponding to the total acidity.
Acidity was expressed as Total acidity = (volume
of NaOH Normality 100)/ 0.1(mEq/L).12

The ulcer score was determined by using a 10
magnifying hand lens. The scoring of severity of
ulceration was as follows: 1 mm (pin point)= 1;
1-2 mm=2; >2 mm=3; >3 mm=4. The mean ulcer
score was determined by dividing the total ulcer
indices in a group by the total number of animals
in that group. Ulcer score = total ulcer index (UI)
in a group/ total number of animals in that group.
The curative ratio of an ulcer was determined by
subtracting the test ulcer score from the control
ulcer score divided by the control ulcer score.
The result was multiplied by 100.13
Statistical analysis: The results obtained were
expressed as MeanSEM and were analyzed by
the application of One-way Analysis of Variance
(ANOVA)
RESULTS
Pylorus ligation method: Extract of Momordica
Dioica (150mg/Kg, 300mg/Kg) treated animals
has shown significant reduction in Ulcer Index,
Volume of Gastric juice (p<0.001), total acid and
free acid (p<0.001) and also it increases the pH
(p<0.001), percentage protection (61.66%) when
compared with the control group. Standard drug
treatment with ranitidine (60mg/Kg) also showed
significant reduction in Ulcer Index, Volume of
Gastric juice, total acid and free acid and also
increases in pH and percentage of protection
(92.37%).
764
Raveendra et al.,
Table 1: Effect of Momordica Dioica on pylorus ligation ulcer model (n=6, MeanSEM)
Grou
p
Treatment
Control-2%
GA
StandardRanitidine
Test-T1extract
Test-T2extract
2
3
4
Dose
Vol. of
gastric juice
Gastric contents (MeanS.E.M)

Total acid
Free acid
pH
Ulcer
index
% of ulcer
protection
2ml/100g
4.700.34
94.333.59
32.331.56
2.030.12
4.33
0%
60mg/kg
2.980.15**
53.334.07
191.36*
4.790.14
0.33
92.37%
**
4.150.27*
79.834.14
27.830.98*
3.460.26
2.8
35.33
632.54**
25.501.89*
3.980.13
1.66
61.66
150mg/kg
300mg/kg
3.180.21**
**
**
P<0.05, **P<0.01, ***P<0.001 compared to Control.
Ibuprofen induced ulcer model: Extract of

Momordica Dioica (150mg/Kg, 300mg/Kg)
treated animals has showed significant reduction
in Ulcer Grades (p<0.001), Ulcer Index (10.66)
with high dose (300mg/Kg) and increase in
percentage of protection (72.09%) when

compared to control group. Standard drug
treatment with ranitidine (60mg/Kg) also showed
significant reduction in Ulcer Index and increase
in percentage of protection (95.65%).
Table: 2. Effect of Momordica Dioica in Ibuprofen induced ulcer model

Groups
Treatment
Dose
Control-2% GA
2ml/100g
2
Standard-ranitidine
60mg/kg
3
Test-T1-extract
150mg/kg
4
Test-T2-extract
300mg/kg
*
**
***
P<0.05, P<0.01, P<0.001 compared to Control.
Ulcer grade
(MeanSEM)
33.333.33
Ulcer index
38.2
% of ulcer
protection
0
1.661.66**
26.662.10*
104.47*
1.66
27.99
10.66
95.65
26.72
72.09
DISCUSSION
In spite of tremendous development in the field
of synthetic drugs during recent era, they are
found to have some or other side effects, whereas
plant products or homeo drugs still hold their
own unique place by the way of having no side
effects. Peptic ulcer disease is a chronic
inflammatory disease characterized by ulceration
in the upper GI.14 The pathophysiology of ulcers
is due to an imbalance between aggressive
factors (acid, pepsin, H.pylori and NSAIDs) and
local mucosal defensive factors (mucous,
bicarbonate, blood flow and prostaglandins). The
integrity of gastro duodenal mucosa is
maintained through a hemostatic balance

between these aggressive and defensive factors.
The major cause of gastric ulcer is the chronic
use of NSAIDs. Therapeutic& adverse effects of
NSAIDs have been attributed to the ability of
these drugs to inhibit the action of
cyclooxygenase (COX). COX is responsible for
the synthesis of prostaglandins that normally
inhibit acid secretion, as well as having a
protective effect on gastric mucosa. Infection of
the stomach mucosa with H.pyloria gram
negative spiral shaped bacterium is now
generally considered as the major cause of gastro
765
Raveendra et al.,
intestinal ulcers. Treatment includes H2-receptor

antagonists (Cimetidine), proton pump inhibitors
(Omeprazole) and cytoprotectives (Misoprostol).
Antacids like Aluminium hydroxide &
magnesium hydroxide are used often to
neutralize excess gastric acidity in the stomach.
Due to problems associated with recurrence after
treatment, there is a need to seek an alternative
drug against gastrointestinal ulcers. 15 The
present investigation demonstrated the efficacy
Momordica Dioica of plant extract against
gastric ulceration induced by two experimental
models viz. Pylorus ligation induced gastric
ulceration and Ibuprofen induced ulceration.
In pylorus ligation model, the plant extract of
Momordica Dioica produces a decrease in the
ulcer number, total gastric volume, total acid,
and free acid and increases the pH and
percentage of ulcer protection (61.66%) and in
standard drug (Ranitidine) treated animals the
percentage of ulcer protection (92.37%) when
compared with control group (0%). High dose of
extract (300mg/Kg) more active than low dose
(150mg/Kg) but less active than standard drug
(Ranitidine).
In Ibuprofen induced ulcer model, the plant
extract of Momordica Dioica produces a
decrease in the ulcer number and increase in
percentage of ulcer protection (72.09%) and with
standard drug the percentage of ulcer protection
(95.65%) when compared to control group (0%).
High dose of extract (300mg/Kg) more active
than low dose (150mg/Kg) but less active than
standard drug (Ranitidine).
The anti ulcer property of Momordica Dioica in
both the experimental models explained above, is
due to presence of flavonoids, terpenoids,
tannins, and triterpenes. The triterpenes are
known as an anti-ulcer agent and their action has
been mentioned to be due to activation of cellular
proteins, reduction of mucosal prostaglandin
metabolism, cytoprotective actions and reduction
of gastric vascular permeability and remaining
compounds have been shown to scavenger free
radicals.16-18 The results in the present study

seem to provide support for the use of
Momordica Dioica as an anti-ulcer drug in folk
medicine. Therefore, also in view of its large use
in India further investigations are needed to
know about its anti-ulcer activity in human
beings.
CONCLUSION
The present study indicates that the plant

Momordica Dioica has potential anti-ulcer
activity against pylorus ligation and Ibuprofen
induced ulcers in experimental animals. So this
activity of plant probably due to the compounds
present such as Flavonoids and triterpenes. So
the plant Momordica Dioica uses for both
Ayurvedic and Modern drug development areas
because of its phyto-medicinal uses but it needs
further clinical trials before complete trust and
usage.
ACKNOWLEDGEMENT
The author Dr. Raveendra Kumar expresses

extreme pleasure and thanks to management of
ASRAM, Eluru for giving the opportunity to do
this research work. And also thanks to co-authors
and technicians for their support throughout this
work.
REFERENCES
1. Colin W. Howden and Richard H Hunt,

James H. Lewis: Peptic Ulcer Disease. A
Pharmacological approach to gastrointestinal
disorders.1994; 1st ed.:3-21
2. Lawrence
and
Bennett:
Clinical
th
Pharmacology. 8 ed. ELBS Publication;
Churchill Livingston; Edinburgh, 1997; 567.
3. Aggarwal KK, Chopra K.L: Peptic ulcer
disease: Changing concepts from pH to HP.
Speciality issue of Ind. J. of Clinical Practice
on Gastroenterology. 1995;9-10.
4. Marshal BJ, Warren JR. Unidentified curved
Bacilli in the stomach of patients with
766
Raveendra et al.,
gastritis
and
peptic
ulcer
Lancet
1984:1(8390):1311-1315.
5. Kumar A, Nirmala V. Gastric anti ulcer
activity of the leaves of Caesalpinia
pulcherrima. Indian J. Pharm.1992;(4)67-68
6. Shreedhara CS, Vaidya VP. Screening of
Momordica dioica for hepatoprotective, antiinflammatory, anti oxidant activities. Natural
product science. 2006; 12(3):157-61
7. Asli Semiz, Alaattin SEN. Antioxidant and
chemoprotective properties of Momordica
charantia L. (bitter melon) fruit extract.
African Journal of Biotechnology. 2007;
6(3): 273-277.
8. Ramesh L Londonkar. Studies on activity on
various extracts of Mentha arvensis Linn.
Against drug induced gastric ulcer in
mammals,
World
J
gastrointestinal
Oncology. 2009; 1(1): 82-88.
9. Hegde DA, Khosa RL, Goel RK. Antiulcer
and cytoprotective action of Wedelia
calendulace Less. Ancient Sci. Life. 1994;
14:7781.
10. Sastri BN. The wealth of India-raw materials.
CSIR, New Delhi.1962;.2:408.
11. Nwinyl FC, Binda L, Ajoku GA. Evaluation
of aqueous extract of Boswollia dalzielii stem
bark for anti microbial activities and
gastrointestinal effects. African J of
Biotechnol.2004;3;284-88
12. Antonial J, Sertie A. Anti ulcer activity of
ethanol extract of Sesbania grandiflora.
Brazilian J Pharm Sci. 2007;37:20-26.
13. Khayaei M, Salehi H, Protective effect of
falcaria vulgaris extract on ethanol induced
gastric ulcer in rats. Iranian J Pharmacol Ther
2006;5:43-46.
14. Cola- Miranda M. Anti-ulcerogenic activity
Indigo for a truxillensis kunth. Biota
neotropico 2006; 6 available from URL:
http:// www.biotaneotropica.org.br
15. Enaganti S. Peptic ulcer disease. Hospital

Pharmacist 2006; 3:16-18.
16. Ashok P, Rajani GP, Sinnathambi A, Hulkoti
B, Desai B, Rajendran R. Studies on corneal
permeation and oculo-hypotensive effect of
benazepril in chronic and acute models of
glaucoma. Iranian J Pharmacol Ther. 2006;
5:141-44.
17. Rajkapoor B, Anandan R, Tayakar B. Antiulcer effect of Nigella sativa Linn. against
gastric ulcers in rats. Cur Sci 2002;(77)82:25
18. Rajkapoor B, Tayakar B, Anandan R,
Murugesh N. Anti-ulcer effect of dried fruits
of Carrica papaya Linn. in rats. Ind. J.
Pharmaceutical Sci. 2003; 52: 122-25.
767
Raveendra et al.,
DOI: 10.5958/j.2319-5886.2.4.123

&
Health Sciences
Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
th
Accepted: 24 Aug 2013
STUDY AMONG BETEL QUID CHEWERS FROM INDIAN POPULATION

*Adhikari Aniket1, De Auley1, Podder Gargi1, De Madhusnata2
1
Research Scholar, 2Professor, Department of Genetics, Ramakrishna Mission Seva Pratishthan,

Vivekananda Institute of Medical Sciences, 99 Sarat Bose Road, Kolkata - 700026
*Corresponding author email: aniket_adhikari@rediffmail.com
ABSTRACT
Background: Oral cancer is most common in males and also in females. Betel quid (BQ) is the main
causative agent of oral cancer. Areca catechu, a major component of BQ, contains certain alkaloids that
give rise to nitrosamines. Mitotic index (MI) and Micronuclei (MN) were studied among the studied
population. Methods: In this present study subjects were screened from Department of E.N.T. &
Department of Oral and Facio maxillary of RKMSP hospital, and different areas of Eastern and North
Eastern states of India. For mitotic index (MI) blood leukocyte cultures were analyzed and for
micronuclei (MN) buccal mucosa were examined. Results: Some of them had more than one addiction.
Micronuclei percentage and mitotic index both higher than normal. Conclusion: Betel quid play a role
in changing the oral pathology and thus causes oral cancer.
Keywords: Oral cancer, betel quid, micronuclei, mitotic index
INTRODUCTION
Oral premalignancies are very common in betel

quid chewers and is the most common cancer
worldwide. 45% and 60% mortality depend upon
the patient group and the disease frequently
associated with tobacco smoking, chewing. Lip,
tongue, palate, gum and cheek these parts of the
oral cavity are effected from tobacco chewing .
Malignancies of the oral cavity arise from the
precancerous lesion such as leukoplakia,
erythroplakia and pre cancerous condition such
as oral submucous fibrosis. Oral squamous cell
carcinoma and the most common oral
premalignancies such as leukoplakia and oral
submucous fibrosis appear to be related to the
habit of betel quid (BQ) chewing in South East
Aniket et al.,
Asia, whereas in Western countries cigarette

smoking and heavy alcohol consumption are the
main causative agents. Areca nut (Areca
catechu), a major component of BQ. Areca nut
contains certain alkaloids that give rise to
nitrosamines, some of which such as Nnitrosoguvacoline,
3-(methylnitrosamino)
propionitrile,
3-methylnitrosamino
propionaldehyde and N-nitrosoguvacine, are
shown to be carcinogenic.1These BQ-specific
nitrosamines may act as an adjunct to tobaccospecific nitrosamines that are strongly implicated
as an etiologic factor for leukoplakia and oral
submucous fibrosis. Metabolic activation of
several nitrosamines was reported to be catalyzed
768
Int J Med Res Health Sci. 2013;2(4): 768- 772
by cytochrome P450 enzymes (CYPs), large

multi-gene family enzymes important in phase I
metabolic activation reactions. Furthermore,
reactive oxygen species are generated in the oral
cavity during BQ chewing due to the addition of
slaked lime [Ca(OH)2] into BQ.2Among
xenobiotic metabolizing enzymes, the CYP2A
family is characteristic of its catalytic properties
to nitrosamines.3 Several workers have
investigated the chemopreventive action of tea
against cancer.4,5,6 Consumption of black tea has
been shown to exert a protective effect against
oral precancerous lesions.7 Epigallocatechin-3gallate (ECG), is one of the major component of
green tea which inhibit cell growth and also
reduce tumor incidence. Since the formation of
micronuclei in the eukaryote cells is an end point
of chromosomal damage or segregation errors.8
The presence of micronuclei reflects a genotoxic
or carcinogenic exposure. Association with
chromosomal aberrations, micronuclei acts as a
good indicator of genotoxic exposure. The assay
is reliable and technically easy to perform. The
present study was carried out by the Department
of Genetic Toxicology, in collaboration with the
Departments of ENT and Oral Maxillofacial
surgery, of the Ramakrishna Mission Seva
Pratishthan (RKMSP) Hospital, Kolkata.
The purpose of this study is to see whether
percentage and chromosomal damage are more
in oral cancer.
PATIENTS AND METHODS
After the Institutional Ethics committee

approval, study was conducted in ENT and Oral
Maxillofacial department of RKMSP Hospital.
Inclusion criteria: Screening of subjects was
carried out in 3 settings:I) Camp in Eastern India: 220 subjects were
screened at a camp held in Bankura, Purba
Midnapur, North West Bengal. Out of them, 133
were betel quid chewers were included in the
study
Aniket et al.,
II). North East camp: 56 subjects were screened

at a camp held in Karimganj, Assam. Out of
them, 33 were betel quid chewers.
III) RKMSP Hospital: 35 subjects were screened
out of them 24 cases were betel quid chewers.
Out of 24, 7 subjects had pre cancerous lesion, 6
subjects had squamous cell carcinoma, 11
subjects had pre cancerous condition.
Total 311 subjects were screened from different
areas of Eastern India, North East India and
E.N.T and Oral Maxillofacial OPD of RKMSP
hospital. Among them total 190 subjects included
for study who were betel quid chewers, from
each person conform consent was taken.
Exclusion criteria: The subjects who had no
betel quid chewing habit. The subjects who had
betel quid chewing habit and any type of
precancerous lesion, precancerous condition
related with betel quid was included in this study.
Screening of subjects was carried out by
administering questionnaires.
Methods: Detailed history was taken from all
cases by filling up questionnaire.
Parameters studied:
Leukocyte culture,
Micronuclei (MN) study
Leukocyte culture: - Peripheral blood was
collected from all subjects. Human leucocyte
culture was carried out by the method of
Moorhead PS et al 9 modified by the method of
Sharma and Talukder.10 A total of 4 ml of
peripheral venous blood was collected from each
patient under aseptic condition with the help of a
sterile disposable needle and transferred to a
heparinized vial. Leucocyte rich plasma (0.5 ml)
was added to a 5 ml of culture media (RPMI
1640, Sigma, St. Louis, USA) supplemented with
20 % foetal bovine serum (Sigma) and
Phytohaemagglutinin M (0.04 ml / ml of culture
media, GIBCO BRL). The cultures were
incubated at 37o C. After 70 hours incubation,
colchicines (0.2 ml of 0.04% / ml) was added.
Two hours later, cells were centrifuged at 1000
rpm for 5 min, treated with prewarmed KCL
(0.075M) for 15 min, centrifuged at 1000 rpm for
5 min, and fixed in methanol: acetic acid (3:1).
769
Fixed cell suspension was taken on clean grease

free glass slide and air dried. The preparation
was stained with aqueous Giemsa. All slides
were coded and 1000 blast cells were scored to
determine mitotic index per individual.
Micronuclei (MN) study: - For Micronuclei
study Premoistened wooden spatula was used to
sample cells from the oral mucosa. The spatula
was applied to a precleaned microscope slide.

After air dried the smear fixation was done by
methanol. Slides were stained by the Giemsa
solution and the MN frequency was scored using
the criteria described by Sarto et al.11 The same
person scored 1000 cells blindly in each case to
determine the MN Percentage.
RESULTS
Table 1: Detailed history of subjects of different areas
31-40
41-50
51-60
61-70
Above 70
Smoking
Alcohol
Betel Quid
No BQ Addiction
Tea Drinker
Non Tea Drinker
Addiction
Below 30
AGE GROUP
( in years)
56
12
24
11
33
23
40
16
34
20
16
14
19
15
34
East Midnapur,
Bibhisanpur
North, Atghara
46
22
13
28
29
36
10
40
89
28
18
21
15
27
56
33
73
16
Narrah, Bankura
51
13
12
14
22
29
49
RKMSP hospital
35
11
20
24
11
29
TOTAL
311
66
73
64
65
32
11
114
65
190
121
265
46
PLACE
NO
North East camp

(Assam, Karimganj)
Eastern India camp
1) Bankura,Dhulai
Table 2: Micronuclei and Mitotic Index of betel quell chewers.
PLACE
Micronuclei (%)
Mitotic Index
(Mean SE)
(Mean SE)
Dhulai, Bankura
26.29 1.95
3.94 0.23
Bibisanpur, East Midnapore
12. 31 2.75
8.66 0.67
Atghara
4.76 1.26
5.07 0.60
RKMSP Hospital
----- *
4.54 0.33
Narrah, Bankura
4.61 2.82
4.28 0.62
(Normal values of MI are < 4% and MN is < 1%)
*Study of micronuclei of oral cancer cases was not possible due to severe ulceration and bleeding and
cases were unable to open their mouth. Mean value of mitotic index of all cases having betel quid
chewing habit was 5.29 0.49 and mean percentage of micronuclei were 12 2.19
Aniket et al.,
770
Total 311 subjects studied (Table 1), out of

which 56 subjects from North East camp
(Karimganj, Assam), 220 subjects from East
India and 35 subjects from RKMSP hospital. Out
of 56 subjects from North East 58.92% were
betel quid chewers and 71.42% were tea drinker.
They took betel quid more than once. Out of 33
betel quid chewers, 6 cases took betel quid
occasionally, rest of them took BQ 3-4
times/day. Out of 34 subjects from Dhulai,
Bankura, 55.88% were betel quid chewers and all
of them were tea drinker. Out of 19 betel quid
chewers, 13 cases took betel quid occasionally,
rest of them took BQ 2-5 times/day. Out of 46
subjects from East Midnapore 78.26% were betel
quid chewers and 86.95% were tea drinker. Out
of 36 betel quid chewers, 5 cases took betel quid
occasionally, rest of them took BQ 7-16
times/day. Out of 89 subjects from North 24 Pgs
62.92% were betel quid chewers and 82.02%
were tea drinker. Out of 56 betel quid chewers,
19 cases took betel quid occasionally, rest of
them took BQ 6 -10 times/day. Out of 35
subjects from RKMSP hospitals 68.57% were
betel quid chewers and 82.85%were tea drinker.
Out of 24 betel quid chewers, 12 subjects took
betel quid occasionally, rest of them took BQ 4-9
times/ day.
90% subjects were coming from rural areas at
Karimganj. All subjects were from Dhulai,
Bibhisanpur, Narrah, Atghara under rural areas.
10% subjects were coming from rural areas of
RKMSP Hospital and rests on them were from
urban areas.
Mean value of mitotic index (MI) of all cases
having betel quid chewing habit was 5.29 0.49
and mean percentage of micronuclei (MN) were
12 2.19 (Table 2)
countries. 12 In another study the prevalence of

head and neck cancers was found to be
significantly high at 54.48% in the population of
North Eastern India. Gurkha and pan masala has
been shown to be carcinogenic in experimental
animals, causing tumors in various organs. No
effective techniques have yet been developed for
making direct chromosome preparation from
epithelial tissues. They concluded that the
gradual increase in Clinical chemoprevention
trials on oral pre-malignancies have used MN in
oral mucosa as a surrogate endpoint of cancer
.13These findings clearly suggest a causal link
between MN and cancer.Micronuclei are the
small extra nuclei cells which is formed in
metaphase and anaphase stage. The presence of
micronuclei
reflects
a
genotoxic
and
carcinogenic exposure since it is associated with
chromosome aberrations.14 Micronuclei have
been used as an important marker. In our study
we have seen that mitotic index of all subjects
having betel quid chewing habit and mean
percentage of micronuclei were higher than
normal. Normal values of MI are < 4% and MN
is < 1%.
M. Sulkowska,15 observed that mitotic index
count was high in oral squamous cell carcinoma
cases. Mitotic activity has proven to be an
efficient prognostic indicator of squamous cell
carcinoma of various sites.
DISCUSSION
ACKNOWLEDGEMENTS
According to World Health Organisation (WHO)

data, the standardized mortality rate for 2002 was
2.2 deaths per 100,000 populations. Oral cancer
is one of the leading cancers in most Asian
The authors are thankful to the Secretary,

Ramakrishna Mission Seva Pratishthan, for kind
permission to use the laboratory for this work.
The authors are also thankful to the National Tea
Aniket et al.,
CONCLUSION
Betel quid has an immense role in changing the

oral pathology and developing oral cancer. In
this present study it has been found that the
micronuclei percentage can be used as a
biomarker. The Micronuclei percentage and
mitotic were higher than normal.
771
Research Foundation, India for financial support

of this work.
REFERENCES
1. Hoffmann D, Brunnemann KD, Prokopczyk

B, Djordjevic MV. Tobacco-specific Nnitrosamines
and
Areca-derived
Nnitrosamines:
chemistry,
biochemistry,
carcinogenicity, and relevance to humans. J.
Toxicol Environ Health .1994; 41:1-52.
2. Nair U J, Nair J, Mathew B , Bartsch H.
Glutathione S-transferase M1 and T1 null
genotypes as risk factors for oral leukoplakia
in ethnic Indian betel quid/tobacco chewers.
Carcinogenesis .1999; 20:74348.
3. Fujita K, Kamataki T. Role of human
cytochrome P450 (CYP) in the metabolic
activation
of
N-alkylnitrosamines:
Application of genetically engineered
Salmonella typhimurium YG7108 expressing
each form of CYP together with human
NADPH-cytochrome P450 reductase. Mutat
Res. 2001; 483:3541.
4. Lambert
JD,
Yang
CS
.Cancer
chemopreventive activity and bioavailability
of tea and tea polyphenols. Mutat Res. 2003;
523-524: 201-8.
5. Talukder G, Sharma A .Tea as a protectant in
human cancer. National Tea Research
Foundation. Special Issue. 2004.
6. Mukherjee P, Podder S, Talukder G, Sharma
A .Protection of black tea extract against
chromosome damage induced by two heavy
metals in mice. Pharmaceutical biology.
1999; 37: 243- 7.
7. Halder A, Roychowdhury R, Ghosh AK, De
M. Black Tea (Camellia sinensis) as a
Chemo preventive agent in oral precancerous
lesions. Journal of Environmental Pathology,
Toxicology and Oncology, USA. 2005;
24(2):103- 6.
8. Geard CR, Chen CY. Micronuclei and
clonogenecity following low and high dose
Aniket et al.,
rate -irradiation of normal human fibroblasts.

Radiat Res .1990; 124: 856-61.
9. Moorhead PS, Nowell PC, Mellman WJ,
Battips DM, Hungerford DA. Chromosome
preparation of leucocyte culture from human
peripheral blood. Exper Cell Res.1960; 20:
613 -6.
10. Sharma A, Talukder G. Chromosome
methodology .Lab Procedures Hum Genet.
1974; 61- 75.
11. Sarto F, Tomanin R, Giacomelli L, Canova
A, Raimondi F, Guiotto C, Fiorentino MV.
Evaluation of chromosomal aberrations in
lymphocytes
and
micronuclei
in
lymphocytes, oral mucosa and hair root cells
of patients. Mutat Res.1990; 228: 157-69.
12. Lin Sc, Chen YJ, Kao SY, Hsu MT, Lin CH,
Yang SC, et al. Chromosomal changes in
betel associated oral squamous cell
carcinoma and their relationship to clinical
parameters . Oral Oncol. 2002; 38: 266 -73.
13. Fenech M. Nutritional treatment of genome
instability: a paradigm shift in disease
prevention and in the setting of
recommended dietary allowances. Nutrition
Res
Rev.2003; 16:109 22.
14. Roberts DM .Comparative cytology of the
oral cavities of Snuff users. Acta Cytol.
1997; 41:1008 -014.
15. Mariola Sulkowska, Waldemar Famulski,
Stanislaw Sulkowski, Joanna Reszed,
Maruisz Koda, Marek Baltaziak, et al .
Correlation between Bcl -2 protein
expression and some clinico pathological
features of oral squamous cell carcinoma.Pol
J Pathol. 2003; 54(1):49 -52.
772
DOI: 10.5958/j.2319-5886.2.4.124

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Research article
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STUDY OF PALMAR DERMATOGLYPHICS IN PATIENTS

HYPERTENSION BETWEEN THE AGE GROUP OF 20-50 YEARS
WITH
ESSENTIAL
Rudragouda S Bulagouda1, Purnima J Patil2, *Gavishiddppa A Hadimani3, Balappa M Bannur4, Patil

BG5, Nagaraj S. Mallashetty6, Ishwar B Bagoji3
1
Asso. Prof Dept, 2Undergraduate Student, 3Lecturer, 4Professor & HOD, 5Professor, 6Post Graduate
Student, Dept. of Anatomy, Shri B M Patil Medical College Hospital and Research Centre BLDE
University Bijapur, Karnataka India
*Corresponding author email: gavish.hadimani@yahoo.com
ABSTRACT
Background: In present study, we tried to determine significant palmar dermatoglyphic parameters in

case of essential hypertensives in age group between 20-50 years and whether the parameters can be
used for screening purpose i.e., early detection of hypertension. Method: With the use of modified
Purvis Smith method, Black duplicating ink (Kores, Bombay) was smeared on both hands one by one
and prints will be taken by rolling the hands from wrist creases to finger tips on the roller covered
with bond paper. While crystal bond paper, applied firmly over a wooden pad, was used for recording
the inked epidermal ridge patterns. Rolled finger prints were recorded after applying uniform
pressure on white bond paper from ulnar to radial side. Complete palm impression, including the
hollow or the palm was obtained over paper. Thus one set of finger prints and palm prints was
obtained. The prints obtained were immediately examined with hand-lens. Result: Right hand and left
hand of the both male and female study group showed more number of arches than controls. Right
hand and left hand of the both male and female study group showed more number of Radial loops than
controls. The right hand and left hand of both male and female control group showed more number of
ulnar loops than study group. The right hand and left hand of the male control group showed more
number of Whorls than study, while in females, the right hand study group showed more number of
whorls than control group and the left hand study group showed less number of Whorls as
compared to control group. Conclusion: The present study indicates that there are some genetic factors
which are involved in the causation of essential hypertension and it is possible to certain extent to
predict from dermatoglyphics individuals chance of acquiring essential hypertension. Like clinical
history, examination and investigations, the dermatoglyphics will play an important role revealing the
genetic susceptibility to essential hypertension.
Keywords: Palmar Dermatoglyphics, Essential Hypertension, Arches, Loops, Whorls
773
Rudragouda et al.,
INTRODUCTION
MATERIALS & METHODS
The term Dermatoglyphics [from the Greek,

Derma = skin, glyphic = carvings] is the
scientific term coined by Prof. Harold
Cummins. The analysis of dermal ridges and
their configurations by studying prints of them
is called Dermatoglyphics1. The term is also
used as a collective name for all the features of
ridged skin. The skin patterns are studied from
prints or impressions2. In ancient India,
palmistry, an art of fortune telling by reading
the pattern of friction ridges and palmar lines,
dates
from
about
2000
B.C.3.
Dermatoglyphics has been studied extensively
in chromosomal disorders, single gene disorders
and those disorders whose genetic basis is not
clear.
Amidst oceans of causes of human suffering,
hypertension the silent killer of mankind is a
public health problem. If untreated, it produces
a lot of complications like heart attack, heart
failure, stroke and kidney diseases. The
prevalence of hypertension is 59.9 and 69.9 per
1000 in males and females blood pressure in
hypertensives even by 2mm can reduce the
overall mortality by 3%4.Twin studies have
shown that genetic factors play an important
role in the pathogenesis of essential
hypertension5. By analyzing various parameters
of dermatoglyphics in the palms and fingers, it
is aimed to prevent the ill effects of the disease
by modifying the risk factors. Dermatoglyphics
helps in the early detection of cases of
essential hypertension6. There is a steady
increase in hypertension prevalence over the
last 50 years, more in urban than in rural areas.
It is well recognized that hypertension is now a
major health problem in India7. The relevance
of dermatoglyphics is not to diagnose, but to
prevent by predicting a disease; not for defining
an existing disease, but to identify people with
the genetic predisposition to develop certain
diseases.
The study was carried for a period of 3

months from July 2011 to September 2011,
with diagnosed Essential hypertensive patients
attending out-patient and in-patient, medicine
department, BLDE Universitys, Shri B. M.
Patil medical college, Hospital and Research
Centre, Bijapur were selected. 100 patients [50
Males and 50 Females] between the age group
of 20-50 years were taken up for the study
and 100 healthy people of same age group
included both sexes as control. Informed
consent was taken from individual persons and
the study was approved by Institutional Ethics
Committee of Shri B M Patil Medical College.
Inclusion criteria: Clinically diagnosed cases of
essential hypertension
Exclusion criteria:
1. Any deformities of fingers and palm and
Infected hand
2. Diseases causing secondary hypertension
3. Chromosomal
abnormalities
like
Klinefelters
syndrome,
Turners
syndrome etc.
4. Deep burns of fingers and palms leading
to scars.
Material used: wooden table of suitable
height, kores duplicating ink, roller, white
crystal bond paper, magnifying lens, soap,
needle, scale, water and towel.
Method: The modified Purvis Smith method
was applied. Patients were asked to wash both
their hands with soap and water so as to
remove any oil or dirt. Black duplicating ink
(Kores, Bombay) was smeared on both hands
one by one and prints will be taken by rolling
the hands from wrist creases to finger tips on the
roller covered with bond paper8,9.
Fingerprints: The distal phalanges of persons
right hand were inked over the tile by firm
pressure on the dorsum, starting from little
finger. The distal phalanges of left hand were
similarly inked10.
While crystal bond paper, applied firmly over a
wooden pad, was used for recording the inked
epidermal ridge patterns. Rolled finger prints
774
Rudragouda et al.,
were recorded after applying uniform pressure

on white bond paper from ulnar to radial side.
Palm Print: Palm prints of both hands were
obtained after inking them with help of rubber
roller. A white crystal bond paper was wrapped
around a wooden rod placed on the table. The
hand was horizontally placed against it and the
rod was gradually rolled on the table. Complete
palm impression, including the hollow or the
palm was obtained over paper. Thus one set of
finger prints and palm prints was obtained. The
prints obtained were immediately examined with
hand-lens and care was taken to include all
essential details. Dermatoglyphics of sole and
toes were not recorded (fig 1).
The study included both qualitative and
quantitative tests. Qualitative study includes
finger print patterns (whorls, radial loop, arches,
and ulnar loop) and in the palm includes simian
line and Sydney line. Quantitative study
includes Total Finger Ridge Count, Absolute
Finger Ridge Count and atd angle. To analyze
finger pattern frequency, the fingertip pattern
configurations were classified as arches (A),
Fig.1: Procedure of finger and Palm prints
loops (L), whorls W). The arches were

further recorded as simple (A), or tented (At)
arches depending upon the presence or absence
of a triradius. For statistical purpose, both were
grouped together as arches only. Statistical
calculations were done by arithmetic mean and
standard deviation, Z test and Chi-square test
applied wherever necessary.
OBSERVATION
Development of dermatoglyphic pattern is

under genetic control. Hence qualitative and
quantitative study of dermatoglyphic traits may
give us a clue to the susceptibility of essential
hypertension.
The Quantitative Analysis includes: The
Total Finger Ridge Count (TFRC), Absolute
Finger Ridge Count (AFRC) and atd Angle
(fig 2)
The Qualitative Analysis includes: Analysis
fingertip patterns of Right hand and left hand
separately, right hand and left hand combined
and abnormal palmar creases Sydney line (Sy
line) and simian line(Sm line).
Fig.2: Atd angle measurement
775
Rudragouda et al.,
Table 1: Digit wise frequency of pattern
Male
Female
Study Group
Control Group
Study Group Control Group
Right
Left
Right
Left
Right Left Right Left
Hand
Hand
Hand
Hand
Hand Hand Hand Hand
25
18
04
07
22
19
0
4
Arch
26
30
11
21
31
32
23
21
LoopRadial
115
116
131
120
100
113
129
118
Loop Ulnar
84
86
104
102
97
86
88
112
Whorl
Simian Line absent in right and left hands of both male & female hypertensive individuals
Table 2: Presence of Sydney Line in Right Hand
Male
Female
Study Group Control Study Group Control

Present
Right Hand Absent
Present
Left Hand Absent
14
36
15
35
0
50
0
50
22
28
14
36
0
50
0
50
Table 3: Total finger ridge count (MeanSEM)
Study Group (Hypertensive)
Control (Normal)
Inference
80.3 1.4*
84.7 1.6
84.3 1.4
83.8 1.2
Significant
Not significant
Male
Female
*P<0.05 compared to control group
Table 4: Absolute finger ridge count (Mean S.D)
Study Group
Male
Female
103.9 14
112.6 18.4
Control
109.9 18
110 14.6
t testP value Inference

1.85 0.067 not significant
Table 5: atd Angle (Mean S.D)

Study Group
Control
39.45 7.18
Right Hand 40.76 5.77
41.91 6.38
Left Hand 41.87 5.54
Male
42.84 4.92
Right Hand 41.03 8.59
39.34 6.5
Female Left Hand 39.31 6.52
On statistical analysis atd angle was not significant in both the
control group.
DISCUSSION
Hypertension the silent killer of mankind is a

public health problem. If untreated, it produces a
lot of complications like heart attack, heart
failure, stroke and kidney diseases. The
prevalence of hypertension is 59.9 and 69.9 per
t
p
Inference
hands of male and female study and
1000 in males and females blood pressure in

hypertensives even by 2mm can reduce the
overall mortality by 3%4. The relevance of
dermatoglyphics is not to diagnose, but to
prevent by predicting a disease; not for defining
an existing disease, but to identify people with
genetic predisposition to develop certain
776
Rudragouda et al.,
diseases. There are various studies mentioned

about the dermatoglyphic pattern in various
diseases like pulmonary tuberculosis, Diabetes
Mellitus Type II Essential Hypertension,
Eczema, psoriasis and alopecia areata and even
in healthy Indian children11-14. Present study is
compared with a study by K M Godfrey15.
In present study, we tried to determine
significant palmar dermatoglyphic parameters in
case of essential hypertensives in age group
between 20-50 years and whether the
parameters can be used for screening purpose
i.e., early detection of hypertension.
Qualitative Analysis
Arches: Right hand and left hand of the both
male and female study group showed more
number of arches than controls. K M Godfrey
studied dermatoglyphics of hypertensive
patients and found that arches were least
common in the study group15.
Radial loops: Right hand and left hand of the
both male and female study group showed more
number of Radial loops than controls. K M
Godfrey
studied
dermatoglyphics
of
hypertensive patients and found that loops in
general i.e., both radial and ulnar loops were
most common in the study group15.
Ulnar loops: The right hand and left hand of
both male and female control group showed
more number of ulnar loops than study group. K
M Godfrey studied dermatoglyphics of
hypertensive patients and found that loops in
general i.e., both radial and ulnar loops were
most common in the study group15.
Whorls: The right hand and left hand of the
male control group showed more number of
Whorls than study, while in females, the right
hand study group showed more number of
whorls than control group and the left hand
study group showed less number of Whorls as
compared to control group. On study of K M
Godfrey on dermatoglyphics of hypertensive
patients found that whorls were second most
common in the study group.
Sydney Line: 14 cases had Sydney line in male
and 22 in female study group. All the cases in
control had sydney line. There is no study of

sydney line in the available literature.
Simian Line:
No cases in study as well as
control group had simian line. There is no study
of simian line in the available literature.
II) Quantitative Analysis:
Mean The Total Finger Ridge Count (TFRC):
The Mean the Total Finger Ridge Count

(TFRC) in Male patients was lesser 80.3 with
S.D. of 10.1 as compared to male control group
which had TFRC 84.3 with S.D. of 10.0 This
difference was statistically significant (P=.05).
The Mean Total Finger Ridge Count (TFRC) in
female patients was higher 84.70 with S.D. of
11.6 as compared to female control group which
had TFRC 83.38 with S.D. of 8.64. This
difference was statistically not significant
(P=0.515).
Mean Absolute Finger Ridge Count (AFRC):
The Mean Absolute Finger Ridge Count (AFRC)
in Male patients was lesser 103.9 with S.D. of 14
as compared to male control group which had
AFRC 109.9 with S.D. of 18. This difference
was statistically not significant (P=0.067). The
Mean Absolute Finger Ridge Count (AFRC) in
female patients was higher 112.6 with S.D. of
18.4 as compared to female control group which
had AFRC 110 with S.D of 14.6. This difference
was statistically not significant (P=0.443).
Mean atd Angle: The Mean atd angle in
right hand of male patients (40.76) was more
than that of controls (39.45). It was less in left
hand of patients (41. 87) than that of controls
(41.97). This difference was not statistically
significant. The Mean atd angle in right hand
of female patients (41.3) was lesser than that of
controls (42.84). Similarly it was less in left
hand of patients (39.31) than that of controls
(39.34). This difference was statistically not
significant.
K
M
Godfrey
studied
dermatoglyphics of hypertensive patients and
found that the mean palmar atd angle was 41.7
(5.5) degrees6.
777
Rudragouda et al.,
CONCLUSION
In present study, we tried to determine

significance
of
palmar
dermatoglyphic
parameters in case of essential hypertension in
age group between 20-50 years and whether
these parameters can be used for screening
purpose i.e. to identify people with genetic
predisposition
to
develop
to
essential
hypertension. The analysis revealed the
following findings:
Significant findings in qualitative and
quantitative analysis of both sexes of essential
hypertension in age group between 20-50 years
were: the Mean Total Finger Ridge Count
(AFRC) in study group of males was lesser when
compared to control group.
The present study indicates that there are some
genetic factors which are involved in the
causation of essential hypertension and it is
possible to certain extent to predict from
dermatoglyphics individuals chance of acquiring
essential hypertension. Like clinical history,
examination
and
investigations,
the
dermatoglyphics will play an important role
revealing the genetic susceptibility to essential
hypertension.
At present there
are
very few studies on
palmar dermatoglyphics
in essential
hypertension. The findings of previous studies
are many ways similar to our present study. But
still the number of studies is limited. Since this is
an interesting subject, more number of studies is
expected. This was a small study consisting of
100 patients. Hence its findings cant be
generalized. So further large case controls are
needed to establish the exact relation between
essential hypertension and dermatoglyphics and
utility of dermatoglyphics in prediction of
susceptibility to essential hypertension.
ACKNOWLEDGEMENT
Authors are thankful to ICMR for selecting

this project for short term studentship (ICMRSTS-2011 Reg. no. 201102292) project and for
funding. Authors are also thankful to Principal

and Anatomy department staff of Shri B M Patil
Medical College Hospital and Research centre
BLDE University for kind support.
REFERENCES
1. Bannister LH, Berry MM, Collins P,

Dyson M, Dussek JE, Ferguson MWJ.
Gray's Anatomy. Integumental system.38th
ed. NewYork: Churchill Livingstone;
2000.p.380.
2. Holt SB. Significance of dermatoglyphics
in
medicine.
Clinical
pediatrics
1973;12(8):471-83.
3. Saha KC. Dermatoglyphics. Indian Med
Associ 1970; 54: 428.
4. Park K. Hypertensive. Parks Textbook of
Preventive and Social Medicine. 18th Ed.
Banarsidas Bhanot; 2005; 295.
5. Chobanian VA, Bakris GL, Black HR,
Cushman WC, Green LA, Izzo JL.
Hypertension. American Heart Association
2003; 42; 1206.
6. Godfrey KM, Barker DJP, Peace J, Cloke J,
Osmond C. Relation of fingerprints and
shape of the palm to fetal growth and adult
blood pressure. British Medical Journal
1993; 307: 405-09.
7. History of dermatologlyphics. Available from
url:
http//www.handanalysis.net/library/
derm_ history. htm accessed on 2005 June
28.
8. Schaumann B, Alter M. Dermatoglyphics in
medical disorders. New York: Springer
Verlag; 1976.p.1-129.
9. William JB. Embryonic development of
epidermal ridges and their ConfigurationsBirth defects: Original Article Series 1991;
27:95-112.
10. Schaumann B, Alter M. Dermatoglyphics in
medical disorders. New York:Springer
Verlag;1976.p.1-129.
11. Desai SD, Hadimani GA. Dermatoglyphics
and Health Anatomica Karnataka; 2013: 7(1),
778
Rudragouda et al.,
01-09
12. Kumar S, Kumar N, Mangal BD.
Dermatoglyphics in healthy Indian children:
An analysis of finger prints, palm prints,
axial triradii, and atd angle, sole and toe
prints. Indian J Pediatric 1974; 41:249-56.
13. Babu SS, Powar BP, Khare ON, Palmar
Dermatoglyphics in Pulmonary Tuberculosis.
J. Anat Soc.India 2005; 54:64-6.
14. Pour Jafari H, Farhed DD, Yazdani A, Hashe
Mzadeh CM. Dermatoglyphics in patients
with eczema, psoriasis and alopecia areata.
Skin Res Technol 2003; 9:240-44.
15. Oladipo GS, Osogba IG, Bobmanuel I,
Ugboma HAA, Sapira MK, Ekeke ON.
Palmar Dermatoglyphics in Essential
Hypertension Amongst Rivers Indigenes.
Australian J of Basic and Applied Sci.
2010;4(12): 6300-05
779
Rudragouda et al.,
DOI: 10.5958/j.2319-5886.2.4.125

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Health Sciences
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Coden: IJMRHS
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Received: 1 Aug 2013
Research article
Copyright @2013
ISSN: 2319-5886
Accepted: 1st Sep 2013
A STUDY OF MORPHOLOGY OF VERMIFROM APPENDIX IN 200 CASES

Chaudhari Manisha L1, Kapadia Divyesh M2, *Kanani Sanjay D3, Patel Jitendra P4, Shah Ritesh K5,
Nirvan Ashok B6
1
Assistant Professor, Department of Anatomy, Gujarat Adani Institute of Medical Sciences, Bhuj, Gujarat
Assistant Professor, 4Associate Professor, Department of Anatomy, Smt.N.H.L.Municipal Medical College,
Ellisbridge, Ahmedabad, Gujarat, India
3
Tutor, Department of Anatomy, GCS Medical College, Naroda road, Ahmedabad, Gujarat, India
5
Assistant Professor, Department of Anatomy, GCS Medical College, Naroda road, Ahmedabad, Gujarat
6
Associate Professor, Department of Anatomy, B.J.Medical College, Asarwa, Ahmedabad, Gujarat
2
* Corresponding author email: drsanjaykanani@gmail.com

ABSTRACT
Aims: To study the various positions of vermiform appendix, and its relation to various diseases of the
vermiform appendix, and average length and external diameter of the vermiform appendix.
Materials & Methods: This study was conducted on 200 cases 100 cadavers from the dissection
laboratory with an age range of 50 90 years. The dissection was performed in the dissection hall of Smt.
N.H.L. Municipal Medical College, Ahmedabad, B. J. Medical College, Ahmedabad, A.M.C.M.E.T.
Medical College, Ahmedabad, and 100 cases from postmortum room of V. S. Hospital from August 2009 to
December 2012. Result and Observation: classic coeliac trunk with emission of the left gastric, splenic and
hepatic arteries was found in 76(76 %) cadavers. Haller's tripod, in which the three arteries originated at the
same level and in the terminal portion of the coeliac trunk was observed in 18(18%) cadavers. In 16 cadavers
inferior phrenic arteries originated from coeliac trunk was observed. In 8 cadavers variations regarding
disposition of the left gastric, splenic and hepatic arteries also regarding the number of emitted arteries
observed. Conclusion: Appendix is only organ in our body which has not constant anatomical position.
From various positions of vermiform appendix we can understand the possible outcome of the appendicitis
specifically location of site of pain.
Key words: Appendix, Position, Length, Diameter

INTRODUCTION
The Appendix is a narrow worm like structure

present in the right iliac fossa, arising from the
posteromedial wall of the caecum about 2 cms
below the ileo-caecal junction and has no
constant anatomical position. The length of

appendix varies from 2 to 20 cms with an
average 2 of 9 cms. A variation in the position of
the appendix, along with the degree of
780
Manisha et al.,
inflammation makes the Clinical presentation of

appendicitis
notoriously
inconsistent.
Misdiagnosis in different age groups is from 10
to 33%1. The attachment of the base of appendix
remains fairly constant, but the tip can be found
anywhere in Retrocaecal, Pelvic, Subcaecal, Para
caecal, Post ileal and Preilea positions.
Appendicitis in different positions may mimic
other diseases in retrocolic colitis, Post ileal
ureteric colic, Pelvic inflammatory disease2,
Torsion of ovarian cyst & Ruptured tubal
gestation, Sub hepatic hepatitis, biliary colic3.
The only invariable feature is its origin from the
caecum at the site of coalescence of all three
taenia coli4. Though considered by most to be a
vestigial organ, its importance in surgery is
mainly due to its propensity for inflammation
that results in the clinical syndrome known as
acute appendicitis, and is the most common
cause of acute abdomen in young adolescents3.
MATERIALS AND METHOD
Material: This study was conducted on total 200

cases, 100 cases taken from dissection laboratory
of the anatomy department, Smt. N.H.L.
Municipal Medical College, Ahmedabad, B. J.
Medical
College,
Ahmedabad,
and
A.M.C.M.E.T. Medical College, Ahmedabad
with an age range of 50-90 years of both sexes.
The cadavers were embalmed through the carotid
and femoral arterial perfusion of formaldehyde
solution, spirit, water and glycerine and
preserved in a weak formalin solution before
dissection, and remaining 100 cases are taken
from postmortem room of Sheth V. S. Hospital

from August 2009 to December 2012.
Method: Length of vermiform appendix was
measured by nylon thread from root to tip of
appendix. Threads length was measured by
vernier caliper. External diameter was measured
by vernier caliper at a maximum external
diameter of the appendix. Dissection done
according to cunninghams manual of practical
anatomy.
RESULTS
Keeping in view the aim of the study mentioned

earlier, following observations were recorded: In
the present study the total number of cases was
200 (136 Males and 64 Females). Table.1 shows
the position of vermiform appendix in present
study (Figure.1 Retrocoecal position, Figure.2
Pelvic position, Figure.3 Post ileal position,
Figure.4 Subcoecal position, Figure.5
Paracoecal position, Figure.6 Subhepatic
position). In present study most common position
in male and female was retrocaecal founded in
75 cases (55.14%) and 36 cases (56.25%)
respectively; and least common position in male
was subhepatic founded in 01 case (0.007 %) and
in female was paracaecal founded in 03 cases
(0.04%). No case of preileal and promontory
position was found.
Table.2 shows the calculation of external
diameter and length of vermiform appendix in
present study. In present study the average length
of vermiform appendix was 5.436 cm in 200
cases and average external diameter was
7.0450cm in 200 cases.
Table 1: Position of vermiform appendix
Serial number
1
2
3
4
5
6
Total
Position
Retrocaecal
Pelvic
Postileal
Subcaecal
Paracaecal
Subhepatic
Male
75
32
14
07
07
01
136
Female
36
15
04
06
03
00
64
Total
111
047
018
013
010
001
200
Percentage
55.5 %
23.5 %
9%
6.5 %
5%
0.5 %
100 %
781
Manisha et al.,
Table 2: Calculation of external diameter and length of vermiform appendix
MALE
External
Diameter (mm)
15
3
7.3014
7
2.8029
Maximum
Minimum
Mean
Median
SD
FEMALE
Length
(Cm)
9
2
5.5647
5.6
1.3348
External
Diameter (mm)
14
4
6.5000
6
2.2253
Length
(Cm)
7
2.4
5.1625
5.4
1.1086
Table 3: Comparison of different positions of the vermiform appendix of present study with other studies
Author
No.of
Retro- Pelvic
specimen caecal
125
38.4% 31.2%
Solanke TF8
Postileal Preileal Subcaecal

12%
4%
11.2%
Paracaecal
2.4%
Subhepatic
-
Varshney S et 600
al.9
Golalipour MJ2 117
19%
53%
1%
2%
7%
18%
32.4%
33.3%
2.6%
18.8%
12.8%
Cecil P G10
65.28% 31.1%
0.40%
1.00%
2.26%
67.3%
21.6%
3.8%
4.9%
2.4%
62%
31%
0.4%
11%
2%
74%
21%
0.5%
1%
1.5%
2%
55.5%
23.5%
9%
6.5%
5.0%
0.5%
10,000
Clegg Lamptey 1358

JNA et al11
Shah& Shah12
591
Bailey Love
13
In Present Study 200
0.5%
Table 4: Comparison of length of the vermiform appendix of present study with other studies
Year
Author
Shortest
Centimeters
Longest
Centimeters
Mean
Length (cm)
Mean External
Diameter (mm)
1891
1895
1913
1918
1923
Ferguson14
Berry15
Deaver16
Lewis17
Arthur
Robinson18
2.2
3.1
1.0
2.0
1.8
13.3
23
20
23
10.13
8.3
8-9
8.3
9.2
8
3-5
1927
1932
Royster19
2.5
Donald C. Collins20
29.4
24.5
7.5
8.2
2012
Present
Study
5.436
7.035
782
Manisha et al.,
Fig 1: Retrocaecal Position of Appendix (1appendix, 2-caecum, 3-ileum)
Fig 4: Subcaecal position of appendix (1-caecum,

2-appendix)
Fig 2: Pelvic position of appendix (1-appendix, 2caecum, 3-ileum)
Fig 5: Paracaecal position of appendix (1-caecum,

2-appendix)
Fig 3: Post-ileal position of appendix (1-appendix,

2-ileum, 3-caecum)
Fig 6: Subhepatic position of appendix (1-liver, 2bile, 3-appendix, 4-caecum )
DISCUSSION
The ultimate position of the appendix is

profoundly influenced by the changes in the
position and shape which the caecum undergoes
during development
and
growth. The
primordium of cecum and vermiform appendix
i.e. caecal diverticulum appears in the 6th week
as a swelling on the antimesentric border of the
caudal limb of the midgut loop. After the

completion of the gut rotation, the caecal
diverticulum occupies a position on the right side
of the abdominal cavity5.
Table.3 shows the comparison of different
positions of the vermiform appendix of present
study with other studies
783
Manisha et al.,
Retrocaecal and retrocolic positions of the

appendix were by far the commonest6 (58%).
Incidence of postileal position was also fairly
common (10%)6. Probably the common position
of the appendix (retrocaecal) is its resting
position. It might rest in this position if there is
no infection in the abdomen. A surgeon or an
anatomist can see the position of the appendix
only during the surgery or dissection. There are
no studies on various positions of the appendix in
the
same
individual
on
different
days/weeks/months/years. Studies of the
positions of appendix every month in an
individual using a scanner might confirm the
hypothesis that vermiform appendix keeps
changing its position according to the presence of
infection7.
Table.4 shows the comparison of length of the
vermiform appendix of present study with other
studies.
CONCLUSION
Appendix is the only organ in our body which

has not constant anatomical position. Various
positions of vermiform appendix are useful to
understand the location of site of occurrence of
pain during appendicitis. Retrocaecal appendix
has symptoms of upper urinary tract infection,
due to irritation of the adjacent ureter. In pelvic
position pain may be felt when the thigh is flexed
and medially rotated, because the obturator
internus is stretched. Pelvic appendix may irritate
the bladder or rectum causing suprapubic pain,
pain with urination, or feeling the need to
defecate. Postileal position in some males, can
irritate the ureter and cause testicular pain. In
sub-hepatic position, the patient have pain in the
right hypochondriac region. From various
positions of vermiform appendix we can
understand the possible outcome of the
appendicitis specifically location of site of pain.
Appendix is supplied by end artery which is one
of cause of occurrence of appendicitis.
Appendicular artery which is branch of inferior
division of iliocolic artery goes through appendix

along mesoappendix.
ACKNOWLEDGEMENTS
We sincerely thankful to our Professor and Head

of the Department of Anatomy, Smt.N.H.L.
Municipal Medical College, B.J.Medical College
and AMC MET Medical College, Ahmedabad,
Professor and Head of the Department of
Forensic Medicine, Smt.N.H.L. Municipal
Medical College who not only acted as guide but
also as a mentor for successfully completing this
research.
REFERENCES
1. Karpelowsky JS, Bickler S, Rode H.

Appendicitis pitfalls and medicolegal
implications. South Afr MED J. 2006; 96 (9):
866- 872.
2. Golalipour MJ. Arya B, Azarhoosh R,
Jahanshahi M. Anatomical Variations Of
Vermiform Appendix In South-East Caspian
Sea. Journal of Anatomical Society India.
2003; 52 (2): 141-43.
3. Thyagaraj J. A Study of Anatomical position
in normal population and in inflamed cases
[Thesis]. Bangalore Medical College;
RGUHS; 2005.
4. Snell RS. Clinical Anatomy 7th edition.
Baltimore: Lippincot William and Wilkins;
2004: 215-217.
5. Moore KL and Persaud T V N. Before we are
born- Essentials of embryology and birth
defects. 5th edition. Philadelphia: W.
B.Saunderscompany; 1998:273-280.
6. Ajmani ML, Ajmani K. The position, length
and arterial supply of vermiform appendix.
Anat Anz. 1983; 153(4):369-74.
7. Geethanjali HT, Lakshmi Prabha Subhash,
Tumkur Anatomica. A Study of Variations in
the Position of Vermiform Appendix.
Karnataka. 2011; 5(2):17-23.
784
Manisha et al.,
8. Solanke TF. The position, length, and content

of the vermiform appendix in Nigerians. Brit.
J. Surg. 1970;57:100-10.
9. Varshney S, Jhonson CD, Rangnekar GV.
Retrocaecal appendix appears to be less
prone to infection. Br J Surg. 1996; 83:223224.
10. Cecil P.G Wakeley. The position of the
vermiform appendix tip obtained by analysis
of 10,000 Cases. Journal Anat. 1933; 67:277.
11. Clegg-lamphey JN, A Harmah ,S.b.Naaeder
and Adu-Aryee NA. The position of the
Vermiform appendix in Nigerians with a
review of the literature. East African
Medical Journal. 2006;83(12)
12. Shah MA, Shah M. The position of
vermiform appendix. Ind Med Gaz.
1945;80:494-95.
13. Baily & Love Practice of Surgery, 24edition,
chapter 70.The Vermiform Appendix. 2004;
1205 07
14. Ferguson, John. Some Important Points
Regarding the Appendix Vermiformis. Am.
Jour. MED. Sc. 1891;26:61-62.
15. Berry RJA. The Anatomy of the Vermiform
Appendix. Anat. Anz. 1895; July: 761-69.
16. Deaver JB. Appendicitis, Fourth Edition.
Philadelphia: P. Blakistons Son and Co.
1913
17. Lewis WH. Anatomy of the Human Body,
Twentieth Edition. Philadelphia: Lea and
Febiger; 1918.
18. Arthur Robinson. Cunningham's Textbook of
Anatomy, Fifth Edition. Edinburgh: William
Wood and Co; 1923.
19. Royster HA. Appendicitis. New York:
Appleton and Co.; 1927.
20. Donald C. Collins. The Length and position
of the vermiform appendix - A Study of
4,680 Specimens. Ann Surg. 1932; 96(6):
104448.
785
Manisha et al.,
DOI: 10.5958/j.2319-5886.2.4.126

&
Health Sciences
www.ijmrhs.com
rd
Volume 2 Issue 4 Oct - Dec

Research article
Coden: IJMRHS
nd
Copyright @2013
ISSN: 2319-5886
Accepted: 3rd Sep 2013
A COMPARITIVE STUDY ON CRYO, PULSED ULTRASOUND AND ITS COMBINATION

THERAPIES ON DELAYED ONSET OF MUSCLE SORENESS
*Shaji J. Kachanathu1, Manoj Kumar2, Pavas Jaiswal3, Shibili Nuhmani4, Sajith Vellappally5
1,5
College of Applied Medical Sciences, King Saud University, KSA

Faculty of Applied Medical Sciences, Manav Rachna International University, India
4
Department of Physiotherapy, Jamia Hamdard, New Delhi, India
2,3
*Corresponding author e-mail: johnsphysio@gmail.com

ABSTRACT
Objectives: Individuals engage in strenuous physical activity to which they are unaccustomed usually
land up in a phenomenon called Delayed Onset of Muscle Soreness (DOMS) and results in pain, muscle
stiffness and swelling. The current study was aimed to see the effect of cryo, ultrasound and its
combination therapies on the reduction of symptoms of DOMS. Materials and Methods: A total of 30
subjects with the mean age of 22.1 5.9 years participated in the study. Subjects were randomly
allocated to three groups A, B and C (n=10) and induced DOMS by a standard exercise protocol. Each
group received different treatment application i.e. ultrasound (US), cryotherapy (CT) and combination
(C) of both. Study outcomes were measured by Perceived Muscle Soreness (PMS), Relaxed-Elbow
flexion angle (rEFA), Plasma Creatine Kinase (CK) level at 0 hours (pre-exercise), 24hrs, 48hrs, 72hrs
and at 92hrs. Results: All three groups showed improvement with respect to their interventions, whereas
the C group, after 96 hours of post-exercise the rEFA return to its near normal range as compared to the
other two groups. Although there was a rise in the plasma CK level in all three groups, however the C
group was effective in minimizing the rising level of CK and also in the reduction of muscle soreness at
successive time intervals and reaches to baseline after 96 hours of post-exercise. Conclusion: The
combined application of cryotherapy and pulsed ultrasound immediately after exercise induced muscle
damage is a better choice of treatment, It is also observed that cryotherapy was more effective than
pulsed ultrasound alone treatment in reduction of symptoms.
Key words: Muscle soreness, Cryotherapy, Ultrasound, Range of motion, Creatine Kinase
INTRODUCTION
Delayed onset muscle soreness (DOMS) refers to

the skeletal muscle pain that follows novel
eccentric exercise.1,2 The intensity of soreness
increases during the first 24 hrs, peaks at 2448
hrs, and subsides within five to seven days of

postexercise.1 The sore muscles are described as
feeling stiff, tender, and aching especially after
palpitation or movement but these common
Shaji et al.,
Int J Med res Health Sci. 2013;2(4): 786-792
786
symptoms rarely require medical attention.1,3

DOMS is typically experienced by all individuals
regardless of fitness level, and is a normal
physiological response to increased exertion, and
the introduction of unfamiliar physical activities.
It can occur any number of times throughout
ones life4. Researchers hypothesis that DOMS is
related to muscle structural damage that is
followed by ion imbalance, inflammation, and
pain1,2,3. Muscle damage includes disrupted
sarcolemma, T-tubules, myofibrils, cytoskeletal
protein, and sarcoplasmic reticulum (SR) 3,5,6.
Immediate soreness may be due to biomechanical end products of metabolism affecting
nerve endings or temporary hypoxia due to
muscle ischemia. Severity of the soreness
depends upon the complexity of the exercise7.
Due to the sensation of pain and discomfort,
DOMS can impair physical fitness and
performance, so prevention and treatment of
DOMS is of great concern to coaches, trainers,
and therapists8.
Some strategies proposed to alleviate DOMS
include pre and post-exercise stretching, light
exercise, ultrasound, topical analgesics, and it is
also common for the clinician to recommend
NSAIDs to decrease the magnitude of these
characteristics. None of these treatments,
however, completely attenuate DOMS7,9,10.
Studies also reported that sports massage reduces
DOMS and CK when administered 2 hours after
the termination of eccentric exercise11.
Present clinical practice, cryotherapy and
ultrasound therapy are used as the focal point for
the immediate management of musculoskeletal
injuries. The objectives of the current study were
to track the efficacy of ultrasound, cryotherapy
and its combination on CK levels, PMS, and
rEFA during DOMS.
The current study approved by the Institutional

Ethics Committee, a total thirty healthy subjects
of 15 males and 15 females with a basic
characteristic of 22.1 5.9 years of age, 169.5

10.3 cm of height, and weight of 62.8 19.5 kg.
None of the subjects had performed upper body
weight training within the last 6 months,
experiencing any musculoskeletal injury and
pain, under any medication and phases of the
menstrual cycle. The present study was obtained
ethical committee clearance from the parent
organization. Each subject was clearly explained
about the DOMS-inducing exercise protocol and
informed written consent was also collected from
all the subjects prior to the study. Subjects were
randomly allocated into three groups A, B and C
(n=10) with equal gender distribution. Each
group received different treatment application i.e
ultrasound (US), cryotherapy (CT) and
combination (C) of both with respective to their
group. After completing the pre-exercise
evaluation by the investigator and self arm
stretching by each subject then asked to perform
an exercise of elbow flexors to induce DOMS by
eccentric exercises in non-dominant arm.
Subjects began with a 13.5-kg (30-lb) dumbbell.
Beginning in full elbow flexion, subjects were
instructed to lower the dumbbell to full extension
over 3 seconds. Upon reaching full extension, the
investigator assisted the subjects in returning the
weight to the starting position. Subjects
performed continuous repetitions until they could
no longer control the weight during the 3-second
period. At this point, the weight was reduced by
2.25 kg (5 lb), and the protocol was repeated. As
subjects continued to fatigue, the weight was
sequentially lowered in 2.25-kg (5-lb) increments
until a total weight of 2.25 kg (5 lb) was reached.
At this weight, subjects were asked to perform
repetitions either to fatigue or until 10 repetitions
completed. Treatment was applied (respective to
their groups). On successive 24 hours interval
treatment was repeated. Cryotherapy was given
by ice bag (crushed ice) method. Ice crushed and
filled in the polythene bag. One layer of towel
wrapped around the ice bag to avoid direct
contact of skin to the bag. Cryotherapy was
Shaji et al.,
787
applied for 20 minutes continuously. Pulsed

ultrasound treatment with frequency of 1 MHz,
duty cycle of 20%, ratio 1:4, intensity of 0 .8
w/cm2, was given on the muscle belly for 7
minutes. Treatment head of 3cm diameter is used
for the treatment. Ultrasonic gel is used to as
transmission medium. In combination therapy,
cryotherapy was given for 10 minutes, and then
pulsed US applied for 4 minutes with five
minutes of interval after cryotherapy. Study
outcomes were measured by Perceived Muscle
Soreness (PMS), Relaxed-Elbow flexion angle
(rEFA), Plasma Creatine Kinase (CK) level at 0
hours (pre-exercise), 24hrs, 48hrs, 72hrs and at
92hrs.
RESULTS
Data analysis of outcome variables was done

with the help of one-way ANOVA, post hoc test,
and Chi-square test for all three groups named as
Group AU. S, Group BCryo, and Group C
Cryo +US (Table:4 and 5). After 96 hours of
post exercise statistical analysis using one-way

ANOVA indicated significant differences (p=.
001) between all three treatment groups, with
maximum recovery in C Group. Results showed
a rise in the plasma CK level at successive level
in the three different treatment groups, although
the minimal rise in the C Group (Table:1;
Figure:1.). After 96 hours of post-exercise
analysis showed significant difference (p=.000)
between the plasma CK levels of three different
groups. PMS value was higher in the Group-A
and this value was peak during the 24-48 hours
of post-exercise, although there was least
increased in the value in the Group-C and it
reached toward near normal level at 96 hours of
post exercise in C group (Table:2; Figure:2.).
rEFA value was again higher in the Group-A
and this value was peak during the 24-48 hours
of post-exercise in A group, although there was
least increased in the Group- B and C and it
reached toward near normal level at 96 hours of
post exercise in C group (Table:3; Figure:3.).
Table.1: Plasma CK level (IU/L) in groups at different time interval

Groups 0Hrs.
24 Hrs.
48Hrs.
72Hrs.
G-A
149.010.9 880.690.7 1520.672.0 1784.294.8
G-B
150.110.5 805.696.5 1487.876.6 1684.488.5
G-C
145.015.6 685.867.9 1276.465.9 1467.092.2
Table: 2. PMS (cm) level in groups at different time interval
Groups
0Hrs.
24 Hrs.
48Hrs.
G-A
0.00.0
3.40.52 3.40.52
G-B
0.00.0
2.60.69 2.30.48
G-C
0.00.0
2.50.50 2.10.31
Table: 3. rEFA (degrees) in groups at different time interval
Groups
0Hrs.
24 Hrs.
48Hrs.
G-A
14.1 1.4 20.01.9 20.12.0
G-B
14.01.6 18.11.1 7.6 0.8
G-C
13.41.5 17.01.4 7.6 0.8
72Hrs.
2.60.51
1.40.48
1.10.31
72Hrs.
18.41.5
16.21.0
14.81.1
96Hrs.
2010.688.7
1796.290.0
1547.096.4
96Hrs.
1.60.69
0.50.52
0.30.48
96Hrs.
16.41.5
15.21.2
13.91.1
788
Shaji et al.,
Table: 4. rEFA and Plasma CK level within and between groups

One-way ANOVA
Sum
of df
Mean
Post 96 hrs.
Squares
Square
rEFA
Between Groups
31.27
2
15.63
Within Groups
46.90
27
1.74
Total
78.17
29
Between Groups
1076643.20 2
538321.60
CK
Within Groups
281526.00
27
10426.89
Total
1358169.20 29
Sig.
9.00
.001
51.63
.000
Table: 5. PMS analysis in groups

Chi-Square Tests
Value
df Asymp.Sig (2-sided)
Pearson Chi-Square
19.000(a) 4 .001
Likelihood Ratio
23.755
4 .000
Linear-by-Linear Association 14.586
1 .000
N of Valid Cases
30
A 9 cells (100.0%)have expected count less than 5. the minimum expected
count is 2.00
Perceived Muscle Soreness
Plasma CK
2500
1500
G-A
1000
G-B
Axis Title
2000
G-C
500
4
3.5
3
2.5
2
1.5
1
0.5
0
G-A
G-B
G-C
0
0Hrs. 24 Hrs. 48Hrs. 72Hrs. 96Hrs.
Fig:1. Plasma CK level in groups at different

time interval
Fig:2. PMS level in groups at different time interval
rEFA
25
20
15
G-A
10
G-B
G-C
5
0
0Hrs.
24 Hrs.
48Hrs.
72Hrs.
96Hrs.
Fig:3. rEFA in groups at different time interval

789
Shaji et al.,
DISCUSSION
The objectives of the present study was to track

the efficacy of ultrasound, cryotherapy and its
combination on CK levels, PMS, and rEFA
during DOMS. The treatment of cryotherapy and
pulsed ultrasound therapy immediately after
exercise induced muscle damage is effective in
reducing stiffness as relaxed arm angle, and
reduction in muscle soreness level, and lower
value of plasma CK activity. In the current study
all three groups results showed improvement
with respect to their interventions, whereas the C
group, after 96 hours of exercise the rEFA return
to its near normal range as compared to the other
two groups. Although there was a rise in the
plasma CK level in all three groups, however the
C group was effective in minimizing the rising
level of CK at 96 hours of post-exercise and the
muscle soreness was reduced significantly in
both B and C groups and reached almost to
baseline after 96 hours of post-exercise.
The present study used pulsed US as an
intervention and its positive effects on the results
were supported by the mechanical effects, stable
cavitations, and micro streaming are believed to
aid tissue regeneration and healing8. Acoustic
micro streaming and cavitation increase the
diffusion of ions and metabolites across the cell
membranes and enhance the reparative process12.
Changes in calcium permeability are associated
with enhanced tissue healing12. Increased sodium
permeability may reduce pain and spasm by
altering neural activity12. In the current study
these factors might have improved the muscle
soreness.
Until little researches have been performed on
rEFA and its role with pulsed US, Cryo
therapies. Continues US with its thermal effect
was normally used to increase range of
motions13. In the previous studies also observed
that any reduction of significant evidence of
perceived soreness and relaxed elbow angle
indicates healing and treatment effect. Our
finding also supports with the data from US

alone treatment for an acute inflammation
response is effective for DOMS8. Elbow range of
motion was actually a function of subjective
soreness in this study. Subjects were asked to
actively extend the elbow to physiological
limitation or to pain tolerance. Because no
subject recovered full extension (relative to
pretest values) by 96 hrs, pain undoubtedly
played a role in rEFA. Joint stiffness and
decreased mobility are common following
muscle injury, and movement may be more
discouraged by the stiffness than by pain, but the
subjects were extending the elbow to the point
that any further extension would be too painful;
thus, rEFA was an indicator of how much pain
subjects were experiencing.
Studies indicated the positive results of
cryotherapy with pulsed ultrasound in the
treatment of acute muscle injuries and pulse
ultrasound therapy helped in regeneration of
muscle fibers, which ultimately reduce the
healing time8,13,14. In case of muscle soreness
combined therapy almost improved the muscular
function by means of near normal relaxed arm
angle and with minimal muscle pain. However in
the case of plasma CK level, there was minimal
raised in the value of combined group as
compared to the other two groups, but failed
completely to decrease in the value at successive
time interval.
CK levels depend on age, gender, race, muscle
mass, physical activity and climatic condition15.
High levels of CK in apparently healthy subjects
may be correlated with physical training status,
as they depend on sarcomic damage; strenuous
exercise that damage skeletal muscle cells results
in increased CK total CK activity is markedly
elevated for 24 hours after the exercise bout16.
Although previous researches indicated that it
was not a good indicator of DOMS because it
varies with many possibilities and sometimes it
790
Shaji et al.,
did not relate to other symptoms of DOMS.

Pulsed ultrasound therapy helps in the
regeneration of skeletal myofibers after DOMS.
By reducing the symptoms of DOMS this study
indicated that if deep temperature at tissue level
was reduced and pulse ultrasound used without
heating effect it can facilitate the recovery of
muscle soreness and regeneration of muscle
fibers17. A study suggested that sports massage
will reduce DOMS and CK when administered 2
hours after the termination of eccentric exercise.
This may be due to a reduced emigration of
neutrophils and/or higher levels of serum
cortisol11, the micro massage effect of US also
contributed to the positive result.
Gulick et al. (1996) was reported that there was
decreased in the muscle soreness level in the
cryotherapy group after treatment and on the next
day and stated that was because of numbing
effect of cold modality depress the excitability of
the free nerve ending and peripheral nerves
which increases the threshold and decreased
pain. This was proved in previous studies as they
measure local pain thresholds after treatment
with ice give varying results, with the effects
lasting from 30 minutes to 12 hours. Cold also
slows the conduction velocity of peripheral
nerves18.
In our study observed the effect of pulsed
ultrasound therapy and cryotherapy individually
and in its combination form by reducing the
symptoms of DOMS. It is also observed It is also
observed that cryotherapy was more effective
than pulsed ultrasound alone treatment in
reduction of symptoms. Studies also proved
immediate application of cryotherapy reduced
the tissue temperature as well as the demand of
oxygen at injured cell. This helps in the
minimizing secondary damage to muscle due to
hypoxia and increased in temperature. And if
there is less damage to muscle and less edema
formation at the cellular level, recovery will be
easy as compared to high temperature at tissue
level. This effect of cryotherapy was supported
in the past studies as they provide evidence for

secondary injury in tissue due to exercise
induced muscle soreness and effective way of
treatment19,20.
CONCLUSION
The combined application of cryotherapy and

pulsed US immediately after exercise induced
muscle damage, was effective to reduce the
symptoms of DOMS and it facilitated the tissue
healing. It is also observed that cryotherapy was
more effective than pulsed ultrasound alone
treatment in reduction of symptoms. This showed
through the reduction in the presence of
symptoms and their severity. Only plasma CK
level showed persistent increased in all groups at
successive intervals. Although that was least
raise in the cryotherapy with a pulse ultrasound
group, but this group also unable to completely
decrease the persistent increase in CK level. It
helps in maintaining the plasma CK level at
minimal value compared to other two groups. So
if cryotherapy with pulse ultrasound used in
appropriate methods it will show positive results
in the reduction of symptoms of DOMS.
REFERENCES
1. Armstrong RB. Mechanisms of exerciseinduced delayed onset muscular soreness: a

brief
review.
Med
Sci
Sports
Exerc.1984;16:529-38.
2. MacIntyre DL, Reid WD, McKenzie DC.
Delayed onset muscle soreness: the
inflammatory response to muscle injury and
its
clinical
implications.
Sports
Med.1995;20:24-40.
3. Clarkson PM, Sayers SP. Etiology of
exercise induced muscle damage. Can J Appl
Physiol.1999;24:234-48.
4. Kolt GS. Physicaltherapies in sports and
exercise book ,1st edition,2004.
791
Shaji et al.,
5. Child RB, Saxton JM, Donnelly AE.

Comparison of eccentric knee extensors
muscle actions at two muscle lengths on
indices of damage and angle specific force
production
in
humans.
J
Sports
Sci.1998;16:301-8.
6. Newman DJ, Jones DA, Ghosh G, et al.
Muscle fatigue and pain after eccentric
contractions at long and short muscle
lengths.Clin Sci.1988;74:553-7.
7. Grossman JM, Arnold BA, Perrin DH,
Kahler DM. Effect of ibuprofen on pain,
decreased range of motion, and decreased
strength associated with delayed onset
muscle soreness of the elbow flexors. Journal
of Sport Rehabilitation.1995;4:253-263.
8. Stay JC, Richard MD, Draper DO, EdD,
Schulthies SS, Durrant E. Pulsed Ultrasound
Fails To Diminish Delayed-Onset Muscle
Soreness Symptoms. J Athl Train.
1998;33(4): 341346.
9. Bougie JD. Management of delayed onset
muscle soreness: a review of literature.
Sports
Chiropractic
and
Rehabilitation.1997;11:110.
10. Gulick DT, Kimura IF, Sitler M, et al.
Various treatment techniques on signs and
symptoms of delayed onset muscle soreness.
Journal of Athletic Training.1996;31:145-52.
11. Smith LL, Keating MN, Holbert D. The
effects of athletic massage on delayed onset
muscle soreness, creatine kinase, and
neutrophil count: a preliminary report. J
Orthop Sports Phys Ther. 1994;19:93-99.
12. Dyson M. Mechanisms involved in
therapeutic
ultrasound.
Physiotherapy.
1987;73:116-120.
13. Rose S, Draper DO, , Schulthies SS, Durrant
E. The Stretching Window Part Two: Rate of
Thermal Decay in Deep Muscle Following 1MHz Ultrasound. J Athl Train. 1996; 31(2):
139-43.
14. Mickey CA, Bemier JN, Perrin DH. Ice and

ice with nonthermal ultrasound effects on
delayed-on
set
muscle
soreness.
JAthlTrain.1996;31(1):19.
15. Brancaccio P, Limongelli F, Maffulli N.
Monitoring of serum enzymes in sport,
British journal of sports medicine.
2006;40(2):96-97.
16. Brancaccio P, Limongelli F, Maffulli N.
Creatine kinase monitoring in sports
medicine, British Medical Bulletin. 2007;8182:209-230.
17. Stauber WT .Delayed-onset muscle soreness
and muscle pain. In Zachazewski J, Magee D
and Quillen W (Eds): Athletic Injuries and
Rehabilitation. Sydney: WB Saunders
Company, 1996;pp.92-97.
18. Gulick DT, Kimura IF, Sitler M, Paolone M,
Paolone A, Kelly JD. Various treatment
techniques on signs and symptoms of delayed
onset muscle soreness. J Athletic Training.
1996;31:145-152.
19. Olson JE, Stravino VD: A review of
cryotherapy. Phys Ther. 1972;52:840-853.
20. Oliveira NML, Rainero EP, Salvini TF.
Three intermittent sessions of cryotherapy
Reduce the secondary muscle injury in
skeletal Muscle of rat. Journal of Sports
Science and Medicine . 2006;5:228-34.
792
Shaji et al.,
DOI: 10.5958/j.2319-5886.2.4.127

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
th
Research article
Copyright @2013
ISSN: 2319-5886
th
Accepted: 5 Sep 2013
MORPHOLOGICAL STUDY ON SUPRASCAPULAR NOTCH

TRANSVERSE SCAPULAR LIGAMENTS IN HUMAN SCAPULAE
AND
SUPERIOR
*Vasudha TK1, Ashwija Shetty1, Sadashivana Gowd1, Rajasekhar SSSN 2

1
Department of Anatomy, Subbaiah Institute of Medical Sciences & Research Centre, Shimoga,
Karnataka, India
2
Department of Anatomy, Melmaruvathur Adiparasakthi Institute of Medical Sciences and Research,
TamilNadu, India
*Corresponding author email: tkvasudha75@gmail.com
ABSTRACT
Background: The scapula is a flat triangular bone situated on the posteroleteral aspect of thoracic wall
between second and seventh rib. The coracoid process of scapula projects upward and, medial to the
base of coracoid process is the Suprascapular Notch (SSN). Morphology of SSN is considered to be a
risk factor for Suprascapular Nerve (SN) entrapment in combination with an anomalous Superior
Transverse Scapular Ligament (STSL). Aim: To review and document the morphology of suprascapular
notch, degree of ossification of superior transverse scapular ligament and its clinical correlation.
Materials and Methods: The study was carried out by visual observation on 115 dried human scapulae.
Result: It was observed that 115 scapulae showed different shapes with symmetrical U, the most
common type (34.78%). There was a unique variation in one left scapula, where SSN was replaced by a
narrow groove (0.86%). Conclusion: This study will help to correlate suprascapular nerve entrapment
with a specific type of SSN.
Keywords: Suprascapular notch, Superior transverse scapular ligament, suprascapular nerve
entrapment.
INTRODUCTION
Suprascapular notch is situated at anterolateral

end of the superior border of scapula, separating
the root of coracoid process from superior border
of scapula. The notch is bridged by the STSL,
which is attached laterally to root of coracoid
process and medially to the limit of the notch.
This ligament converting the notch into the
foramen, transmits suprascapular nerve to
supraspinous fossa, whereas the suprascapular

vessels pass backwards above the ligament1.The
morphology of the suprascapular notch is
considered to be a risk factor for suprascapular
nerve entrapment either in combination with an
anomalous STSL or as a narrowed notch2.
Accordingly this notch is an important landmark
of the suprascapular nerve during arthroscopic
793
Vasudha et al.,
shoulder operation3. Previously SSN has been

classified by many researchers based on complex
geometrical calculations. Studies reveals, 6
different types of anatomical variations of the
suprascapular notch, including complete absence
of notch have been reported in Nigerian
population4,5. Koepell and Thompson (1959)
were the first to describe the SN entrapment
syndrome6 .They reported that abduction or
horizontal adduction of the shoulder exerted
traction on the SN, which led to its compression
against the STSL. The anatomical variation of
the SSN includes the variation in shape,
complete or partial ossification of STSL.
Rengachary et al observed 6 basic types of SSN
in 2011 scapulae7. The purpose of this study was
to document the incidence, morphology and
clinical significance of SSN and the existence of
ossified STSL.
The study was conducted on 115 dried human

scapulae (54 right and 61 left) obtained from
bone library, Department of Anatomy, Subbaiah
Institute of Medical Sciences and Research
Centre, after obtaining clearance from the

Institutional Ethics Committee. This is an
observational study, conducted from January
2012 to February 2013. Scapulae were analyzed
for morphology of SSN and degree of
ossification of STSL, irrespective of age, sex and
race. Scapulae with damaged SSN were excluded
from the study. The results were documented by
photographs.
RESULTS
In the present study different shapes of SSN and

degree of ossification of STSL were documented
in Table 1 and Table 2. Table 1 shows different
types of SSN. Among different types
symmetrical U shape is most common followed
by J shaped notch. In one of 115 dry human
scapulae, SSN was replaced by a narrow groove,
which extended from lateral end of superior
border to the spinoglenoidal notch. Table 2
shows different degrees of ossification of STSL,
which includes both complete and partial
ossification. In one left scapulae out of 115, there
was notch with foramen.
Table.1: Different types Suprascapular Notch
Shape of SSN
Symmetrical U shaped
Shallow U
J shape
Wide notch
Indented
Hockey stick
Deep U
Absence
Groove
No. of Scapulae
[Right & Left]
39
[22 & 07]
07
[03 & 04]
22
[10 & 12]
08
[04 & 04]
09
[04 & 05]
06
[04 & 02]
07
[04 & 03]
07
[05 & 02]
01
[00 & 01]
Percentage (%)
34.78
6.08
19.13
6.95
7.82
5.21
6.08
6.08
0.88
Table.2: Types of different degrees of ossification
Degree of Ossification
Complete
Partial
Notch with foramen
No. of Scapulae
05
02
01
Percentage (%)
[Right & left]
[ 02 & 03 ]
[ 01 & 01 ]
[ 00 & 01 ]
4.34
1.73
0.86
794
Vasudha et al.,
Table.3: Comparison of different shapes of SSN and degree of ossification of STS of previous studies with
present study.
Shapes
SSN
of Previous studies (%)
Present study
(%)
Sinkeet et al Polguj et al Iqbal et al Soni et

2010
2010
2010/11
2012
Symmetrical 29
2.3
14/13.2
58
Shallow U
21
J shape
00/22
27
Wide notch
57.7
Indented
00/27.5
03
Hockey stick 22
Deep U
24.4
Absence
2.12
10/23
02
Groove
V shape
5.18
68/20
07
SSN: Suprascapular Notch, STS: Superior Transverse Scapular Ligament.
al
34.78
6.08
19.13
6.95
7.82
5.21
6.08
6.08
0.88
-
Fig 1: Different Shapes of SSN. a) Width and breadth of SSN equal, b) Width is greater than breadth,
c) One edge of SSN was longer, d) Width is more wider,
e) Almost like a shape of hockey stick, f)
SSN was absent, g) slight notch was present, h) a groove replacing SSN,
i) breadth is greater than
the width.
795
Vasudha et al.,
a) Complete
b) Partial
c) Notch with foramen
Fig 2: Different degrees of ossification of STSL a) STSL was completely calcified, b) partially calcified
STSL c) Ossified band of STSL dividing the SSN into foramen below and notch above
DISCUSSION
Study on morphology of SSN and degree of

ossification of STSL, is done by many
researchers. Joe De Beer, in his study stated that,
the shape of the notch and calcified STSL has
been shown to be associated with increased risk
of SN entrapment, resulting in weakness and
wasting of supraspinatus and infraspinatus
muscles8. Dunkelgrun et al stated that U shaped
notches had a larger area than the V shaped
notches, leading to the assumption that a V
shaped notch is more likely to be connected with
nerve entrapment9.
A study by Sinkeet et al (2010, in Kenyan
population)10 classified 6 types of SSN with
description, which also includes degree of STSL
ossification. According to their study Type I
represent wide U, Type II represents J shape,
Type III, which has explained has most common,
represents symmetrical, Type IV represents V
shape, Type V&VI are related to the degree of
ossification of STSL, to the present study.
Polguj et al (2010)11 found that, in 21 (24.4%)
scapulae the maximal depth(MD) of notch is
more than superior transverse diameter
(STD),which represents deep U of present
study. Two scapulae (2.3%) had equal MD and
STD, represents symmetrical of present, in 47
(57.7%) scapulae the STD was longer than MD,
represents wide U of present.
In a study by Iqbal et al12, 13 2011-12 in Pakistani
population, in their two different studies showed
that 4 types of notches, with 10% without notch
(type 1), 14% symmetrical ( type 2), 68% V
shape ( type 3) and 8% inverted V ( type 4)

which is having a greater inferior maximum
length as compared to superior length. Soni Garg
et al (2012) reported that, symmetrical is most
common type, with V shape least common14.
Regarding degree of ossification, complete
ossification of STSL was reported, 30.76%, 3%,
7%, and 3% by Silva et al 200715, Sinkeet et al
201010, polguj et al 201011, and Soni Garg et al
201214, respectively. Partially ossified STSL is
reported by Sinkeet et al 18% and G. Soni et al
11%.
Notch with foramen is described by Natsis et al
as bony bridge, which limit the area of SSN and
divide it into a bony foramen inferiorly and a
notch superiorly16. He found such type of
variation in 2 scapulae out of 204 scapulae
(0.98%).
In the present study we have explained different
shapes of notch depending on size and shape and
also different degrees of ossification which are
illustrated in Table 1and Table 2, and compared
with previous studies in Table 3. These various
shapes are thought to play a part in the
predisposition for SN entrapment, assuming that
a small notch gives a larger chance of nerve
impingement than a large notch.
Our study also showed a unique variation found
in one left scapulae that, presence of groove
extending from lateral end of superior border to
its spinoglenoidal notch, where SSN was absent.
Assuming this groove in living bridged by
ligament, converting groove into osseofibrous
796
Vasudha et al.,
tunnel which may cause increased risk of SN

entrapment.
CONCLUSION
The shape of SSN and ossified STSL has been

shown to be associated with increased risk of SN
entrapment, resulting in weakness and wasting of
supraspinatous and infraspinatous muscles. A
reduction in the height of the SSN substantially
narrows the suprascapular foramen, should be
considered as a possible etiologic factor in SN
entrapment. Anatomical knowledge of such
variations should be kept in mind by a
radiologist, Orthopaedicians and neurosurgeons
as these variations may alter the technique of
surgery.
ACKNOWLEDGEMENT
We sincerely thank the management and staff of

the Dept. of Anatomy of Subbaiah Institute of
Medical Sciences and Research Centre, Shimoga,
Karnataka in India.
Declarations: Funding: None
Competing interests: None declared
REFERENCES
1. Standring S, Grays, The Anatomical Basis

of Clinical Practice 40th edition.2008, 79495.
2. Bayramoglu A, Demiryurek D, Tuccar E,
Erbil M, Aldur MM, Testik O, Doral MN.
Variations in anatomy at the suprascapular
notch possibly causing suprascapular nerve
entrapment: an anatomical study. Knee Surg
Sports Traumatol Arthroscopy, 2003; 11:39398.
3. Bigliani LU, Dalsey RM, McCann PD, April
EW. An anatomical study of the
suprascapular nerve. Arthroscopy. 1990;
6:301-05.
4. Natsis K, Totlis T, Tsikaras P, Appell H G
Skandalakis P, Koebke J. Proposal for
classification of SSN: a study on 423 dried
scapulae. Clin Anat 2007; 20:135-39.
5. Ofusori DA, Ude RA, Okwuonu

Cu,
Adesanya OA. Complete absence of SSN in a
Nigerian scapule: a possible cause of
suprascapular nerve entrapment. Int. J
Shoulder Surg. 2008; 2:85-86.
6. Kopell HP, Thompson WA. Pain and frozen
shoulder. Surg Gynecol Obstet 1959; 109:9296.
7. Rengachary SS, Neff JP, Singer PA, Brackett
CF.
Suprascapular
nerve
entrapment
neuropathy: A clinical, anatomical and
comparative study. Part 1: Clinical study.
Neurosurg. 1979; 5:441-46.
8. Joe De Beer and associates. Current trends in
management
of
suprascapular
nerve
entrapment Cape Shoulder Institute, South
Africa.
9. Dunkelgrun M, Lesaka K, Park SS, Kummer
FJ, Zuckker-man JD. Interobserver reliability
and
intraobserver
reproducibility
in
suprascapular notch typing. Bull Hosp Joint
Dis.2003; 61: 118-22.
10. Sinkeet SR. The suprascapular notch: its
morphology and distance from the glenoid
cavity in a Kenyan population; Folia
Morphol, 2010; 69:241-45.
11. Polguj M. Correlation between Morphometro
of
the
SSN
and
anthropometric
measurements of the scapula. Folia Morphol,
2011; 70,109-15.
12. Khadija
Iqbal
and
Rameez
Iqbal.
Classification of Suprascapular Notch
According to Anatomical Measurements in
Human Scapulae; J of the college of
physicians and surgeons Pakistan 2011, 21
(3): 169-70.
13. Iqbal K, Iqbal R, Khan SG. Anatomical
variations in shape of suprascapular notch of
scapula; J Morphol.Sci. 2010,27(1): 1-2.
14. Soni G, Malik VS, Shukla L, Chabbra S,
Gaur N. Morphometric Analysis of the
Suprascapular Notch. The Internet Journal of
Biological Anthropology. 2012; 5(1): DOI:
10.5580/2b19 797
Vasudha et al.,
15. Silva JG. High Incidence of Complete

Ossification of the Superior Transverse
Scapular Ligament in Brazilians and its
Clinical Implications. Int. J. Morphol., 2007;
25(4):855-59.
16. Natsis K. A bony bridge within the
suprascapular notch. Anatomic study and
clinical relevance Case report. Aristotle
University Medical Journal, 2008; 35(1):2933.
798
Vasudha et al.,
DOI:10.5958/j.2319-5886.2.4.128

&
Health Sciences
www.ijmrhs.com Volume 2 Issue 4 Oct-Dec Coden: IJMRHS
Received: 9th Aug 2013
Research article

Accepted: 7th Sep 2013
VERTEBROBASILAR VARIANTS AND THEIR BASIC CLINICAL IMPLICATIONS

*Iqbal S.
Professor, Department of Anatomy, Amala Institute of Medical Sciences, Amala Nagar, Thrissur,
Kerala, India.
*Corresponding author email: dr.iqbal.s@gmail.com
ABSTRACT
Objectives: Cerebrovascular diseases are the leading illness affecting the modern world with a high
mortality rate. The posterior circulation of the brain consists of vertebrobasilar system, shows a high
incidence of anomalies in the form of hypoplasia, fenestrations and asymmetry of the vessels, which
precipitate the development of vertebrobasilar insufficiency and posterior circulation stroke. A detailed
knowledge of the vertebrobasilar variants is essential in the diagnosis, treatment as well as in educating
the patients suffered from posterior circulation stroke. The present study is aimed to analyze the size,
asymmetry and anomalies of the vertebrobasilar system and their implications in posterior circulation
infarcts. Materials and methods: Fifty adult brains were studied during routine dissection of the
cadavers. The base of the brain with intact vertebral, basilar and posterior cerebral arteries were
dissected, preserved in 10% formalin and analyzed for the variations in the size, length and asymmetry
in the configuration. The dimensions of the vessels were measured using graduated calipers. Results:
Anomalies of the basilar artery were found in 14% of the brains, in the form of hypoplasia, fenestration
and terminal expansion at its bifurcation. The vertebral arteries showed asymmetry with right vertebral
were hypoplastic in majority of the brains. Conclusions: The variations of the vertebrobasilar system
increase the risk of vertebrobasilar insufficiency and posterior circulation stroke. Anomalies of the
vertebrobasilar arteries were also found to be associated with aneurysms. The right vertebral artery has
been frequently hypoplastic and there was no consistent correlation between the left vertebral
dominance and right handedness of the person. Hypoplastic vessels were frequently associated with
vertebrobasilar territory ischemic stroke.
Keywords: Hypoplasia, Fenestration, Dolichoectasia, Asymmetry, Dimensions, Infarction.
INTRODUCTION
Cerebrovascular disorders are one of the leading

ailments affecting the modern mankind with high
incidence of mortality rate; with high levels of
disabilities
among
those
who
survive
1
cerebrovascular
accidents .
Vertebrobasilar
Iqbal et al.,
system constitutes the posterior circulation of the

brain, supplies brainstem, cerebellum and
occipital lobes of the cerebrum, shows a high
incidence of anomalies. Anomalies of the
vertebrobasilar system may precipitate the
799
development of cerebrovascular diseases viz.,

stroke and aneurysms. Variations in the form of
hypoplasia and duplications are often prevalent.
Asymmetry of vertebral arteries is quite
common, but the amount of blood reaches the
basilar artery remains constant due to the contra
lateral large vertebral artery2. Vertebral artery
hypoplasia or asymmetry is frequently associated
with posterior circulation stroke (PCS) 3, 4. The
basic knowledge of vertebrobasilar variants is
essential in diagnosis, treatment as well as in
educating and training the patients suffered from
posterior circulation stroke. In the cases of
occlusion of an internal carotid artery, the
principal source of blood supply is through the
vertebrobasilar system, but the size and patency
of these arteries are quite variable. The vertebral
asymmetry can cause insufficiency in the
posterior circulation, which results in
vertebrobasilar ischemia. Asymmetrical vertebral
arteries are also considered to be one of the risk
factors for pontine infarction. Various types of
anomalies exist in different populations, but the
anomalies of the vertebrobasilar complex in
Indian population have been reported only by
few authors previously, based on cadaveric
analysis. So the objective of the present study is
to analyze the size, asymmetry and anomalies of
the vertebrobasilar system and their implications
in posterior circulation infarcts. The surgical
importance lies in its application during the
exposure of the vertebrobasilar territory and a
thorough knowledge of the vascular variants will
increase the success of the procedure. The
inference obtained from this work is also useful
for the sonologists in improving their diagnostic
skills and for anatomists in enhancing their
knowledge in teaching.
Fifty adult brains were studied from the regular

dissection hall cadavers over a period of Jan
2008-2013. The cadavers were obtained by
following the procedures in accordance with the
ethical standards of experimentation. The bases
of the brain including the brain stem with intact

vertebral, basilar and posterior cerebral arteries
were fixed in 10% formalin for 10 days. The
intra cerebral portion of the vertebral, basilar and
the proximal posterior cerebral arteries were
dissected carefully under water, dried and
painted with fevicryl red colour. The subarachnoid portions of the vertebral and basilar
arteries were then analyzed for the variations in
the size, length and any asymmetry in the
configuration. The dimensions of the component
vessels were measured using graduated calipers
(sensitivity: 0.1 mm). We focused on the basilar
artery and the upper segment of the vertebral
artery. The results obtained were recorded and
tabulated.
OBSERVATIONS
Basilar artery: The basilar artery was normal in

43 circles (86%). Anomalies were found in 7
cases (14%). Progressive narrowing of the basilar
artery was seen in two circles (4%) [Fig-1.A]. A
cobra-hood like terminal expansion at its
bifurcation was found in 4 circles (8%) [Fig1.B]. Partial duplication of the basilar artery in
the form of fenestration, in its proximal part was
found in one circle (2%) [Fig-1.C]. In this circle
the proximal segment of the basilar artery
duplicated immediately into two unequal
divisions. The larger division (thickness 2.8 mm)
occupied the basilar sulcus, while the smaller one
(thickness 1.6mm) deviated slightly to the right
and ran forwards for a short distance, and then
joined the main division 6mm away from its
origin. The rest of the basilar artery showed
progressive narrowing. The vertebral arteries in
this case were unequal in size. The origin of
basilar artery was at the ponto-medullary
junction in 35 circles (70%). In 13 circles it was
1 cm below ponto-medullary junction (upper
medulla) and in 2 circles it was 1cm above the
ponto-medullary junction. The basilar artery
terminated opposite to the ponto-mesencephalic
junction in 32 circles (64%). It bifurcated at the
upper pons in 16 circles and in 2 circles at the
800
Iqbal et al.,
level of mammillary bodies. The length and

diameter of the basilar artery was given in Table1
Vertebral artery: Bilateral symmetrical
vertebral arteries were encountered in 28 circles
in this series (56%). Asymmetry was observed in
22 circles (44%). The left vessel was larger than
the right in 14 circles and the right larger than the

left in 8 circles. Hypoplastic vertebral arteries
were seen in 5 brains (10%). The left vertebral
artery was hypoplastic in 2 brains (4%) [Fig-1.D]
and the right one was narrow in 3 brains (6%)
[Fig-1.E]. The average diameter of the vertebral
artery was given in Table-1.
Table: 1. Average dimension of vertebral and basilar arteries
Name of the vessel
Length (mm)
Range
Average
Diameter (mm)
Range
Average
Basilar artery
18-37
30
2.8-5.1
3.9
Vertebral artery
1.6-3.9
2.1
Table: 2. Average dimensions of basilar and vertebral arteries as reported in literature

Diameter of vertebral
Length of the basilar artery
Diameter of basilar artery
artery
Name
of
the
author
Range
Average
Range
Average
Range
Average
(mm)
(mm)
(mm)
(mm)
(mm)
(mm)
3.4 (L) &
Pai et al22
24 - 35
24.9
3-7
4.3
3.15
2.9 (R)
Idowu et al19
20 - 40
31.42
2.5 - 5.5
3.82
2.98
Present study
18 - 37
30
2.8 - 5.1
3.9
1.6 - 3.9
2.1
Fig.1: A-Progressive narrowing of (hypoplastic) basilar artery, B-Cobra-hood like terminal expansion of
the basilar artery at its bifurcation, C-Partial duplication (Fenestration) of the basilar artery at its
proximal portion, D-Hypoplastic left vertebral artery & E-Hypoplastic right vertebral artery.
801
Iqbal et al.,
DISCUSSION
In the present study 86% of the brains displayed

a normal basilar artery with a uniform diameter
throughout its length. Anomalies of the basilar
artery were rare and include duplication or
fenestration, rarely hypoplasia, segmental aplasia
and plexiform channels5. An unusual anomaly in
the form of a fenestration in the proximal part of
basilar artery was noted in 2% of the brains. The
proximal portion of the vessel was divided into
two unequal divisions. The larger division
(2.8mm) lies in the basilar sulcus and the narrow
smaller division (1.6mm) deviates slightly to
right and then fuses with main division with a
fenestration window of about 6mm. There was
no associated aneurismal dilatation in these
cases. The occurrence of this anomaly can be
explained on the basis of embryological
development. During the development of the
intracranial arteries, two bilateral, longitudinal
vascular channels differentiate along the ventral
surface of the hind brain from a plexus fed by
intersegmental and transitory pre-segmental
branches of the dorsal aorta and its forward
continuation. These longitudinal channels are
later connected cranially with the terminal
branches of the internal carotid arteries and
caudally with the vertebral arteries through the
first cervical intersegmental arteries. Fusion of
these two longitudinal channels results in the
formation of the basilar artery. The incomplete
fusion of two longitudinal vascular channels in
its proximal portion may result in the formation
of this anomaly. This type of anomaly seemed to
be reported rarely in the literature reviewed.
Dodevski et al6 reported two cases of
fenestrations of the basilar artery out of the 50
patients analyzed under computed tomography
angiography (CTA), an incidence of 4%. The
fenestration windows in these cases were 3.68
mm and 8 mm. There were no associated
aneurysms in these cases. Sanders et al7 in their
retrospective review of 5190 cerebral
angiograms, reported 37 patients with 38
fenestrated arteries viz., 16 basilar, 10 vertebral,
Iqbal et al.,
9 middle cerebral and 3 anterior cerebral arteries.

The angiographic incidence of basilar artery
fenestration was 0.3%. In 5 cases the fenestration
was at the proximal basilar artery, in 7 cases in
the mid basilar artery and in 4 cases in the distal
part of the basilar artery.
Fenestration is the partial/complete duplication
of a part of a vessel with or without a common
adventitial layer. It appears in different forms,
with a small mass of vascular tissue separating
the two lumens to the actual duplication of a part
of the affected vessel7. Fenestration of the basilar
artery was most frequent, followed by vertebral
and middle cerebral artery duplications8. The
reported incidence of basilar artery fenestrations
range from 0.02% to 0.6% in angiographic
series, 2.0% on magnetic resonance angiography
and from 1.3% up to 6.0% in autopsy studies.
The reason for the wide range in the incidences
can be explained by the fact that in some cases
the duplication is not complete and in others it is
not angiographically evident. The commonest
site of basilar fenestration was in its proximal
part close to the junction of the vertebral arteries.
Basilar fenestration was commonly found
associated with aneurysms. There were local
defects in the medial walls of the duplicated
segment at proximal end of the fenestration. The
tunica media was deficient with discontinuity of
the elastic fibers. These structural changes in the
proximal end of the fenestration are similar to
those seen in arterial bifurcations and were
consistent with the causes of intracranial
aneurysms6.
Sanders et al7 found a 7% incidence of aneurysm
in basilar fenestration. In all intracranial
fenestrations, the overall incidence of aneurysms
at the fenestration site was 3%. A majority of
aneurysms arises at the proximal junction of the
fenestration. So in patients with vertebrobasilar
aneurysms, the associated fenestrations should
always be looked for. The basilar artery
fenestrations may sometimes misinterpreted for
dissecting aneurysms or thrombosis in patients
with stroke leading to incorrect diagnosis and
mismanagement8.
Vertebrobasilar
artery
802
fenestrations may also found to be associated

with brain stem ischemia or infarctions.
Collateral branches may arise from the limbs of
the fenestrated vessels. These findings should be
analyzed in detail and the fenestrations should be
differentiated from aneurysm before surgery in
order to prevent inadvertent clipping of a limb of
the fenestration including these branches6.
The cause of the basilar hypoplasia is still not
known as other arterial abnormalities.
Embryologically, the posterior circulation begins
as two paired plexiform longitudinal neural
arteries and they start to fuse to form the basilar
artery at 5 weeks of gestation, while the
trigeminal artery begins to involute9. The size of
an artery depends on the area that ultimately
irrigates and an artery becomes unnecessary
during development if the area undergoes
regression. Therefore basilar artery hypoplasia is
believed to be the consequence of the persistent
primitive trigeminal artery (PPTA)10. It has also
been
suggested
that
large
posterior
communicating artery, which was commonly
seen in these cases, may show the persistent flow
from carotid to vertebrobasilar circulation and
this may cause vertebrobasilar hypoplasia. In
addition, malformations, injuries that effect
acting either in the perinatal period (such as basal
meningitis, arteritis and arterial occlusion) or in
the early childhood trauma, may impede the
normal reproduction of the smooth muscle cells
in the media from maintaining the capacity of the
artery to grow with the brain, have been
suggested in development of hypoplastic
arteries11. When associated with persistent
primitive trigeminal artery, basilar artery
hypoplasia occurs commonly at proximal part of
the vessel and usually associated with vertebral
artery hypoplasia12.
Previous studies of stroke in young adults have
not so far included hypoplastic cerebral vessels
among the potential causes of cerebral ischemia.
Chaturvedi et al13 had suggested that hypoplastic
basilar artery might be a predisposing factor for
ischemic stroke and the mean age of all cases
was 49.8 out of 4000 cases he has examined.
Iqbal et al.,
Szdzuy and Lehmann14 described angiographic

findings of incomplete fusion of the distal part of
the basilar artery associated with vertebral artery
hypoplasia in two cases presented with
symptoms of brain stem ischemia and termed this
condition as distal hypoplasia. It was speculated
that poor retrograde flow due to hypoplastic
distal basilar artery might make easy occurrence
of infarction. Demonstration of these hypoplastic
narrowing is also of importance since
atherosclerotic disease may also appear at an
earlier age if the native vessel is hypoplastic and
would become stenosed sooner than a large
vessel15. Moreover, embolic occlusions tend to
involve the distal basilar segment and usually
result in fatal consequences. It has been recently
concluded that magnetic resonance angiography
(MRA) can demonstrate entire/partial hypoplasia
of the basilar system. Moreover, the
demonstration of these hypoplastic vessels may
be clinically important, since it has been
suggested that hypoplastic vertebrobasilar
vessels should be considered among the potential
causes of cerebral ischemia in young adults13. In
reviewing the literature, symptomatic entire
basilar artery hypoplasia has been described only
in 13 cases by three previous reports11, 13, 14.
Hypoplastic basilar arteries were encountered in
4% of circles in this series. We conclude that
hypoplastic basilar arteries as a predisposing
factor should always be investigated in posterior
circulation stroke patients, and MRA as a noninvasive tool, should be considered in diagnosis
of these basilar abnormalities.
Dolichoectasia is the dilated, elongated and
tortuous vessels affecting vertebrobasilar
systems. It is also known by other names such as
megadolichoectasia, fusiform aneurysms or
tortuous vertebrobasilar system. It may compress
the cranial nerves, causes ischemia, subarachnoid
hemorrhage (SAH) and sometimes obstructive
hydrocephalus. On reviewing literature, the
incidence of VBD was to be 4.4%, and it usually
affects women. The basilar trunk was commonly
involved (40%), followed by vertebral arteries.
VBD is caused by either a congenital
803
vasculopathy of the tunica intima or hypertensive

stress on the vessel wall deranging the collagen
and elastin meshwork of the media and
downgrades the vessel. Neurological symptoms
manifest in 10% of the patients, in the form of
ischemic stroke, temporary/permanent motor
deficits, hydrocephalus, cerebellar dysfunction
and brain stem compression, which may be mild
to severe. The most frequent clinical picture is
due to cranial nerve compression or brain stem
ischemia or intracranial bleeding16,17. Tomoyuki
Nishizaki et al18 reviewed 23 patients with VBD
and found seven cases (30%) of intracranial
aneurysms. It was in the form of fusiform as well
as multiple and giant aneurysms. Rupture of the
dolichoectatic basilar artery is considered
unlikely and rarely presented with cerebellar
hemorrhage. In our studies we have found a
cobra-hood like terminal expansion of the basilar
artery at its bifurcation in 8% of the circles.
Idowu et al19 also observed that the diameter of
the basilar artery was relatively constant
throughout its course except for the widening at
its terminal bifurcation. These terminal
widenings/expansions were probably in the form
of minor variants of the above mentioned
dolichoectasia. And we are not sure about the
antemortem history of these patients with regard
to hypertension or any other congenital
malformations of the vasculature to explain the
above anomalies, since our specimens were
randomly collected from the dissection hall
cadavers.
The basilar artery terminates at the pontomesencephalic junction in 64% of the cases. In
32% of the brains the vessel bifurcated at the
upper pons and in the remaining 4% of the cases,
opposite to the mammillary bodies. Stopford20
found that the basilar artery had bifurcated at the
upper border of pons in 97.5% of the specimens
and below this level, ie, at the upper pons in the
remaining 2.5% of the cases. Sacki and Rhoton21
have reported that the vessels had bifurcated
opposite to the interpeduncular fossa in 88% of
the specimens, at the upper pons in 10% of the
brains and in the remaining 2% of the cases, the
Iqbal et al.,
bifurcation has indented the mammillary bodies.

Idowu et al19 stated that the basilar artery extends
from the lower to the upper border of the cisterna
pontis in 98% of the brains; and early bifurcation
at the mid pontine region in 2% of the cases. It
terminates at the ponto-mesencephalic junction
by running a straight course in 60% of the cases,
convex to the right in 18% and convex to the left
in 18% of the cases and forming a loop in 4% of
the cases. The dimensions of the basilar artery
were compared with that of other workers in
Table-2. Our measurements were more or less
coincides with that of other workers.
Asymmetrical vertebral arteries were commonly
encountered and were found in 44% of the brains
in this series. The left vertebral artery was larger
in diameter than the right in 28% of the cases and
the right vessel was larger in 16% of the brains.
Cloud and Markus23 concluded that the left VA
was dominant in approximately 50%; the right in
25% and only in the remaining quarter of cases
was the two vertebral arteries of similar caliber.
Seydel24 found that the vertebral arteries were
asymmetrical in 39.79% of the specimens and
further reported that the left vessels was larger
than the right in 26.53% and the right vessels
was larger in 13.26% of the cases. Stopford20
gave the ratio of left to right vertebral arteries
was 51:41 for diameter predominance and stated
that it was equal on both sides in only 8% of the
cases, out of the total 150 specimens they have
examined. Gillilan25 also stated without giving
any figures, that the cranial vertebral arteries
were frequently unequal in size, the right being
more often smaller. Kirgis et al26 have reported a
case of congenitally small vertebral artery and a
relatively large contra lateral vertebral artery and
further added that the discrepancy in the caliber
of the vertebral arteries was not uncommon and
there was no consistent correlation between the
asymmetry of these arteries and the asymmetry
of the circle of Willis. So from the present
observation as well as from the findings of
others, it is inferred that the cranial vertebral
arteries are usually unequal in size, the left vessel
is generally larger than the right. There was no
804
clear cut reason for the existence of this

asymmetry. But the development of this
asymmetry was related to vascular requirements
of the brain. Numerous authors had investigated
the correlation between the dominance of the left
vertebral artery and right handedness and vice
versa. But there is no definite evidence to
correlate the vertebral dominance and
handedness. So based on the findings of the
present study and also from others observations,
it is inferred that there seems to be a possibility
of a greater flow on the left side in the cranial
vertebral arteries and there is no consistent
relation between the asymmetry of these arteries
and the asymmetry of the circle of Willis.
Hypoplasia of vertebral artery (HVA) is not rare
in normal population, but is more frequent in
patients with posterior circulation stroke (PCS).
Congenital variations in the size of the vertebral
arteries were frequently encountered ranging
from asymmetry to severe hypoplasia of one
vertebral artery. In reviewing the literature most
of the workers agreed, that the external diameter
of 2mm or less was considered to be
hypoplastic15. Other workers with the help of the
colour duplex ultrasonography defined the HVA
with flow volume less than 30-40 ml/min in the
vertebral artery. The absence of uniform
description of HVA is due to the lack of studies
on the healthy individuals, smaller size of sample
groups and inadequate sonographic findings to
support HVAs. In the more recent observations
using colour coded ultrasonographic studies, a
diameter of less than 2.2mm was considered
hypoplastic, which was mainly based on
hemodynamic changes and supported by
ipsilateral flow resistance, contralateral diameter
and flow volume27. In our study we fixed that the
external diameter of less than 2mm was
considered hypoplastic. On reviewing the
literature, we found that about 1.9% to 35.2% of
the brains have unilateral HVA and makes little
contribution to basilar artery flow. It is also
worthwhile to mention that in all the above
works the right vertebral artery was more
hypoplastic than the left vessel. Hypoplastic
Iqbal et al.,
vertebral artery was found in 10% of the total 50

brains analyzed in our study. Hypoplasia was
commonly observed on the right side (6%),
which was consistent with findings of other
workers.
Chaturvedi et al13 suggested that a hypoplastic
vertebrobasilar system was considered to be a
predisposing factor in the posterior circulation
ischemia. Ipsilateral hypoplasia of vertebral
artery was more frequent in patients with lateral
medullary syndrome and concluded that HVA
conferred an increased probability of ischemic
stroke3. In the studies conducted by other
workers, HVA was significantly more frequent in
posterior territory ischemic stroke compared with
healthy subjects or patients with anterior
circulation stroke3, 4, 28. Chuang et al28 examined
191 acute ischemic stroke patients in the age
group 55.8 14.0 years, with the help of the
magnetic resonance angiogram (MRA) and
duplex ultrasonography and confirmed the
overall increase in the incidence of a unilateral
congenital HVA in the cases of brainstem /
cerebellar infarction. They also postulate that
hypoplastic VA might cause a decrease in the net
flow volume which conditions the development
of ischemic stroke in posterior cerebral
circulation. In addition, HVA with additional risk
factors such as hypertension, hyperlipidemia,
diabetes and smoking was also reported to
contribute to ischemic brainstem stroke, even in
young patients29.
Watanabe et al30 correlated asymmetry of
vertebral artery and pontine infarction in
Japanese population and concluded that patients
with small diametric VA of the right side
significantly had infarctions in the same side of
the pons and suggest that VA asymmetry is
considered to be one of the risk factors of pontine
infarction and that MRA can be useful in the
examination of the cerebral artery as a valuable
and non-invasive screening method. The average
diameters of the vertebral artery were compared
with the values of other authors in Table 2.
The end results of the anomalies of the
vertebrobasilar system in this study was not a
805
true reflection of the general population in the

frequency of the vertebrobasilar anomalies,
because our data were limited to only 50 adult
cadaveric brains without any neurological
diseases. In addition our sample group was so
small and Indian origin, it may also limit
generalizations of these anomalies based on our
study results. The inference of this study will
inform neurosurgeons, sonologists and patients
about the potentially vulnerable vertebrobasilar
circulation and further autopsy, angiographic,
and magnetic resonance imaging analysis were
needed to augment these clinical implications.
CONCLUSION
Cerebrovascular diseases are one of the leading

problems in modern medicine with high
incidence of mortality rate. The vertebrobasilar
system which supplies one fourth of the brain
shows a high incidence of variations in the form
of hypoplasia, fenestrations and asymmetrical
configuration. These variations increase the risk
of vertebrobasilar ischemia and posterior
circulation stroke. Our study was conducted to
analyze the size, asymmetry and anomalies of the
vertebrobasilar system, using fifty adult
cadaveric brains. The common variations
encountered were hypoplasia of vertebrobasilar
arteries, fenestrations of basilar artery and
asymmetrical vertebral arteries. The role of these
anomalies was discussed in causing the posterior
circulation stroke. The left vertebral artery was
significantly larger in diameter than the right and
there seems to be more blood flow on the left
side than on the right half of the brain and there
was no consistent correlation between the
vertebral
dominance
and
handedness.
Hypoplastic vertebral artery was frequently
common in the normal population and there was
a high incidence of its association with
vertebrobasilar territory ischemic stroke.
ACKNOWLEDGEMENTS
We acknowledge Prof. Mini Kariappa, Professor

and HOD of Anatomy, Dr. Ajith. TA Professor
of Biochemistry, Mr. Remith RP Assistant

Professor of Anatomy, Dr. Sugathan KR, Tutor
in Anatomy, Smt. Sindu CD, Smt. Lissy CD and
Mr. Mathews PP of Amala Institute of Medical
Sciences, Thrissur, Kerala for their valuable help
and assistance to make this work a reality.
ABBREVATIONS
CT: Computerized tomography, CTA: Computed

tomography angiography, MRA: Magnetic
resonance angiography, PPTA: Persistent
primitive trigeminal artery, MRI: Magnetic
resonance imaging, VBD: Vertebrobasilar
dolichoectasia, VA: Vertebral artery, HVA:
Hypoplasia
of
vertebral
artery,
SAH:
Subarachnoid hemorrhage
Conflict of Interest: Nil
REFERENCES
1.
2.
3.
4.
5.
6.
Voljevica A, Kulenovic A, Kapur E.

Angiography analysis of variations of the
posterior segment of the circle of Willis. Bos
J Basic Med Sci.2005; 5: 30-34.
Gillilan LA. Anatomy and embryology of
the arterial system of the brain stem and
cerebellum. In: Vinken PJ, Bruyn GW
(editors), Handbook of clinical neurology,
Amsterdam, Netherlands, 1975, pp.24-44.
Park JH, Kim JM, Roh JK. Hypoplastic
vertebral artery: Frequency and associations
with ischemic stroke territory. J Neurol
Neurosurg Psychiatry. 2007; 78: 954-958.
Perren F, Poglia D, Landis T, Sztajzel R.
Vertebral artery hypoplasia: A predisposing
factor for posterior circulation stroke?
Neurology. 2007; 68: 65-67.
Stehbens WE, editor. Pathology of the
cerebral blood vessels, St. Louis: CV Mosby
Co; 1986.
Dodevski A, Lazareska M, TosovskaLazarova D, Zhivadinovik J, Stojkoski A.
Basilar artery fenestration. Folia Morphol.
2011; 70 (2): 80-83.
806
Iqbal et al.,
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
Sanders WP, Sorek PA, Mehta BA.

Fenestration of intracranial arteries with
attention to associated aneurysms and other
anomalies. Am J Neuroradiol. 1993; 14:
675-80.
Scherer A, Siebler M, Aulich A. Virtual
arterial endoscopy as a diagnostic aid in a
patient with basilar artery fenestration and
thrombo embolic pontine infarct. Am J
Neuroradiol. 2002; 23: 1237-39.
Padget DH. The development of the cranial
arteries in the human embryo. Contrib
Embryol.1948; 32: 205-61.
Fields WS. The significance of persistent
trigeminal artery. Radiology. 1968; 91:
1096-101.
Hegedus K. Hypoplasia of the basilar artery.
Eur Arch Psychiatr Neurol Sci. 1985; 234:
395-398.
Boyko OB, Curnes JT, Blatter DD, Parker
DL. MRI of basilar artery hypoplasia
associated
with
persistent
primitive
trigeminal artery. Neuroradiology. 1996; 38:
11-14.
Chaturvedi S, Lukovits TG, Chen W,
Gorelick PB. Ischemia in the territory of a
hypoplastic
vertebrobasilar
system.
Neurology. 1999; 52: 980-983.
Szdzuy D, Lehmann R. Hypoplastic distal
part of the basilar artery. Neuroradiology.
1972; 4: 118-20.
Fischer CM, Gore I, Okabe N, White PD.
Atherosclerosis of the carotid and vertebral
arteries extracranial and intracranial. J
Neuropathol Exp Neurol. 1965; 24: 45576.
Ubogu EE, Zaidat OO. Vertebrobasilar
dolichoectasia diagnosed by magnetic
resonance angiography and risk of stroke
and death: A cohort study. J Neurol
Neurosurg Psychiatry.2004; 75: 22-26.
Ritesh Kansal, Amit Mahore, Nitin Dange,
Sanjay
Kukreja.
Dolichoectasia
of
vertebrobasilar arteries as a cause of
hydrocephalus. J Neurosci Rural Pract.
2011; 2(1): 62-64.
Iqbal et al.,
18. Tomoyuki Nishizaki, Norihiko Tamaki,

Naoya Takeda, Takayuki Shirakuni, Takeshi
Kondoh,Satoshi Matsumoto. Dolichoectatic
Basilar Artery: A review of 23 cases.
Stroke.1986; 17: 1277-81.
19. Idowu OE, Malomo AO, Akang EEU.
Surgical Anatomy of the Vertebrobasilar
Territory and Posterior Circle of Willis.
West African Journal of Medicine. 2010;
29(4):230-34.
20. Stopford JSB. Arteries of the Pons and
Medulla Oblongata. J Anat and Physiol.
1915;50: 131-64.
21. Sacki N, Rhoton AL. Microsurgical
anatomy of the upper basilar artery and
the Posterior Circle of Willis. Journal of
Neurosurgery. 1977; 46: 563-78.
22. Pai BS, Varma RG, Kulkarni RN, Nirmala
S, Manjunath LC, Rakshith S. Microsurgical
anatomy of the posterior circulation. Neurol
India. 2007; 55(1): 31-41.
23. Cloud GC, Markus HS. Diagnosis and
management of vertebral artery stenosis. Q J
Med. 2003; 96: 27-34.
24. Seydel GH. The Diameters of the Cerebral
Arteries of the Human Foetus. Anatomical
Record.1964; 150: 79-88.
25. Gillilan
LA.
Significant
superficial
anastomosis of the arterial blood supply to
the human brain. J Comp Neurol. 1959; 112:
55-74.
26. Kirgis HD, Fisher WL, Llewellyn RC,
Peebles E.McC. Aneurysms of the Anterior
Communicating
Artery
and
Gross
Anomalies of the Circle of Willis. J
Neurosurg. 1966; 25: 73-78.
27. Jeng JS, Yip PK. Evaluation of vertebral
artery hypoplasia and asymmetry by
colorcoded
duplex
ultrasonography.
Ultrasound in Med Biol.2004; 30: 605-09.
28. Chuang YM, Huang YC, Hu HH, Yang CY.
Toward a further elucidation: role of
vertebral artery hypoplasia in acute ischemic
stroke. Eur Neurol. 2006; 55:193-97.
29. Giannopoulos S, Markoula S, Kosmidou M,
Pelidou SH, Kyritsis AP. Lateral medullary
807
ischemic events in young adults with

hypoplastic vertebral artery. J Neurol
Neurosurg Psychiatry.2007; 78: 987-89.
30. Watanabe M, Takahashi A,Hashizume Y,
Motegi Y, Furuse K. The correlation
between vertebral artery asymmetry and
pontine infarction: an MR angiography
study. Rinsho Shinkeigaku.1992; 32(7):
708-12.
808
Iqbal et al.,
DOI:10.5958/j.2319-5886.2.4.129

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
nd
Revised: 2 Sep 2013
Research article
Copyright @2013
ISSN: 2319-5886
th
LIGHT EXPOSURE AT NIGHT AND ROTATING NIGHT SHIFT ASSOCIATED WITH

CIRCADIAN DISRUPTION OF 6-SULFATOXY MELATONIN
Anjum B1, Verma NS2, Tiwari S3, Singh R1, Fatima G1, Singh P2, Mishra S2, Mahdi AA1
1
Departments of Biochemistry, 2Departments of Physiology, 3Departments of Surgery, King Georges

Medical University, India
*Corresponding author email: drnsvermakgmu27@gmail.com
ABSTRACT
Background: Alterations in the sleep-wake cycle leads to decreased melatonin secretion and it may be
associated with sleep disorders and cancer risk. Exposure of light at night and rotating night shift
decrease the melatonin production due to acute suppression of pineal melatonin secretion during night
work has been suggested to increases cancer risks. Aims & Objectives: The objectives of the present
study were to investigate the effect of light exposure at night on circadian pattern of 6-Sulfatoxy
melatonin levels in night shift nursing professionals. Material and Methods: 62 healthy nursing
professionals of both genders performing day and night shifts (continuous 9 days night shift with
alternate day shifts) were recruited. Urine samples were collected at around 8 hour intervals (afternoon
sample: between 13:00 to 15:00, night samples between 22:00 to 01:00 and morning samples between
05:00 to 08:00) while they were performing night duties and repeated when they were assigned day
duties. Night melatonin level was decreased as compared to morning melatonin. Results: Night
melatonin level was found declined as compared to morning level and this pattern was significant when
compared night melatonin between night (16.71 11.98) vs day shift (22.71 13.25) and morning
melatonin level between night (20.07 14.13) vs day shifts (28.26 14.14) (p<0.001). Conclusion:
Light exposure at night disrupts the circadian rhythm of melatonin secretion during night shift leads to
internal desynchronization.
Key words: Rotating night shift; Light at Night; Circadian rhythm; 6-Sulfatoxy melatonin.
INTRODUCTION
Rotating night shift disrupts the circadian

rhythms and has been associated with fatigue,
stress and sleep disturbances. Alterations in the
sleep pattern leads to decreased melatonin which
might be associated with sleep disorders, anxiety,
depression, and stress and cancer risk. Those
who work in night shift may attempt to sleep

when their body clock is adjusted for the
awakening phase.1 This attempt disturbs the body
clock resulting in a contradictory relationship
between sleep time and circadian schedule. It is
possible that the circadian sleep propensity
809
Anjum et al.,
rhythm and hormonal rhythm are under influence

of circadian pacemaker as well as sleep habit.2
Majority of the circadian rhythms in our body
have both an endogenous component regulated
by an internal clock, viz. the suprachiasmatic
nuclei (SCN), and it synchronized with an
exogenous component composed of a light-dark
cycle.3,4
Melatonin is a hormone (N-acetyl 5 methoxytryptamine) synthesized and secreted principally
by the pineal gland at night under normal
environmental conditions. The pineal gland
decides whether or not to secrete melatonin and
the amount of melatonin secretion based on
information directly sent from the retina of the
eye. The Retina of the eye contains a unique
subset of cells other than rods and cones, this
unique subset of cells produce a pigment called
melanopsin. Melanopsin allows a cell to detect
light and dark. Information collected by the
unique subset of cells is sent along the
retinohypothalamic tract (RHT), a sort of
information highway that extend from the retina
to the hypothalamus. In hypothalamus, this
information is transmitted to a cell called the
suprachiasmatic nuclei (SCN). The SCN of the
hypothalamus have melatonin receptors and
melatonin may have a direct action on SCN to
influence circadian rhythm.5
Melatonin secretion is enhanced in darkness and
decreased by light exposure. Exposure to
artificial light at night and disruption of the
endogenous circadian rhythm with suppression
of the melatonin synthesis has been suggested
mechanisms.6 Melatonin gives a measure of day
length, it can reset the clock by acting as
chemical zeitgeber. Melatonin is metabolized to
6-hydroxy-mel in the liver and the main
metabolite excreted in urine is 6-Sulphatoxymelatonin are more stable than 6-hydroxy
melatonin in serum. The concentration of 6Sulfatoxy melatonin or 6- hydroxyl melatonin
sulphate in urine correlates with the total level of
melatonin in the blood during the collection
period. Melatonin levels in individuals with
normal sleeping patterns begin to increase during

the evening (~ 9:00 p.m.). Melatonin levels peak
at around 2:00 a.m. and return to baseline around
sunrise (~ 6:00 a.m.).7 Irregular sleeping patterns
can lead to circadian disruption and shift the
amplitude and timing of peak melatonin levels.
The hypothalamic-pituitary adrenal axis (HPA),
has been identified as a potential mechanism of
neuroendocrine system that influenced by night
shift work through which circadian desynchrony
may lead to stress and ill-health.8 The present
study was planned to investigate the effect on
light exposure at night and rotating night on
circadian pattern of 6-sulfatoxy melatonin in
night shift nursing professionals.
MATERIAL & METHODS
The study was approved by the institutional ethic

committee (Ref. code: XXXIV ECM/B-P3), a
detailed proforma was explained to all
volunteers; written informed consent was
obtained from all the subjects. The study
volunteers willing to participate in the study were
recruited from Trauma Centre, GM and
Associated Hospitals, KGMU, Lucknow, UP,
India. Sixty two healthy night shift nursing
professionals, aged 20-40 year, performing
rotating night shift duties (continuous 9 days
night shift with alternate day shifts) from past 56 years, the duration and pattern of shift work
were same among all the subjects. Inclusion
criteria: Subjects were working in continuous 9
days light at night exposure in each month. We
recruited nurses of both genders, age between
20-40 yrs from different wards and units viz.
Intensive care unit (ICU), surgical emergency,
Neurosurgery,
Neurotrauma,
Orthopaedics
emergency and Medicine emergency, who
worked in rotating night shift.
Exclusion criteria: Subjects with any
acute/chronic illness, known patients of diabetes
mellitus,
other
endocrinal
disorders,
hypertension, coronary artery disease, subjects
taking oral contraceptive pills and chronic renal
810
Anjum et al.,
diseases were excluded from this study.

Study design: The present prospective
observational study was planned to investigate
the effect of light exposure at night and rotating
night shift on circadian pattern of 6-sulfatoxy
melatonin in night shift nursing professionals and
whether they are reversible in due course of time.
Collection of Urine samples: Urine samples
were collected at around 8 hours interval in their
night shift and day shift schedules (afternoon
sample: between 13:00 to 15:00, night samples
between 22:00 to 01:00 and morning samples
between 05:00 to 08:00). The volunteers
themselves collected the samples in different
colour vials. For collection of urine samples, a
notebook was provided to each subject with all
details regarding the timing and procedure for
sampling and their sleep-awake timing. Samples
were analyzed for 6-Sulfatoxy Melatonin by the
ELISA method.
RESULTS
There were total 62 (32 male and 30 females)

night shift nursing professionals recruited in the
present study. The effect of light at night
exposure on rotating night shift was investigated
by analyzing urinary 6-sulfatoxy melatonin
levels. All the data were summarized as Mean+
SD & baseline characteristics of male and female
night shift workers are given in Table 1. Groups
were compared by applying paired t test. A two
tailed (=2), p<0.05 was considered significant,
p<0.01 moderate/very significant and p<0.001
highly significant. P value elucidate that if it is <
0.05, < 0.01, < 0.001 then the null hypothesis
would be rejected at 5 %, 1 % or 0.1 %
respectively. Statistical analysis was carried out
by using INSTAT 3.0 (Graph pad prism
software; San Diego, CA). Association of
variable between different shifts was done by
Pearson correlation analysis.
Table 1: Baseline characteristics of night shift workers.
Baseline Characteristics
Age (years)
Weight (kg)
Height (cm)
Body mass index (BMI)
Marital Status
Married
Unmarried
Diet
Vegetarian
Non-Vegetarian
Data are presented as means SD.
Night Shift Workers (n = 62)

24.74 3.81
53.21 8.85
160.44 8.16
20.59 2.40
16 (25.80%)
46 (74.19%)
23 (37.10%)
39 (62.90%)
Table 2: Correlation of Urinary Melatonin between Nights versus Day shift

Measured Variables
Night Shift (NS) versus Day Shift (DS)
6-Sulfatoxy Melatonin
( n=62 )
Afternoon Melatonin: NS vs DS
r =0.13ns
Night Melatonin: NS vs DS
Morning Melatonin:NS vs DS
r =0.51***
r =0.18ns
ns= Non significant, ***p<0.001 highly significant
811
Anjum et al.,
Fig 1: Mean Afternoon, Night and Morning melatonin during night and day shift
(AML: Afternoon Melatonin level; NML: Night Melatonin level; MML: Morning Melatonin level),
(*p<0.05, ***p<0.001; By paired t test; - Bar of the standard deviation).
Melatonin hormone also shows diurnal variation,
its level increases from midnight to early
morning and decreases in the late morning and in
day hours. This pattern was found altered in
rotating night shift workers during night shift.
Melatonin synthesis directly depends upon
transport of signal of light in the day time and
conversion of serotonin into melatonin depends
upon signals of darkness received at night.
However, its level may differ from individual to
individual. Normal range of melatonin is 0.8-40
ng/ml, its levels increases at midnight and
declines in day time. Night 6-sulfatoxymelatonin
level was found declined as compared to
morning level and this pattern was significant
when
compared night 6-sulfatoxymelatonin
between night (16.71 11.98) vs day shift (22.71
13.25) and morning melatonin level between
night (20.07 14.13) vs day shifts (28.26
14.14) (p<0.001) (Figure 1). 6-sulfatoxy
melatonin level of evening and morning time
during night shift was positively associated with
that of during day shift. Since the pattern of
melatonin secretion was altered in early morning
time during night shift hence this positive

association did not reach at significant level
(p>0.05);(Table 2). 6-sulfatoxy melatonin level
of night time during night shift was positively
associated with that of during day shift and this
association was highly significant (p<0.0005).
The result show that light exposure at night
effect on melatonin production during night shift.
Altered 6-sulfatoxymelatonin levels were found
at night and in the morning samples during night
shift.
DISCUSSION
Previous studies have reported that subjects

exposed to light and who remain awake at night
have lower levels of melatonin at night , as
melatonin synthesis always occurs at night,
particularly in the darkness. On the basis of the
finding of the previous studies, it has been
hypothesized that exposure of light at night
(LAN) is one of potential mechanisms of breast
carcinogenesis in the night shift workers through
decreased melatonin synthesis.6 Findings of the
recent study indicates that two nights of rotating
812
Anjum et al.,
shift work may not change the timing of

melatonin production to the day among those
working at night.9 While the results of the
present and other studies indicate that working
six to eight or more night shifts per month may
disrupt the synthesis of melatonin.6 Finding of
our study in agreement with previous study
indicate that night shift workers have
substantially lower level of 6-sulfatoxymelatonin
at night work and daytime sleep during night
shift, and levels remain low when night shift
workers sleep at night during day shift. Long
term chronic reduction in melatonin among night
shift workers may be an important carcinogenic
mechanism, which could affect the cancer
risk.10,11 Other studies have also reported higher
incidence of poorer sleep and its complications in
night shift workers.12-14 These findings reinforce
previous studies which reported elevated
exposure to cortisol on early shifts, relative to
normal later working days and rest days, might
promote pathogenic processes including insulin
resistance.15 and help to elucidate the increased
risks of cardiovascular diseases in rotating night
shift workers.16 In other study, the related
neurotransmitters like Urinary norepinephrine
and Epinephrine were higher during work than
non-work in the day, but in evening shift and
night shift workers, the difference was lesser and
in opposite direction. Working evening or night
shift are independent predictors of Non dipper
status.17 During night shift the hormones are
more sensitive to endogenous components like
catecholamine, prolactin, and growth hormones
which showed an immune response to the shifted
sleep/activity cycle, evidencing a masking
effect due to the work activity. In another study,
hormones
having
stronger
endogenous
components, such as cortisol and Melatonin,
showed a more stable pattern, with a slight
tendency for partial adjustment of cortisol during
the second night.18 The onset of sleep was
consistently followed by a decrease in
concentration of cortisol. While both sleep-wake
and light-dark transitions were consistently
associated with cortisol secretary pulses.19 It is

also reported that the sleep factor (time of onset
and/or period) seemed to be more potent in
modifying the circadian rhythm of serum
cortisol, especially with the night shift.20 Sleep
was initiated (on average) about three hours prior
to the onset of melatonin production in night
shift workers while in day-active subjects
initiated sleep (on average) about three hours
after their melatonin onset. Thus, the sleep times
availed for night shift workers may not be wellsynchronized to their melatonin secretion
rhythm, assumed to mark the phase of their
underlying circadian pacemaker.21
The change in the Acrophase of 6-sulfatoxymelatonin was associated with different shifts.22
The overall advance of Melatonin profile was
primarily achieved during the initial exposure to
an 8h period of darkness. The present data
suggested that exposure to dark affects human
circadian phase.23 In the present study, subjects
with rotating shifts of 12 hrs night works had
complained of difficulty in sleep, decreased
calculative tasks, impaired cognitive functions,
decreased alertness, constipation, stress and
mental fatigue which is in accordance with the
other studies.24, 25 Quality and quantity of sleep
are also affected by rotating night shift. Duration
of sleep was shorter during day time at night shift
(3-4 hours less as compare to night time sleep
during day shift). Night shift nurses have
experience changes in aMT6s levels after six to
eight nights in a month and the findings might be
related to the increased cancer risk reported in
night-shift workers and suggest that a short nap
during night-shifts may exert a positive effect to
night shift workers.26 The long term higher
intensity of light exposure during night work
may have decreased total melatonin production,
possibly by initiating re-entrainment and leads to
internal desynchronization that could be the
mediator between night shiftwork and cancer
risks.27 In brief, it is possible that rotating night
shift appears to have adverse effects on bodys
813
Anjum et al.,
physiological rhythm leads to hormone related

disorders and cancer risk.
CONCLUSION
In present study, we concluded that rotating night

shift disrupt the circadian pattern of melatonin
particularly at night and in the morning time
during night shift due to desynchronization.
However, recovery was found when subjects
went back to the day shift. Prolonged exposure of
light at night leads to decreased melatonin level
may be one factor contributing to an increased
risk of cancer and other endocrinal disorders in
rotating night shift workers.
ACKNOWLEDGEMENT
The authors gratefully acknowledge the

invaluable contributions of the nursing staff to
various aspects of the study. We would also like
to thank the Council of Science & Technology,
UP for financial support for this study.
Conflicts of interest: The authors declare that
there is no conflict of interest.
REFERENCES
1. Lamond N, Dorrian J, Roach GD, McCulloch
K, Holmes A L, Burgess et al. The impact of
a week of simulated night work on sleep,
circadian phase and performance. Occup
Environ. Med; 2003;60: 13.
2. Kudo Y, Uchivama M, Okawa M, Shibui K,
Kamei Y, Hayakawa T, et al. Correlation
between the circadian sleep propensity
rhythm and hormonal rhythm under ultra
short sleep-wake cycle. Psychiatry Clin
Neurosci. 1999;53:253-55.
3. Nagai K, Nagai N, Sugahara K, Niijima A,
Nakagawa H. Circadian rhythms and energy
metabolism and special reference to the
suprachiasmatic nucleus. Neurosci Biobehav
Rev. 1994;18:579-84.
4. Santhi N, Jeanne F, Duffy Todd, Horowitz,
Charles A, Czeiser. Scheduling of
sleep/darkness affects the circadian phase of

night shift workers. Neuroscience letters.
2005;384: 316-20.
5. Kara Rogers. Cancer on the night shift; Why
night workers are at risk. The Lancet
Oncology.http://www.britannica.com/blogs/2
007/12/cancer-on-the-night-shift-whyworkers-are-at-risk
6. Peplonska B, Bukowska A, Gromadzinska J,
Sobala W, Reszka K, Lie JA, et al. Night
shift work characteristics and 6 sulfatoxy
melatonin (MT6s) in rotating night shift
nurses and midwives. Occup and Environ
Med. 2012; 69(5): 339-46.
7. Zee and Manthena. The brains master
circadian
clock:
Implications
and
opportunities for therapy of sleep disorders.
Sleep Medicine Reviews.2007;11(1): 59-70.
8. Nader N, Chrousos GP, Kino T. Interactions
of the circadian clock system and the hpa
axis. Trends Endocrinol. Metab. 2010;21(5):
277-86.
9. Grundy A, Sanchez M, Richardson H,
Tranmer J, Borugian M, Charls H. et al.
Light intensity exposure, sleep duration,
physical activity, and biomarkers of
melatonin among rotating night shift nurses.
Chronobiol Int. 2009; Oct 26: (7):1443-61.
10. Mirick DK, Bhatti P, Chen C, Nordt F,
Stanczyk FZ, Davis S. Night shift work and
level of 6- sulfatoxy melatonin and cortisol in
men Cancer Epidemiol Biomarkers Prev.
2013:22. (6):1079-87.
11. Davis S, Mirick DK, Chen C, Stanczyk FZ.
Night shift work and hormone level in
women Cancer Epidemiol Biomarkers. Prev.
2012; 21(4):609-18.
12. Hennig J, Kieferdarf P, Moritz C, Huwe S,
and Netter P. Changes in cortisol secretion
during shift work :implication for tolerance
to shift work. Ergonomics.1998; 41(5):61021.
13. Akerstedt T. Sleepiness as a consequence of
shift work. Sleep.1988;11:17-34.
814
Anjum et al.,
14. Rutenfranz J, Colquhoun WP, Knauth P,

Ghata JN. Biomedical and physiological
aspects of shift work. Scand J Work Environ
Health. 1977; 3:165-82.
15. Sack RL, Blood ML, Lewy AJ. Melatonin
rhythm in night shift workers. Sleep.
1992;15(5):434-41.
16. Anagnostis P, Athyros VG, Tziomalos K,
Karagiannis A, Mikhailidis DP. Clinical
review: The pathogenetic role of cortisol in
the metabolic syndrome: A hypothesis. J Clin
Endocrinol Metab 2009;94(8): 2692-01.
17. Fujino Y, Iso H, Tamakoshi A, Inaba Y,
Koizumi A, Kubo T,et al. A prospective
cohort study of shift work and risk of
ischemic heart disease in Japanese male
workers. Am. J. Epidemiol. 2006;164(2):
128-35.
18. Yamasaki,F., Schwartz,J.E., Gerber,L.M.,
Warren,K., and Pickering,T.G. Impact of
shift work and race/ethnicity on diurnal
rhythm
of
blood
pressure
and
catecholamines. Hypertension:1998; 32(3):
417-23.
19. Costa G, Bertoldi A, Kavocic M, Ghirlanda
G, Minors DS, Waterhouse JM. Hormonal
secretion of nurses Engaged in fast rotating
shift system.
Int J Occup Environ
Health.1997; (Supll 2):S35-S39.
20. Coufrei Z, Moreno-Reyes R, Leproult R,
Vertongen F, VanCauter E, Copinshi G.
Immediate effects of an 8-hours advance shift
of the rest activity cycle on 24h profile of
cortisol. Am.J.physiol Enocrinol Metab.
2002;282(5):E1147-53.
21. Fujiwara S, Shinkai S, Kurokawa Y,
Watanable T. The acute effects of
experimental short-term evening and night
shifts on human circadian rhythm: the oral
temperature, heart rate, serum cortisol and
urinary catecholamines levels. Int.Arch
Occup Environ Health.1992;63(6):409-18.
22. Quera Salva MA, Guilleminault C, Claustrat
B, Defrance R, Gajdos P, McCann CC. et al.
Rapid shift in peak melatonin secretion
associated with improved performance in

short shift work schedule. Sleep.1997;
20(12):1145-50.
23. Yan Cauter E, Moreno-Reves R, Akseki EL,
Hermite Baleriaux M, Hirchfeld U, Leproult
R. et al. Rapid phase advance of the 24 h
melatonin profiles in response to afternoon
dark exposure. Am J Physiol:1998;275 (1
pt1):E48-54.
24. Takahashi M, Fukuda H, Milki K, Haratani
T, Kurabayashi L, Hisanga N. et al. Shift
work related problems in 16h night shift
nurses (2);Effects on subjective symptoms,
physical activity, heart rate and sleep.
Ind.Health:1999;37(2): 228-36.
25. Anjum B, Verma NS, Tiwari S, Singh R,
Mahdi AA, Singh RK, et al. Association of
salivary cortisol with chronomics of 24 hours
ambulatory blood pressure/heart rate among
night shift workers. Bioscience Trends.2011;
5(4):182-88.
26. Bracci M, Copertaro A, Manzella N,
Staffolani S, Strafella E, Nocchi L, et al.
Influence of night-shift and napping at work
on urinary melatonin, 17-ß-estradiol
and clock gene expression in pre-menopausal
nurses. J Biol Regul Homeost Agents. 2013;
27(1): 267-74.
27. Dumont M, Lanctt V, Cadieux-Viau R,
Paquet J. Melatonin production and light
exposure of rotating night workers.
Chronobiol Int. 2012;29(2):203-10.
815
Anjum et al.,
DOI:10.5958/j.2319-5886.2.4.130

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Revised: 5th Sep 2013
Research article
Copyright @2013
ISSN: 2319-5886
SEROPREVALENCEOF HBV, HCV AND HIV INFECTIVITY AMONG BLOOD DONORS IN

IBN SINA TEACHING HOSPITAL IN SIRT REGION OF LIBYA
Ismail Mahmud Ali1, *Amirthalingam R2
1
Hospital Director, Head, Assistant Professor, Department of Surgery, 2Specialist, Department of

Molecular biology, Ibn Sina Teaching Hospital, Sirt University, Libya. P.O.Box 705.
*Corresponding author email:amrith2002@rediffmail.com
ABSTRACT
Background &Aim:Numerous infectious diseases are spread by blood transfusion, particularly viral
infections. The hepatitis B virus (HBV), hepatitis C virus (HCV), and human immunodeficiency virus
(HIV) and other pathogenic organisms are transmitted through inappropriate screening of blood product.
These infected blood products are causing fatal, persistent and life frightening disorders. The
predominance of these viruses differs by ethnic group and geography. Scheme of the current study was
to statistical estimation of the incidence of HBV, HCV and HIV along with blood donors. Materials &
Methods: The existing review was approved in Ibn Sina Teaching Hospital, Sirt Region of Libya. A
total of 16,929donors were analyzed by enzyme immune assay (EIA) kits from TaytecInc, Canada, for
the predominance of human immunodeficiency virus, hepatitis B and C virus, over a period of 17
months from January2012 to May 2013.Results: Among the blood donors, 81.40% were unpaid donors
and 18.60% were alternative donors. The total incidence in blood donors was 3.18%. The
seroprevalence of hepatitis B was uppermost (1.98%) followed by hepatitis C (1.20%) and
seroprevalence of HIV was nil among unpaid and surrogate donors. Conclusion: Present study was
emphasized the prevalence rates of HBV and HCV between charitable and alternative blood donors and
the HIVwas not detected in the current study.The prevalence rate was more in male among the blood
donors.
Keywords: Human immunodeficiency virus, Hepatitis B&C virus, Seroprevalence, Blood donors
INTRODUCTION
Blood transfusion is the transfer of blood and its

components such as red blood cells, platelets,
and plasma from donor to recipient. Donation of
the blood saves the life of millions of people
universally, and it is essential to the helpfulness
of the health system by supporting current
Ismail et al.,
medicine as its key role in patient contribution 12

.Today, the medical and surgical procedure like
organ transplantations, heart surgery, trauma,
cancer and hematologic condition such as severe
anemia, leukemia, sickle cell disease, and others
health emergency depends extremely on blood
816
transfusions worldwide. Hence, in developing

countries,
blood
transfusion-transmitted
infections (TTIs) frequently terrorize the defense
of patients demanding blood transfusion, and
healthcare facility supplier faces serious
challenges with blood availability and protection
because of an improper facility. It is estimated
about 45% of 80 million blood donations through
the world are collected every year in rising
nation that included almost 80% of the worlds
population3-4.
In universal healthcare service provider, the
blood safety studies have integrated procedure
for clinical laboratory screening of HIV1&2;
human T-lymphotropic virus 1&2(HTLV);
hepatitis B&C virus; West Nile virus,
cytomegalovirus; human herpes virus 8,
parvovirus B19, malaria; Creutzfeldt-Jakob
disease, influenza, chikungunya; dengue,
trypanosomacruzi
and
other
viruses.
Furthermore, the very important subject that
making difficulties of transfusion because of
bacterial contamination of platelets in blood
products5.This screening protocol might be
differing from country to country and depend on
epidemiological condition. In addition to
infectious diseases threat, clinicians should also
supervise other risk, such as post blood
transfusion reactions. These include transfusionrelated lung injury (TRALI); transfusion
associated circulatory overload (TACO), and
transfusion-related immune modulation (TRIM),
post transfusion iron overload and graft versus
host diseases (GVHD) 6.
The blood transfusion department contains
clinical methods and guidelines for screening of
blood before transfusion. If the screening
procedure and other regulation are not followed
well there is possibility to carry the risk of
spreading
blood
transfusion
contagious
pathogens like HIV, HBV, HCV, Bacteria
(syphilis) and others7. Also, there is a 1% of
chance of transfusion related infection in each
unit of blood even if the procedure followed
well8.Therefore, the risk of blood transfusionIsmail et al.,
transmitted infection today is minimized than

constantly, the delivery of safe blood products
stays behind inquiry to infection with accepted
and until now to be predictable human
pathogens9.
To supply of safety blood product for
transfusion, it's compulsory to introduce an
advanced technology like a nucleic acid test
(NAT) because of an excellent clinical sensitivity
and good specificity to detect infected blood
components as it identified pathogens prior in the
'window period' than enzymes immune assay10.
Even though, it has some margin in blood
components with lesser range of viremia, which
can even free quantifiable by NAT11. Even with
this margin, the grouping of both enzymes
immune assay and NAT has notably condensed
the hazard of pathogen spread during transfusion
12-13
.Also many scientific research data showed
that the comparison between p24 antigen
detection or conventional serological testing, it is
estimated that the use of NAT reduces the
detection time from 22 to 11 days for HIV; from
70 to 10 days for HCV and from 60 to 30 days
for HBV infection. Final outcome of this, the
prevalence risk for HIV is between 0.14-1.1 and
for HCV between 0.10-2.33 per million units
transfused13-14.The greater risk of HBV spread
through blood transfusion differ between the
countries. The HBV infection through blood
transfusion differs among 0.75 per million blood
donations in Australia, 3.6-8.5 in the USA and
Canada.0.91-8.7, also from North region 7.5-13.9
in the Southern region of Europe; up to 200 per
million blood contributions in Hong Kong,
mostly reflecting the universal epidemiology15.
The objective of this study is to statistical
estimations of those pathogenic viruses such as
HBV, HCV and HIV in well blood contributor.
Hence, it needs to authenticate how well we are
responsibility in clinical laboratory and
proficiently in work with medical ethics. This
statistic may possibly assist in creating the state
health plan to advance improve the background
and method to instruct the public concerning the
817
subject matter of these burdens therefore to

reduce the incidence of illness and death formed
by these
viral pathogens through blood
transfusion.
Study Population: In the present study were

incorporated 16,929 blood donors (99% of male).
All the donors have been screened with medical
consultant before donation, who attended as
voluntary and replacement in blood transfusion
department at Ibn Sina Teaching Hospital, a
tertiary care hospital Sirt region of Libya during
the period of January 2012 to May 2013.The
ethics committee and an internal appraisal panel
of the organization approved the procedure.
Informed consent obtained from individual
patients.
Sample Collection: Five milliliters (5ml) of
venous blood was collected from each patient
using plain vacationer tubes after taking history
and clinical examination. All samples were
allowed to clot and centrifuged at 3000 rpm for
10 minutes. All serum samples were separated
into sterile 2ml cryovial containers and stored at
-20C until ready for use.
Serology:All donors samples were screened by
enzyme immune assay (EIA) kits from
TaytecInc, Canada, for HIV-1 antigen and HIV-2
antigen; HBsAg and Anti-HCV antibodies. The
EIA was authenticated by the approval standard
instructed by the manufacturer for the optimal
density of reagent blank and optimal density
mean value of positive and negative controls
given with the test protocol. The least value (cut
off) was considered as per company guideline for
reporting positive and negative outcomes.
Confirmed positive and negative samples were
used subjectively as an outside run in each
screening for our laboratory intention. The
donated blood was discarded if the serum sample
was found positive for any infectivity. The
statistical analysis was done using Microsoft
ware office excel 2007.
Ismail et al.,
RESULTS
A total 16,929 donors were integrated in the
study. Of these, 3152 (18.60%) were replacement
and 13777 (81.40%) were voluntary donors.All
of the samples were collected within transfusion
department not from any other branch of
requirement of blood donation. Males blood
donorsmore than female with16, 862(99.6%)
donations while only 67(0.4%) donors were
females. Among these, most of the donors aged
from 18 to 40 years. Out of the 16,929 blood
donors, 535 were tested positive for donated
healthy blood samples (3.18%).Out of these, 61
were alternative donors. In general, the
predominance of HIV, HBsAg,HCV and total
positivity in blood screening was 0%, 1.98%,
1.2% and 3.18%,in assenting order (fig-1).The
prevalence of HBsAg in total donors was 1.98%
(333 cases). Substitute donors (44 cases) had a
high incidence with low frequency of patients as
compared to the voluntary donors (289 cases).
The seropositivity of HCV in total donors was
1.20% (202 cases). Replacement donors (17
cases) had a low incidence with low frequency of
patients as compared to the voluntary donors
(185 cases). Zero prevalence of HIVwas zero
among all blood donors. The infectivity rate of
male blood is higher than female blood donors.
The agreeing rates for seropositivity were peak
for HBsAg infection followed by HCV infection
in descending order. The co-infection of
transfusion transmitted infectious diseases has
not been studied among blood donors.
1.98% 1.20%
Negative
96.82%
HBsAg Positive
HCV Positive
Fig.1: Distribution of seroprevalence
818
DISCUSSION
Blood transfusion is a branch of medicine in the

healthcare sector. An incorporated strategy for
blood safety is required for elimination of
transfusion transmitted infections and for
provision of safe and adequate blood. The
infectious agents such as HIV, HBV and HCV
are important blood born and transfusion
transmitted infections throughout the world
including Libya. The previous research statistical
data has been established that prevalence rate of
HBsAg, anti-HCV and anti-HIV among blood
donors or the general population varied from
country to country16.
In the present study, the prevalence of HBsAg
and anti-HCV antibodies was 1.98% and 1.20%
respectively. These prevalence rates can be
compared with other provincial studies from
Central Hospital (Tripoli), and from Libyan
National Center for Infectious diseases were
2.2%, 1.2%17 and others studies 22.7% was
reported with HCV infection through blood
transfusion18.Also, these rates can be compared
with other studies from Egypt, from the Eastern
Mediterranean region and elsewhere, the antiHCV in Egyptian blood donors studies found
13.6% were anti HCV antibodies detected as
infection18.In Saudi Arabia the prevalence of
anti-HCV and HBsAg infection in blood donors
was 0.4% and 4%19.
In current study none of the donors had a
confirmed positive result for HIV infections. The
comparisons of the prevalence of transfusion
viruses among different sex blood donors may
not be valid because of high percentage of male
donors; this is due to low hemoglobulin in
females and the fact that women are less willing
to donate blood. The most of the donors (99%)
were male, which is similar to the preceding
report20, 21.The differences in the incidence
between current and past studies may be credited
to differences in the sensitivities of the assay
used, and the criteria of positivity in the degree
Ismail et al.,
to which individuals with risk factors for bloodborn viral infections may have been excluded.
In general, the prevalence rates of hepatitis B and
C were lower among young donors than older
donors. This confirms the results reported earlier
by other investigators22.In contrast, most of the
blood donors in Libya are young men (1840years of age). It is recognized that this age
group is generally arrogant group example of
misusing of drug, insecure sex, and other
misbehavior habits for the transmission of the
virus. This may be explained on the essential of
increased exposure with age and on the fact that
a high awareness of blood born viral infections
has developed and a comprehensive vaccination
program against hepatitis B has been
implemented in Libya. It should be noted that the
carrier rate of HBV was higher than the carrier
rate of HCV in this study and in other studies23.
These data suggested that the mode of
transmission and the efficiency of transmission
of HBV may be different from that of HCV.
The predominance of HBV and HCV between
blood donors was lower than it is in other
countries. The prevalence of hepatitis B among
blood donors was 3.8% in Syria23, 9.8% in
Yemen24, 2.1% in Egypt25, >5.0% in Sudan26,
10.7%in Cameroon27, 8.8% in Tanzania28and
(Africa 5-15%). Similarly, the prevalence of
HCV was 2% in Yemen24, 4.8% in Cameron27,
1.5% in Tanzania28, and high in Egypt 13.6%25.
This was probably due to the compulsory
screening of all emigrants prior to granting
residency in Libya. The other infectious agent of
blood transfusion is HIV causes major health
problem in sub Saharan Africa where the
prevalence of HIV among blood donors ranges
between 2-20% in Kenya29, and 5.9% in
Ethiopia30.However, our results showed no
confirmed HIV in the analyzed blood donors.
Hence, the previous blood donors study in Libya
reported the prevalence rates of HIV was 0.4
%31.The frequency of HBsAg is more compared
to the anti-HCV.There is no way to ignore that
blood donation which is collected in the
819
window period of infectious might be

transmittable even though a negative antibody
test. Therefore, the introduction of screening
procedures for hepatitis B core antigen and
performance of NAT are advised in the blood
transfusion division in this locality.
In feature direction, the implementation of new
technology like
MALTI-TOF32MS(MatrixAssisted Laser desorption/Ionization, Time of
Flight Mass Spectrometry) for the genomic
detection of the 101 blood groups antigen;DNA
microarray33 for complete blood groups typing;
and
integrated
microchip
arrays
or
34
nanotechnology
are being developed to
enhance rapid screening of donated blood for any
numbers of infectious diseases to get paramount
donors for blood transfusion and get free from all
kinds of risk including viruses, bacteria and
blood typing. Further, taming public, generating
notice, consoling unpaid blood donation, highquality blood bank practice and employing a
meticulous donor range condition according to
blood transfusion by National Infectious
Diseases control Organization is an important
factor.
CONCLUSION
In 17 months period, 16929 units of blood

werecollected. A total positivity of blood;
HBsAg, anti-HCV and anti HIV were 3.18%,
1.98%, 1.20 % and 0% respectively. The
seroprevalence rate was tall in unpaid donors as
compared to surrogate donors because of most of
them charitable donors.The major limitation of
this study is the fact that there is no previous
study and or data available in this region for
comparison.
ACKNOWLEDGEMENT
We acknowledge the support provided by

technical staff from Blood Bank and Serology
division of Ibn Sina Teaching Hospital, Sirt
Region of Libya.
Ismail et al.,
REFERENCES
1. Eyles J, Heddle N, Webert K, Arnold E,

McCurdy B. Do expert assessments
converge? An exploratory case study of
evaluating and managing a blood supply
risk.BMC Public Health.2011; 11:666.
2. Gharehbaghian A, Abolghasemi H, Namini
MT. Status of blood transfusion services in
Iran. Asia J Transfus Sci.2008; 2(1):13-7.
3. Reynolds L, McKee M. Matching supply and
demand for blood in Guizhou province,
China: an unresolved challenge. Public
Health (Oxf).2010; 32(1):103-9.
4. World
Health
Organization.
Blood
transfusion safety (updated 2012 June 14);
Available from: http://www.who.int/blood
safety/en.
5. Klein man S, King MR, Busch MP, Murphy
EL,GlynnSA. National Heart Lung Blood
Institute Retrovirus Epidemiology Donor
Study; Retrovirus
Epidemiology
Donor
Study-II.Twenty years of research to advance
blood
product
safety
and
availability.Transfuse. 2012 Oct; 26(4):28104.
6. Naomi LC, Luban. Childrens National
Medical Center, Washington, DC; Advances
in Transfusion Medicine.2008; 4:421445.
7. Jain C, Mogra NC, Mehta J, Diwan R, Dalela
G. Comparison of seropositivity of HIV,
HBV, HCV and Syphilis and Malaria in
replacement and voluntary blood donors in
Western India. IJCRR. 2013;5:43-46.
8. Widman FK (eds.), Technicalmanual.
American Association of Blood Banks,
Arlington, 1985, pp. 325-344.
9. Florian Bihl,DamianoCastelli, Francesco
Marin cola, Roger Y Dodd and Christian
Brander.Transfusion-transmitted infection.
Journal of Translational Medicine. 2007; 525.
10. Stramer SL, Glynn SA, Kleinman SH, Strong
DM, Caglioti S, and Wright DJ et
al.Detection of HIV-1 and HCV infections
820
among antibody-negative blood donors by

nucleic acid amplification testing. N Engl J
Med.2004; 351(8):760-68.
11. Schuttler CG, Caspari G, Jursch CA, Willems
WR, GerlichWH,and Schaefer S, et
al.Hepatitis C virus transmission by a blood
donation
negative
in
nucleic
acid
amplification tests for viral RNA.
Lancet.2000;355(9197):41-42.
12. Allain JP, Bianco C, Blajchman MA, Brecher
ME, Busch M, Leiby D,et al. Protecting the
blood supply from emerging pathogens: the
role of pathogen inactivation. Transfus Med
Rev.2005;19(2):110-26.
13. Dodd RY, Notari EP, Stramer SL: Current
prevalence and incidence of infectious
disease markers and estimated windowperiod
risk in the American Red Cross blood donor
population. Transfusion.2002;42(8):975-79.
14. Alvarez do Barrio M, Gonzalez Diez R,
Hernandez Sanchez JM, Oyonarte Gomez S:
Residual risk of transfusion-transmitted viral
infections in Spain, 1997-2002, and impact of
nucleic
acid
testing.
Euro
Surveill.2005;10(2):20-22.
15. Coste J, Reesink HW, Engelfriet CP,
Laperche S, Brown S.Implementation of
donor screening for infectious agents
transmitted by blood by nucleic acid
technology: update to 2003. Vox Sang.2005;
88(4):289-303.
16. Luksamijarulkul P,Thammata N,Tiloklurs
M.Seroprevalence of hepatitis B,hepatitis C
and human immunodeficiency virus among
blood donors,Phitsanulok Regional Blood
Centre,Thailand. Southeast Asian J Trop Med
Public Health.2002;33:272-9.
17. NilimaSawke,
Sawke
GK,
Chawala.Seroprevalence
of
common
transfusion-Transmitted infections among
blood donors. Peoples journal of scientific
research.2013;3(1):5-7.
18. Abudher A,Esmeo MN,Sammud M,Elzouki
A,Tashani O,El-Gadi S.Prevalence of
hepatitis B,C and HIV infections in Libya:
Ismail et al.,
how big are the problem? Submitted to XVII

International AIDS Conference in Mexico
City, 3-8 August 2008.
19. Gurol E. Trends in hepatitis B and hepatitis C
virus among 12. Blood donors over 16 years
in
Turkey.
European
Journal
of
Epidemiology. 2006; 21:299305.
20. Saeed AA, Fairclough D, Al-Admawi AM,
Bacchus R, Osoba A, Al-Rasheed A, et al.
Hepatitis C virus in Saudi Arabia a
preliminary survey. Saudi Med J. 1990; 11:
331-332.
21. Arora D, Arora B, Khetarpal A,
Seroprevalence of HIV, HBV, HCV and
Syphilis in blood donors in Southern
Haryana. Indian J Pathol Microbial. 2010;
53(2):308-09.
22. Rao P, Annapurna K, HIV status of blood
donors and patients admitted in KEM
Hospital Pune.Indian J Hemat Blood Transf.
1994; 12:174-76.
23. Sarkodie F, Adarkwa M, Adu-Sarkodie Y,
Candotti D, AcheampongJW,Allain JP.
Screening for viral markers in volunteer and
replacement blood donors in West Africa.
Vox Sang. 2001; 80: 142-147.
24. Haidar NA. Prevalence of hepatitis B and
hepatitis C in blood donors and high risk
groups in Hajjah, Yemen Republic. Saudi
Med. J 2002; 23:1090-94.
25. Darwish MA, Raouf TA, Rushdy P,
Constantine NT, Rao MR, Edelman R.Risk
factors associated with a high seroprevalence
of hepatitis C virus infection in Egyptian
blood donors. Am J Trop Med Hyg. 1993;
49: 440-447.
26. Mahgoub.Hepatitis B virus infection and
recombination between HBV Genotypes
DandE in Asymptomatic Blood Donors
fromkhartoum,Sudan.JClin
Microbiol.2011;49(1):298-306
27. Mbanya DN, Takam D and Ndumbe
PM.Serological findings amongst first time
blood donors in Yaounde Cameroon are safe
821
donation a reality or myth? Transfusion

Medicine.2003; 13(5):267-73.
28. Mecky IN Matee, Pius M Magesa and Eligius
F Lyamuya.Seroprevalence of human
immunodeficiency virus hepatitis B and C
viruses and syphilis infections among blood
donors at the Muhimbili National Hospital in
Dar Es Salaam. Tanzania BMC Public
Health.2006; 6:21.
29. Moore A, Herrera G, Nyamongo J, Lackritz
E, Granade T, Nahlen B, et al. Estimated risk
of HIV transmission by blood transfusion in
Kenya.Lancet. 2001; 358: 657-60.
30. Sentjens R, Sisay Y, Vrielink H, Kebede D,
Ader HJ, Leckie G, et al. Prevalence of and
risk factors for HIV infection in blood donors
and various population subgroups in
Ethiopia. Epidemiol Infect. 2002; 128:221228.
31. Zaid A, Elneihonum A, Elzouki A. Routine
screening for anti-HIV antibodies, hepatitis
Bsurface antigen and anti-hepatitis C
antibodies among general hospital in
patients.JMJ.2010; 8-12.
32. ChristophGassner,Stefan Meyer, Beat M.
Frey,CarenVollmert; Matrix-Assisted Laser
Desorption/Ionization, Time-of-Flight Mass
SpectrometryBased
Blood
Group
GenotypingThe Alternative Approach.
Transfusion Med. 2013;27: 29.
33. Hashmi G, Sharif T, Seul M.A flexible array
format for large-scale, rapid group DNA
typing. Transfusion 2005; 45:680-88.
34. Clewley JP. A role for arrays in clinical
virology: fact or fiction? J ClinVirol 2004;
29:2-12.
Ismail et al.,
822
DOI:10.5958/j.2319-5886.2.4.131

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
A STUDY ON HEARING THRESHOLD PROFILE IN TRAFFIC POLICE PERSONNEL

*Shelke BN1, Aundhkar VG2, Adgaonkar BD3, Somwanshi SD4, Gavkare AM1, Ghuge SH1
1
Assistant Professor, 3 Professor and Head, 4Associate Professor, Dept of Physiology, MIMSR Medical
College, Latur, Maharashtra, India
2
Professor and Head of Dept, Dept of Physiology, Govt. Medical college, Miraj, Maharashtra, India
* Corresponding author email: bhagwat.shelke@gmail.com, dr.bhagwat@yahoo.co.in
ABSTRACT
Introduction: Noise is one of the causes of preventable sensori-neural loss. The traffic police
personnel(TPP) busy in controlling traffic at heavy traffic junctions suffer from the ill effects of noise
and air pollution. Aim and objectives: The objective of this study was to assess the hearing threshold at
various frequencies of the traffic police persons exposed to the vehicular noise and comparison with
controls not exposed to noise. Material and methods: Thirty TPP and thirty controls were evaluated by
clinical methods and subjected to the Pure Tone Audiometry (PTA) in ENT department. Audiogram
recorded by using conventional techniques in both ears. RESULTS: There was a significant difference
in the hearing thresholds at frequency 2000 Hz, 4000 Hz and 8000 Hz of right and left ear between the
two groups. Conclusion: This study concludes an increased risk of noise induced hearing loss (NIHL)
for the environmental noise exposed subjects.
Keywords: Traffic police personnel, TPP, Hearing threshold, NIHL
INTRODUCTION
Automobile vehicles are the major sources of

noise in the city, which originates from engines,
air turbulence and frictional contact of the
vehicle's tiresto the ground. Noise is one of the
causes of preventable sensori-neural loss. The
attention has to be given towards the problem as
no cure is available for noise induced hearing
loss because of irreversible damage to the hair
cells.1-4Studies carried out by various workers
showed an average traffic sound in the city is
about 60-102 dB.5,6The traffic police personnel
busy in controlling traffic at heavy traffic
junctions suffer from ill effects of noise and air

pollution. Irritation of upper respiratory tract
provokes them to use a mask to prevent the ill
effects of air pollution. However, the insidious
nature of the noise induced hearing loss keep the
majority of them unaware of the effects of noise
pollution. 7,8
With this background, this study was carried out
to evaluate hearing threshold profile of traffic
police personnel serving at busy parts of streets
in the city.
Shelke et al.,
Int J Med Res Health Sci. 2013; 2(4): 823-827
823
MATERIAL AND METHODS
as an audiogram. Audiogram recorded by using

conventional techniques in both ears. The test
begun at 1000 Hz and then other frequencies
were tested in the following order 20004000Hz repeated again followed by 500Hz
and 250 Hz. The examiner first familiarizes the
subject with the tone by delivering the sound at
an arbitrarily presumed supra-threshold level
oftesting frequency. When the subject hears
the tone, the tone is reduced by 10 dB till
subject stops hearing or fails to give a
response. Once this stage is reached the tone
raised by 5 dB. If the subject hears this tone, the
sound is again decreased by 10 dB. If he does not
hear it, the tone was again raised by 5 dB. In
this way by several threshold crossings
(between 10-110 dB), the exact hearing
threshold was obtained when one gets at
least 3 out of five responses correct.
After the approval from Secretary of ethical

committee this study was conducted in Miraj,
city of Maharashtra (India), between July to
December 2010 in 30 traffic police personnel
(TPP) and 30 normal healthy individuals as a
control from the same city and residing in the
College campus. Written informed consents were
obtained from all the subjects.
Inclusion criteria: Age between 25 to 45 years.
Five years of exposure to traffic pollution, with
spending average 8 hours in busy traffic areas.
The thirty normal healthy individuals (control
group) were of the same age and sex. The
study and control group belonged to the
same ethnic group. All the subjects were males.
Exclusion criteria: A primary screening was
done in the medicine and ENT outpatient
department by personal history and otoscopic
examination. By taking detailed personal
RESULTS
history subjects having smoking habits,
diabetes
mellitus and hypertension were
The age, height, body weight and BMI were
excluded from the study. Subjects having
compared between the control and study group
conditions that may affect the hearing like ear
using two tailed un-paired Students t test in
drum perforation, acute or chronic suppurative
Microsoft Excel 2007. It was found that there
otitis media, wax and suffering from ear diseases
was no significant difference between two
were excluded from the study.
groups for age in years , height in
Thirty traffic police personnel and thirty controls
centimeters, weight in kg BMI in kg/m2
underwent a pure tone audiometry (PTA).
(Table1).
Audiometer used was Elkon EDA-3N3 Giga 3.
The audiometry data was calculated in an excel
Audiometric testing was conducted in a
spreadsheet which was then exported R 3.0.1
dedicated room that met the audiometer
version for analysis. The collected audiometry
manufacturers
specifications,
in
ENT
data was analyzed by using two tailed undepartment. Test was conducted in the morning
paired Student's t-test
and the values were
hours before joining the duty hours to minimize
expressed as mean SD of observed value.A
the effect of temporary threshold shift (TTS). Air
P-value of less than 0.05 was taken as significant
conduction was assessed by placing ear phones
(Table II).
on the ears. Each ear was evaluated separately
and the results were reported on the graph known
Table.1: Anthropometric parameters of control and study groups
Control group (n=30)
Study group (n=30)
( p Value)
Age (years)
34.577.47
35.038.13
> 0.05
Height (cm)
171.95.55
172.634.71
> 0.05
Weight (kg)
BMI (kg/m2)
Shelke et al.,
71.68.66
24.24 2.88
75.537.96
25.1 2.67
> 0.05
> 0.05
824
Table II - Average hearing threshold at different frequencies in study and control groups
Hearing Thresholds Frequencies in Hertz
Study group(n=30) Control group(n=30)
23.835.52
25.57.11
250
R
25.835.26
24.836.08
L
500
23.55.11
23.166.88
R
24.334.49
255.41
L
1000
21.665.14
21.665.62
R
23.54.38
24.165.09
L
2000
17.834.29
214.43
R
17.163.86
21.335.07
L
4000
17.334.86
33.8315.57
R
17.504.50
33.8317.89
L
15.55.62
23.3310.61
8000
R
14.58.02
22.1612.77
L
* Significant R- right ear L- left ear
p value
>0.05
>0.05
>0.05
>0.05
>0.05
>0.05
<0.05*
<0.05*
<0.05*
<0.05*
<0.05*
<0.05*
Fig.1: Study group subjects audiogram (Right & Left)

DISCUSSION
In the present study tested for the hearing

threshold audiometrically in right and left ear
separately. Mean hearing level at each tested
frequency was compared between noise exposed
TPP and non exposed groups using un-paired
Student t tests. There was a significant difference
in the hearing threshold at frequency 2000 Hz,
4000 Hz and 8000 Hz of right and left ear
between the two groups.This is in agreement
with the finding of Jayesh et al who showed an
increased hearing threshold mainly affected
higher frequencies concentrated at 4000Hz in
textile workers exposed to industrial noise in
Gujrat9. Frequency specic analysis by McBride
et al10andFrancois-Xavier Lesage et al 11showed
notches at 4 kHz in electrical transmission
workers and France Motorcycle police officers
respectively who had the expected associations

with exposure to noise. Similar raised hearing
thresholds at higher frequency were recorded in
Liquefied Petroleum Gas (LPG) Cylinder
Infusion Workers exposed to noise in Taiwan12.
Our study confirmed the presence of 4000Hz
notch5 which is the classic sign of NIHL. Since
most significantly affected frequency was 4000
Hz for both right and left ears, paired t test was
conducted to evaluate whether there was any
significant difference for hearing loss between
right and left ears of study subjects. This showed
no significant difference of hearing loss between
right and left ears of study subjects. This finding
was similar with studies conducted on workers of
chromite mines13. In the early stages of NIHL,
the speech frequencies are less affected and the
patients have a very few symptoms and hence
Shelke et al.,
825
they are usually unaware of the deleterious

effects of sound. Frequency area 4000-6000 Hz
is usually affected first with maximum at 4000
Hz. Any level of NIHL may muffle highfrequency sounds such as whistles or buzzers and
may result in difficulty discriminating speech
consonant sounds such as those in the words fish
and fist, particularly in noisy environments with
background noise, many voices, or room
reverberation6,9.
The
observed
hearing
impairment was most probably related to the
prolonged exposure to road traffic noise. Daily
noise exposure, over long period affects the
hearing ability. The mechanism involved in noise
inducing hearing loss includes mechanical
damage to cochlear structure and metabolic
overload due to excessive stimulation. The
severity of hair cell damage depends on sound
intensity. Exposure to noise at sub-traumatic
level exhibit a temporary threshold shift in
hearing, reversible with time away from the
hazardous exposure. Higher level of sound leads
to collapse of stereocilia and eventual permanent
damage to hair cell. Non-functioning of outer
hair cells raise the threshold sensitivity of inner
hair cell and greater stimulation is required to
initiate an impulse; which perceived as a
hearing loss5,13.
Limitations: Some technical limitations could
not be avoided in this study. First, the timing of
the audiometry assessment in relation to when
subjects were last exposed to noise could not be
controlled. The French norm recommends
testing hearing 3 days after the last noise
exposure, but it was not possible to achieve
this in this study. Therefore, it is possible that
the effect of temporary threshold shift has led to
an overestimate of the real risk of NIHL.
The second limitation of the present study was
the small sample size of subjects, which was not
ideal for cross-sectional analysis and thus the
statistical significance of the results should
be interpreted with caution. We were
constrained by the inability to find adequate
number of subjects as per criteria of study by
excluding smokers, females and exposure < 5

years within limited number of TPP in the study
area. So, it is important to replicate and extend
our observations to large population. We also
fail to quantify the noise level at the traffic
junctions.
Shelke et al.,
CONCLUSION
This study concludes traffic police personnel

working on busy traffic junctions are at risk of
noise induced hearing loss. They have to make
aware of the ill effects of noise and motivate to
use personal protective devices like ear plugs and
ear muffs.
REFERENCES
1. Thomas A, Nor Mariah A, Fuad S, Kuljit R

Philip. Noise Exposure and Noise Induced
Hearing Loss Among Kuala Lumpur Traffic
Point
Duty
Personnel.
Med
J
Malaysia.2007;62(2):152-55.
2. Omidvari M., Nouri, J. Effects of noise
pollution on traffic policemen. Int. J.
Environ. 2009; 3(4):645-52.
3. Abdel-Aziz Kamal M, SamiaEldamati E,
Ricky Paris. Hearing threshold of Cairo
traffic policemen. International Archives of
Occupational And Environmental Health
2004; 62:54345
4. Itrat Jawed, AyubMusani, RaanaMahmood,
Wadood, YousufKhambaty, MohamadAsim.
The effect of traffic noise on the hearing
level of people on Karachi streets. J Pak Med
Assoc. 2010; 60(10): 813-816.
5. Nandi SS, Dhatrak SV. Occupational noise
induced hearing loss in India. Indian journal
of occupational and environmental medicine.
2008.12(2):53-56
6. Shrestha I, Shrestha BL, Pokharel M, Amatya
RCM, Karki DR. Prevalnace of Noise
Induced Hearing Loss among Traffic Police
Personnel of Kathmandu Metropolitan City.
Kathmandu Univ Med J. 2011;36(4):274-78
826
7. Tripathi SR, Tiwari RR. Self-reported

hearing quality of traffic policemen: a
questionnaire-based study. Indian journal of
occupational and environmental Medicine.
August 2006; 10(2): 82-84.
8. Kavana G, Venkatappa, Vinutha Shankar
MS, NachalAnnamalai. Assessment of
knowledge, attitude and practices of traffic
policemen regarding the auditory effects of
noise. Indian
J
PhysiolPharmacol
2012;56(1):6973
9. Solanki JD, Mehta HB, Shah CJ, Gokhale
PA. Occupational noise induced hearing loss
and Hearing threshold profile at high
frequencies. Indian journal of Otology.
2012;18(3):125-28.
10. D I McBride, S Williams. Audiometric notch
as a sign of noise induced hearing loss.
Occup Environ Med 2001; 58: 4651
11. Francois-Xavier Lesage, Nicolas Jovenin,
Frederic Deschamps, Samuel Vincent. Noiseinduced hearing loss in French police
officers. Occupational Medicine 2009;
59:483486.
12. Shu-Ju Chang, Chin-Kuo Chang. Prevalence
and Risk Factors of Noise-induced Hearing
Loss among Liquefied Petroleum Gas (LPG)
Cylinder Infusion Workers in Taiwan.
Industrial Health 2009; 47: 603610
13. SunamaniKarketta,
RajendraGartia,SomanathBagh. Occupational
hearing loss of the workmen of an open cast
chromite mines. Indian journal of
occupational and environmental medicine.
2012;16(1) :18-21
Shelke et al.,
827
DOI:10.5958/j.2319-5886.2.4.132

&
Health Sciences
www.ijmrhs.com
Volume 2 Issue 4 Oct-Dec Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
A COMPARATIVE STUDY ON LIFESTYLE AND METABOLIC PROFILE IN NORMAL

AND OBESE INDIVIDUALS
* Revathi R1, Swetha S2, MeghalathaTS1, Arunakumari R3
1
Lecturer, 2Assistant professor , 3Professor and Head , Department of Biochemistry, Karpaga Vinayaga
Institute of Medical Sciences, Chinna Kolambakkam, Palayanoor, Madhuranthakam, Tamil Nadu
*Corresponding author email: revathi_3aug@yahoo.co.in
ABSTRACT
Background/Aim: The aim of the present study was to evaluate the lifestyle and metabolic profiles in
normal and obese. Material and Methods: A cross sectional study design was employed. Information
on body weight, height, body fat, food choices, diet and physical activity behavior were collected by a
questionnaire among 100 obese adults aged 18-35 years and compared with healthy individuals as
controls. Blood samples were collected to analyze blood glucose, heamoglobin and total cholesterol.
Result: Mean BMI for obese were 36.25 About 50% reported consuming no fruits or vegetables,
while 80% preferred fried food over other forms of cooked food. The majority (60%) engaged in <40
min of physical activity a day. Significant number of adults had Hb>13mg/dl. Blood glucose levels
(>100) & total cholesterol levels (>200) significantly higher (p<0.05) in obese individuals compared to
control. Conclusions: Dietary and physical activity behaviour of the participants were generally poor.
High blood glucose and cholesterol levels found among obese compared to normal. Innovative ways to
improve consumption of fruits and vegetables and increase physical activity among the obese are
needed.
Keywords: BMI, Waist circumference, Obesity
INTRODUCTION
Obesity has reached epidemic proportions in

India in the 21st century with morbid obesity
affecting 5% of the countrys population 1. India
is following a trend of other developing countries
that are steadily becoming more obese. The rate
of growth alarming considering that overweight
and obesity is a major health problem among
adults, but weight and dietary problems usually
start when people are children or adolescents.
There has been a steady increase in the
prevalence of overweight since the mid 1960s

and the drastic increase is particularly notable in
recent years.2 If obesity extends into adulthood, it
puts individuals at risk for serious health
consequences, including type 2 diabetes,
osteoporosis and some cancers3-6.
There are several eating patterns developed
during childhood and adolescence that can have
an immediate impact on overall health as well as
the noted long term consequences, such as type2
Revathi et al.,
828
diabetes. A high consumption of soft drinks and

juices may contribute to an imbalance between
intake and expenditure due to reduced effect on
satiety as compared to solid foods. Other dietary
patterns, which may be associated with increased
risk of obesity in adolescents, include skipping
breakfast and a low intake of fruits and
vegetables. Moreover, research indicates that
unhealthy dietary patterns (eg. dieting, high fat
diet, fast food, limited fruits and vegetables and
skipping breakfast) are linked to other high-risk
activities such as tobacco and drug use. 7,8
This study therefore sought to assess lifestyle and
metabolic profile overweight/obesity as well as
their nutritional status.
The study was conducted in the department of

biochemistry in Karpaga Vinayaga Institute of
Medical Sciences, after the permission of the
Institutional Ethics Committee, Karpaga
Vinayaga Institute of Medical Sciences and
further sample processing has been done after
getting approval from the patient.
Study design: A cross sectional study
Study population: 100 overweight/obese
individuals aged 18-35yrs were randomly
selected from sub rural hospital. Normal healthy
individuals with age matched controls were
taken.
Exclusion criteria: Hypertension, aneamia,
diabetes mellitus and other endocrine disorders.
A
semi-structured
questionnaire
was
administered to solicit information on sociodemographic variables like age and gender of
individuals, educational and occupational status
of parents as well as on food choices, diet and
physical activity.
To assess overweight and obesity in different age
groups, including adolescents, weight for height
is considered statistically valid measure9. The

preferred measure of weight for height is body
mass index (BMI).
BMI is accepted internationally as a standard for
the assessment of overweight and obesity in
adults because it correlates very highly with body
fat10, and it is especially well suited for
adolescents9 and adults. Waist circumference was
measured midway between the lowest rib and the
superior border of the iliac crest with a flexible
tape.
Dietary habits: To evaluate dietary habits, a
semi structured questionnaire was used to solicit
information on frequency of meal (breakfast,
lunch, supper and snacks) consumption.
Physical activity (PA) behavior: To estimate
the PA habits, individuals were asked about the
number of minutes spent watching television,
walking, running, skipping, bicycle riding,
dancing or any indoor games.
Collection and preparation of samples:
Blood samples were collected after a twelve hour
fasting period (Overnight fasting) under aseptic
conditions, the obtained blood sample was
centrifuged and plasma was separated.
The plasma was analysed for the metabolic
parameters that includes, Glucose estimated by
GOD-POD method11, Lipid profile analysis12,
Haemoglobin
by
Acid
Haematin
13
method (SAHLIS Haemoglobinometer).
Statistical analysis:
All the data was analyzed by using SPSS
(version 16 for windows).continues variables are
presented as mean values and their standard
deviations (SD) and categorical variables as
frequencies, percentages or proportions. For all
comparisons-values<0.05
was
considered
statistically significant.
829
Revathi et al.,
RESULT
Table 1: Physical profile of the participants
Variables
Age (years)
BMI (kg/m)
Waist circumference (cm)
Normal (n=100)
29.8 10.3
21.5 2.0
35.5 2.0
Obese (n=100)
29.5 9.8
36.2 5.0
120.2 9.0
P- value
0.04
0.010
Hip (cm)
Waist/hip ratio
45.2 0.72
0.77 0.05
130.0 8.0
0.92 0.03
0.010
Table 1 shows increased BMI & waist/ratio compared to controls (p<0.05).The levels of BMI,
Waist/Hip ratio was significantly higher (p<0.05) in obese compared to normal subjects.
Table.2: Biochemical profile of the participants
Biochemical profile
Normal
(n=100)
Obese (n=100)
Hb (g/dl)
13.2 1.2
14.7 0.9
0.05
Blood glucose (mg/dl)
87.5 13.3
172.6 19.2
0.02
Total Cholesterol (mg/dl)
179.6 22.5
213.4 30.3
0.02
Triglycerides (mg/dl)
120 12.5
170 20.5
0.03
HDL (mg/dl)
60 25.8
35 15.6
0.04
LDL (mg/dl)
95 33.2
145 20.2
0.02
p-value
Table 2 shows increased levels of Heamoglobin in obese compared to normal. Blood glucose and lipid
profile. The levels of Blood glucose and lipid profile was significantly higher (p<0.05) in obese
individuals compared to normal subjects.
DISCUSSION
Evidence in recent years suggests that obesity is

growing rapidly across the globe. Obesity is one
of the most important health related problems
facing humans today. Obesity is associated with
increased mortality and morbidity through its
association with cardiovascular disease14 and a
variety of related conditions such as type 2
Diabetes Mellitus, musculoskeletal problems,
various malignancies and polycystic ovary
syndrome15.The increasing prevalence of obesity
is a global phenomenon that is showing no signs
of abatin 16.Therefore, the public health
implications of obesity and its pathological
sequelea are set to become even more of a
priority for future governments and health-care

providers.
In our study, although we observed a regular
eating pattern for most of the participants, food
choices were generally poor as these participants
preferred high calorie foods to diet rich in fruits
and vegetables. We observed that this age group
often remembered and purchased foods like
French fries, sweet and salty snacks, soft drinks
and fast foods. In a personal communication with
some participants, they revealed that they do not
consume fruits and vegetables daily because they
dont find them in colleges/home.
Revathi et al.,
830
Among various indices, the BMI was selected as

an indicator for total obesity. Furthermore, in this
particular population the BMI is significant and
highly correlated with other indices used for
estimation of total body fatness17.The WC, the
waist hip ratio was selected as an indicator of
obesity since WC is easy to measure and the
measurement error is low due to large
circumference.
In our findings we found significantly higher
hemoglobin levels among obese compared to
non-obese. The mechanism underlying the
relationship between obesity and hemoglobin
level is not well established. It has been
suggested that obese individuals have higher
food consumption and therefore, ingest more
iron18 .
In our study we also found that blood glucose
and total cholesterol was significantly higher in
obese compared to control. However, obesity is
known to be more common among individuals of
poor socioeconomic status of whom their diet is
usually characterized by higher carbohydrate
intake19and high saturated fat in their diet
increases chances of having weight problems20.
Several studies have confirmed that overweight
and obese are at a risk of nutrient deficiencies as
a consequence of inadequate dietary intake
related to poor education or social factors, eating
disorders, unbalanced weight- reducing diets or
comorbidities21.
behaviors among the obese. Innovative ways to

improve consumption of fruits and vegetables
and increase physical activity among obese
individuals are urgently needed.
REFERENCES
Our findings show that overweight and obese

individuals have inadequate dietary and physical
activity behaviors. These behaviors may have
resulted in the poor nutritional status observed ie.
The prevalence of averagely high BMI, High
percentage body fat and high levels of
heamoglobin. This suggests that obesity control
to be achieved, concerned efforts of stakeholders
like the family, school, community, media,
government and food industry is crucial to create
an environment that encourages healthy eating
1. India facing obesity epidemic: experts.

http://hindu.com/2007/10/12stories/20071012
60940600. htm).
2. Lobstein T, Baur L and UauyR. Obesity in
children and young people: A crisis in public
health. Obes. Rev. 2004;5(1): 4-10.
3. Reilly JJ, Methven, McDowell ZC, Hacking
B, Alexander D. Health consequences of
obesity. Arch. Dis. Child. 2003,88: 748-52
4. Viana V, Sinde S and Saxton JC .Children's
eating behavior questionnaire: Associations
with BMI in Portuguese children. Brit. J.
Nutr., 2008.100:445-450.
5. Freedman DS, Khan LK, Dietz WH,
Srinivasan SR, Berenson GS. Relationship of
childhood obesity to coronary heart disease
risk factors in adulthood: The bogalusa heart
study. Pediatrics, 1997; 108: 712-18.
6. Must A, Jacques PF,Dalal CE, Bajema CJ,
Dietz WH. Long- termmorbidity and
mortalityo f overweighta dolescentsN. Eng J
Med. 1992 ;327:1350 55.
7. Heald F. Fast food and snack food: beneficial
or deleterious. J Adol Health. I 992:l 3:380383.
8. LytleL A, Roski J, Un healthy eat in agndo
their risk- takin behavior: are they related?
Annals New York Academy of Sciences.
1997 : Bl7 496.
9. Himes JH, Dietz WH. Cuidel inesfor over
weight in adolescent preventive services:
Recommendat ions from an expert commrttee
Am J Clin Nutr. l994; 5 9 : 3 0 7 3.
10. Guillaume M . Def in obesity in childhood:
current practice. Am J Clin Nutr. 1999;70
(l2):6l -13 0
11. Carl
A.Burtis,
Edward
R.Ashwood,
Estimation of glucose by glucose oxidase
Revathi et al.,
CONCLUSION
831
method.Tietz., Text book of clinical

chemistry.1994,chapter 24:778-780.
12. Carl A.Burtis, Edward R. Ashwood,
Measurement of lipids, lipoproteins and
apolipoproteins Tietz.,Text book of clinical
chemistry 3rd edition.1994,chapter 25:837845.
13. G.K. & Pal, Pravati, Sahlis acid heamatin
method.Text book of practical physiology 2nd
edition.2006:13.
14. Hubert HB, Feinleib M, McNamara PM,
Castelli WP. Obesity as an independent risk
factor for cardiovascular disease: a 26-year
follow-up of participants in the Framingham
Heart Study. Circulation 1983, 67:968-77.
15. TM Barber, MI McCarthy, JA Wass, S
Franks: Obesity and polycystic ovary
syndrome. Clin
Endocrinol
(Oxf) 2006,
65:137-45.
16. Bessesen DH. Update on obesity. J Clin
Endocrinol Metab 2008, 93:2027-34.
17. Khalid MEM, Mahmoud MSW, Elbagir
MahmadK. Fat indices in high and low
altitude populations in south western soudi
Arabia. Ann Saudi Med 1997;17:312-15
18. Camitta BM, Nathan DG. Anemia in
adolescence. Postgrand Med J 1975;57:151155
19. Theodore
B.health
implications
of
overweight and obesity in the unitedstates.
Ann intern Med 1985;103:983-88
20. Katherine M, Flegal et al. Journal of
American medical association prevalence and
trends in obesity among U.S adults 19992008; January 20,2010.
21. Allard J. Should nutritional status be
routinely assessed and corrected before
bariatric
surgery?
Nat
Clin
Pract
Gastroenterol Hepatol. 2007;4:13031
832
Revathi et al.,
DOI:10.5958/j.2319-5886.2.4.133

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Health Sciences
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Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
nd
HAEMODYNAMIC RESPONSE TO NASOTRACHEAL INTUBATION UNDER GENERAL

ANAESTHESIA: COMPARISON BETWEEN FIBEROPTIC BRONCHOSCOPY AND DIRECT
LARYNGOSCOPY
*Tushar Bhavar1, Punia TS2, JPS Bhupal3, Harpreet Babrah4, Banreet Bagri5, Abhishek Singla6
1
Assistant Professor, 6Resident, Dept. of Anaesthesia & Intensive Care, Rural Medical College, PIMS
Loni, Maharashtra, India
2
Professor & Head, 3Professor, 4Resident, 5Resident, Dept. of Anaesthesia & Intensive Care GMC,
Rajindra Hospital, Patiala.
*Corresponding author email: tganesh55555@gmail.com
ABSTRACT
Study Objective: To compare haemodynamic response in nasotracheal intubation under general

anaesthesia between FOB and DLS as one accomplished with a FOB is thought to attenuate the
circulatory responses to intubation as stimulation of the oropharyngeal structures may be avoided.
Design: Randomized, prospective study. Patients: 50 ASA grade I and II patients of both sexes in the
age group of 18 - 60 years scheduled for an elective surgery under general anesthesia. Interventions:
Patients were randomly allocated to nasotracheal intubation facilitated with either the FOB [Group I] or
the DLS [Group II]. A uniform protocol of anesthesia was used. Measurements: Heart Rate [HR],
Systolic Blood Pressure [SBP], Diastolic Blood Pressure [DBP] & Mean Arterial Pressure [MAP] in
the two groups were compared at their baseline, post-induction values, at the time of insertion of the
scope, immediately after intubation & at 3, 5 and 10 minutes after intubation. Results: Haemodynamic
response in the form tachycardia, increase in SBP, DBP & MAP occurred in nasotracheal intubations
with both the fiberoptic bronchoscope and with direct laryngoscope. Tachycardia of similar magnitude
was noted in both the groups following insertion of scope and after intubation whereas SBP, DBP &
MAP were significantly high in Group II [p<0.01] at the time of intubation & SBP immediately after
intubation was significantly high in Group I[p<0.05] Conclusions: Fiberoptic bronchoscopy provides no
advantage over conventional laryngoscopy, in terms of decreasing the hemodynamic response to
nasotracheal intubation under general anaesthesia.
Keywords: Nasotracheal intubation, General Anaesthesia, Hemodynamic Responses, Fibreoptic
Bronchoscope, Macintosh Direct Laryngoscope, Difficult Intubation.
INTRODUCTION
Alfred Kirstein [18631922] first described

direct visualization of the vocal cords on 23
April 1895 and fiberoptic assisted tracheal

intubation was introduced into anaesthetic
833
Tushar et al.,
practice by Murphy in 1967 and Taylor & Towey

in 19721-3. The popularity of fiberoptic intubation
has increased since the introduction of delicate
flexible fiberoptic laryngoscopes. However, it
remains a skill possessed by a minority of
anaesthetists in this country, the principal
obstacles to dissemination of competence being
the relatively fragile nature of a costly instrument
and the difficulties of training. Fiberoptic
nasotracheal intubation can avoid the mechanical
stimulus to oropharyngolaryngeal structures
thereby it is likely to attenuate haemodynamic
response.4
After the Institutional Ethics Committee

approval, the study was conducted in Rajindra
Hospital Patiala in 50 patients of either sex, aged
18 to 60 yrs of ASA grade I and II scheduled to
undergone elective surgery under general
anaesthesia requiring intubation. A written
informed consent was obtained from each
patient. The patients were divided in two groups
randomly of 25 patients each.
Exclusion criteria: Patients refusing; those with
anticipated
difficult
airway,
obesity,
cardiovascular and endocrine diseases, bleeding
disorders, history of nasal surgery or trauma,
nasal polyp or on drugs known to produce
changes in heart rate and blood pressure like beta
blockers, digitalis, calcium channel blockers, oral
contraceptives were excluded from study.
After a proper pre-anaesthetic checkup and
assessing fasting status patients were premedicated with inj Glycopyrolate [0.2mg] I.M,
inj Midazolam [2mg] + Promethazine [25mg] IM
30 min before the elective surgery. Fifteen
minutes before shifting the patient to the OT
table, 0.1% Oxymetazoline nasal drops where
instilled in both the nasal passages. All patients
received tab. Alprazolam 0.25 mg before sleep
and 6 am on the day of surgery. After the patient
is brought to operation table baseline
measurements of heart rate, blood pressure and
Spo2 were taken. Fentanyl in a dose of 1.5g/kg
was administered intravenously 5 minutes before

induction. Patients were pre oxygenated with
100% O2 for 3 minutes.
General anaesthesia was induced with an
intravenous injection of Propofol, 2mg/kg and
intubation was facilitated with the use of
Rocuronium 0.9 mg/kg intravenously. Then
patient were ventilated with 100 % oxygen.
Intubation was commenced exactly after 90
seconds of giving inj. Rocuronium.
In group I, nasotracheal intubation was carried
out with the aid of fiberoptic bronchoscope and
in group II with the aid of laryngoscope. A 7.00
mm internal diameter, cuffed endotracheal tube
[ETT] was used for female patients and 7.5 mm
internal diameter cuffed ETT for male patients.
In group I the ETT lubricated with lignocaine
jelly was threaded over the fiberoptic
bronchoscope. The fiberoptic bronchoscope was
then introduced in the more patent nasal passage
and once in nasopharynx, glottis identified and
scope then advanced 5 to 7 cm beyond the
laryngeal inlet till carina is visible. The ETT was
then advanced into the trachea over the scope
and fiberoptic bronchoscope removed gently
through the endotracheal tube looking for
position of ETT.
Similarly in group II, ETT was introduced
through the more patent nasal passage. Direct
laryngoscopy was performed to visualize the
glottis and the endotracheal tube advanced into
trachea with the help of Magill's forceps. In both
the groups, after introduction of ETT,
anaesthesia was maintained with O2:N2O:40:60
along with 1% isoflurane. The following
parameters were observed: heart rate [HR],
systolic blood pressure [SBP], diastolic blood
pressure [DBP] and mean arterial blood pressure
[MAP]. These parameters were recorded at
following time intervals: baseline value, after
induction, at the time of insertion of
laryngoscope/fiberoptic
bronchoscope,
immediately after intubation and thereafter at 3,
5 and 10 minutes. ECG and SPO2 were
monitored continuously as per the intervals
834
Tushar et al.,
mentioned above. The study was terminated at

the end of 10 minutes after intubation. However
vitals were monitored throughout the surgery.
Time of intubation from cessation of mask
ventilation to connection of breathing circuit to
ETT was noted. And postextubation epistaxis if
any noted.
Statistical analysis: Data was analyzed with
Graph Pad Prism 6.01 statistical softwares. The

male/female distribution & epistaxis between the
two groups were compared using fishers exact
stastical test. Demographic data, blood pressure,
heart rate, time of intubation & Spo2 were
compared between the two groups using
unpaired Students t-test.
RESULT
Table.1: Comparison demography, time of intubation, epistaxis & Spo2
Variables
Group I
Group II
P value
Age [yrs]
36.84 22.28
37.04 21.06
0.9483
Sex [M:F]
9:16
3:22
0.0955
Weight [Kg]
60.2 9.66
59.08 13.9
0.5112
Time req for intub.
69.5237.18
18.2 7.12
<0.0001*
Epistaxis
3[12%]
1[4%]
0.6092
Spo2
98.726.1
99.960.4
0.048*
Table.2: Comparison of haemodynamics FOB vs DLS Group.
Group I
Group II
HR (bpm)
Baseline
Aft. Induct.
At Insertion
Imm. Aft intub.
3min
5 min
10 min
SBP (mmHg)
Baseline
Aft. Induct.
At Insertion
Imm. Aft intub.
3min
5 min
10 min
DBP (mmHg)
Baseline
Aft. Induct.
At Insertion
Imm. Aft intub.
3min
5 min
10 min
MAP(mmHg) Baseline
Aft. Induct.
At Insertion
Imm. Aft intub.
83.1614.7
77.7613.7
88.9615.85
86.0815
83.0414.58
8114.44
79.8414
122.4814.24
108.612.87
127.9615.05
141.416.4
121.3614.54
118.813.61
116.5213.81
7913.65
67.9611.41
82.5614.46
91.2416
78.6414
76.7213
76.613.53
93.513.5
81.511.5
97.714.28
107.9615.72
92.8813.81
90.7512.85
89.9113.3
3min
5 min
10 min
*Significant (P<0.05), values=MeanSD
82.7216.83
76.1213.88
88.5621.99
85.820.39
82.2813.4
80.5212.65
79.412.62
122.0414.67
107.9219.06
14028.67
133.1631.23
116.6421.3
114.1222.8
114.3622.71
79.618.77
68.1619.61
91.9626.28
87.2424.25
75.2421.8
74.4419.73
75.424.8
93.7515.68
81.416.93
107.9724.56
102.5524.69
89.0420.53
87.6718.1
88.3922.8
P value
0.84
0.40
0.88
0.91
0.70
0.80
0.81
0.83
0.76
0.0005*
0.02*
0.07
0.08
0.42
0.79
0.93
0.002*
0.17
0.19
0.33
0.67
0.90
0.96
0.0007*
0.07
0.12
0.17
0.56
835
Tushar et al.,
Mean age, weight & M:F were statistically

insignificant and so both groups were
comparable demographically. Epistaxis was seen
in both groups and was statistically insignificant.
It depends on proper preparation of patients.
Spo2 was continuously monitored during
intubation using either technique and it was
found that patients maintained 100% saturation
during induction, at the time of insertion of
FOB/DLS, at 3min, 5min and 10 min in both
Groups. In Group I, 4 patients and in group II, 1
patient had lower reading immediately after
intubation. Difference was statistically analysed
and found to be significant [p<0.05]. Mean time
for intubation in Group I using FOB was high
comparing that with DLS Group II. Difference in
intubation time was found to be statistically
significant [p<0.0001]. There was significant fall
of all parameters after induction comparing with
baseline [p<0.0001] in both groups. Comparing
both groups there was no significant difference.
At the time of insertion of FOB/DLS there was
significant rise of HR, SBP, DBP & MAP.
There was no statistically significant difference
of HR between two groups whereas SBP, DBP &
MAP were significantly high in Group II
[p<0.01]. HR remained high even after
intubation and returned to baseline value at 3min
in both groups. SBP, DBP & MAP further
increased after intubation and returned to
baseline value at 3min in FOB group while HR,
SBP, DBP & MAP
remained high after
intubation but didnt increase and returned to
baseline value at 3min in DLS group. Similarly
maximum mean HR was noted at the time of
insertion of FOB while maximum mean SBP,
DBP & MAP were seen immediately after
intubation using FOB in Group I. whereas
maximum readings of all parameters were noted
at the time of insertion of DLS in Group II.
Comparing both groups SBP immediately after
intubation was significantly high in Group I
[p<0.05]. In both groups HR, SBP, DBP and
MAP were at baseline level at 3min and there
was no statistically significant difference
between two groups. In both groups HR, SBP,

DBP and MAP was below baseline at 5min and
10min.
DISCUSSION
Flexible fiberoptic intubation of the trachea is

now the method of choice when direct
laryngoscopy is expected to be difficult. The
cardiovascular response to tracheal intubation,
although transient, may be harmful to some
patients, mainly those with myocardial or
cerebrovascular disease. So we have conducted a
study to find out whether FOB has some
beneficial effect attenuating this hemodynamic
effect of intubation. Spo2 immediately after
intubation was low in group I and is due to
longer intubation time required for FOB.
Difference in intubation time was found to be
statistically significant [p<0.0001]. Our findings
were consistent with most of the studies
conducted.5-11 This difference is because FOB is
more technical, requires hand eye coordination
and one has to reach till carina using FOB and
then guide ETT over it and then withdraw FOB
looking for tube position whereas in DLS we
have direct vision of vocal cords, and also in
FOB the field of view is restricted.5 At the time
of insertion of FOB/DLS there was significant
rise of HR, SBP, DBP & MAP. This increase is
due
to
stress
response
to
9
laryngoscopy/bronchoscopy. There was no
statistically significant difference of HR between
two groups whereas SBP, DBP & MAP were
significantly high in Group II [p<0.01]. This
finding is not in acceptance with study by Michal
Barak, et al.
which shows no significant
differences this may be due to different route of
intubation as they had used oral route for
intubating.9 Our results are consistent with study
conducted by J. E. Smith, et al. These differences
may arise because of the combined effects of
differences in airway stimulation and differences
in the duration of laryngoscopy between the two
techniques. The fibrescope may produce less
mechanical pressure on the tissues of the anterior
836
Tushar et al.,
pharynx, which may therefore induce less reflex

sympathetic activity.6 SBP, DBP & MAP further
increased after intubation and returned to
baseline value at 3min in FOB group while HR,
SBP, DBP & MAP
remained high after
intubation but didnt increase and returned to
baseline value at 3min in DLS group. Comparing
both groups SBP immediately after intubation
was significantly high in Group I [p<0.05]. This
findings are consistent with study conducted by
J. E. Smith which shows that the increase in
systolic pressure was sustained for a longer
period in the fiberoptic group and concluded that
the cardiovascular responses associated with
fiberoptic intubation under general anaesthesia
appear to be more severe.5 This findings are also
consistent with study conducted by J. E. Smith,
et al. which shows that highest mean systolic
pressure in the fiberoptic group was delayed until
the second minute.6 This findings are also
consistent with most other studies.12,13 This may
be due to following reasons:
1. It has been shown that the longer the
intubation time the more likely is it to
develop hypercapnia, which can result in
hypertention and tachycardia.4 Longer time
may tend to produce more sympathetic
activity6
2. FOB necessitates the lifting of the jaw
upward to make a clear passage for the FOB
and for the tracheal tube to enter the glottis.
Lifting of the jaw upwards itself is sufficient
to cause a cardiovascular response similar to
those observed in the laryngoscopic
intubation.4,13
3. The advancement of the tracheal tube over
the FOB is often impeded when the
Murphys tip catches on the downward
sagging epiglottis, arytenoid cartilage, vocal
cords and anterior tracheal wall. On such
occasions, the successful intubation often
requires some specific maneuvers e.g.
rotating the tracheal tube, further lifting jaw
upward and adjusting the patients head-neck
position.4,13
4. During the fiberoptic intubation, the insertion

cord of the FOB must be placed into the
trachea for guidance followed by advancing
the tracheal tube over the insertion cord into
the trachea and then the FOB is removed.
This can cause repeated friction and irritation
to the trachea.4
5. The traction on the tongue which is necessary
to clear the airway which itself is a potent
stimulus as the Macintosh blade.5
6. Tracheal tube insertion itself is most invasive
stimuli.14
7. Longer intubation time may also cause
weaning of anaesthetic effect of inhaled
anaesthetic agent, hypoxia & hypercarbia in
FOB group and minimal or negligible
interruption of inhaled anaesthetic agent in
DLS group this drawback was eliminated by
using a mask adapter by Makoto Imai, et al.
and found that FOB resulted in milder
hemodynamic
changes
compared
to
conventional laryngoscopy, as they were able
to maintain anaesthesia during intubation.15
Even though there was significant high
haemodynamic response to laryngoscopy
compared to bronchoscopy at the time of
intubation which may be due to sudden severe
stress response to DLS compared to FOB during
intubation and also in DLS oropharyngeal
structures alongwith nasopharyngeal ones are
stimulated, there is no advantage of FOB in
attenuating haemodynamic response as there was
significant high SBP after intubation and SBP,
DBP and MAP remained high for longer time.
This has been shown by most of the studies.4-9,
12,13, 16-19
CONCLUSION
Fiberoptic bronchoscopy provides no advantage

over conventional laryngoscopy, in terms of
decreasing the hemodynamic response to
nasotracheal
intubation
under
general
anaesthesia.
837
Tushar et al.,
ACKNOWLEDGEMENT
It gives me pleasure to render my thanks to my

parents, and esteemed teachers Dr.T.S.Punia,
Dr.JPS Bhupal, Dr. Parmod Kumar & Dr. Rahul
Kunkulol. I thank my friends Dr.Subhash,
Dr.Vishal, Dr.Nidhi, Dr.Jeevraj, Dr.Pavan,
Dr.Ruhi, Dr.Divya and all my department staff
for their support and help. Lastly, I thank all the
patients undergoing treatment who volunteered
to participate in this study and without which this
work would have not been possible.
REFERENCES
1. Vlajkovic G, Sindjelic R, Markovic D, Terzic
M. A look into the larynx-two centuries
along the path of laryngoscopy. Acta Chir
Iugosl. 2009; 56(1): 61-66.
2. Murphpy P. A fibre-optic endoscope used for
nasal intubation. Anaesthesia 1967; 22: 48991.
3. Taylor PA, Towey RM. The bronchofiberscope as an aid to endotracheal
intubation. British journal of anaesthesia.
1972; 44; 611-2.
4. Zhang Guo-hua, Xue Fu-shan, LI Ping, SUN
Hai-yan, LIU Kun-peng, XU Ya-chao. Effect
of fibreoptic bronchoscope compared with
direct laryngoscope on haemodynamic
responses to orotracheal intubation. Chin
Med J 2007; 120(4): 336-38.
5. Smith JE. Heart rate and arterial pressure
changes during fibreoptic tracheal intubation
under general anaesthesia.
Anaesthesia
1988; 43: 629-32.
6. Smith JE, Mackenzte AA, Sanghera SS,
Scott-knight. Cardiovascular effects of
fibrescope-guided nasotracheal intubation.
Anaesthesia 1989;44: 907-10.
7. Finfer SR, MacKenzie SI, Saddler JM,
Watkins TG. Cardiovascular responses to
tracheal intubation: a comparison of direct
laryngoscopy and fibreoptic intubation.
Anaesth.Intens.care 1989: 17: 44-48.
8. Schaefer HG, Marsch SCU. Comparison of

orthodox
with
fibreoptic
orotracheal
intubation under total i.v. anaesthesia. British
Journal of Anaesthesia 1991; 66(5): 608-10.
9. Michal Barak, Avishai Ziser, Avital
Greenberg, Sophie Lischinsky, Beno
Rosenberg.
Haemodynamic
and
Catecholamine Response to Tracheal
Intubation: Direct Laryngoscopy Compared
with Fibreoptic Intubation. Journal of
Clinical Anesthesia 2003; 15: 13236.
10. Jakusenko, Kopeika, Mihelsons, Nagobade,
Vija Putnia, Pavars. Comparison of stress
response performing endotracheal intubation
by direct laryngoscopy, fibreoptic intubation
and
intubation
by
the
glidescope
laryngoscope. 2008;62(4):176-81.
11. Aghdaii N, Azarfarin R, Yazdanian F, Faritus
SZ. Cardiovascular responses to orotracheal
intubation in patients undergoing coronary
artery bypass grafting surgery. Comparing
fiberoptic
bronchoscopy
with
direct
laryngoscopy. Middle East J Anesthesiol.
2010;20(6):833-38.
12. Xue FS, Zhang GH, Sun HT, Li CW, Li P,
Liu KP et al. A comparative study of
haemodynamic responses to orotracheal
intubation with fibreoptic bronchoscope and
laryngoscope
in
children.
Pediatric
Anesthesia 2006; 16: 74347.
13. Ranju Singh, Pramod Kohli, Sunil Kumar.
Haemodynamic Response to Nasotracheal
Intubation under General Anaesthesia A
Comparison
between
Fibreoptic
Bronchoscopy and Direct Laryngoscopy. J
Anaesth Clin Pharmacol 2010; 26(3): 335-39
14. Kapil Gupta, Kiran Kumar Girdhar, Raktima
Anand, Sumanth Mallikarjuna Majgi,
Surinder Pal Gupta, Payal Bansal Gupta.
Comparison of haemodynamic responses to
intubation: Flexible fibreoptic bronchoscope
versus bonfils rigid intubation endoscope.
Clinical Investigation. 2012;56(4):353-58.
15. Makoto Imai, Chihoko Matsumura, Yukari
Hanaoka, Osamu Kemmotsu. Comparison of
838
Tushar et al.,
Cardiovascular Responses to Airway

Management: Fibreoptic Intubation Using a
New Adapter, Laryngeal Mask Insertion, or
Conventional Laryngoscopic Intubation.
Journal of Clinical Anesthesia 1995; 7: 14-l8.
16. Staender S, Marsch SCU, Schumacher P,
Schaefer HG. Haemodynamic response to
fibreoptic versus laryngoscopic nasotracheal
intubation
under
total
intravenous
anaesthesia.
European Journal of
Anaesthesiology 1994: 11(3): 175-79.
17. Yushi UA, Isao Takamatsu,
Kazuhiko
Watanabe, Yoshitaka Uchihashi, Hideyuki
Higuchi, Tetsuo Satoh. Evaluation of the
Cardiovascular Responses to Fibreoptic
Orotracheal Intubation with Television
Monitoring: Comparison with Conventional
Direct Laryngoscopy. Journal of Clinical
Anesthesia 2000; 12: 50308.
18. Xue FS, Zhang GH, Sun HY, Li CW, Li P,
Sun HT, et al. Blood pressure and heart rate
changes during intubation: A comparison of
direct laryngoscopy and a fibreoptic method.
Anaesthesia May 2006; 61(5): 444-48.
19. Arash
Farbood,
Hamid
Kamalipour,
Mohammad Ali Sahmeddini Kazem Samadi.
Comparison of the haemodynamic changes
following tracheal intubation with direct
laryngoscopy and fibreoptic bronchoscopy
method in hypertensive patients. Journal of
Iranian society anaesthesiology and intensive
care 2009; 31(67): 50-57.
839
Tushar et al.,
DOI:10.5958/j.2319-5886.2.4.134

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
MUPIROCIN RESISTANCE IN CLINICAL ISOLATES OF STAPHYLOCOCCUS AUREUS IN

A TERTIARY CARE HOSPITAL SET UP IN NORTH INDIA
*Singh Amit K, Venkatesh Vimala, Singh Mastan
Postgraduate Department of Microbiology, King George Medical University, Lucknow, U.P, India
*Corresponding author email: amit.singh.dr@gmail.com
ABSTRACT
Background: Mupirocin is a topical antibiotic used for nasal decolonisation of methicillin resistant
Staphylococcus aureus (MRSA). While resistance to mupirocin has been described it is usually not
tested for in most clinical laboratories. Aim: The present study was carried out to detect the occurrence
of mupirocin resistance in clinical isolates of Staphylococcus aureus in a tertiary care hospital set up in
northern India. Materials and Methods: Staphylococcus aureus isolates obtained from clinical samples
received in the microbiology laboratory over a period of one year were included in this study. Mupirocin
resistance was detected by three phenotypic methods; disk diffusion method using 5g and 200g
mupirocin disk to determine low-level and high-level resistance, broth microdilution method and an agar
dilution method for determining minimum inhibitory concentrations. Methicillin sensitivity was also
determined in the study isolates. Results: Of 250 non-duplicate Staphylococcus aureus isolates
obtained, 5 (2%) were found resistant to mupirocin. All mupirocin resistance isolates were shown to
have high-level resistance (minimum inhibitory concentration > 512g/ml). All mupirocin resistant
isolates were also resistant to methicillin. Results obtained by all three phenotypic methods showed
good correlation. Conclusion: High-level mupirocin resistance is present in the northern Indian
population which may be of major concern to prevent the spread of MRSA in hospitals and community.
Keywords: Mupirocin resistance, MuH, MRSA
INTRODUCTION
Methicillin-resistant Staphylococcus aureus

(MRSA) is one of the major nosocomial
pathogen in healthcare institutions and
increasingly reported from hospitals and the
community worldwide.1, 2 Carriage of MRSA in
nose, axilla, perineum and hands of patients and
health care personnel is an important risk factor
for
MRSA
acquisition
and
spread.3
Amit et al.,
Decolonisation from the site of carriage is one of

the modalities for prevention of MRSA
infections in healthcare settings.4 Mupirocin
(pseudomonic
acid
A)
derived
from Pseudomonas fluorescens is an important
topical antibiotic ointment for the nasal
decolonisation of MRSA in carriers.5-8 It acts by
binding specifically to the bacterial isoleucyl840
tRNA synthetase (IRS) enzyme and inhibits its

protein synthesis.9 Along with its use as a
decolonising agent in health care personnel and
patients, it has also been used for treatment of
staphylococcal skin and soft tissue infections.10,11
Resistance to mupirocin is being increasingly
found due to its irrational use, which leads to
improper decolonisation of MRSA from the site
of carriage and spread of infection.12,13
Although there is no such guidelines published
for mupirocin susceptibility testing, traditionally
susceptible strains have minimum inhibitory
concentration (MIC) 2 g/ml while those
having a MIC of 4 g/ml were designated as
resistant, and by disk diffusion method those
with zone diameter of 14 mm with a 5g disk
were taken as susceptible while zones of 14 mm
were considered resistant14. However, recently
mupirocin-resistant strains have been grouped
into two distinct phenotypes: low-level resistance
(MuL) with MICs of 8-256 g/ml, and high-level
resistance (MuH) with MICs 512 g/ml. An
isolate with MIC 4 g/ml is considered as
mupirocin-sensitive. With the previously used 5
g mupirocin disk, MuL and MuH strains cannot
be differentiated. However it can be performed
by concomitant use of 5 g and 200 g
mupirocin disks.15
MuH strains have been found to be associated
with failure of mupirocin as a decolonising agent
as well as for treatment of skin and soft tissue
infections.16 Plasmid-mediated mupA encoding a
novel isoleucyl RNA synthetase is a major
genetic mechanism seen in high-level mupirocin
resistance isolates.17,18 Whereas base pair
changes in native isoleucyl RNA synthetase gene
is seen in low-level mupirocin resistance
isolates18. Various studies suggest that during
mupirocin prophylaxis transfer of mupA gene
from normal commensal flora of skin such as
Staphylococcus epidermidis to MRSA is
responsible for emergence of mupirocin
resistance.19
Thus, this study was carried out to determine the
rates of high-level and low-level mupirocin
Amit et al.,
resistance in Staphylococcus aureus by disk

diffusion and MIC methods and to evaluate its
association with methicillin-resistant isolates.
Staphylococcus aureus isolates recovered from

clinical specimens comprising pus, blood,
various swabs and sterile body fluids received in
the Postgraduate Department of Microbiology,
King George Medical University, Lucknow,
during a one year period from August 2011 to
July 2012 from patients who attended the
outpatient department (OPD) or were admitted to
various inpatient departments (IPD) of Gandhi
Memorial & Associated Hospitals were included
in the study. Isolates from urine were not
included.
Clinical specimens were processed and isolates
were identified as Staphylococcus aureus by
routine microbiological procedures. Nonduplicate Staphylococcus aureus isolates were
tested for mupirocin resistance by disc diffusion
method, broth microdilution method and agar
dilution method.
In the disk diffusion method, mupirocin disks of
5g (SD748, Himedia Labs, India) and 200g
(CT0523B, Oxoid, India) concentration were
used. Zone diameter of > 14 mm for both disks
was taken as susceptible for mupirocin. Whereas,
isolates that showed zone diameters < 14 mm in
the 5 g disk but > to 14 mm in the 200 g disk
were considered to be low-level mupirocin
resistant strains.15 All isolates with zone
diameters < 14 mm for both 5g and 200g disks
were considered to be high-level mupirocin
resistant strains15 (Fig. 1).
The broth microdilution method was done for
determination
of
Minimum
Inhibitory
Concentration (MIC) on Mueller-Hinton broth
(MHB) with a final mupirocin concentration
ranged from 0.25 g/ml to 512 g/ml (Fig. 2).
Similarly agar dilution method was done for
determination of MIC on Mueller-Hinton agar
(MHA) with same concentration. Mupirocin
MIC of < 4g/ml was taken as susceptible, that
841
of 8g/ml to 256g/ml as low-level resistance

and > 512 g/ml as high level resistance (Fig. 3).
Detection
of
methicillin
resistance
in
Staphylococcus aureus isolates were performed
as per Clinical Laboratory Standards Institute
(CLSI) 2012 guidelines by using cefoxitin (30g)
disk20. Antimicrobial susceptibility testing was
done as per CLSI guidelines by Kirby-Bauer disk

diffusion method for the following antibiotics:
ampicillin (10 g), ciprofloxacin (5 g),
clindamycin (2 g), erythromycin (15 g),
linezolid (30 g), tetracycline (30 g), septran
(1.25/23.75 g), vancomycin (30 g). Statistical
test of significance applied z-test.
Fig.1: Demonstration of high-level mupirocin resistance and mupirocin sensitive phenotypes by disk
diffusion method
Fig.2: Broth microdilution method for determination of MIC of mupirocin in Staphylococcus aureus
isolates
Fig.3: Agar dilution method for determination of MIC of mupirocin in Staphylococcus aureus isolates
Amit et al.,
842
RESULTS
Among the 250 non-duplicate Staphylococcus aureus isolates included in study, 133 (53.2%) were
MRSA. Of these, 5 i.e., 3.76% of MRSA were mupirocin resistant Staphylococcus aureus (MupRSA).
Mupirocin resistance was not detected in methicillin sensitive Staphylococcus aureus (MSSA) isolates.
Table.1: MupRSA and MRSH strains among total Staphylococcus aureus isolates in different samples
Samples
S. aureus MRSA (%)
MuH (%) MuL (%) 95% CI
Pus
142
78 (54.93)
2 (1.4)
0.9-6.06
Blood
48
27 (56.25)
3 (6.25)
0.7-22.96
Genitourinary 11
1 (9.09)
specimens
Respiratory
39
23 (58.97)
specimens
Miscellaneous 10
4 (40.0)
TOTAL
0.53-6.99
250
133 (53.2)
5 (2.0)
MRSA= Methicillin resistant Staphylococcus aureus, MuH= High-level mupirocin
MuL= Low-level mupirocin resistance, CI= Confidence Interval, * = Significant
P-value
<0.0001*
<0.0001*
<0.0001*
resistance,
Table.2: Distribution of S. aureus, MRSA and MupRSA in different clinical wards
WARDS
S. aureus MRSA (%)
MupRSA
(%)
2 (1.73)
0
95% CI
P-value
Surgical
1.06-6.86
<0.0001*
115
69 (60)
54
23(42.59)
General
surgery
21(72.41)
1(3.44)
4.35-13.87
<0.0001*
Orthopaedics 29
20 (62.5)
1(3.12)
4.55-14.55
<0.0001*
Neurosurgical 32
Gynaecology
11
5 (45.45)
0
Paediatrics
0.74-20.74
<0.0001*
67
30 (44.77)
3 (4.47)
Medicine
20
11 (55)
0
OPD
37
23 (62.16)
0
Total
0.53-6.99
<0.0001*
250
133 (53.2)
5 (2.0)
MRSA= Methicillin resistant Staphylococcus aureus, MupRSA=Mupirocin resistance
Staphylococcus aureus, CI= Confidence Interval, * = Significant
Table.3: Antimicrobial sensitivity pattern of MRSA and MupRSA isolates
Antibiotics
Sensitive (%)
Intermediate (%)
MRSA
MupRSA MRSA
MupRSA
Ampicillin
7 (5.26)
7 (5.26) Ciprofloxacin 36 (27.06) 10(7.52) Clindamycin
46 (34.58) 1 (20)
9 (6.77) 1 (20)
Erythromycin 44 (33.08) 1 (20)
6 (4.51) 1 (20)
Linezolid
133 (100) 5 (100)
Septran
44 (33.08) 3 (60)
12(9.02) 1 (20)
Tetracycline
68 (51.13) 3 (60)
9 (6.77) 1 (20)
Vancomycin
133 (100) 5 (100)
MRSA= Methicillin resistance Staphylococcus aureus,
MupRSA= Mupirocin resistance Staphylococcus aureus
Amit et al.,
Resistant (%)
MRSA
119(89.47)
87 (65.41)
78 (58.65)
83 (62.41)
77 (57.89)
56 (42.11)
-
MupRSA
5 (100)
5 (100)
3 (60)
3 (60)
1 (20)
1 (20)
-
843
Amongst the mupirocin resistant isolates, all the

5 isolates were high-level mupirocin resistant.
Percentage of methicillin resistant and mupirocin
resistant Staphylococcus aureus isolates among
different samples is documented in the Table 1.
Distribution of samples according to the wards
from where they were received is documented in
Table 2. Amongst other antibiotics, percentage
resistance is documented in Table 3, with a
maximum resistance seen for ampicillin.
Vancomycin and linezolid were found to be the
most sensitive drugs across all staphylococcal
species.
DISCUSSION
Staphylococcus aureus is one of the most
frequently isolated pathogen from both
nosocomial and community associated infections
causing a wide range of infections from
abscesses, impetigo and cellulitis to deep seated
pyogenic lesions, pneumonias, meningitis and
septicaemias.1 Increasing number of infections
caused by MRSA strains has led to poorer
treatment outcome.2 Mupirocin is an important
topical antibiotic widely used for treatment of
skin and soft tissue infections caused by
Staphylococcus aureus.11 In healthcare institute it
is used for nasal decolonisation of health care
personnel to prevent the spread of MRSA among
co-workers and the patients.10 Emergence of
resistance to mupirocin is likely to worsen the
problem. Studies suggest mupA gene which
encodes mupirocin resistance is transferred from
commensal flora of skin to MRSA during
mupirocin therapy.19 This could be a threat to
irrational use of mupirocin as it may lead to the
development and spread of mupirocin resistance.
In this study, out of total 250 Staphylococcus
aureus isolates, 5 i.e. 2% showed mupirocin
resistance by disk diffusion method. All the
mupirocin resistant Staphylococcus aureus
isolates are high-level resistant strains as
determined by disk diffusion method and two
Amit et al.,
different MIC methods: broth microdilution

method and agar dilution method.
The percentage rate of high-level mupirocin
resistance in this study is consistent with other
studies conducted in different regions of India.2,21
Low-level resistance is not found in this setup
which is in agreement with the study conducted
in Chennai by Oommen et al., but in contrast
Krishnan, et al., and Gadepalli, et al., has shown
1.5%
and
1%
low-level
resistance,
2,21,22
respectively.
In this study, none of MSSA
isolates showed resistance to mupirocin (either
high-level or low-level), and it is seen only in
MRSA isolates. Also, there was no significant
association seen between mupirocin resistance
with resistance to other antibiotics in this study,
which is in contrast to studies conducted by
MCDougal etal and Cadilla etal.23,24
Efficacious nasal clearance of MRSA for a
significant duration in carriers is shown in
mupirocin sensitive isolates. Emergence of highlevel mupirocin resistance has shown to be
associated with the failure of decolonisation
therapy among carriers and patients and offers
fewer topical treatment options16. However,
studies has suggested that low-level mupirocin
resistance strains can still be controlled with
normal dosage schedule of mupirocin ointment,
as it contains a higher concentration of mupirocin
(2000 g/ml) than the MICs of low-level
mupirocin resistance strains.25
CONCLUSION
The present study has demonstrated the presence

of high-level mupirocin resistance in a major
tertiary care setup of northern India which is a
concern to prevent the spread of MRSA in
hospitals and community. This may be attributed
to irrational use of antibiotics as well as over the
counter sale of drugs. Nasal decolonisation of
MRSA in healthcare personnel is performed by
using 2% mupirocin ointment along with absence
from duty till culture reports are documented
negative and since low-level mupirocin
resistance can be treated with the normal dosage
844
of mupirocin ointment, thus detection of highlevel mupirocin resistance seems to be

mandatory. Hence, it would be advisable to
detect mupirocin resistance by using both 5 g
and 200 g mupirocin disks from carriers before
starting mupirocin decolonisation therapy so that
alternatives may be used.
ACKNOWLEDGEMENTS
Our thanks to Ms. Shubhra Mishra, Msc, PhD for

technical help during the study
REFERENCES
1. Grunden N. MRSA, a short history of a

monster microbe. Pittsburgh Regional
Healthcare Initiative. Reprinted from PRHI
Executive Summary, December 2003.
Available:
http://www.prhi.org/docs
/MRSAa%20short%20history%20of%20a%2
0monster%20microbe12-1-2003.pdf
2. Gadepalli R, Dhawan B, Kapil A, Sreenivas
V, Jais M, Gaind R, Chaudhry R, Samantaray
JC, Udo EE. Clinical and molecular
characteristics of nosocomial meticillinresistant Staphylococcus aureus skin and soft
tissue isolates from three Indian hospitals. J
Hosp Infect. 2009;73(3):253-63.
3. Hill RLR, Casewell MW. Local treatment of
MRSA carriage and colonization. In:
Cafferkey
MT,
ed. Methicillin-resistant
Staphylococcus aureus. New York: Marcel
Dekker, 1992:14970
4. Hingst V, Vergetis W, Bommer J, Borneff M.
Prospective randomised placebo-controlled
study concerning the elimination of
Staphylococcus aureus by means of
mupirocin
in
patients
undergoing
hemodialysis (poster). International Congress
on Management of Infection. Amsterdam. 59 April 1992; Abstract p2: 110
Amit et al.,
5. Ellis MW, Grifth ME, Dooley DP, et al.

Targeted intranasal mupirocin to prevent
colonization and infection by communityassociated
methicillin-resistant
Staphylococcus aureus strains in soldiers: a
cluster
randomized
controlled
trial.
Antimicrob Agents Chemother. 2007;
51:35918
6. Lally RT, Lanz E, Schrock CG. Rapid
control of an outbreak of Staphylococcus
aureus on a neonatal intensive care
department using standard infection control
practices and nasal mupirocin. Am J Infect
Control. 2004; 32:4447
7. Paule SM, Robicsek A, Thomson RB Jr,
Kaul KL, Peterson LR. Three years of
universal surveillance and decolonization: the
effect on mupirocin resistance [abstract C21069]. In: Program and abstracts of the 48th
Annual ICAAC/IDSA 46th Annual Meeting
2008 (Washington, DC):171
8. Doebbeling B, Breneman D, Marsh R,
Reagen D, Wenzel R. Multicentre study of
elimination of Staphylococcus aureus nasal
carriage with calcium mupirocin ointment in
healthy subjects. Proceedings of the 32nd
Interscience Conference on Antimicrobial
Agents and Chemotherapy. Oct 1992; 11-14
9. Yanagisawa T, Lee JT, Wu HC, Kawakami
M. Relationship of protein structure of
isoleucyl-tRNA synthetase with pseudomonic
acid resistance of Escherichia coli. A
proposed mode of action of pseudomonic
acid as an inhibitor of isoleucyl-tRNA
synthetase. Journal of Biological Chemistry.
1994; 269, 243049
10. West SK, Plantenga MS, Strausbaugh LJ.
Use
of
decolonization
to
prevent
staphylococcal
infections
in
various
healthcare settings: results of an Emerging
845
Infections Network survey. Infect Control

Hosp Epidemiol. 2007; 28:11113
11. Chase McNeil J, Kristina G. Hulten, Sheldon
L. Kaplan and Edward O. Mason. Mupirocin
Resistance in Staphylococcus aureus Causing
Recurrent Skin and Soft Tissue Infections in
Children. Antimicrob. Agents Chemother.
2011;55(5):2431-33
12. Elaine S. Walker, Foster Levy, Mahmoud
Shorman,
Gerard
David,
Jehad
Abdalla and Felix A. Sarubbi. A Decline in
Mupirocin Resistance in MethicillinResistant
Staphylococcus
aureus
Accompanied Administrative Control of
Prescriptions.
J.
Clin.
Microbiol. 2004;42(6):2792-95
13. Jacob S. Hogue, Patricia Buttke, LoRanee E.
Braun, and Mary P. Fairchok. Mupirocin
Resistance Related to Increasing Mupirocin
Use in Clinical Isolates of MethicillinResistant Staphylococcus aureus in a
Pediatric Population. J. Clin. Microbiol.
2010;48(7):259900
14. Creagh S, Lucey B. Interpretive criteria for
mupirocin
susceptibility
testing
of
Staphylococcus spp. using CLSI guidelines.
Br J Biomed Sci. 2007; 64:15.
15. de Oliveira NE, Cardozo AP, Marques De A,
dos Santos KR, Giambiagi-deMarval M.
Interpretive criteria to differentiate low- and
high-level
mupirocin
resistance
in
Staphylococcus aureus. J of Medical
Microbiol. 2007;56:937-39
16. Perez-Roth E, Lopez-Aguilar C, AlcobaFlorez J, Mendez-Alvarez S. High-level
mupirocin resistance within methicillinresistant Staphylococcus aureus pandemic
lineages. Antimicrob Agents Chemother.
2006; 50: 320711
17. Hodgson JE, Curnock SP, Dyke KG, Morris
R, Sylvester DR, Gross MS. Molecular
Amit et al.,
characterization of the gene encoding highlevel mupirocin resistance in Staphylococcus

aureus
J2870.
Antimicrob
Agents
Chemother. 1994; 38:120508.
18. Udo EE, Jacob LE, Mathew B. Genetic
analysis
of
Staphylococcus aureus expressing high- and
low-level mupirocin resistance. J Med
Microbiol. 2001;50:90915
19. Hurdle JG, O Neill AJ, Mody L, Chopra I,
Bradley SF. In vivo transfer of high-level
mupirocin resistance from Staphylococcus
epidermidis
to
Staphylococcus aureus associated with
failure of mupirocin prophylaxis. J
Antimicrob Chemother. 2005;56:1166-68.
20. Clinical Laboratory Standard Institute.
Performance Standards for Antimicrobial
Susceptibility
Testing;
Twenty-Second
Informational Supplement. 2012;32(1):70-71
21. Oommen SK, Appalaraju B, Jinsha K.
Mupirocin resistance in clinical isolates of
staphylococci in a tertiary care centre in
south India. Indian J Med Microbiol.
2010;28(4):372-5.
22. Krishnan PU, Miles K, Shetty N. Detection
of methicillin and mupirocin resistance in
Staphylococcus aureus isolates using
conventional and molecular methods: a
descriptive study from a burns unit with high
prevalence of MRSA. J Clin Pathol. Oct.
2002;55(10):745-8
23. Adriana Cadilla, Michael Z. David, Robert S.
Daum, and Susan Boyle-Vavra: Association
of High-Level Mupirocin Resistance and
Multidrug-Resistant
Methicillin-Resistant
Staphylococcus aureus at an Academic
Center in the Midwestern United States. J.
Clin. Microbiol. 2010; 50: 95100
24. McDougal LK, Fosheim G, Patel JB; Team
ABCs. Emergence of resistance among USA
846
300 MRSA isolates causing invasive disease

in the US [abstract C1-166]. In: Program and
abstracts of the 48th Annual ICAAC/IDSA
46th Annual Meeting (Washington, DC,
2008):103.
25. Hudson IR. The efcacy of intranasal
mupirocin
in
the
prevention
of
staphylococcal infections: a review of recent
experience. J. Hosp Infect. 1994; 27, 8198
Amit et al.,
847
DOI:10.5958/j.2319-5886.2.4.135

&
Health Sciences
Coden: IJMRHS
st
Research article
Copyright @2013
ISSN: 2319-5886
th
A STUDY TO ANALYZE THE PREVALENCE OF MARTIN GRUBER ANASTOMOSES

AMONG MEDICAL STUDENTS
*Rupanjali B1, Vijayalakshmi B2, Chandrasekhar M3
1
Student, 2Professor, 3Dean and Head, Department of Physiology, Meenakshi Medical College and
Research Institute, Kanchipuram, Tamilnadu, India
*Corresponding author email: rupanjali1992@gmail.com
ABSTRACT
The most frequently occurring anomaly in the upper extremities has been the Martin Gruber
Anastomoses (MGA) which occurs due to the crossover of nerve fibers from the median nerve to ulnar
nerve. This study was performed to investigate the prevalence of MGA in 100 healthy medical students
as it acts as an etiology to carpal tunnel syndrome and other hand injuries. A nerve conduction study for
median and ulnar nerve was performed by placing the surface electrodes on the Thenar, Hypothenar and
first dorsal interosseus muscle with their Compound Muscle Action Potential (CAMP) and their
amplitudes being evaluated. MGA was found in 23 out of 100 volunteers. This relatively high incidence
demonstrates the necessity for healthcare specialists to factor the MGA into their diagnosis.
Keywords: Martin Gruber Anastomoses, Nerve Conduction study, Compound Muscle Action Potential
INTRODUCTION
The Martin Gruber anastomoses is a

communicating nerve branch between the
median nerve and the ulnar nerve in the forearm.
It
is
one
of
the
most
common
anastomotic anomalies that occur between these
two nerves. This connection carries motor nerve
fibers. In case of nerve lesions of the median or
the ulnar nerves, the Martin Gruber anastomoses
can serve as a channel for alternative
innervations of portions of the forearm and hand.
This inconstant pattern of connection can serve
as an explanation for challenging differential
diagnosis1.
Median-ulnar nerve anastomosis in the forearm
is the most common form of anomalous
innervations which was first described by

Swedish anatomist R.Martin in 1763 and later by
Gruber in 1870 and thus referred to as MartinGruber anastomoses. These anastomoses involve
axons leaving either the main trunk of the
median nerve or the anterior interosseous nerve,
crossing through the forearm to join the main
trunk of the ulnar nerve and ultimately
innervating the intrinsic hand muscles2-4. It is to
be noted that not all the axons of the median
nerve will be involved in this anomalous route.
In the type I anastomosis the cross over fibers
terminate in the Hypothenar muscles, in the type
II anastomosis the cross over fibers terminate in
the first dorsal interosseous, in the type III
Rupanjali et al.,
848
anastomosis the cross over fibers terminate in the

Thenar muscles5.
The main purpose of this study is to draw
attention of clinicians or surgeons from
neurophysiology field to this anastomosis and to
avoid misinterpretations of different studies of
needle electromyography and other nerve
conduction studies. Therefore for the assessment
of traumatic and entrapment lesions of median
and ulnar nerve and for surgical landmarks the
knowledge of this anastomosis is important.
100 healthy medical student volunteers of age
group 17-22 years were selected for this study.
Among them 40 students were male and 60
students were females. An informed consent was
taken from the students to whom the study was
performed. Subjects with peripheral neuropathies
and patients having diabetes mellitus, neuropathy
was not included.
The procedure followed to test for MGA is
outlined below:6
Surface electrodes were placed on the right hand
Thenar, Hypothenar and on the First Dorsal
Introsseous (FDI) muscles and were left in the
same position during the whole of the
electrophysiological testing. The median and the
ulnar nerves were stimulated supramaxilly at the
wrist and the elbow and the compound muscle
action potential (CMAP) were recorded with
their amplitudes being evaluated.
The electrodes were placed in standard
recording, reference and stimulation points.
Rectangular pulses of 0.2 m Sec duration were
used and the stimulus strength was
supramaximal.
The compound muscle action potentials (CMAP)
were recorded and the amplitude of each CMAP
was measured from the negative to the positive
peak of the response (peak to peak amplitude).
CMAP from the FDI, Thenar and Hypothenar
muscles larger (at least 1 mv) upon median nerve

stimulation at the elbow then at the wrist and
CMAP from one or more of these sites larger (at
least 1mv) upon stimulation of ulnar nerve at the
wrist than at the elbow were accepted as
indicators of presence of MGA.
MGA criteria2
A person is said to have Martin Gruber
Anastomoses based on the following:
If, on median nerve stimulation on the three
muscles-first dorsal interossei, hypothenar and
thenar, the amplitude at the wrist is greater than
the amplitude at the elbow, or If, on ulnar nerve
stimulation on the three muscles-first dorsal
interossei,hypothenar and thenar, the amplitude
at the elbow is greater than the amplitude at the
wrist.
Classification of Martin Gruber Anastomoses
In Type I anastomoses the crossover nerve fibers
terminate in Hypothenar muscles.
In Type II anastomoses the crossover nerve
fibers terminate in first dorsal interossei muscles.
In Type III anastomoses the crossover nerve
fibers terminate in thenar muscles5.
RESULTS
MGAs were found in 23 out of 100 subjects

tested: Out of these, 5 students were found to be
having type I (nerve fibers terminate in
Hypothenar muscles), 17 students were found to
be having type II (nerve fibers terminate in first
dorsal interossei muscle), and 1 student was
found to be having type III (nerve fibers
terminate in thenar muscles). In the group of 60
women 11 (18.3%) were found to have MGA. In
the group of 40 men, 12 (30%) were found to
have MGA. There are no significant racial or
gender differences in the prevalence of this
communication.
849
Rupanjali et al.,
25
FEMALE(F)
23
MALE(M)
F+ M
20
17
15
11
10
12
0
TYPE I
TYPE II
TYPE III
TOTAL
Fig 1: Prevalence of different types of MGA

DISCUSSION
MGA has been causing confusion in the

assessment of nerve injuries, carpel tunnel
syndrome and leprosy neuropathy. Because of its
high prevalence and different electro diagnostic
considerations, it can thus be concluded that
MGA is frequently encountered and it should be
kept in mind that abnormal innervations models
might influence the electrophysiological findings
and ultimately gives rise to faulty interpretations,
particularly in case of median and ulnar nerve
lesions. Mannerfelt was the first to use electro
diagnostic techniques to detect MGA and
reported a 15% incidence in a study of 41% 7.
Crutchfeild and Gutmann found an incidence of
28% in the general population and 62% in 29
relatives of 5 subjects with MGA8. Gutmann
studied 13 extremities with MGA and reported
that anomalous innervations were present in all
of Hypothenar and FDI muscles and in 6% of
Thenar muscles 9. Several other authors, using
electro diagnostic techniques have reported
incidences of MGA ranging from 8% to 26% in
patients with carpal tunnel syndrome (CTS) 10, 11.
CONCLUSION
Rupanjali et al.,
Martin Gruber Anastomoses might lead to the

misdiagnoses of many syndromes that affect the
nerve supply of the upper limb especially the
intrinsic muscles of hand. There were absolutely
no noticeable racial or gender differences in the
prevalence of this communication. It is important
to understand the existence of this
communication and its location for correct
patience assistance. In our study the incidence of
type II MGA was relatively high. Fortunately,
this does not present any difficulty in routine
ulnar nerve conduction studies because the
recording electrodes are not placed on this
muscle. A potential difficulty arises in cases of
suspected lesions in the deep palmar branch of
the ulnar nerve, because the recording electrodes
should be placed on the dorsal interosseous
muscle 10.
REFERENCES
1. Unver Dogan, Nadire. The communications
between the ulnar and median nerves in
upper limb. Neuroanatomy 2009; 8:15-19.
850
2. Oh SJ. Clinical Electromyography Nerve

Conduction Studies. Baltimore: Williams
Wilkins; 1993; Ed. 2; 314-333
3. Gutmann L. AAEM Minimonograph:
Important anamolous innervation of the
extremities J Muscle Nerve. 1993; 16:339347.
4. Uchida Y, Sugiyoka Y, Electrodiagnosis of
Martin Gruber Connection and its clinical
importance in peripheral nerve surgery, J
hand surg. 1992; 17(1):54-59.
5. Hatice Rana Erdem, Sevin, Ergurk, Cigdem
Erturk and Sumru Ozel.Electrophysiological
Evaluation of the Incidence of Martin Gruber
Anastomosis in Healthy Subjects. Yonsei
Medical Journal.2002; 43: 291-295.
6. De Lisa JA, Lee HJ, Baran EM, Lai KS,
Speilholz N. Manual of Nerve Conduction
Velocity and Clinical Neurophysiology. New
York: Rven Press; 68-92.
7. Mannerfelt. Studies on the hand in ulnar
nerve paralysis. A clinical experimental
investigation in normal and anomalous
innervation. Acta Ortho Scand.1966;87:23142.
8. Crutchfeild CA, Gutmann L. Hereditary
aspects
of
median-ulnar
nerve
communications. J Neural Neurosurg
Psychiatry1980; 229-235.
9. Gutmann L, Gutierez A, Riggs JE. The
contribution
of
median-ulnar
nerve
communication in diagnosis of mild carpal
tunnel syndrome. J Muscle Nerve. 1986; 9
(4) :319-321.
10. Wilburn AJ, Lambert E. The forearm median
to
ulnar
nerve
communication:
electrodiagnostic aspects (1976); 26: 368.
11. Lambert EH, Diagnostic value of electrical
stimulaton of motor nerves. J.EEG clinical
neurophysiology. 1962;22:9-16.
851
Rupanjali et al.,
DOI:10.5958/j.2319-5886.2.4.136

&
Health Sciences
www.ijmrhs.com Volume 2 Issue 4 Oct-Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886
Received: 23rd Aug 2013
Research article
PREDICTION OF WEIGHT OF CHILDREN AGED UP TO TWO YEARS BASED ON FOOT
LENGHT IN ETHIOPE EAST LOCAL GOVERNMENT AREA OF DELTA STATE OF SOUTHSOUTH NIGERIA
Lilian Ebele Chris-ozoko

Department of Human Anatomy, Faculty of Basic Medical Sciences, College of Health Sciences, Delta
State University Abraka, Nigeria.
Corresponding author email: lilyzoks@yahoo.com
ABSTRACT
Introduction: When a child is in a critical condition, it may not be hundred percent possible to
determine the body weight using weighing scale. Under such a condition, paediatricians estimate weight
using the age of the child. Material and Method: The weight was measured using a weighing scale. In
cases where the babies were too small and unable to stand on the weighing scale alone, the mother was
weighed alone and while carrying the baby and the weight of the baby was determined by subtracting
the weight of the mother from the weight of the mother and the baby. Results: Mean weight for male
children is 10.98kg, Mean foot length for male children is 5.04 inches, R2 = 0.61, F statistics = 7.57,
Probability = 0.0001531, Standard deviation of weight for males is 5.2, Standard deviation of foot length
is 0.009 Conclusion: Base on Foot length, weight of children below two years can be predicted in
emergency condition.
Keywords: Weight, Foot length, Children
INTRODUCTION
In emergency situations drug dosage is very

difficult to calculate for children who are
incapacitated, because their weight, surface areas
and length which are the present available means
of estimating appropriate drug dosages may not
be readily assessable. Although early researchers
have predicted age-based formulas which were
predominantly used for estimation of childrens
weight under emergency medical treatment.1
This method of drug dosage estimation is even
less specific and hence less accurate than the
preceding ones most especially because of the

variability of weight of children across different
tribe and economic situations.
Haftel et al 2 carry out a study on hanging legweight method for weight estimation in
children. Though the method was not like other
work proposed and used before, but could not
attract further interest. For obvious reasons
Mathur et al, 3 showed that foot length can be
used to predict the gestational age of very
premature aborted foetuses.
Bavdekar 4 in India conducted a study on a
novel technique using foot-length to predict the
852
Lilian Ebele Chris-ozoko et al.,
weight of children under the age of 2 years was

developed in India.
Foot length measurement is a potential tool for
evaluating children with low birth weight. 5
Embleton et al 6 work on a research study on the
relationship between foot length and nasotracheal
length. They came out to show that foot length is
a reliable predictor of nasotracheal length.
Other researchers (Amamturk et al 7also
conducted a study on the relationship between
foot length and body weight in adults age
between 17.6 and 82.9 years. And found a
significant relationship between both.
The aim of this study therefore, is to establish a
relationship between foot length and weight of
children below two years in Ethiopia East local
Government Area of Delta State; south-south
Nigeria.
Procedure for weight measurement: The

weight was measured using a weighing scale. In
cases where the babies were too small and unable
to stand on the weighing scale alone, the mother
was weighed alone and while carrying the baby
and the weight of the baby was determined by
subtracting the weight of the mother from the
weight of the mother and the baby.
Procedure for measurement of foot length:
Foot length was measured as a direct distance
from the prominent point of the back of the heel
to the tip of the hallux or to the tip of the second
toe, when the second toe is longer using a vernier
calliper.
Statistical analyzing data: The data obtained
was analyzed using mean, bar chart, frequency
polygon, standard deviation, body mass index,
linear regression and correlation analysis.
Statistical analysis performed using the ordinary
least squares (OLS) technique with its desirable
property of the best linear unbiased estimator
(BLUES) being adopted.
MATERIAL AND METHOD
Sample size : Sample size of the research study

is hundred and ten. Sixty four (64) males and
females (46) were included in the present study.
All the children used in the study were under two
years and their ages ranged from three months to
two years. Healthy children without deformity
were used after permission was obtained from
parents and teachers of sure foundation nursery
and primary school, Abraka- Delta State.
RESULT
Data analysis : Mean weight for male children is

10.98kg, Mean foot length for male children is
5.04 inches, R2 = 0.61, F statistics = 7.57,
Probability = 0.000153, Standard deviation of
weight for males is 5.2, Standard deviation of
foot length is 0.009
Table 1: Showing Weight, foot length and Weight Predicted using regression formula for males
Weight
8kg
9kg
9kg
14kg
9kg
Foot length
2.05 inches
3.83 inches
4.46 inches
5.72 inches
6.90 inches
Weight predicted using regression formula

6kg
10kg
11kg
14.7kg
17kg
Table 2: Summary of Regression Result for Male
Independent
variable
Weight
Constant
Dependent variable
(Foot length male)
Coefficient
0.07
77927
t-statistics
2.88
12.47
Standard Error
0.03
6248.207
Probabilities
0.01
0.00
853
The result in table 4.1 shows that the increase in

weight has a linear relationship with the foot
length. Thus an increase in weight by a unit will
increase the foot length by 0.07 units.
The R2 is the coefficient of determination and it
explains the fitness of the equation. The R2
suggests that 63 percent of the changes in foot
length have been explained by weight. This
means that the equation represents a good fit.
This is because the unexplained variation is just
thirty seven percent (1-063). The R2 is the
adjusted R2 for degrees of freedom and it
suggests that sixty one percent of the changes in
foot length have explained by weight.
The F test is used to test the overall significance

of the equations. The result showed that the F
calculated (7.57) > + critical (2.01) + critical
(2.01). This is an indication that weight is
significant in explaining the changes in foot
length.
R2 = 0.81, R-2= 0.79, F statistics = 10.67,
Probability = 0.000199, Female mean weight is
9.58kg
Female mean foot length is 4.04inches, Standard
deviation of weight in females is 3.9, Standard
deviation of foot length in females is 0.009
Table 3: Showing Weight, Foot length and Weight Predicted using regression formula for Females
Weight
11.5kg
5kg
7kg
12kg
10kg
Foot length
1.09 inches
2.37 inches
3.67 inches
4.21 inches
5.80 inches
Weight predicted using regression formula

4kg
5kg
7.8kg
8.6kg
11.2kg
Table 4: Summary of Regression Result for Female
Independent
variable
Dependent variable
( Foot length male)
Coefficient
Standard Error
t-statistics
Probabilities
Weight
0.81
0.05
16.25
0.0000
Constant
2794.7
1183.3
2.36
0.0228
The results in this table suggest that weight has a
linear equation relating foot length to weight was
positive linear relationship with foot length. Thus
y = 2.4x + 1 and y = 1.6x + 1.9 for females. The
an increase in the weight by a unit will increase
average body mass index for males was 15.70
the foot length by 0.81 units. The regression
and for females is 17.28
Fig 1: Foot length and weight of Males
Fig 2: Foot length and weight of Females

854
DISCUSSION
The finding in this present study shows that the
mean weight in males is higher than the mean
weight in females, while the mean foot length in
males is higher than the mean foot length in
females.
Sandeep et al, 8 working with Indian children
under two (2) years found a coefficient of
determination to be 0.88 while James D.K. et al 9
working in Manchester found a correlation
coefficient of 0.95. This work arrived at a
correlation coefficient of 0.62 in males and 0.81
in females. This is quite similar to the above
finding and suggests that all variability in weight
can be explained by a linear regression model.
The average body mass index for females was
17.28 and for males was 15.70, this all falls
within the fifth percentile for children under two
(2) years which is considered as normal (CDC,
2009). This work also gives a regression line
equation for children under two years in Nigeria.
It is our hope that other writers will derive
equations for other parts of Nigeria since this
work x-rays Ethiope East local Government Area
of Delta State in South- South Nigeria.
The importance of this study cannot be
overemphasized, because it provides the
parameters measured for estimation of weight
and thereby estimation of dosage of drugs for
emergency purposes in health cares. The results
have shown some important implications. It
showed that both for females and for males, the
weight plays significant role in influencing the
changes in foot length for both males and
females. The result showed that when the weight
of the females changes by a unit, the foot length
of males increases by 0.86 units. The result also
indicates that when the weight of the females
changes by a unit, the foot length of males will
increase by 0.07 units.
From the equations derived for both males and
females, it shows that if any of the variables are
known, the other can be determined.
Weight was estimated using the regression

equation derived and was compared with the
actual weight and they were all within the same
range.
CONCLUSION
In conclusion, this study is most useful in

emergency cases for determination of weight for
calculation of drugs doses especially in rural
Nigeria where adequate facilities are not
available in our paediatric wards and the age of
the child is in doubt.
REFERENCES
1. Lubitz DS, Seidel JS, Chameides L, Luten

RC, Zaritsky AL, Campbell FW. A rapid
method for estimating weight and
resuscitation drug dosages from length in the
paediatric age group. Ann Emerg Med
1988;17:576-581
2. Haftel AJ, Khan N, Lev R, Schonfeld N.
Hanging leg weight -- a rapid technique for
estimating total body weight in pediatric
resuscitation.
Ann
Emerg
Med
1990;19(5):523-526
3. Marthur A, Suresh K. Foot length a newer
approach on neonatal anthroprometry.
Journal of Tropical pediatrics. 1984; 30(6):
333 36.
4. Bavdekar SB, Sathe S, Jani P. Prediction of
weight of Indian children aged up to two
years based on foot-length: implications for
emergency
areas.
Indian
Pediatr
2006;43(2):125-30.
5. Marchant T, Jeanie J, suzzane P, Marcel T,
Joanna A S. Measuring newborn foot lengths
to identify small babies in need of extra care:
A cross sectional hospital based study with
community follow up in Tanzania. BMC
Public health. 2010;10: 624.
6. Embletonn et al. Foot length an accurate
predictor of nasotracheal tube length in
neonates. Arch des child fetal, neonatal ed
2001: 85: F60 F64.
7. Atamturk D. And duyar, I. (2008). Agerelated factors in the relationship between
foot measurement and living stature and body
855
weight. Journal of forensic sciences, 53:

1296 -1300.
8. Sandeep B, Shefalis Pranar J. Prediction of
weight of India children aged up to two years
based on foot length: implication for
emerging areas. J. Clin. Pediatrics. 2005; 10:
100 06.
9. James K, Dryburgh F, Chiswick M. Foot
length a new and potentially useful
measurement in the neonate. Arch dis child.
1979; 54: 226 -30.
856
DOI:10.5958/j.2319-5886.2.4.137

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
rd
Revised: 17thSep 2013
Research article
Copyright @2013
ISSN: 2319-5886
Accepted: 29thSep 2013
A STUDY ON PULMONARY FUNCTION TESTS IN WEAVERS

*Rajsri TR1, Gokulram N1, Gokulakrishnan K1,Chandrasekar M2, Nikhil Chandrasekar3
1 nd
II Year M.B.B.S., 2Dean, 3Department of Anesthesia, Meenakshi Medical College and Research
Institute, Enathur, Kanchipuram, Tamilnadu, India,
*Corresponding author email: rsri34@gmail.com
ABSTRACT
Occupation is the one in which person not only earn his daily bread but also spend one third of average
adult life. As the number of industries is on the increase, several industries like cement industries,
chemical industries, textile industries etc, serves mainly man for comfortable living. Health hazards
caused due to a particular occupation is yet to gain importance in public health measures. These diseases
are termed occupational hazards. Weavers are constantly exposed to fine cotton dust generated from the
weaving unit. Inhalation of this dust compromises their lung function greatly. Occupational exposure to
cotton dust has been a great threat to the respiratory function. Pulmonary function tests are set of
parameters to assess the lung function. It measures the function of lung capacity and chest wall
mechanics to determine a fault in lung function. Materials & Method: Spirometry is used to determine
airway disorders and is capable of predicting early damage in lung function. This paper discusses about
the lung impairment in female weavers of below age groups, corresponding to minimum 5 years of
exposure to cotton dust. 50 non smoking female weavers of age groups 25-40 years are chosen
respectively. Pulmonary function was assessed using computerized spirometry and compared with same
age, healthy non weavers. Conclusion: The pulmonary function parameters such as FVC, FEV1,
FEV1/FVC, and FEF25-75 were significantly reduced in weavers.
Key words: Pulmonary function tests, Spirometry, Occupational hazards, etc
INTRODUCTION
Weavers play an important role in a community.

Weaving either its manual or mechanized has
been important in a society which fulfill the
clothing needs. Several studies have found that,
on average, lung function is lower in cotton
workers than in the general population and in
general in those with a history of byssinosis. A
mortality study reported in 1985 of women aged
between 15 and 74 years found a marked excess
in the proportional mortality ratio (PMR) from
all causes of respiratory disease, including

byssinosis, in textile workers, particularly in
those employed as labourers and in fibre
preparation, whose PMR was more than 200 (i.e.
more than twice expected; a PMR of 100 is
equivalent to no excess mortality). The
Occupational Health Decennial Supplement
published in 1995 reported a PMR for chronic
bronchitis and emphysema in female textile
workers of 119 and of byssinosis of 1140.
857
Rajsri et al.,
Int J Med Res Health Sci. 2013; 2(4):857-860
Prevalence of byssinosis was 10.5%, chronic

cough 7.5%, chronic phlegm 12.9%, wheeze
with shortness of breath 22.3%, shortness of
breath (grade 2) 21%, chest tightness ever
33.3%; whereas, a low prevalence of asthma
(4%) was identified in this population1.
Karjalainen et al studied the impact of
occupational factors in the inception of adult
onset persistent asthma, and consequently the
potential for prevention is much larger and more
widely spread than generally assumed2.DrAsaad
Ahmed Nafees et al3studied the pattern and
predictors for respiratory illnesses and symptoms
and lung function among textile workers in
Karachi, Pakistan. This was a cross-sectional
survey of 372 adult male textile workers from the
spinning and weaving sections of 15 textile mills
from Karachi. Data were collected from
November to December 2009 through a
structured,
pretested
questionnaire
and
spirometry3.
Christiani et al conducted their research in
People's Republic of China. Pulmonary function
tests were performed pre and post work shift on
887 textile workers with at least two years of
employment in two cotton mills and one silk mill
in Shanghai, the People's Republic of China.
Environmental sampling was performed with
vertical elutriators, and pulmonary function was
performed with standardized techniques. Cotton
textile workers were found to have greater
across-shift decrements in forced expiratory
volume in 1 s (FEV1.0) than silk workers.
Increasing duration of exposure resulted in
increasing acute decrements in FEV1.0, although
significant acute decrements were found in
workers with less than five years of exposure.
The acute changes in FEV 1.0 were noted in both
symptomatic and asymptomatic cotton workers,
though the difference between the across-shift
change in FEV1.0 (delta FEV1.0%) of the
byssinotics and non byssinotics increased as
work duration increased. There was no difference
in pres hift FEV1.0 between the cotton and silk
workers, but several selection factors likely
influenced the observations4.
Boskabady et al evaluated the respiratory and
allergic symptoms in 66 Iranian carpet weavers
and 66 controls with similar age and gender
characteristics using a questionnaire including
questions on work-related respiratory symptoms
in the past year, allergies, smoking habits, and

work exposure duration. A total of28 carpet
weavers (42%) reported work-related respiratory
symptoms. Incidences of all respiratory
symptoms and most allergic symptoms were
significantly higher in carpet weavers than in
controls (p<0.05 - p<0.001). Moreover, most
respiratory and allergic symptoms in carpet
weavers were significantly more prominent
during working hours (p<0.01 - p<0.001).
Pulmonary function test results ofthe carpet
weavers
showed
significant
impairment
compared with controls (p<0.05 - p<0.001)5.
Rajsri et al.,
Cotton weaving has been a major occupation of

people in Thirupparkadal village in Vellore
district over generations. Almost all the members
of the family are involved in weaving. Cotton
weaving causes excessive development of fine
dust of cotton. Continuous exposure to this fine
dust over years has caused a threat to their lung
function. Reduction in lung function is directly
proportional to years of exposure to cotton dust.
This study mainly focuses on proving that over
the years there is severe impairment in lung
function.
Study population: Present study was conducted
in weaving units at Thirupparkadal village in
Vellore district, Tamilnadu in India. .
Institutional Ethical committee of Meenakshi
Medical College and Research Institute
(MMCH&RI), Enathur Kanchipuram has given
approval for the study. Study group consist of
non smoking female weavers
Group I: female weavers aged 25- 40 yrs (n=50)
Group II: female non weavers aged25-40yrs
(n=50). From all weavers informed consent was
obtained and procedure of the research was
properly explained. Subjects with clinical
abnormalities of the neuromuscular diseases,
known cases of gross anemia, diabetes mellitus,
pulmonary tuberculosis, bronchial asthma,
chronic bronchitis, bronchiectasis, emphysema
and malignancy were excluded from the study.
The subjects who had undergone abdominal or
chest surgery were also excluded from the study.
Inclusion criteria: Non smoker, corresponding
to minimum 5 years of exposure to cotton dust.
Exclusion criteria: Subjects with clinical
abnormalities of the neuromuscular diseases,
858
known cases of gross anemia, diabetes mellitus,

pulmonary tuberculosis, bronchial asthma,
chronic bronchitis, bronchiectasis, emphysema
and malignancy were excluded from the study.
The subjects who had undergone abdominal or
chest surgery were also excluded from the study.
Pulmonary function test: The pulmonary
function tests was carried out using a
computerized spirometer (Helios 401 RMS)
using the standard laboratory methods. The
spirometer was calibrated regularly and a brief
physical and general examination was carried out
and the anthropometric parameters (name, age,
sex, height, weight, occupation, and smoker /
nonsmoker) were entered in the computer. All
the pulmonary function tests were done on the
subjects comfortably in an upright position.
During the test, the subject was adequately
encouraged to perform their optimum level and
also a nose clip was applied during the entire

maneuver. Tests were repeated three times and
the best matching results were considered for
analysis. The parameters measured by the
apparatus were the Forced vital capacity (FVC),
Forced Expiratory Volume in 1st second (FEVI),
FEVI /FVC, Forced Expiratory Flow in 25% 75% (FEF25 -75%) with graphic curves were
obtained.
Statistical analysis
The data of pulmonary function tests were
presented as the Mean Standard Deviation for
each of the parameter. The two groups were
compared by using student t test by SPSS
software. The values obtained are statistically
significant.
RESULT AND DISCUSSION
Parameters
Group I
FVC
66.65 4.793
FEV 1
76.24 5.180
FEV 1 / FVC
115.8 2.600
FEF 25 - 75
40.88 4.442
*significant
The mean values of pulmonary function
parameters of weavers are given in above table.
The table depicts the comparative decline in lung
parameters of group I compared with group II.
The FVC, FEV, FEF25-75, FEV1/FVC (as a
percentage of predicted) was seen to significantly
decreased in group I than group II. The Present
study demonstrates that there is altered lung
function in weavers due to chronic exposure.
When compared to the predicted values there
was statistically significant decline in the values
of FVC, FEV, FEF25-75 and FEV1/FVC.
Inhalation of dust is an important cause of
interstitial lung disease in India.6 The present
study demonstrates that there is a significant
decrease in lung function as the years of
exposure to cotton dust increases. The probable
cause for the decrease in pulmonary function test
is the accumulation in peri bronchial lymphoid
and connective tissues along with varying
degrees of wall thickening and remodeling in
terminal and respiratory bronchioles arising from
each pathway. Bronchiolar walls with marked
Group II(control group)
P Value
83.262.5
86.25 6.292
87.9 10.17
70.64 2.019
< 0.01*
< 0.01*
< 0.01*
< 0.01*
thickening contained moderate to heavy amounts

of carbon and mineral dust and wall thickening is
associated with increase in collagen and
interstitial inflammatory cells including dustladen macrophages.7 The study by Edwards et al
has shown that in larger bronchi of the bysinotics
there was a higher percentage of muscle and
glands with corresponding lower percentage of
connective tissues and cartilage. While in
segmental bronchi no significant changes were
observed.12 Decrese in FVC, FEV1and
FEV1/FVC indicates an obstructive pattern of
lung disease. Decrease in FEF indicates a
pathology involving the larger airways due to
cotton dust. Studies have shown that cotton dust
induces histamine release or immunological
reaction antigen-antibody reaction as mechanism
of cotton dust disease. A growing number of
literatures have confirmed that endotoxin is the
main mediator in byssinosis and obstructive lung
diseases.13- 15.
859
Rajsri et al.,
CONCLUSION
The data suggests that cotton dust inhalation can

account for substantial decrease in lung function.
In order to prevent these among weavers the
strategies of use of mask, regular health check up
and proper awareness about the symptoms of a
particular lung dysfunction can be done
ACKNOWLEDGEMENT
Rajsri thanks Department of Physiology,

MMCH&RI for their guidance. Also thanks
Mr.M.G.K. Danacheriyan, Panchayat president
and Smt. Baby, VHN of thiruparkadal village for
helping out on the field.
REFERENCES
1. The
Occupational
Health
Decennial
Supplement published in 1995.
2. Karjalainen A, Kurppa K, Martikainen R,
Klaukka T, Karjalainen J. Work is related to
a substantial portion of adult-onset asthma
incidence in the Finnish population. Am
JRespirCrit Care Med. 2001;164(4):565-8.
3. Asaad Ahmed Nafees. Pattern and predictors
for respiratory illnesses and symptoms and
lung function among textile workers in
Karachi, Pakistan. Occup Environ Med:
2013; 10.1136/oemed-2011-100561; 99-107.
4. Christiani DC, Eisen EA, Wegman DH, Ye
TT, Gong ZC, Lu PL et al., Respiratory
disease in cotton textile workers in the
People's Republic of China. II. Pulmonary
function results, Scand J Work Environ
Health. 1986;12(1):46-50.
5. Boskabady MH, Karimiani EG, Vostacolaei
HA. Respiratory symptoms and pulmonary
function changes among carpet weavers in
Iran.Int J Occup Environ Health. 2007;
13(4):369-75.
6. Jindal SK, Aggarwal AN, Gupta D. Dutinduced intertitial lung diease in the tropics.
Curr Opin Pulm Med.2001; 7: 272-77.
7. Pinkerton KE, Green FHY, Saiki C,
Vallyathan V, Plopper CG, Gopal V et al.
Distribution of particulate matter and tissue
remodeling in human lung. Environ Health
Perspect 2000; 108:10639.
8. Kauffmann F, Drouet D, Lellouch J, Brille D.
Twelve years spirometric changes among
Paris area workers. Int J Epidemiol 1979;

8:201-12.
9. Mahmoud TM, Hosnia. Abd El Maged. A
study of occupational health hazards among
assuit spinning factory workers; Ass. Univ.
Bull Enviro. Res.2004;1: 63-75.
10. Paramasvam
Parimalam,
Narayani
Kamalamma and Anind kumar Ganaguli
knowledge, attitude and practices related to
occupational health problems among
Garment workers in Tamilnadu, India.
Journal of occupational health. 2007: 49 (6):
528-534.
11. Calvin S, Joseph B. Occupational Related
accidents in selected Garment Industries in
Bangalore city: Indian journal of community
medicine.2006;31(3):150.
12. Edwards C, Macartney J, Rooke G, Ward F,
The Pathology of lung in byssinotics. Thorax
1975:30: 612-23.
13. Khan AJ, Nanchal R, Cotton Dust Lung
Diseases, Corr Opin Pul Med 2007: 13(2);
137-41.
14. Rylander R, Haglind P, Lundholm M,
Endotoxin in Cotton Dust and Respiratory
function on decrement among cotton workers
in an experimental cardroo Am Rev Respir
Dis 1985; 131; 209-213.
15. Niven R McL, Pickering CAC. Occupational
Lung Disease-6; Byssinosis; a reviw: Thorax
1996: 51(6): 632-37.
860
Rajsri et al.,
DOI:10.5958/j.2319-5886.2.4.138

&
Health Sciences
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Coden: IJMRHS
rd
Research article
Copyright @2013
ISSN: 2319-5886
A STUDY OF ANTHROPOMETRIC MEASUREMENTS

OVERWEIGHT AMONGST GIRLS IN AN URBAN SCHOOL
AND
PREVALENCE
OF
*Sukhmeet Minhas1, Priyanshi Chaudhary2, Harinder Sekhon3, George Koshy4, Vandana Gangadharan5
1
Reader, Dept of Community Medicine, Armed Forces Medical College, Pune, Maharashtra, India
Intern, MH Secunderabad,
3
Psychiatrist, Composite Hospital, Central Reserve Police Force, Jammu, Jammu & Kashmir
4
OIC, Station Health Organisation, INS Rajali, Arakkonam, Tamil Nadu
5
Assistant Professor, Department of Pathology, Meenakshi Medical College & Research Institute,
Enathur, Tamil Nadu
2
*Corresponding author email: sukhmeetminhas@yahoo.com

ABSTRACT
Background: Individuals whose Body Mass Index exceeds the age-gender-specific 95th percentile are
overweight; while those with BMI between the 85th and 95th percentiles are at risk of overweight. The
prevalence of obesity is increasing worldwide. Children are becoming overweight at younger age.
Currently 10% of children worldwide are either overweight or obese. The present study was undertaken
to study the anthropometric measurements and determine the prevalence of overweight amongst school
girls in the age group of 5-8 years in a school of Pune. Methods: Anthropometric measurements of the
study subjects were studied by conducting a cross sectional descriptive study. All the 312 girl students,
aged 5 to 8 years enrolled in the school during the study period were studied. Results: 15.4% of the girls
were found to be overweight while 5.4% are at risk of overweight. Conclusion: With increasing age,
more girls become overweight and at risk of overweight. This increase is steady as the age increases
from 5 to 8 years.
Keywords: Anthropometry, overweight, children, urban, girls
INTRODUCTION
Overweight and obesity are by definition,
abnormal or excessive fat accumulation that may
impair health1,2 or simply as a state of excess
adipose tissue3.Another definition says that
obesity is an excessive accumulation of adipose
tissue containing stored fat in the form of
triglycerides4.Limited research has been carried
out in case of childhood overweight. However,

evidence based on surveys indicates that the
rising incidence of overweight and obesity
among children parallels that among adults5.The
prevalence of obesity is increasing worldwide in
almost every country in all the age groups and
children are becoming overweight at a younger
age6. Blood pressure, blood lipid levels, and
Minhas et al.,
861
obesity in childhood track into adulthood. The

increase in type 2 diabetes among children and
adolescents is directly related to the obesity
epidemic1,7,8. There is a secular trend of
childhood obesity to adult life; 41% of obese
adults have been overweight or obese during
their childhood also7,8. The rate of childhood
obesity has increased to a great extent in the last
two decades9. At present, about 10% of children
the world over are either overweight or obese10.
Among Canadian children, the rate of overweight
has increased from 11% in 1980s to over 30% in
1990s. Amongst Brazilian children it has
increased from 4% (1980s) to 14% (1990s)11. In
India, available studies from Chennai, Delhi and
Bhavnagar have shown the prevalence of obesity
as 6.2%, 7.4% and 5.55% respectively. The
prevalence of combined overweight and obesity
is more in girls (16.66%) than in boys
(12.48%)12. A "double burden" of disease exists
now. This is faced more so by many low- and
middle-income countries. While they continue to
deal with the problems of infectious diseases and
under-nutrition, there is a significant increase in
chronic disease risk factors. An upsurge in
obesity and overweight is particularly found in
urban settings. Very often there is under-nutrition
and obesity existing side-by-side within the same
country, the same community and even within
the same household2. According to one study, the
overall prevalence of overweight in urban
children in New Delhi has shown an increase
from 16% (2002) to about 24% (2006-2007)12. In
another study, the prevalence of overweight in
children was 16.75 % in boys and 19.01 % in
girls respectively. Besides, it was observed that
both overweight and obesity started manifesting
as early as 5 years of age13. At the time of entry
to school at 5 years of age, about 9% of boys and
girls were overweight and about 5% were
obese13. Another study found the overall
prevalence of obesity and overweight as 11.1%
and 14.2% respectively14. Similar study found
the prevalence of overweight to be 17.8% in boys
and 15.8 % in girls; and the prevalence of obesity
Minhas et al.,
was 3.6% in boys and 2.7% in girls15. Yet

another study found the prevalence of
overweight among school girls to be significantly
higher compared to the boys of the same age
group16. The available data therefore suggests
that Indian children today are taller and heavier
than their counter parts were fifteen years ago13.
The present study was undertaken to study the
anthropometric measurements and determine the
prevalence of overweight amongst school girls in
the age group of 5-8 years in an urban school.
Assessment of overweight: In the case of
children aged 5 to 8 years, emphasis is placed on
the assessment of physical status by the
measurement of height, weight and mid-upper
arm circumference17.
The anthropometric measurements recommended
for the children aged 5 to 8 years are:
Weight, Height, Body Mass Index, and Mid
Upper Arm Circumference18.
BMI has been recommended as the preferred
measure by many expert and advisory groups, for
evaluating overweight among children and
adolescents 2 to 19 years of age20. BMI is
recommended since it can be obtained easily, is
co-related strongly with body fat percentage
(especially at extreme BMI levels), is associated
only weakly with height, and it identifies the
fattest individuals correctly, with acceptable
accuracy at the upper end of the distribution (e.g.
85th or 95 thpercentile for age and
gender)19,20,21.
The BMI is a derived index and is calculated as
per the guidelines given by the WHO as
follows17:
BMI = Weight (in Kgs) / Height2 (in meters)
Using the above equation, BMI is calculated
until the second decimal value.
Classification
The most commonly used parameter is BMI
which is calculated as weight in kg divided by
the square of the height in meters. After BMI is
calculated, the number is plotted on the CDC
862
BMI-for-age growth charts to obtain a percentile

ranking. These charts are separate for girls and
boys. Percentiles are the most commonly used
indicator to assess the size and growth patterns of
individual children. Percentile indicates the
relative position of a particular childs BMI
number in comparison to children of the same
sex and age. The growth charts show the weight
status categories used with children. They depict
underweight, healthy weight, at risk of over
weight, and overweight, as shown in Table 121.
Table 1: CDC Classification of Weight Status
According to the Percentile Range
Weight
status
category
Underweight
Percentile range
Healthy
weight
At risk of
overweight
Overweight
5th percentile up to the 85th

percentile
85th to less than 95th percentile
Less than 5th percentile
Equal to or greater than the 95th

percentile
Aims and Objectives:

The study was undertaken with the following
aims and objectives:
1. To study the anthropometric measurements of
school girls in the age group of 5-8 years.
2. To determine the prevalence of overweight.
The anthropometric measurements of school girls

in the age group of 5-8 years in an urban school
were studied by conducting a cross sectional
descriptive study. All the 312 girl students, aged
5 to 8 years enrolled in the school during the
study period were studied. Before start of the
study, ethical clearance was obtained from
institutional ethics committee, informed consent
was taken from the parents and the relevant
authorities of the school were briefed about the
scope of the study, with a view to solicit their cooperation. The age was recorded to the nearest
Minhas et al.,
completed year (6 months and above being

rounded off to the next year and less than six
months to the previous year) as per the official
records of the school. Record of the educational
status of the child was restricted to the class in
which the child was studying at the time of data
collection.
Anthropometric
Measurements
recorded during the conduct of the study were
weight, height, Body Mass Index (BMI), Mid
Upper Arm Circumference (MUAC) and was
done with the full uniform on, less the belt and
shoes and was conducted on the guidelines
issued by the World Health Organisation13. Data
was analysed using Epi Info software.
RESULTS
It was observed that out of the total of 312

subjects examined, all the subjects aged 5 years
were studying in class 1, 97% of those aged 6
years were in class 1, while the remaining 3%
aged 6 years were in class 2. 57.1% of those aged
7 years were in class 1, 36.3% in class 2, and the
remaining 6.6% were in class 3, as shown in
Table-2. Out of the 8 year old subjects, 1.6%
were in class 1, 36.3% in class 2 and the
remaining 62.1% were in class 3, respectively.
The distribution of BMI percentiles according to
age of the subjects is as shown in Table2. It was
observed that based on BMI criteria as defined,
overall, 16.7%, 42.4%, 33.0% and 16.5%
subjects had BMI <5thpercentile at the age of
5,6,7, and 8 years, respectively. 83.3%, 45.5%,
51.6% and 57.7% subjects had BMI 5 th - <85th
percentile at the age of 5, 6, 7, and 8 years,
respectively. 9.1%, 9.9% and 19.8% subjects had
BMI 85 th - <95th percentile at the age of 6, 7,
and 8 years, respectively. 3.0%, 5.5% and 6.0%
subjects had BMI 95 th percentile at the age of 6,
7, and 8 years, respectively. It was found that
BMI percentile categories as shown in the table
were homogenous with respect to age (p<0.05).
The distribution of mean MUAC and standard
deviation of the subjects by age, is as shown in
Table3. It was observed that the mean MUAC
863
of the subjects decreased till 7 years and

increased thereafter. Similarly, the median
MUAC decreased from 5 to 6 years of age, and
increased thereafter. It was found that mean
MUAC, median MUAC and standard deviation
as shown in the table were homogeneous with
respect to age of the subjects (p<0.05).
The distribution of percentiles of weight of
subjects according to age is as shown in Fig
1.On plotting the percentile distribution of
weight with respect to age of the subjects; it is
observed that there is an increasing trend in
respective percentile with respect to age. The
weight at 5, 6, 7, and 8 years of age being 17, 14,
14, and 16 kg at the 5th percentile; the same being
21, 18, 20, and 24 kg at the 50th percentile; and
the corresponding weight at the 95th percentile
being 23, 36, 35 and 40 kg. There is a gradual
decrease till the age of 7 years, after which there
is a rapid increase observed to 8 years of age.
Further, this increase in the weight is more
marked at the higher percentiles.
The distribution of percentiles of height of
subjects according to age is as shown in Fig-2.On
studying the percentile distribution of height with

respect to age of the subjects, it is observed that
there is generally an increasing trend in
respective percentile with respect to age. The
height at 5, 6, 7, and 8 years of age being 115,
101, 104, and 106cms at the 5th percentile; the
same being 118, 113, 117, and 124cms at the 50th
percentile; and the corresponding height at the
95th percentile being 121, 129,137, and 140cms.
The distribution of percentiles of BMI of subjects
according to age is as shown in Fig3.On
studying the percentile distribution of BMI with
respect to age of the subjects; it is observed that
there is an increasing trend in respective
percentile with respect to age, except for a slight
dip around 6 years of age. The BMI at 5, 6, 7,
and 8 years of age being 12, 10, 12, and 10 kg/
m2 at the 5th percentile; the same being 14, 14,
14, and 15 kg/ m2 at the 50th percentile; and the
corresponding BMI at the 95th percentile being
16, 22, 23 and 24 kg/ m2. The fall and rise in the
BMI is more marked at the lower percentiles.
Table 2: Distribution of BMI percentiles according to age
Age
BMI Percentiles
Total
th
th
th
th
th
th
<5
5 - <85
85 - <95
95
1 (16.7)
5 (83.3)
0
0
6 (100)
5
14 (42.4)
15 (45.5)
3 (9.1)
1 (3.0)
33 (100)
6
30 (33.0)
47 (51.6)
9 (9.9)
5 (5.5)
91 (100)
7
30 (16.5)
105 (57.7)
36 (19.8)
11 (6.0)
182 (100)
8
75 (24.0)
172 (55.1)
48 (15.4)
17 (5.4)
312 (100)
Total
2
X = 20.6024, df = 9, p < 0.05
Note: As per CDC 2000 guidelines, percentile of the BMI define Underweight, Healthy weight, At risk
of overweight and Overweight in case of children. The figures in parenthesis refer to the percentages.
Table: 3 Distribution of MUAC Mean Standard Deviation according to age of the subject
Age
(completed years)
5
6
7
8
Minhas et al.,
Observations
Mean SD
6
33
91
142
17.661.40
16.992.07
16.962.55
17.992.47
864
X2 = 21.0258, df = 3, p < 0.05

45
40
Weight (kg)
35
30
P5
25
P25
20
P50
15
P75
10
P95
5
0
6
7
Age in completed years
Fig 1: Distribution of percentiles of weight of subjects according to age

150
140
130
P5
P25
110
P50
100
P75
90
P95
Height
(cms)
120
80
5
6
7
8
Fig 2: Distribution of percentiles of height of subjects according to age

30
BMI
25
20
P5
P25
15
P50
10
P75
P95
5
0
5
6
7
8
Fig: 3Distribution of percentiles of BMI of subjects according to age
Minhas et al.,
865
Table 4: Comparison of median height of subjects
Age Present
Study
Agarwal
al26
et Rath et al29
Marwaha Vijaya
et al13
Raghavan et al28
CDC23 WHO31
5
117.830.0223 104.9227.38 109.694.84 111
112.243.91
108
110
6
114.760.0639 110.544.34 118.784.65 117
117.735.08
115
115
7
116.700.0633 11542.10
122.994.74 122
122.655.79
122
121
8
124.400.0582 123.835.51 127.796.83 128
127.226.58
128
127
Note: The values in parenthesis correspond to the mean and SD. The values of SD are not available in
respect of the other studies.
Table 5: Comparison of median weight of subjects
Age Present
Agarwal
et Rath et al29 Marwaha Vijaya
al26
et al26
Raghavan et al28
Study
5
20.332.14 15.7711.14
18.722.4 19
18.671.89
6
19.084.21 17.8918.72
21.723.85 21
21.563.44
7
20.154.09 19.3423.40
23.033.49 24
24.454.41
8
23.824.54 22.3422.56
26.396.11 27
25.974.87
Note: The values in parenthesis correspond to the mean and SD. The values of SD
CDC23 WHO31
18
18
20
20
23
22
26
25
are not available in
Table 6: Comparison of median BMI of subjects
WHO31
Age
Present Study
5
14.631.32
13
6
14.382.05
13
7
14.722.07
13
8
15.302.13
13
Note: The values in parenthesis correspond to the mean
CDC23
Marwaha et al13
13
12
13
12
13
12
13
13
and SD. The values of SD are not available in
Table 7: Comparison of means of MUAC of subjects
Age
5
6
7
8
Present Study
17.66 1.40
16.99 2.07
16.962.55
17.992.47
Shrivastava et al32
15.3 1.1
15.9 1.3
16.5 1.2
17.2 1.5
Rath et al29
16.34 1.24
17.72 1.71
17.58 1.76
18.57 2.82
Vijaya Raghavan et al28

16.3 1.31
16.96 1.60
17.70 2.14
18.00 2.16
DISCUSSION
The comparison of median height of subjects is
as shown in Table4.On comparing with other
studies, it was observed that the median height of
the subjects in the present study is higher at all

ages than that observed by KN Agarwal et al26, 27
whereas it is lower at all ages than that observed
Minhas et al.,
866
by Marwaha et al13, VijayaRaghavan et al28 and

Rath et al23 at all ages except at the age of 5
years. On the whole, it was observed that the
median height of the girls in the present study is
comparable to the other studies.
The comparison of median weight of subjects is
as shown in Table5.On comparing with other
studies, it was observed that the median weight
of the subjects in the present study is higher at all
ages than that observed by KN Agarwal et al26
whereas it is lower at all ages than the median
weight observed in the other studies, except at
the age of 5 years.
The comparison of median BMI of subjects is as
shown in Table6.On comparing the median
BMI with respect to age of the subjects, it was
observed that the median BMI of subjects in the
present study is generally more than that in the
CDC standards23, the WHO standards31, and the
BMI observed by Marwaha et al13 at all ages.
The comparison of MUAC of subjects is as
shown in Table7.On comparing with other
studies, it was observed that the mean MUAC of
the subjects in the present study is higher at 5
years of age, than the mean MUAC of the
subjects observed in the studies by DK
Shrivastava et al32, Rath et al29 and
VijayaRaghavan et al28. However, there is a dip
at 6 and 7 years of age, after which it again rises.
and at risk of overweight. This increase is steady

as the age increases from 5 to 8 years.
ACKNOWLEDGEMENT
This study is part of a research project funded by

grant from the Indian Council of Medical
Research.
REFERENCES
In the present study we have observed that at the

age of 6 years, 3.0% of the subjects are
overweight while 9.1% of the subjects in the
study population are at risk of overweight.
Similarly, at the age of 7 years, 5.5% of the
subjects are overweight while 9.9% of the
subjects in the study population are at risk of
overweight. The similar figures at 8 years of age
are 6.0% and 19.8% respectively. Overall, 15.4%
of the girls were found to be overweight while
5.4% are at risk of overweight. From the present
study we can conclude that with increasing age
during childhood, more girls become overweight
1. Donohoue AP. Obesity. In: Behrman E

Richard, Kleigman M Robert and Jenson B
Hal editors. Nelson: Textbook of Pediatrics.
18th Edition. Saunders (Elsevier), 2008: 232242.
2. World Health Organisation. Fact Sheet No.
311. Sep 2006. Accessed on 10 Oct 2006.
http://www.who.int/mediacentre/factsheets/fs
311/en/
3. Flier SJ, Maratos-Flier E. Obesity. In: Kasper
L Dennis, Braunwald Eugene, Fauci S
Anthony, Hauser L Stephen, Longo L Dan
and Jameson J Larry editors. Harrisons
Principles of Internal Medicine. 17th Edition.
McGraw Hill: Medical Publishing Division,
2008: 462-473.
4. Weaver AK, Piatek A. Childhood obesity. In:
Samour Patricia Queen, Helm Kathy King
and Lang E Carol. Handbook of Pediatric
Nutrition.2nd Edition. Jones and Bartlett
Publications, 2004: 173-89.
5. Kafatos A, Codrington CA, Linardakis M.
Obesity in Childhood:
The Greek
Experience. In: Simopoulos P Artemis editor.
World Review of Nutrition and Dietetics
Nutrition and Fitness: Obesity, the Metabolic
Syndrome, Cardiovascular Disease and
Cancer (Volume - I). Karger, 2005: 27-35.
6. Astrup A. Obesity. In: Geisler Catherine and
Powers Hilary editors. Human Nutrition.11th
Edition. Elsevier (Churchill Livingstone),
2006: 379-99.
7. Ramachandra A, Snehalata C, Vinitha R.
Prevalence of overweight in urban Indian
Minhas et al.,
867
CONCLUSION
adolescent school children. Diabetes Res

ClinPract 2002; 57: 185- 90.
8. Kapil U, Singh P, Pathak P. Prevalence of
obesity amongst affluent adolescent school
children in Delhi. Indian Paediatrics.2002;
39: 449-452.
9. Han JC, Lawlor DA, KimmSY. Childhood
obesity. Lancet. 2010;375:1737-48.
10. Bessesen DH. Update on obesity. J Clin Endo
crinol Metab. 2008;93(6):2027-34.
11. Flynn MA, McNeil DA, Maloff B. Reducing
obesity and related chronic disease risk in
children and youth: a synthesis of evidence
with 'best practice' recommendations. Obes
Rev. 2006;7(Suppl 1):1-5.
12. Shah C, Diwan J, Bhabhor M, Gokhale P,
Mehta H. Assessment of obesity in school
children.
Calicut
Medical
Journal
2008;6(3):e2.
13. Bhave S, Bavdekar A, Otiv M. IAP National
Task Force for Childhood Prevention of
Adult Diseases: Childhood Obesity. Indian
Paediatrics.2004; 41: 559-75.
14. World Health Organisation. Obesity:
preventing and managing the global
epidemic, Geneva; June 1997: 3-5.
15. Chhatwal J, Verma M, Riar SK. Obesity
among pre-adolescent and adolescents of a
developing country (India). Asia Pac J
ClinNutr. 2004;13(3):231-35
16. Heird CW and Donohoue AP. Nutrition. In:
Behrman E Richard, Kliegman M Robert and
Jenson B Hal editors. Nelson: Textbook of
Pediatrics. 17th Edition. Saunders (Elsevier),
2004: 153-177.
17. World Health Organisation. Physical Status:
The
use
and
interpretation
of
Anthropometry. WHO Tech Report Series,
No.
854.
WHO
Geneva
1995.
http://www.who.int/childgrowth/
publications/physical_status/en/index.html
18. Jelliffe BD and Jelliffe EFP editors.
Anthropometry: methods. In: Community
Nutritional Assessment. Oxford Medical
Publications, 1989: 64-104.
Minhas et al.,
19. Bhasin SK, Singh S, Kapil U. Height and

Weight of Well to do Children in
Haryana. Indian Paediatrics.1990; 27: 108993.
20. Krebs N, Himes JH, Jacobson D et al.
Assessment of Child and Adolescent
Overweight and Obesity. Pediatrics 2007;
120: Supplement 4.
21. Child Growth Standards. National Centre for
Health Statistics .National Health and
Nutrition Examination Survey. Centers for
Disease
Control
and
Prevention.
http://www.cdc.gov/nchs/ nhanes.htm
22. Mercedes de Onis, Adelheid WO, Elaine
Borghi, Amani Siyam, Chizuru Nishida &
Jonathan Siekmann. Development of a WHO
growth reference for school-aged children
and adolescents. Bulletin of the World
Health Organization 2007; 85: 66067.
23. BMI Body Mass Index: About BMI for
Children and Teens. Centres for Disease
Control (CDC) Atlanta. Division of Nutrition
and Physical Activity, National Centre for
Chronic Disease Prevention and Health
Promotion..
http://www.cdc.gov/healthyweight/assessing/
bmi/
24. Reaven GM. Role of insulin resistance in
human disease. Diabetes 1988; 37: 1597-07.
25. Guyton CA, Hall EJ. The Cell and Its
Functions. In: Textbook of Medical
Physiology. Elsevier (Saunders), 11th Edition;
2006: 12; 842: 872-74.
26. Agarwal KN, Manwani AH, Khanduja.
Physical Growth of Indian Children. Indian
Pediatrics. 1970; 7 (3): 146 55.
27. Marwaha RK, Tandon N, Singh Y, Aggarwal
R, Grewal K, Mani K. A study of growth
parameters and prevalence of overweight and
obesity in school children from Delhi. Indian
Pediatrics. 2006;43 (11): 943-52.
28. Vijaya Raghavan K, Singh D, Swaminathan
MC. Heights and Weights of Well- nourished
Indian School Children. Indian Journal of
Medical Research. 1971; 59 (4): 648-654.
868
29. Rath B, Ghosh S, Mohan M. Anthropometric

Indices of Children (5 15 years) of a
Privileged Community. Indian Pediatrics.
1978; 15 (8): 653 65.
30. Donohoue AP. Groth and Development. In:
Behrman E Richard, Kleigman M Robert and
Jenson B Hal editors. Nelson: Textbook of
Pediatrics. 17th Edition. Saunders (Elsevier),
2004: 46 -49.
31. Growth reference charts. World Health
Organisation 2008. http://www.who.int/
childgrowth/ standards/en/
32. Shrivastava DK, Thawrani VP, Gupta K.
Health Examination of primary School
Children at
Gwalior
Part
III:
Anthropometric
Assessment.
Indian
Pediatrics. 1978;15 (8):67179.
33. VijayaRaghavan K, Singh D, Swaminathan
MC. Arm Circumference and Fat Fold at
Triceps in Well- nourished Indian School
Children. Indian Journal of Medical
Research. 1974; 62 (7): 994 - 1001.
34. Park K. Parks Textbook of Preventive and
Social Medicine. 21st edition. 2011. 366-70
Minhas et al.,
869
DOI:10.5958/j.2319-5886.2.4.139

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Health Sciences
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Volume 2 Issue 4 Oct - Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886
th
Research article
EVALUATION OF TRENDS IN THE PROFILE OF GYNAECOLOGIC MALIGNANCIES AT

A TERTIARY CARE HOSPITAL IN KARNATAKA, SOUTH INDIA
Hemalatha AL1, Gayathri MN2, *Deepthi B Ramesh3, Neelima P Chamarthy3, Giripunja M3, Nayana
NS3
1
Professor and Head, 2Assistant Professor, 3Post Graduate, Department of Pathology, Mysore Medical
College and Research Institute, Mysore, Karnataka, India
*Corresponding author email: halingappa@gmail.com
ABSTRACT
Objective: Comprehensive estimates of the incidence of gynecological malignancies reported from
India are very limited due to limitation in record maintenance. Auditing of the results on the incidence
rates provided by the Population Based Cancer Registries has shown variation in the patterns of
gynecologic malignancies. The present study was undertaken to establish the profile of gynecologic
malignancies reported in our centre, with reference to incidence, histological subtypes and frequency of
involvement at various sites. Another objective was also to compare the procured data with those from
other national and international centers. Materials and Methods: In this descriptive study, the records
pertaining to all the pathological specimens categorized as ovarian, uterine corpus and uterine cervical
cancers from January 2003 to December 2012 at our tertiary center were studied and compared with the
available international data. Results: Cervical malignancies were the commonest at our center, as
compared to the uterine malignancies, which were commoner as per the data available from Surveillance
Epidemiology and End Result (SEER) programme of the United States and the European Union.
Keywords: Gynecological malignancy; South India; Cervical Malignancy.
INTRODUCTION
The cancer has already emerged as one of the

most important health problems with an alarming
rate of over 800,000 new cases occurring every
year.1 According to the data collected the Cancer
Registries, it has been noted that >70% of the
cancers in women according occurs in middle
aged women ranging from 35 to 64 years,
thereby suggesting the impact of cancer as a
major public health issue in the most productive
age group of women. Data from the population
bases registries under the National Cancer

Registry Program indicate that the leading sited
of cancer among women are the cervix, uterus,
breast and oral cavity.2
70% of women present at an advanced stage of
the disease, which results in poor survival and
high mortality rates.2 India, being one of the
developing countries, need to take active
measures to decrease the rate of gynecological
malignancies, thereby decreasing the rate of
Hemalatha et al.,
Int j Med Res Health Sci. 2013; 2(4): 870-873
870
morbidity in women. The first step in this

process is to assess the incidence and prevalence
of cancers. It is of utmost importance in our
country to detect the cancers early and take
active treatment measure. But illiteracy, lack of
awareness about the symptoms of the underlying
grave disease and lack of access to health centers
with treatment and prevention facilities,
prevalence of poverty, results in failure to elicit
the expected response and results in Indian
women.
Regional variability in cancer incidence, the
mean age at which women present with
gynecological symptoms, stage at presentation,
the common sites of occurrence is noted from the
data available from the a good number of centers
worldwide. Studies regarding these issues are
available in registries from developed countries
but reliable data from developing countries, such
as India, is lacking. Keeping this need in view,
the present study was designed to determine the
relative frequency of the malignant tumors of the
female genital tract to study the various
histological types and characteristics of these
tumors among the patients at our center. An
attempt has also been made to compare our data
with those available from cancer registries in
India and across the world.
Detailed relevant information regarding the

clinical history and findings such as patient age,
site of affliction, histopathological diagnosis and
subtypes were collected. The 475 cases included
in the study had a definite histological diagnosis,
made either on biopsy or resection specimens.
Cancer diagnosed by aspiration and cervical
scrape smears but not followed by
histopathological confirmation were excluded
from the study.
The data was analyzed using Microsoft Excel
Software and SSPS 16. For the purpose of
comparison of incidence, our data was curtailed
to the corresponding periods, for which the
international data was also available.
RESULTS
A total of 475 cases of gynecologic malignancies

were reported and treated at our centre, in
between January 2003 to December 2012. The
age ranged from 7 to 85 years (Median age = 47).
The sites of involvement in the order of
prevalence of occurrence included Cervix (358),
Ovary (73), Corpus Uteri (27), Vagina (9) and
Vulva (8).
Out of the total number of 475 cases, the cervix
was a common site affected (Median age = 48
years). Patients between 25 years and 35 years of
age constituted the commonest age group
affected. 8.4% of the cervical cancers occurred in
women <30 years of age.
Ovarian malignancies constituted 14.94% of all
the gynecological malignancies reported, with a
median age of 45 years. The histological
subtypes encountered in the study are as shown
in the table. Uterus was the primary site of
involvement in 5.6% of cases. Nine malignancies
of vaginal origin and 8 malignancies of the
vulval origin were identified. Two cases of
bilateral Krukenberg tumor of the ovary were
encountered.
Table 1: Histologic distribution of gynecologic
malignancies
Histologic types
Uterine cervix
Squamous
cell
carcinoma
Adenoma
Others
Ovary
Epithelial
Germ cell
Stromal
Uterus
Epithelial
Mesenchymal
Vagina
Vulva
Secondary tumors
No. of cases
358
339
%
75.36
71.36
16
3
71
36
7
8
27
24
3
9
8
2
3.36
0.36
14.94
11.78
1.47
1.68
5.68
5.05
0.63
1.89
1.68
0.42
871
Hemalatha et al.,
DISCUSSION
Gynecological malignancies form a huge burden,

contributing significantly to the morbidity and
mortality around the world. Studies based on
cancer incidence in India revealed that the
incidence is >70 per 100,000 population. 1, 3
Nearly 70% of the Indian population lives in
rural areas where the socioeconomic living
standards are low and the quality of health care is
limited. Owing to these factors, women in India
are more vulnerable to most of the risk factors
for cervical cancer such as early marriage, early
childbirth, multiparity and chronic infections
with genital disease, mostly transmitted
sexually.3,4 In the cohort of patients in our study,
cervix was the commonest site of affection
among the gynecologic malignancies. Other
registries in India and South Asia also reported
similar observation.5,6
Cervical cancer remains the commonest
gynecologic cancer and the second most
common cancer among females, first being the
breast cancer as recorded in the consolidated
report from the National Cancer Registry
Programme.7,8 The small number of cases of
vulval and vaginal cancer in our study is not
suitable for making statistical comparison or
estimated due to their small numbers.
Ovary was the second commonest site amongst
gynecologic malignancies at our center. The age
specific incidence rate of ovarian cancer revealed
that, the disease increases from 35 years of age
and reaches a peak between the ages of 55 to 64
years.9 Western data from the GLOBOCAN
2002 reveals a higher number of cases of ovarian
malignancies recorded as compared to the data
recorded in our study, and also the NRCP and
other cancer registries in India.7,8,10
Uterine malignancies were the commonest ones
reported as per the SEER programme of United
Stated and European Union which was
significantly higher in their population as
compared to those reported at our center.11,12 It
was also noted that all the gynecological
malignancies expect those involving the cervix

affected the younger age group in our study as
compared to the studies done in United States
and other developed countries.
Table 2: Leading sited of cancers in females,
pooled aar/100,000 in india 3
SITE
AAR
Breast
25.1
Cervix
21.2
Ovary
6.7
Oral cavity
6.4
Esophagus
5.5
Stomach
3.4
Gall bladder
3.2
Leukemia
2.9
Lung
2.7
Corpus uteri
2.5
CONCLUSION
The present study includes an extensive data of

gynecologic malignancies. Although the
comparative study with the population based
international registries like Seer and Globocan
may not offer a totally accepted comparison,
considering the vast socio-economic and cultural
differences, it nevertheless provides a
comprehensive understanding of the current
scenario of gynecological malignancies in India.
In our country, lack of widespread population
based data has led to a greater reliance on
hospital based registries for the epidemiological
information. The need of the hour is more studies
on gynecologic cancer to help formulate better
cancer detection strategies towards specific age
groups and risk factors.
ACKNOWLEDGEMENTS
We acknowledge the technical help in the

statistical calculations, extended by Dr. Sumanth
MM, Assistant Professor, Department of
Community Medicine, Mysore Medical College
and Research Institute, Mysore.
872
Hemalatha et al.,
REFERENCES
1. Consolidated report of hospital based cancer

registries 2001-3, national cancer registry
program. New Delhi; Indian Council of
Medical Research; 2007.
2. Uma Devi K. Current status of gynecological
cancer care in India. Journal of Gynecologic
Oncology.2009; 20(2), 77-80.
3. Agarwal S, Malhotra KP, Sinha S, Rajaram
S. Profile of gynecologic malignancies
reported at a tertiary care center in India over
the past decade: Comparative evaluation with
international data. Indian journal of cancer.
2012;49(3); 298.
4. Momtahen S, Kadivar M, Kazzazi AS,
Gholipour F. Assessment of gynecologic
malignancies: A multi-center study in
Tehran. Indian journal of cancer.2009; 46(3):
226.
5. Nandakumar A, Ramnath T, Chaturvedi M.
The magnitude of cancer cervix in
India.2009;
6. Moore MA, Ariyaratne Y, Badar F, Bhurgri
Y, Datta K, Mathew A et al. Cancer
epidemiology in South Asia-past, present and
future. Asian Pac J Cancer Prev.2010;11(2),
49-66.
7. Indian Council of Medical Research
(homepage on the internet). Bangalore:
National Cancer Registry Programme 2007.
Consolidated Report of Hospital Based
Cancer Registries 2001-2003. Available
from: www.icmr.nic.in/ncrp/report.
8. Chhabra S, Sonak M, Prem V, Sharma S.
Gynaecological malignancies in a rural
institute in India. Journal of Obstetrics &
Gynaecology. 2002;22(4), 426-29.
9. Murthy NS, Shalini S, Suman G, Pruthvish S,
Mathew A. Changing trends in incidence of
ovarian cancer-the Indian scenario. Asian Pac
J Cancer Prev. 2009;10:1025-30.
10. Ferlay J, Bray F, Pisani P, Parkin DM.
Globocan: Cancer Incidence, Mortality and
Prevalence Worldwide. Lyon, France: IARC

Press; 2004.
11. Seer.cancer.gov (homepage on the internet).
Bethesda, Maryland: North American
Association of Central Cancer Registries;
c2000. SEER Cancer statistics review 19752007. Available from: http://www.seer.
cancer.gov/resources
12. Boyle P, Ferlay J. Cancer incidence and
mortality in Europe, 2004.Annals of
oncology.2005;16(3), 481-488.
873
Hemalatha et al.,
DOI:10.5958/j.2319-5886.2.4.140

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
Research article
Copyright @2013
ISSN: 2319-5886
A PROSPECTIVE STUDY OF AN EFFECT OF SEPTORHINOPLASTY /RHINOPLASTY ON

DEVIATED EXTERNAL NASAL PYRAMID IN KASHMIRI POPULATION
Nazir A khan1, AyazRehman1, MushtaqSangoo1, Sajad Hamid2
1
Department of Otorhinolaryngology, 2Department of Anatomy, SKIMS Medical College, Bemina
*Corresponding author email: drsajadk@rediffmail.com

ABSTRACT
Most studies show that objective measures to quantify and determine surgical success in the treatment of
External nasal deformity with /without nasal obstruction do not correlate with subjective improvement
as reported by patients. Aim: To evaluate the subjective& objective improvement in patients undergoing
septorhinoplasty or rhinoplasty Materials and Methods: It is a prospective study in which we evaluate
100 patients who had to undergone septorhinoplasty /rhinoplasty; various angles of nose & face were
evaluated both preoperatively & postoperatively. In cases selected for Septorhinoplasty, the patients
answered a questionnaire preoperatively and 2 months after surgery with questions about the main
symptoms of nasal obstruction (nasal obstruction, coryza, pruritus, sneezing, facial pain, snoring, sleep
disorders, daytime drowsiness), and a score of each. The intensity of symptoms was scored from 1 to 4,
as follows: 1 - absence of symptoms; 2 - mild symptoms; 3 - moderate symptoms; 4 - severe symptoms.
Results: An improvement of all symptoms was observed after surgery, where there was nasal
obstruction associated with external nasal deformity i.e; NOSE (Nasal obstructive symptom evaluation
were 45.010.2 (preoperatively) &10. 04.23 (post-operatively) with p- value < 0.005 whereas NASE
(Nasal appearance surgical evaluation) were 41.811.25 (pre-operatively) &7. 85.29 (postoperatively) with p-value < 0.005 Conclusions: The external nasal appearance as well as symptoms of
nasal obstruction (in c/o =septorhinoplasty) improved.
Keywords: nasal septum, External nasal deformity, NOSE score, NASE
INTRODUCTION
Patients seeking nasal surgery come for a variety

of reasons. Some have trouble breathing through
the nose. Others have suffered injuries of some
sort, and would like to restore better symmetry
and correct the damage. Finally, many are
looking to alter the size or shape of the nose to
make it more harmonious with their features, to
improve their appearance. The goal of

rhinoplasty is to improve the nose aesthetically,
creating harmony with the other facial features.
Before the nose is altered, a young patient must
reach full growth, usually around age fifteen or
sixteen. Exceptions are cases in which breathing
is severely impaired.
874
Nazir A khan et al.,
Before deciding on rhinoplasty, additional

surgery might be recommended to enhance the
appearance of face. Many patients have chin
augmentation in conjunction with rhinoplasty to
create a better balance of features.
In cases of Nasal obstruction associated with
external nasal deformity, the nasal septum
deviation is one of its most frequent causes.
Other causative conditions are: adenoid
hypertrophy; turbinate hypertrophy; nasal
tumors; and nasal polyps1. Nasal septum
corrective surgery (Septoplasty) was started in
the 19th century, and has been modified and
improved since. The techniques have attempted
to provide maximum functional and respiratory
improvement at the same time preserving other
physiologic functions of the nose (filtering,
warming, and moisturizing the air) to improve
nasal flow.2
Submucosal resection (SMR) was first defined
by Freer in 1902, as the resection of
quadrangular cartilage, the perpendicular lamina
of ethmoid bone and total resection of the vomer.
The era of modern septal surgery began in 1940s
with Cottle, Goldman, and Smith who recognised
the disadvantages of submucous resection.3 The
inadequate surgery for nasal obstruction is still a
dilemma. The surgery specified to the obstructive
pathology should be emphasized. The surgical
correction of nasal septum does not always
guarantee a successful outcome. The literature
supports a reevaluation of surgical paradigms in
patients with the physical findings of both a
septal deviation and turbinate hypertrophy. 2,4
The corrective nasal valve surgery results in
significant improvement in disease specific
quality of life and the high satisfaction level. 5
Some other studies have been performed to
assess the impact of the surgery for nasal
blockage on the quality of life of the patient. 6,7
Objective measures to quantify and establish the
success of surgery have been a challenge.
Several methods have been proposed; the two
most common are rhinomanometry and acoustic
rhinometry. Rhinomanometry measures nasal
flow resistance during breathing. Acoustic

rhinometry measures nasal permeability and
quantifies the cross-sectional area of the nostrils
up to the nasopharynx, as well as the nasal cavity
volume between any two chosen cross-sections6.
Most studies have shown that these methods do
not correlate with the patient's reported
subjective improvement6,7. A few studies have
shown, however, that septoplasty is generally
effective for treating nasal obstruction, and that
most patient show improvements in nasal
symptoms3,4,7-11. The aim of this study is to
evaluate the surgery of External nasal deformity
with/ without nasal obstruction in the patient's
perception, and exhibit our results. We used the
Nasal Obstructive Symptom Evaluation (NOSE)
score and NASE (Nasal angle Surgical
Evaluation) to indicate the impact of surgery. 8-10
After approval by the ethics committee of our

hospital, the study was performed prospectively
between 2012 June 2013 July in a tertiary
hospital. SKIMS Medical college/hospital all
enrolled patients gave signed informed consent.
This study included 100 patients which met the
inclusion criteria as follows: Indications that are
covered:
1) For cosmetic purposes
2) Medically indicated as in
A) When it is being performed to correct a nasal
deformity secondary to congenital cleft lip
and/or palate for patients 18 years of age and
younger.
B) To correct chronic non-septal nasal airway
obstruction
from
vestibular
stenosis
(collapsed internal valves) due to trauma,
disease, or congenital defect, when all of the
following criteria are met:
1. Prolonged, persistent obstructed nasal
breathing; and
2. Physical examination confirming moderate to
severe vestibular obstruction; and
875
3. Airway obstruction will not respond to

Septoplasty and turbinectomy alone; and
4. Nasal airway obstruction is causing
significant
symptoms
(e.g.,
chronic
rhinosinusitis, difficulty breathing); and
5. Obstructive symptoms persist despite
conservative management for 3 months or
greater, which includes, where appropriate,
nasal steroids or immunotherapy; and
6. Photographs demonstrate an external nasal
deformity; and
7. There is an average 50 % or greater
obstruction of nares (e.g., 50 % obstruction
of both nares, or 75 % obstruction of one
nare and 25 % obstruction of other nare, or
100 % obstruction of one nare), documented
by nasal endoscopy, computed tomography
(CT) scan or other appropriate imaging
modality.
C) When rhinoplasty for nasal airway
obstruction is performed as an integral part of
a medically necessary septoplasty and there
is documentation of gross nasal obstruction
on the same side as the septal deviation.
Revision cases: Patients who have any of the
following conditions or met any of the
following criteria are excluded from the
study: The history of allergy, Adenoid
hypertrophy,
Undergoing
concurrent
endoscopic sinus surgery, polypectomy, With
a main preoperative complaint other than
nasal obstruction(e.g. snoring, facial pain,
nasal discharge, postnasal drip syndrome,
sinonasal malignancy etc.), nasosinusal
tumors, head and neck radiotherapy, nasal
septum; insufficient nasal valve, nasosinusal
granulomatous
disease,
hyperplasic
pharyngeal
tonsils,
snoring
surgery,
craniofacial malformation, pregnancy.
After selecting, the patients were assessed
preoperatively and on the 7th, 14th, 30th, and
60th postoperative day. This evaluation consisted
of an otorhinolaryngologica examination,
measurement of NASE (Nasal appearance
surgical evaluation) & NOSE SCORE (Nasal

obstructive symptom evaluation) in cases of
those who underwent septorhinoplasty whereby,
a questionnaire with questions about the main
symptoms of nasal
obstruction (nasal
obstruction, coryza, pruritus, sneezing, facial
pain, snoring, sleep disorders, daytime
drowsiness), were asked and a score given for
each answer. The intensity of symptoms was
scored from 1 to 4, as follows: 1 - absence of
symptoms; 2 - mild symptoms; 3 - moderate
symptoms; 4 - severe symptoms. Data were
gathered on sex, age, and the degree of septal
deviation. Also, the patient factors are to be
taken into consideration. During assessing a
patient for potentialrhinoplasty, a full
concentration was given on the patients
expectations
prior
to
performing
the
comprehensive facial analysis. Although there
are different methods for integrating the patient
in the surgical process. The computer imaging of
the face was done as it provides an excellent way
to gain a realistic understanding of the
anticipated outcome these images were combined
with standardized anterior, lateral, oblique, and
basal
photographs.
Nonsteroidal
antiinflammatory agents and certain herbal
supplements
may
increase
bleeding
complications after surgery and should be
discontinued at least 710 days before a
rhinoplasty. Furthermore, patients are instructed
to avoid consumption of salicylic derivatives for
3 weeks prior and 1 week following surgery.
A critical facial analysis was also done in order
to preserve nasofacial harmony & any natural
facial asymmetries was pointed out so that the
patient gains a better understanding of what is
present before any operative intervention. 12,13
Prior to surgery we convert our operative plan
into a graphic representation to assist us in the
operating room. Modifications to the plan are
documented intraoperatively, transposed to the
graphic depictions postoperatively, and placed in
the patient's chart for future reference. Cefazolin
1 g was administered intravenously as a
876
perioperative antibiotic. We prefer general

anesthesia for our patients, though local
anesthesia with intravenous sedation is a viable
alternative. After the administration of
anesthetic, the nasal vibrissae are clipped and the
nares are prepared with povidone iodine solution.
The anticipated incision approach is marked and
injected with approximately 10 ml of 1%
lidocaine with 1: 100 000 epinephrine into the
nasal mucosa, along the septum and the soft
tissue envelope. Next, the mucosa is treated with
cottonoidpledgets soaked in oxymetolazone
Operative approach: We select the two basic
incisional approaches to rhinoplasty: 1. The open
technique 2. The closed (endonasal) technique.
Each has its advocates who use them
successfully in the practice of rhinoplasty.
The open approach involves a transcolumellar
incision, which can assume varying geometries,
depending on surgeon choice. Our preference is a
stair step configuration, which facilitates
reapproximation while breaking up the scar and
preventing contracture deformities. The open
approach also involves skeletonizing the
underlying osseocartilaginous framework, which
gains enormous exposure for the manipulation
and correction of deformities. The closed (or
endonasal) technique can be performed using a
cartilage-delivery approach or a nondelivery
approach.
Osteotomy techniques: Osteotomies are a
powerful technique in rhinoplasty.14-16 The
indications to perform osteotomies, regardless of
technique are: 1. To narrow the lateral wall of
nose 2. To close an open roof deformity (after
dorsal hump reduction) 3. To create symmetry
by straightening the nasal bony framework
Contraindications: 1. Patients with short nasal
bones 2. Elderly patients with thiin fragile nasal
bones 3. Patients with heavily eye glasses
There are several osteotomy techniques,
including medial, lateral, transverse, or a
combination of these. Furthermore, they can be
performed through either an external or internal
approach 17-19
Closure: After hemostasis was achieved and any

excess debris removed, the skin envelope was
redropped. If the patient has thick skin, and
especially if the patient is a woman, we choose to
place a single 5-0 Vicryl suture from the dermis
(underside of the skin envelope) to the
underlying cartilaginous framework in an attempt
to recreate a supratip break.
The transcolumellar incision was closed using 60 nylon suture in simple interrupted fashion,
making sure the coaptation of the incision
margins is precise. The stair stepping of the
original incision helps us close this accurately.
The
infracartilaginous
incisions
were
reapproximated using 5-0 chromic suture in
simple interrupted fashion. We take special care
to prevent overbiting with the suture, which can
create contour irregularities and notching,
especially in the soft triangle area. In septal
work, we place intranasal silastic splints coated
with antibiotic ointment.
Alar base surgery: In certain cases Alar base
abnormalities were seen &include wide or
excessive nostril sills, a wide alar base,
asymmetric or malpositioned alar bases, or any
combination of these, so alar base surgery was
necessary, & was performed after closure of the
transcolumellar and infracartilaginous incisions,
but before intranasal and external splints are
placed.
Depressor septi translocation: Some patients
had a tension tip (foreshortened upper lip with
decreased tip projection), a depressor septi
translocation was done
Postoperative care: All preoperative and
postoperative instructions were given to the
patients in writing before and on the day of
surgery. Postoperatively, we put them on :
Cephalexin 500mg orally, 8 hourly for 3 days,
Medrol dose pack for 7 days to minimize
postoperative edema,
Acetaminophen500mg
every 4-6 hourly for post-operative pain, Normal
nasal saline solution for post-operative nasal
congestion. The patient is instructed to keep the
head of the bed elevated at an angle of 45
877
beginning immediately after surgery to help

minimize
postoperative
swelling.
Cool
compresses are used periorbitally during the day
for the first 48 hours. The patient is instructed to
change the drip pad under the nose as necessary
until the drainage stops, at which time the drip
pad and tape can be discontinued. Any
manipulation of the nose, including rubbing,
blotting, or blowing, is discouraged for the first 3
weeks postoperatively.
Statistical Analysis
Analyses were conducted in NCSS (Number

Cruncher Statistical System) 2007&PASS 2008
Statistical Software (Utah, USA). The predictors
of improvement for quantitative data, parameters
showing the normal distribution between groups
compared with the One-way Anova test. As well
as descriptive statistical methods (mean, standard
deviation) are used. Parameters which are not
showing the normal distribution between groups,
Mann-Whitney U test is used. To assess the
qualitative data, chi-square test is used. A p<0.05
is considered as statistically significant.
RESULTS
Table 1: Showing information regarding various parameters among selected cases
Parameter
Sex distribution
Male
Female
Area-wise distribution
Rural areas
Urban areas
Types of cases
Primary cases
Revision cases
Main indications
Saddle nose deformity
Dorsal hump
Supratip depression
Nasal valve area weakness
Type operative procedure Septorhinoplasty
Rhinoplasty only
Type
of
operative Open
approach
Close
Chief complaints
External nasal deformity with nasal obstruction
External nasal deformity
Aetiological factors
Post-traumatic
Developmental
Post-operative
Post-infective
No of patients
67
33
70
30
86
14
20
55
5
20
80
20
55
45
80
20
54
40
5
1
Table 2: Shows the type of graft material used
Graft material used ( only in 45 cases)

Autologous septal cartilage
Autologous Conchal cartilage
Autologous iliac crest
Autologous septal bone
35
5
1
4
878
Table 3: Shows the different techniques used
Various surgical techniques used

Dorsal augmentation
Supratip augmentation
Spreader graft
Only graft
Goldhens tip procedure
Intra & Inter dermal suturing
Table 4: Shows evaluation of operation in terms of pre-operative and post-operative nasal angles
Nasal angles
Nasolabial
Nasofrontal
Nasofacial
Pre-operative
94.2 7.7
134.57.4
32.0 5.2
Post-operative
97.16.8
133.16.9
31.2 4.9
p-Value
1.042
1.058
1.020
Table 5: Shows evaluation of operation success by analysing pre-operative & post-operative NOSE score
and NASE score23,24
Score
NOSE (Nasal obstructive symptom evaluation)
NASE (Nasal appearance surgical evaluation)
Fig. 1a: Deviated External nose (pre-op.)
Fig 2a: Deviated External nose (pre-op.)
Pre-operative Post-operative p- Value

45.010.2
10.04.23
< 0.005
41.811.25
7.85.29
< 0.005
1b: Corrected deformity (Post-op.)
2b: Corrected deformity (Post op.)
879
Fig 3a: Deviated External nose (pre-op.)
3b: Corrected deformity (Post op.)
DISCUSSION
Owing to its central location on the face, the nose
plays an intimate role in all social interactions.
Early surgical correction of nasal deformities
improves psychosocial development and
opportunities for normalized social integration
and removes the stigma of an abnormal
appearance. Pre and intraoperative planning are
essential in order to achieve good results; the
surgeon must carefully examine the nose in order
to determine which pathological condition there
is and which surgical procedure is needed 20.
In the present study 67% of patients were male
vs. 33% female. (Table 1) This agrees with the
study for objective evaluation of a deviated
septum, Erdem & Ozturan 21 reported that the
number of males was more than females, 21 that
may be explained because this study dealt only
with patients seeking functional correction of
deviated septum which is more common in males
due to more exposure to trauma. (Table 4) In
contrast to females, male patients seem to lack a
clear body concept and an in-depth awareness of
their physical appearance. As a result, they often
have difficulty articulating their objectives for
cosmetic surgery.
In the current study there was a statistically
significant difference between pre-operative and
postoperative measurements for nasofacial,
nasolabial & naso frontal angles. (Table 4) This
agrees with Okur, et al.22 who stated that the
angle measurement method may be helpful in
evaluating the effectiveness of surgical

techniques and the results for correction22. In
another study by Ozkul & Ozkul et al.,23 five
parameters (nasofrontal, nasomental, nasolabial,
nasofacial angles and nasal projection ratio) were
used to induce a facial harmony index, which is
to generate a score for the patient before and
after the rhinoplasty operation so that the
improvement due to rhinoplasty operation can be
determined objectively 23 .
In the current study, we found that 20% of
patients with saddle nose deformity, 55% had
dorsal hump, 5% had supratip depression & 20%
had nasal valve area v weakness. (Table 1) And
excellent results were seen in in post-operative
measurements. This agrees with Okur et al.
(2004) who found that 66.7% of the patients with
crooked noses had good and excellent results
after surgery.
Also, Erdem & Ozturan (2008) found that 27.7%
of his patients had excellent results and 30.5%
had good results after measuring the angle of
septal deviation post-operatively21,22. The
approach for the management were open (55%)
& close approach in (45%) (Table 1)with the
operative procedure septorhinoplasty done in
(80%) cases & rhinoplasty alone in (20%) cases
(Table 1) & includes wide exposure through
external septorhinoplasty, release of all
deforming forces for the septum, straightening of
the septum while maintaining an adequate dorsal
880
and caudal strut, realigning and reinforcing the

nasal structures with sutures or grafts, and
performing adequate osteotomy.
Although not being necessary for indicating
surgery, the classification of patients as being
candidates or not to the procedure, may predict
results which are more or less satisfactory.
Patients with high scores in the pre-op may not
be very pleased after the surgery, and they may
even have a risk of worsening in their initial
situation. This agrees with Izu, et al. 24
CONCLUSION
This study along with other studies emphasizes

the importance of using the evaluative tools to
subjectively and objectively assess patients
undergoing septorhinoplasty / rhinoplasty. Both
subjective and objective evaluation tools are
important for identifying the best candidate for
rhinoplasty operation, though most of the
surgeons depend on their aesthetic eye only. It
should be taken into consideration that the
aesthetic eye is a skill that needs a lot of time to
be developed.
REFERENCES
1. Uppal S, Mistry H, Nadig S, Back G,
Coatesworth A. Evaluation of patient benefit
from nasal septal surgery for nasal
obstruction.
AurisNasus
Larynx.
2005;32(2):129-137
2. Dinis PB, Haider H. Septoplasty: Long-term
evaluation of results. Evaluation studies. Am
J Otolaryngol 2002;23:8590.
3. Devaiah AK, Keojampa BK. Surgery of the
nasal septum. In: Stucker FJ, De Souza C,
Kenyon GS: Rhinology and Facial Plastic
Surgery. 1st ed.Berlin: Springer; 2009:18185
4. Harrill WC, Pillsbury HC, McGuirt WF,
Stewart MG. Radiofrequency turbinate
reduction: a Nose evaluation. Laryngoscope.
2007;117(11):1912-19.
5. Rhee JS, Poetker DM, Smith TL, Bustillo A,

Burzynski M, Davis RE. Nasal valve surgery
improves disease-specific quality of life.
Laryngoscope. 2005;115(3):437-40.
6. Arunachalan PS, Kitcher E, Gray J, Wilson
JA. Nasal septal surgery: evaluation of
symptomatic and general health outcomes.
Clin Otol 2001;26:36770.
7. Siegel N, Gliklich R, Taghizadeh F, ChangY.
Outcomes of septoplasty. Otolaryngol Head
Neck Surg 2000;122(2):22932.
8. McKiernan DC, Banfield G, Kumar R,
Hinton AE. Patient benefit from functional
and cosmetic rhinoplasty. ClinOtolaryngol
2001;26(1): 5052.
9. Stewart EJ, Robinson K, Wilson JA.
Assessment of patient benefit from
Rhinoplasty. Rhinology 1996;34(1):5759.
10. Likert, Rensis. A technique for the
measurement of attitudes. Archives of
Psychology 1932;140:5155.
11. Constantian MB, Brian CR. The relative
importance of septal and nasal valvular
surgery in correcting airway obstruction in
primary and secondary rhinoplasty. Plast
Reconstr Surg 1996;98(1):3854
12. Gunter JP, Hackney FL: Clinical assessment
and facial analysis. In: Dallas rhinoplasty:
nasal surgery by the masters, St
Louis: Quality Medical Publishing; 2002:53.
13. Rohrich RJ, Gunter JP, Shemshadi H: Facial
analysis for the rhinoplasty patient. Dallas
Rhino plasty Symp. 1996; 13:67.
14. Goldfarb M, Gallups JM, Gerwin JM: Perfor
ating osteotomies in rhinoplasty. Arch
Otolaryngol Head Neck Surg 1993; 119:62427.
15. Parkes ML, Kamer F, Morgan WR: Double
lateral osteotomy in rhinoplasty. Arch Oto
laryngol 1977;103:342-48.
16. Sullivan PK, Harshbarger RJ, Oneal RM: Na
salosteotomies. In: Gunter JP, Rohrich RJ, A
dams Jr WP, ed. Dallas rhinoplasty: nasal
881
surgery by the masters, St Louis: Quality

Medical Publishing; 2002:595.
17. Rohrich RJ, Janis JE, Adams WP. An update
on the lateral nasal osteotomy in rhinoplasty:
an anatomic endoscopic comparison of the
external versus the internal approach. Plast
Reconstr Surg 2003; 111:2461-62
18. Rohrich RJ, Krueger JK, Adams WP. Achiev
ing consistency in the lateral nasal osteotomy
during rhinoplasty: an external perforated
technique. Plast Reconstr Surg 2001; 108:
2122-2130.
19. Rohrich RJ, Krueger JK, Adams Jr WP: Impo
rtance of lateral nasal osteotomy: an external
perforated technique. Dallas rhinoplasty:
nasal surgery by the masters, St
Louis: Quality Medical Publishing 2002:61531.
20. Konstantinidis I, Triaridis S, Triaridis A,
Karagiannidis K, Kontzoglou G. Long term
results following nasal septal surgery: Focus
on patients' satisfaction. AurisNasus Larynx.
2005;32(4):369-74.
21. Tamer Erdem, Orhan Ozturan. Objective
measurement of the deviated nose and a
review of surgical techniques for correction.
Rhinology. 2008; 46; 56-61
22. Okur E, Yildirim I, Aydogan B. Outcome of
surgery for crooked nose: An objective
method of evaluation. Aesth Plast Surg.
2004; 28: 203207.
23. Ozkul T and Ozkul MH. A study towards
fuzzy logicbased assessment of nasal
harmony of rhinoplasty patients. Journal of
the Franklin Institute.2006;343:329-39
24. Izu SC, Kosugi EM, Brando EV, Lopes AS,
Garcia LBS, Suguri VM et al., Normal values
for the Rhinoplasty Outcome Evaluation
(ROE)
questionnaire.
Braz
J.
Otorhinolaryngol. 2012;78(4):76-79
882
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Coden: IJMRHS
th
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A STUDY ON MORBIDITY PROFILE OF SCISSOR MANUFACTURING WORKERS

*Keerti S Jogdand1, Pravin N Yerpude1, Mohini Jogdand 2
1
Associate Professor, Dept of Community Medicine, Gujarat Adani Institute of Medical Sciences, Bhuj,
Gujarat, India
2
Assistant professor, Dept of Community medicine, SRTR Medical College and Hospital, Ambajogai,
Maharashtra, India
*Corresponding author email: drkeertijogdand@gmail.com
ABSTRACT
Introduction: In India, the life of the vulnerable and the marginalized working population is at risk as
there is a lack of awareness about occupational safety and environmental hazards. The scissor
manufacturing workers sector is one of the important but unorganized parts of industry of India and
mainly run by private establishments. The scissors manufacturing workers hardly ever benefit from
occupational health and safety provisions. Materials and methods: The present community based,
cross-sectional study was conducted among 218 scissor manufacturing workers of small scale industry
of urban slum area, Malvani in South Mumbai. The study period was from June 2010 to September
2010. Results: In the present study, 52.75% workers were in the age group of 20-30 yrs followed by in
the age group of 30-40 yrs (32.57%). Majority, 92.66% were males. Regarding the history of addiction,
77.52% workers were using tobacco related products. The commonest health problem present in
workers was acute respiratory infection (ARI) (34.86%) followed by musculoskeletal problems in
25.68% workers. Conclusion: As scissor manufacturing workers suffering from various morbidities, it
is necessary to monitor the occupational environment and health status of the workers periodically. It is
also necessary to create awareness regarding the ill effects of industrial hazards.
Key words: Morbidity profile, scissor manufacturing workers
INTRODUCTION
In the world, one of the leading causes of

morbidity and mortality is occupational health
risks and they are more common in developing
countries 1.
In India, the life of the vulnerable and
marginalized working population is at risk as
there is a lack of awareness about occupational
safety and environmental hazards. In small scale

industries worldwide, over 1000 million people
are employed. 2
The scissor manufacturing workers sector is one
of the important but unorganized parts of
industry of India and mainly run by private
establishments. The scissors manufacturing
Keerti S et al.,
883
workers hardly ever benefit from occupational

health and safety provisions. As they work for
long hours, they may suffer from various health
problems. Most of the health problems among
them are due to the dust particles produced
during various processes like heat treatment,
processing, grinding, polishing, plating, edging,
packing. Scissor manufacturing workers mostly
suffer from various illnesses such as respiratory
problems, musculoskeletal problems, eye
diseases, skin problems.
The various
socioeconomic factors such as poverty, lack of
education, poor diet, addictions, and poor
working conditions also contribute to the ill
health of the workers 3. The present study was
conducted among scissor manufacturing workers
with the objective of finding common morbid
conditions among them.
The present community based, cross-sectional

study
was
conducted
among
scissor
manufacturing workers of small scale industry of
urban slum area, Malvani in South Mumbai. The
study period was from June 2010 to September
2010. Before the start of the study, ethical
clearance was taken from the Institutional Ethics
Committee. The study consists of 218 workers
working in scissor manufacturing units. This
includes all workers involved in all stages of
scissor manufacturing. The workers involved in
other units like cotton were not included in the
study. Out of 218 workers, 202 were males and

16 were females. A pre-designed, pre-tested semi
structured schedule was used during interview of
the workers. Before interview of the workers,
they were explained clearly the purpose of the
study and then verbal consent was obtained from
them. Health status of the workers was assessed
by asking questions regarding their health
problems in the past 3 month period followed by
clinical examination that included respiratory
examination, eye check up. The data was
analyzed using Microsoft excel and the results
were expressed in percentages.
RESULTS
In the present study, 52.75% workers were in the

age group of 20-30 yrs followed by in the age
group of 30-40 yrs (32.57%). Majority, 92.66%
were males. Religion wise, the majority were
Muslims (90.83%). 12.39% were illiterate,
74.77% were married (Table1).
Regarding history of addiction, 77.52% workers
were using tobacco related products. 17.43%
were alcoholics. The commonest health problem
present in workers was acute respiratory
infection (ARI) (34.86%) followed by
musculoskeletal problems in 25.68% workers.
Asthma was present in 23.39% workers.
Tuberculosis was present in 8.26% workers. Skin
diseases were present in 16.05% workers. Eye
problems were present in 10.55% workers
(Table 2).
Table1: Socio-demographic characteristics of workers
Characteristics
Age (years)
Sex
Religion
Education
Marital status
20-30
30-40
Above 40 yrs
Male
Female
Muslim
Hindu
Illiterate
Literate
Married
Unmarried
No (%)
115 (52.75%)
71 (32.57%)
32 (14.68%)
202 (92.66%)
16 (7.34%)
198 (90.83%)
20 (9.17%)
27 (12.39%)
191 (87.61%)
163 (74.77%)
55 (25.23%)
884
Keerti S et al.,
Table 2: Morbid conditions of workers
Diseases
Persistent cough
Asthma
Tuberculosis
COPD
Musculoskeletal problems
Skin diseases
Eye problems
No (%)
76 (34.86%)
51 (23.39%)
18 (8.26%)
6 (2.75%)
56 (25.68%)
35 (16.05%)
23 (10.55%)
DISCUSSION
In the present study, Majority, 92.66% workers

were males. Religion wise, the majority were
Muslims (90.83%). 12.39% were illiterate.
74.77% were married. Similar results were found
in a study done in Meerut on the health status of
scissor workers by Goel K et al 4.
The prevalence of tobacco use among workers
was 77.52%. In a study by Goel K et al 4in
Meerut , the prevalence of tobacco use was found
to be 85%. According to NFHS III, in India,
55.8% males in the age group of 12-60 years
have been found to be consuming tobacco. The
reasons of tobacco consumption may be low
educational status, occupation involving hard
labour work during night shift work and low
socioeconomic status.
In our study, 34.86% workers were having cough
followed by asthma in 23.39% workers. TB was
present in 8.26% workers. In a study by Goel K
et al 4on scissor manufacturing workers in
Meerut,40% worker were suffering from
persistent cough .Asthma was present in 28%
workers. In a study of Qurratul et al5,100 %
workers were suffering from lung diseases. The
reason for such high prevalence may be due to
reason that the workers working in the scissors
industry come in direct contact with the iron
sparkles, suspended particles of metal, iron and
cotton dust and fumes of acids, kerosene oil.
In our study apart from respiratory infections,
other health complications present were
musculoskeletal problems (25.68%), skin
diseases
(16.05%)
and
ear
problems
(10.55%).Mismatch between man and machine
may be one of the major factor contributing to

musculoskeletal problems.
Keerti S et al.,
CONCLUSION
In scissor manufacturing workers, commonest

morbidities detected were respiratory and
musculoskeletal problems. In scissor industry,
several hazardous conditions exist like poor
ventilation, overcrowding and poor illumination
which synergistically affects the health and
comfort of the workers ultimately decreasing the
work efficiency and hence productivity. It is
necessary to monitor the occupational
environment and health status of the workers
periodically. It is also necessary to create
awareness regarding the ill effects of industrial
hazards. Use of personal protective equipments
(PPE) like masks or respirators, ear plugs,
earmuffs should be regularly used by workers.
ACKNOWLEDGEMENT
We would like to thank the study participants for

their co-operation
Conflict of interest: Nil
REFERENCES
1.
2.
World health report, 2002.Reducing risks,

promoting healthy life. Geneva WHO; 2002.
Available from http://www.who.int/peh/
occupational health4. htm
Occupational health: The workplace health
and
environment
in
sustainable
885
3.
4.
5.
development.
Geneva
WHO;
1997.
Available from http://www.who.int/peh/
occupational health2.htm
ILO Encyclopedia. Occupational health and
safety 4th ed.1998.pg.89-90.
Goel K, Ahmad S, Goel P, Parashar P,
Maroof KA, Ali AA. Study on social and
health status of scissor manufacturing
workers of Meerut, UP. International J of
Contemporary Medicine 2003;1(1):51-54.
Qurratul A, Shama P, Verma RK.
Prevalence of lung disease in the workers of
scissors manufacturing industries in Meerut
city. The Pharma research. 2009;4(3):57-60.
886
Keerti S et al.,
DOI:10.5958/j.2319-5886.2.4.142

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th
Research article
CLINICO HISTOPATHOLOGICAL CORRELATION WITHIN THE SPECTRUM OF

HANSEN'S DISEASE: A MULTICENTRIC STUDY IN NORTH INDIA
*Nitesh Mohan1, Nitin Mishra2
1
Associate Professor, Department of Pathology, Rohilkhand Medical College & Hospital, Bareilly, U.P.
India
2
Assistant Professor, Department of Dermatology, SRMS Institute of Medical Sciences, Bareilly, U.P.,
*Corresponding author email: drnitesh@gmail.com
ABSTRACT
Background: Leprosy is one of the oldest and chronic infectious diseases known to human being
caused by Mycobacterium leprae. Leprosy is widely prevalent in all parts of India and it presents with
different clinico-pathological forms. However a great variation is seen in interpretation of clinical and
histopathological examination of these lesions. The present research was taken to study the correlations
between the clinical and histological diagnosis and to evaluate the importance of skin biopsy as an
important diagnostic and spectrum defining tool. Methods: A prospective hospital based study was
conducted among patients attending Dermatology OPD of two tertiary care centres in this region over a
period of two years. All clinically suspected new leprosy patients were included in the study. A detailed
clinical history and examination was carried out and skin biopsies were taken from the most active part
of lesions. Sections were stained with Hematoxylin & Eosin stain and Fite-Feracco stain.
Histopathological findings were compared with clinical diagnoses. Results: A total of 190 cases were
studied, out of which 137(72.10%) were males and 53(27.9%) were females. The histopathological
diagnosis of leprosy was established in 99.47% of clinically diagnosed cases. Clinico-histopathological
concordance was seen maximum in LL (97.22%), followed by BT (79.76%), TT (71.43%), BL
(66.67%), BB (66.67%) and least in IL (50.00%). Overall concordance was 56.54% Conclusion:
Clinical diagnoses of Leprosy still pose a significant problem, especially the Intermediate subtypes of
the disease spectrum. Histopathological examination of the active skin lesions should be done in all new
cases to confirm the spectrum of disease and expected duration of therapy.
Keywords: Leprosy, Lepromatous leprosy, Skin biopsy
INTRODUCTION
Leprosy is one of the oldest and chronic

infectious diseases known to human being caused
by Mycobacterium leprae. The disease still
carries a grave social stigma and ostracism which

compels the patients to hide the disease. Leprosy
887
Nitesh Mohan et al.,
continues to be an important public health

problem in most parts of Asia, especially India.1
Leprosy is a progressive, chronic granulomatous
disease of the peripheral nerves and skin and
other tissues such as mucous membranes,
muscles and reticuloendothelial system. The
disease presents in various clinico-pathological
forms depending on the immune status of the
host. The disease spectrum has been
characterised in a number of classification
systems, most widely being the Ridley-Jopling
classification. In this classification, leprosy has
been
divided
into
five
groups
as
Tuberculoid(TT), Borderline tuberculoid(BT),
Mid-bordrline (BB), Borderline Lepromatous
(BL), and Lepromatous (LL).2
The Classification has been accepted worldwide
and is highly recommended. Though the clinical
diagnosis is based on characteristic skin lesions
with sensory loss, a great variation is seen in
interpretation of these lesions, both clinically and
histopathologically. 3
The present research was taken to study the
correlations between the clinical and histological
diagnosis of the tissue sections from clinically
suspected patients in this region, and to evaluate
to the importance of skin biopsy as an important
tool in diagnosing leprosy in these patients. 3
A prospective hospital-based study was
conducted
among
patients
attending
Dermatology OPD of Rohilkhand Medical
College & Hospital, Bareilly and SRMS Institute
of Medical Sciences, Bareilly and few others
private hospitals in this region, between January

2012 to December 2012. The study was approved
by the Institutional Ethics Committee, and is
informed consent from taken from all the
participants
Unit of Study: Both sex patients of all age groups
between 2 to 70 years, having clinically
suspected leprosy were included in the study.
Exclusion criteria: Patients already treated with
anti-leprosy medications at any time earlier were
excluded.
Nature of Study: The study includes all patients
with clinically diagnosed leprosy and was
subjected to history and examination after taking
informed consent and approval from Institutions
Ethical Committee.
Sample Size: Total no. of cases studied was 190.
Study Schedule: A detailed clinical history and
examination was carried out. Clinical
examination included the type, number and site
of lesion, type of disease and neural involvement.
All the patients were subjected to skin biopsies
from the most active part of the lesions. Biopsies
were fixed in 10% formalin & processed. Serial
sections of 5 thickness were cut and stained
with routine Haematoxylin and Eosin and FiteFeracco stains. The Ridley & Jopling
classification was followed in both clinical and
histopathological diagnosis. Histopathological
evaluation included invasion of epidermis,
involvement of sub-epidermal zone, character &
extent of granulomas, density of lymphocytic
infiltrate, epitheloid cells and other cellular
elements, nerve involvement and presence of M.
leprae.
RESULTS
Table 1: Clinical presentation in various types of leprosy
Clinical diagnosis
Hypopigmented
Erythematous
plaque/ No.of
patch (No. of cases) papule/nodule (No. of cases) cases
Tuberculoid Leprosy (TT)

Borderline Tuberculoid (BT)
Mid Borderline (BB)
Borderline Lepramatous (BL)
Lepramatous Leprosy (LL)
Intermediate Leprosy (IL)
06
75
02
10
16
08
09
11
02
16
29
06
15
86
04
26
45
14
7.89
45.26
2.12
13.68
23.68
7.37
888
Table 2: Histopathological distribution of leprosy cases
Histopathological diagnosis
Mid Borderline (BB)
Total
No. of cases
14
84
03
24
36
28
189
%
7.40
44.44
1.6
12.70
19.05
14.82
100
Table 3: Observation of AFB in different types
Type of Leprosy
No. of Positive cases
Percentage
--
--
08
8.42
Mid Borderline (BB)
11
11.58
28
29.47
34
35.79
14
14.73
Total
95
100
No acid fast bacillus could be demonstrated in any case of TT

Table 4: Distribution of Site of lesions
Site of Lesion
Number of cases
Percentage
Head & Neck
40
21.05
Upper limb
65
34.21
Lower limb
30
15.79
Trunk
25
13.16
Multiple sites
30
15.79
Total
190
100
Table 5: Comparison of clinical and histopathological diagnosis
Histological Clinical Types

Types
TT
BT
BB
TT (14)
10
04
BT (84)
03
67
BB (03)
01
02
BL (24)
03
01
LL (36)
IL (28)
02
11
01
Total (189)
15
86
04
BL
LL
IL
Percentage
of
concordance
71.43
10
04
79.76
66.67
16
04
66.67
01
35
97.22
14
26
45
50.00
14
889
Table 6: Comparison of Sex Distribution
Authors
Males (%)
Moorthy et al (2001) 6
65.05
Bhushan et al (2008) 5
Mathur MC et al (2011)
72.34
2
53.8
Gridhar M et al (2012) 3
77.6
Present study (2013)
72.10
Table 7: Comparative Analysis of Overall Concordance with other similar studies
Studies
Kalla G et al 7
Tailor et al
M Giridhar et al
Present Study
Year
Overall Concordance %
2000
60.6
2008
58
2012
60.23
2013
56.54
Fig1: Grenz zone and macrophage granuloma in

Borderline tuberculoid leprosy (H&E)
Fig3: A case of BT leprosy with satellite lesion
Fig 2: Non caseating granulomas & Langhans
Fig 4: Case of Mid Borderline Leprosy
890
DISCUSSION
In the present study, a total of 190 clinically
diagnosed leprosy patients were examined and
were subjected to clinical and histopathological
examination, which included various aspects of
the lesions, like number and site of lesions, type
of disease.
The studied showed the most common clinical
presentation to be with hypopigmented patch
(61.58%) followed by erythematous plaque or
nodule (38.42%). This correlated well with study
done by M Gridhar et al.3 and Ocampo and
Francisco.4
The sex ratio was heavily skewed towards males
(72.10%). This is similar to other Indian studies
undertaken by Gridhar M et al (77.6%) 3] &
Bhushan et al (72.34%)5. Mathur MC et al.2
however observed 53.8% males in their study
while Moorthy et al. observed 65.05% males.6
In the present study concordance between
clinical and histopathological diagnosis for
individual type of leprosy was found to be TT
(71.43%), BT (79.76%), BB (66.67%), BL
(66.67%), LL (97.22%) and IL (50.00%).
Maximum concordance was observed in LL type
of leprosy, which was similar in studies by
Mathur MC et al.2, Gridhar M et al3 and Moorthy
et al.6 However, concordance differed variably
when compared with other types of Leprosy,
which may be due to more precise diagnostic
criteria laid down in histopathology with
emerging microbiological and immunological
techniques. The observations strongly suggest the
importance of histopathological diagnosis in
these cases, as lesions are easy to diagnose
clinically towards Lepromatous pole of the
disease.4
In our study, histological diagnosis of leprosy
was established in 99.47% cases. One case
(0.53%) was diagnosed as Lupus Vulgaris.
Similar observations have been made by different
authors in their studies, however with lesser
specificity. The discrepancy, whenever seen may
be due to clinical overdiagnosis of leprosy and
misinterpretation of many skin lesions presenting

with hypopigmented patches. 3,4,6
CONCLUSION
Leprosy is a chronic granulomatous disease

widely prevalent in India and is present in
different clinico-pathological forms. Study of
these lesions has contributed a great deal in
understanding the disease. Many cases can be
diagnosed clinically; especially those towards the
Lepromatous pole of the disease, however, other
types of Leprosy pose a significant problem in
clinical diagnosis. Histopathological examination
of the lesions confirms the exact subtype of the
disease and should be done in all cases so as to
facilitate the institution of accurate mode of
therapy.
REFERENCES
1. Mohite RV, Mohite VR, Durgawale PM.

Differential Trend of Leprosy in Rural and
Urban Area of Western Maharashtra. Indian J
Lepr. 2013;85:11-18.
2. Mathur MC, Ghimire RBK, Shrestha P,
Kedia
SK.
Clinicohistopathological
Correlation in Leprosy. Kathmandu Univ
Med J. 2011;36(4):248-51.
3. Giridhar M, Arora G, Lajpal K, Chahal KS.
Clinicohistopathological concordance in
Leprosy- A Clinical, Histopathological and
Bacteriological study of 100 cases. Indian J
Lepr 2012;84:217-25.
4. Vargas-Ocampo, Fransisco. Analysis of 6000
Skin Biopsies of the National Leprosy
Control Program in Mexico. Int J Lepr Other
Mycobact Dis. 2004;59:28-35.
5. Bhushan P, Sardana K. Diagnosing
multibacillary leprosy: A comparative
evaluation of diagnostic accuracy of slit-skin
smear, bacterial index of granuloma and
WHO operational classification. Indian J
Dermatol Venereol Leprol 2008; 74:322-26.
891
6. Moorthy BN, Kumar P, Chatura KR.

Histopathological correlation of skin biopsies
in leprosy. IJDVL 2001; 67:299-301.
7. Kalla G, Salodkar A, Kachhawa D. Clinical
and histopathological correlation in leprosy.
Int J Lepr 2000; 68:184-85.
8. Pandya
A,
Tailor
HJ.
Clinico
histopathological correlation of leprosy.
Indian J Dermatol Venereol Leprol 2008;
74:174-76.
892
DOI:10.5958/j.2319-5886.2.4.143

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Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
A STUDY ON HEARING LOSS IN TYPE II DIABETICS

Jankar DS1*, Bodhe CD2, Bhutada TB3
1
MD Physiology, 2Asst. Professor, 3Asso. Professor, Dept. of Physiology, Govt. Medical College, Miraj,
Maharashtra, India
* Corresponding author email: dr.deepalijankar@gmail.com
ABSTRACT
Diabetes-related sensorineural hearing impairment affects peoples ability to hear and understand
sounds. We carried out this case control study with the purpose of determining the hearing loss in type II
diabetes mellitus in relation to the age and gender of the patients and duration of the illness using tuning
fork tests and pure tone audiometry. Aim: To study the hearing loss in type II diabetics and controls.
Objectives:1. To study the hearing loss in relation to different age groups in diabetics and controls. 2.
To study the hearing loss in relation to gender in diabetics and controls. 3. To study the hearing loss in
relation to duration of diabetes. Material and Methods: 200 diabetic patients and 200 age and sex
matched controls took part in the study. They were evaluated by Tuning fork tests and Pure Tone
Audiometry. Results: The hearing of diabetics was significantly impaired than the non-diabetic control
group. This hearing impairment was noted in all the frequencies tested. The hearing acuity was not
influenced by the duration of diabetes, age or sex of the subjects. Discussion: The possible mechanisms
underlying the hearing loss in diabetic individuals are microangiopathy, demyelination, hyperglycemia,
etc. Conclusion: Type 2 diabetes causes significant hearing loss in the patients, but it is not affected by
the age and sex of the patient or duration of the illness.
Key words: Audiometry, Diabetes, Sensorineural hearing loss
INTRODUCTION
Diabetes mellitus is a heterogeneous group of

metabolic disorders characterized by chronic
hyperglycemia that results from defects in insulin
secretion, insulin action or both. Diabetes
mellitus leads to long term damage, dysfunction
and failure of various organs, especially the eyes,
kidneys, heart and blood vessels.1
Diabetes-related
sensorineural
hearing
impairment affects peoples ability to hear and
understand sounds. Although evidence from as
early as the mid-19th century linked diabetes
with hearing loss, a degree of controversy has
surrounded this association.2
Various tests are available for the clinical
assessment of hearing loss. Localization and type
Jankar DS et al.,
893
of hearing loss can be known by use of simple

tests like the tuning fork tests, while audiometry
gives the graphic recording of hearing
quantitatively and qualitatively.3-5
We carried out this case control study with the
purpose of determining the hearing loss in type II
diabetes mellitus in relation to the age and
gender of the patients and duration of the illness
using tuning fork tests and pure tone audiometry.
Aim: To study the hearing loss in type II
diabetics and controls.
Objectives:
1. To study the hearing loss in relation to
different age groups in diabetics and controls.
gender in diabetics and controls.
duration of diabetes.
Control: non-diabetic healthy controls, Age

above 40 yrs, both genders.
Exclusion criteria: Diabetes other than type2,
patients with conductive hearing loss, or hearing
loss associated with other causes.
Interpretation of tuning fork tests3-5 Initial
screening of hearing loss in the study and control
group was done by tuning fork tests.
Then they were subjected to pure tone
audiometry
Pure Tone Audiometry3-5: Instrument:- Elkon
EDA-3N3 Giga 3 Audiometer 5a was used in the
study.
I. Air conduction tests: The Conventional 5up-10-down method was followed. In this
procedure the tones are lowered in 10 dB
steps and increased in 5 dB steps for each
frequency. The exact hearing threshold is
obtained when one gets at least 3 out of 5
responses correct.
II. Bone conduction tests: Technique:- the 5up-10-down method is followed for bone
conduction study.
Participants were labeled as having sensoryneural hearing impairment if the average of the
pure-tone thresholds in either ear exceeded 25 dB
HL and the airbone gap less than 15 dB.5
Statistical Analysis: Analysis was done by chi
square test using Microsoft Office Excel 2010.
A p value of < 0.05 was considered statistically
significant.
The present study was conducted on patients

attending the ENT and Medicine OPD and IPD
of civil hospital, Miraj after proper consent. 200
diagnosed diabetic patients (Fasting plasma
glucose 126 mg/dl or 2 hour plasma glucose
200 mg/dl during an oral glucose tolerance test)
and 200 age and sex matched controls took part
in the study. The Ethical Committee of the Govt.
Medical College and Hospital, Miraj approved
this study.
Inclusion criteria: Case: Diagnosed cases of type
2 diabetes, Age above 40 yrs, both genders.
Table1: Interpretation of tuning fork tests
Test
Normal
Conductive deafness
Rinne
AC > BC
BC > AC
Weber Not lateralized
Lateralized to poorer ear
ABC
Same as examiners
Same as examiners
Sensori-neural deafness
AC > BC
Lateralized to better ear
Reduced
RESULTS
Table 2: mean age of Diabetic and non-diabetic (controls)
Total no.
Mean age (years)
Diabetics
200
50.30 5.78
Non-diabetics
200
50.25 5.69
894
Jankar DS et al.,
Table 3: Age and sex wise distribution of Diabetics and Non-diabetics
Age 41-50 yrs

Age 51-60 yrs
Diabetics
Males
60
60
Non-diabetics
Males
Females
60
40
60
40
Females
40
40
Table 4: Duration wise distribution of Diabetics
Duration < 5 years

Duration > 5 years
Total
79
121
200
Table 5: Comparison of hearing loss in diabetics and non-diabetic controls (chi square test) (Odds
ratio: 2.398)
P value
Hearing Loss
Diabetics
Non-diabetics
Present
absent
Total
p value: 0.0001 (highly significant)
72
128
200
0.0001*
38
162
200
Table 6: Comparison of hearing loss in relation to different age groups in diabetics and non-diabetic
controls (chi square test)
Age
Diabetics
Non-diabetics
41-50 years
29
16
51-60years
43
22
Total
72
38
P value
0.852
-
Table 7: Comparison of hearing loss in relation to sex in diabetics and controls. (chi square test).
Sex
Diabetics
Non-diabetics
Male
42
24
P value
0.6233*
Female
Total
30
72
14
38
Table 8: Comparison of hearing loss in relation to duration of diabetes in diabetics. (chi square test).
Duration
Hearing loss
No Hearing loss P value
< 5 yrs
> 5 yrs
Total
25
47
72
54
74
128
0.2999
-
DISCUSSION
The results of the present study showed that the

hearing of diabetics was significantly impaired
than the non-diabetic control group. All the
frequencies tested demonstrated this hearing
impairment. The hearing acuity was not

influenced by the duration of diabetes, age or sex
of the subjects.
Jankar DS et al.,
895
Thus, statistically highly significant hearing loss

has been observed in the diabetic group than in
the non-diabetic control group and Odds ratio of
2.398. This finding coincides with the findings of
other workers Taylor I and Irwin J6, Wackym
PA7, Kurien M etal 8, Dalton DS etal 9,
Rzaska-Kudelska 10, Kakarlapudi V etal 11,
Panchu P 12, Bainbridge KE et al 13.
Diabetes-related hearing loss is a progressive,
sensorineural impairment typically affecting
audiometric thresholds between 500 and 8,000
Hz.7,13
The pathophysiology underlying diabetesassociated hearing loss may involve the effect of
diabetes-related microvascular disease on the
cochlea.14 Few microscopic studies (obtained
post-mortem) show sclerosis of the internal
auditory artery, thicker vessel walls of the stria
vascularis and of the basilar membrane, damage
to the outer sheath (demyelination) of the
cochlear nerve, and atrophy of the spiral
ganglion (linking the cochlear nerve and the
brain). 7,15
One study among autopsied diabetic patients
shows atrophy of the spiral ganglion and
demyelination of the eighth cranial nerve
indicating a neurological etiology to diabetesrelated hearing impairment.15
Hyperglycemia itself via elevated glucose levels
in the cerebrospinal fluid or in the perilymph can
lead to cochlear dysfunction in diabetic patients.
This is independent of angiopathic or
neuropathiclesion.8
Study on severe diabetic neuropathy has reported
a reduction of Nerve Growth Factor (NGF) in
neuropathic diabetics causing limitation of
axonal retrograde transport and nervous fibres
demyelinization. 16,17
Thus, the possible mechanisms underlying the
hearing loss in diabetic individuals from the
above discussion are as follows:
1. Microvascular disease affecting the stria
vascularis,
2. Thickening of the basilar membrane,
3. Damage to the outer sheath (demyelination)

of the cochlear nerve,
4. Atrophy of the spiral ganglion,
5. The loss of outer hair cells,
6. Neuronal degeneration
or diabetic
encephalopathy,
7. Hyperglycemia,
8. Hyperactivity of oxygen free-radicals,
9. Reduction of Nerve Growth Factor (NGF),
10. Atherosclerotic narrowing of the internal
auditory artery.
The effect of age on auditory thresholds in
diabetic subjects was statistically not significant.
Kakarlapudi11 Dalton9 Rzaska-Kudelska10, and
P. Panchu 12 showed similar findings in their
study. Thus, age of the patient is not related to
hearing loss in diabetics.
The effect of sex on auditory thresholds in
diabetic subjects was statistically not significant.
Similar findings were reported by Kathleen E.
Bainbridge et al.13 Thus, there is no sex
difference as far as occurrence of hearing loss in
diabetics is concerned.
When hearing loss in diabetics is compared with
relation to duration of diabetes, the difference in
the two groups was statistically not significant.
Thus the duration of diabetes does not alter
hearing thresholds. Similar findings were noted
by Pallavi Panchu12, Kurien M et al 8, Dalton S et
al9, Taylor IG and Irwin J.6
The degree of hypergylcemia and the duration of
uncontrolled hyperglycemia are gaining more
importance as causative factors than the duration
of the disease itself as indicated by the studies of
Kakarlapudi11 Frisina et al18, Hsueh19, Panchu
P12, Bainbridge et al.13 Thus, the age or sex of the
subject or the duration of diabetes are not related
to hearing loss in diabetics but the duration and
degree of uncontrolled hyperglycemia may be
related to hearing loss in diabetic patients and it
needs further study.
Jankar DS et al.,
896
CONCLUSION
1. Wild S, Roglic G, Green. Global percentage

of diabetes: estimates for the year 2000 and
projections for 2030, Diabetes care 2004; 27:
1047-1053
2. Kathleen Bainbridge. Hearing impairment
an under-recognized complication of
diabetes? Diabetes Voice.2009;54(1): 13-16
3. Dhingra PL. Diseases of ear, nose and throat,
assessment of hearing. 2004, 3rd Ed:Chapter
5: 23-32
4. Bhargava KB, Bhargava Sk, Shah TM. A
short textbook of ENT diseases. Examination
of the ear; 2003; 6th Ed; Chapter 4: pg 23-32
5. Anirban
Biswas,
clinical
audiovestibulometry 2nd Ed for Otologists and
Neurologists: Pure Tone Audiometry: 1996,
pg 1-17
6. Taylor IG, Irwin J. Some audiological
aspects of Diabetes mellitus, Journal of
Laryngology and Otology.1978; 92;99-113
7. Wackym PA, Linthicum FH. Diabetes
mellitus and hearing loss: clinical and
histopathologic relationships. Am J Otol.
1986;7(3):176-82.
8. Kurien M, Thomas K, Bhanu TS. Hearing

threshold in patients with diabetes mellitus. J
Laryngol Otol. 1989;103(2):164-8
9. Dalton DS, Cruickshanks KJ, Klein R, Klein
BE, Wiley TL. Association of NIDDM and
hearing loss. Diabetes Care. 1998;21(9):1540
10. Rzaska Kudelska M, Chodynicki S,
Kinalska I, Kowalska I. Hearing loss in
patients with diabetes mellitus type II.
Otolaryngol Pol. 2002;56(5):607-10.
11. Kakarlapudi V, Sawyer R, Staecker H., The
effect of diabetes on sensorineural hearing
loss., Otol Neurotol. 2003;24(3):382-86
12. Panchu P. Auditory acuity in type 2 diabetes
mellitus. Int J Diabetes Dev Ctries.
2008;28(4):114-20.
13. Bainbridge KE, Hoffman HJ, Cowie CC.
Diabetes and hearing impairment in the
United States: audiometric evidence from the
National Health and Nutrition Examination
Survey, 1999 to 2004. Ann Intern Med.
2008;149(1):1-10
14. Lisowska G, Namysowski G, Morawski K,
Strojek K. Cochlear dysfunction and diabetic
microangiopathy. Scand Audiol Suppl.
2001:52:199-203
15. Makishima, Tanaka. Pathological changes of
the inner ear and central auditory pathways in
diabetes. Annals of Otology, Rhinology and
Laryngology1971; 80, 218-28.
16. Tomlinson DR, Femyhough P, Diemel LT,
Maeda K. Deficient neurotrophic support in
aetiology of diabetic neuropathy. Diabet
Med.1996;13S:679-81
17. Salvinelli F, Casale M, Greco F, Trivelli M,
Di Peco V, Amendola Tetal., Nerve growth
factor serum level is reduced in patients with
sensorineural hearing impairment: possible
clinical implications. J Biol Regul Homeost
Agents.2002; 16(3):S176-80
18. Frisina ST, Mapes F, Kim S, Frisina DR,
Frisina RD. Characterization of hearing loss
in aged type II diabetics. Hear Res.
2006;211(1-2):103-13
Jankar DS et al.,
The present study shows that type II diabetes

causes significant hearing loss in the patients, but
it is not affected by the age and sex of the patient
or duration of the illness.
ACKNOWLEDGEMENT
Authors thankful to Dr. Aundhkar VG, Professor

and Head, Dept. of Physiology for his constant
support and valuable guidance; Dr. Bhagwat,
Professor and Head, Dept. of Medicine, Dr.
Mahure, Professor and Head, Dept. of ENT for
allowing me perform this study and their timely
guidance. I am very much thankful to the
technical staff of Audiometry and ENT. I am
thankful to the participants without whom this
study would not have been possible.
REFERENCES
897
19. Hsueh W, Abel ED, Breslow JL, Maeda N,

Davis RC, Fisher EAet al. Recipes for
creating animal models of diabetic
cardiovascular
disease.
Circ.
Res.
2007;100:1415-2
898
Jankar DS et al.,
DOI:10.5958/j.2319-5886.2.4.144

&
Health Sciences
Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
COMPARATIVE STUDY ON TEACHING OF BIOETHICS TO HEALTH CARE PERSONS

USING DIFFERENT METHODOLOGIES
Vedavathi H 1, Tejasvi TS2, * Shreenivas P Revankar3
1
Associate Professor, 3Assistant Professor, Department of Pharmacology, Shimoga Institute of Medical

Sciences, Shimoga, Karnataka, India
2
Assistant Professor, Department of General Medicine, Shimoga Institute of Medical Sciences,
Shimoga, Karnataka, India
* Corresponding author email:sprevankar@yahoo.com
ABSTRACT
Introduction: Bioethics has gained lots of importance in the present days and especially very important in the
field of medical research. Doctors, medical students, nursing staff and other paramedical staff are directly or
indirectly involved in the clinical and research activities. A proper training in bioethics is very essential especially
for medical students nursing and other paramedical staff. There are various teaching methodologies like a black
board (lecturing), power point presentations, case discussions, group discussions and film/movie clipping related
to bioethics .Each of the teaching methodology is effective in a particular group. Materials and methods: Four
different teaching methodologies were used to teach bioethics in four different categories namely MBBS students,
doctors/interns, nurses and lab technicians. All were exposed to all types of teaching methodology. An evaluation
was done by performance based and choice based evaluation system. Results: Case discussion was most popular
choice of MBBS students and Doctors/Interns. Among nurses and lab technicians film discussion was best in
terms of performance and choice. Conclusion: Bioethics covers more about abstract issues related to the health
discussion on this topic help in better understanding and clarification.
Keywords: Bioethics, Teaching Methods, Evaluation

INTRODUCTION
Bioethics is a study of typical controversial

issues brought about by advances in biology and
medicine, it relates to medical policy, practice
and research. In general context ethics is about
giving priority to individual needs and moral
values in an attempt to curb and control potential
societal abuses. 1 The term bioethics was coined
in 1927 by Fritz Jahr.2 Van Ransseller Potter
gave it a broader meaning and coined the word
global ethics. It is a link between biology,
ecology medicine and human values in order to
attain the survival of human beings and other

animal species.2,3 The scope of bioethics can
expand with biotechnology including cloning,
gene therapy, life extension, human genetic
engineering and manipulation of basic biology
through altered DNA, RNA and proteins.4
The fundamental principles of bioethics included
in Belmont report are autonomy, beneficence and
justice the others which were added later on are
non malfeasance and sanction of life.5 Medical
ethics is study of moral values and judgements. It
Vedavathi et al.,
899
encompasses its practical applications in clinical

settings as well as work on its history,
philosophy, theology and sociology.6 Bioethics
has addressed a broad swath of human enquiry
ranging from debates over the boundaries of life
care (eg.abortion, euthanasia, surrogacy,
allocation of scare health care resources) to the
right to refuse medical care.7
Teaching and learning are the two sides of the
same coin. There are various teaching methods
like lectures, power-point presentations, group
discussion, seminars, role play, film or
documentary presentations, case discussions etc.8
Each of them has their own advantages and
disadvantages.9 The teaching methodology to be
used also depends on the topic to be covered; i.e.
for a particular topic a particular methodology
may be effective. The effectiveness of teaching is
dependent on individual interest, but more over
the methodology used is also important. 10
The most accepted criterion for measuring good
teaching is the amount of student learning that
occurs. Teaching in the absence of learning is
talking; effective teaching is that which produces
beneficial and purposeful student learning
through the use of appropriate procedures.11
Students are most qualified sources to report on
the extent to which the learning experience was
productive,
informative,
satisfying
and
worthwhile. A meta-analysis of 41 researches
provides validity that, student ratings tend to be
reliable, valid, unbiased and useful.12 Health care
professionals are the ones who are constantly
exposed to various issues related with bioethics.
This group includes the doctors, nurses, and
laboratory technicians, medical and nursing
students. The ability to understand the concepts
of bioethics varies in each of these health care
personals. There is a need for identifying the
proper teaching methodology for each of this
group; hence the present study was undertaken.
The study population was divided into four

groups which included participants from
different categories like medical students,
intern/junior doctors, nursing staff and lab

technicians from the medical college and
hospital. A group consisted of ten candidates
each from each category, It included ten MBBS
students, ten interns/junior doctors, ten nurses
and ten lab technicians (N=40). Boys and girls
were equally distributed in each group. A total
of 160 participants were included in the study.
Inclusion criteria: Students from second year
MBBS were chosen, taking into consideration
that they sufficient knowledge of basic medical
science. Random selection of fourty students was
done; majority of the students had secured first
class in first year examinations. Hence the bias in
selection of the participants was ruled out. Junior
residents/internees, forty in number were
randomly distributed in four groups with ten
members in each group. They had better
knowledge on ethical issues.
The nurses included in the study were from
diploma (General nursing and midwifery)
background, had fair knowledge and good
communication skills in English.
Laboratory technicians, who had completed
DMLTC (diploma in lab techniques course) were
included in the in the study. They had sufficient
knowledge of understanding and communicating
in English but knew very little about ethics. A
total of forty members working in the various
depts. were included in the study.
Exclusion criteria: Those who lacked the above
criterias were excluded from the study. Nursing
staff had no theoretical knowledge of bioethics.
Topics chosen were easy to understand and
formed the core of bioethics. The four topics
chosen were Informed consent, Medical
negligence, and ethical issues of HIV/AIDS and
Clinical trials.13 Four different teaching
methodologies used in the study were Black
board /lecturing, Power-Point presentations, Case
discussions and film clippings followed by
discussions. Lecture is a talk or a verbal
presentation given by a lecturer, trainer or a
speaker to an audience. This method is
economical, can be used for a large number of
900
Vedavathi et al.,
students, material can be covered in a structured

manner and the teacher has a great control of
time and material. Power-point presentations
make use of computer and LCD-projector,
material to be covered is restricted. Discussion is
a free verbal exchange of ideas between group
members or teacher and students. In casediscussion a case related to the topic is explained
followed by discussion. In film discussion a film
or documentary related to the topic is screened
for 25 minutes, followed by discussion on the
ethical issues related
An evaluation was done by two types of analyses
i.e. performance based and choice based.
Performance based evaluation, scores of pre and
post evaluation test were taken into consideration
to access the performance.14,15 Pre and post
evaluation tests were done with the help of
questionnaires designed in each of the topics.
The topic to be taught was not informed to the
participants. Pre-evaluation test was given
simultaneously to all the groups i.e. all the 160
members had to take the pre-evaluation test at

the beginning of the day. Post evaluation was
done immediately at the end of their respective
classes. The type and number of questions asked
in the pre and post evaluation test were same, the
time duration of the class was restricted to forty
five minutes only which was followed by post
evaluation test for fifteen minutes. The questions
asked were of multiple choice and of yes/no type
.The questions were displayed on the screen
using LCD projector. Improvement was
calculated based on difference in pre and post
evaluation scores.15
A choice based evaluation was done on the last
day, after exposing all the candidates to different
teaching methodologies. In this system the
candidates were asked to rate different methods
of teaching used by their teachers on a scale of 14, one being the least important and 4 being the
most important teaching method. The results of
the study were compiled and analyzed by
percentage method.16, 17
Table 1: Schedule of the study
Topic
Day1
Day2
Day3
Day4
Informed consent
Medical negligence
Ethical issues of HIV/ AIDS
Clinical trials
Teaching methodology
Lecture Power point
class
presentation
Group 1 Group2
Group 2 Group 3
Group 3 Group 4
Group 4 Group 1
Case
discussion
Group 3
Group 4
Group 1
Group 2
Film clip followed

by discussion
Group 4
Group 1
Group 2
Group 3
RESULTS
Table 2: Results of performance based evaluation
Teaching
Method
Lecture
Power point
Case disc#
Film/disc#
MBBS students
Post#
Pre*
14.025
9.65
14.050
9.55
14.55
10.10
14.15
9.20
Nurses
Diff*
4.375
4.5
4.45
4.95
% imp$
21.87
22.50
22.25
24.75
Junior residents/interns
Post* Pre*
Diff *
15.7
12.45 3.25
15.85 12.40 3.45
15.55 12.55 3.00
14.85 11.85 3.00
Lab technicians
% imp*
16.25
17.25
15.00
15.00
Lecture
Power point
Case disc#
Film/disc#
9.00
8.75
9.75
10.25
3.00
3.25
3.75
4.00
15.00
16.25
18.75
20.00
5.62
6.00
4.87
7.75
11.25
13.75
8.75
22.50
6.00
5.50
6.00
6.25
3.37
3.25
3.12
3.25
2.25
2.75
1.75
4.50
Pre*-average pre evaluation score; Post*-average post evaluation score, Diff*-difference between average
pre and post evaluation scores, %imp$-percentage of improvement ; disc#-discussion
901
Vedavathi et al.,
Results of the performance based evaluation:

The major improvement in performance was
seen by medical students. It was above 20% with
all teaching methodology used, Maximum with
film discussion (24.75) and minimum with
lecture class (21.87). The other two teaching
methods showed almost same improvement
(22.5). The improvement percentage in junior
doctors/interns was less but almost in the same
range with different methods. It was highest with
power-point (17.25), followed by a lecture
(16.25), while it was 15% with case discussion
and film-discussion. In this category it was noted
that the pre-evaluation scores were in higher
range compared to other categories. So the
relative improvement was less.
Among the nurses highest improvement (20%)
was seen with film-discussion followed with case
discussion (18.75) and power-point (16.25).

They showed less improvement with lecture
classes (15%). As nurses had limited knowledge
on bioethics their pre-evaluation scores were less
compared to doctors and medical students. Lab
technicians had very low improvement compared
to other categories. The pre-evaluation scores
were least as they had no knowledge about
bioethics. The improvement percentage were
8.75 with case discussion,11.25 with lectures and
13.75 with power-point presentations but filmdiscussion brought about marginal improvement
of 22.5%
Results of choice based evaluation: Table
showing the preferences given by different
categories (MBBS, junior doctors/interns, nurses
and lab technicians) for different teaching
methods.
Table 3: Results of choice based evaluation
Teaching
method
Preferences
MBBS
Junior
dr
/internees
Nurses
Lab
technicians
Lecture
Power point
Case discussion
1
13
8
2 3 4 1 2 3
12 8 7 8 11 16
8 13 11 8 14 15
4
5
3
9
4
13 8
8 8
10 9 8
20 6 8
14
16
Film-discussion
1
16
18
2
15
09
3
5
7
4
4
6
1
3
6
2
2
9
3
11
5
4
24
20
8
10 12
5
14
13
10
14
4
14
18
13
10
5
6
8
6
Table 4: Scores and percentage share of different teaching methods
Lecture
Score
MBBS
Junior.doctors/interns
Nurses
Lab technicians
All candidates
Power point
%
share
27.75
23.25
25.25
19.00
23.81
111
93
101
76
381
Score
102
107
99
90
398
%
share
25.5
26.75
24.75
22.50
24.87
Case
discussion
Score %
share
123
30.75
119
29.75
87
21.75
114
28.50
443
27.69
Film/discussion
Score
64
81
113
120
378
%
share
16.00
20.25
28.25
30.00
23.63
Table 5: Concluding results of the study
Sl
no
Category
1
2
3
4
MBBS
Junior.doctors/internees
Nurses
Lab technicians
Best teaching methodology based on

Performance -evaluation
Choice-evaluation
Film followed by discussion

Power point
Case discussion
Case discussion
902
Vedavathi et al.,
Scoring was calculated based on the preferences

given by the candidates. It was calculated on
allocation of points i.e. the 1st preference was
allotted four points, three points for 2nd
preference, two points for 3rd preference and one
point for 4th preference. The sum obtained was
the overall score for each methodology under
each category
The majority of the medical students preferred
case discussions which accounted for highest
score of 123, lectures were their second choice to
score 111 followed by PowerPoint in 102. Film
discussion was their last choice. Doctors/interns
also liked case discussions very much, powerpoint and lectures were subsequent choice and
film-discussion was the last choice. Film
discussion was a popular choice among the
nurses and lab technicians. Nurses hated the case
discussions while lab technicians did not like
lectures the most.
DISCUSSION
In our study the participants were exposed to all

the four different types of teaching methodology.
The topics chosen were also of similar category
there is every possibility of bias as a particular
topic is taught effectively by a particular method.
To overcome this we had opted for a two way
evaluation system i.e. performance based and
choice based evaluation system as compared to
some of the studies. The performance based
evaluation took into consideration the
performance of candidate in pre and post
evaluation. In choice based evaluation system we
gave freedom to the candidates to grade the
teaching methodology.
When overall results were taken into
consideration it was found that film discussion
and case discussion as teaching methodology is a
most effective means of learning compared to the
lectures and power point presentations.
Discussion involves more participation; learning
is more effective and develops creativity among
participants. This may be contradictory to some
of the studies conducted on teaching
methodologies. 9 Lecture as a teaching method

creates new ideas, are good for large class but
useful only when the concept and views of the
topic are clear. Bioethics has more of abstract
concepts.1, 3 In this study, case discussions and
film presentations followed by discussion fared
well mainly because they provide a platform for
better understanding of abstract concepts in a
simplified way.8 Bioethics as such need not be
restricted to health care; it involves various fields
so there is need to evaluate similar studies in
other areas. In our study only four teaching
methods were tried, this study can be improved
upon by experimenting with other methods of
teaching.
CONCLUSION
In our study we found that lectures and power

point presentations are not much importance in
imparting the knowledge of bioethics. The
concepts involved in bioethics are abstract and it
requires more of discussion for better
understanding and clarifications. The topics of
bioethics must be reserved for panel discussions
in the CME and workshops, so as to improve the
knowledge of bioethics among medical and
paramedical personnel.
ACKNOWLEDGEMENTS
We thank ICMR (Indian council of medical

research) for giving me an opportunity to
participate in a one month long training
programme and taking up the above study as a
part of project. My special thanks to Dr Nandini
kumar and Dr Vasanta Muthuswamy of ICMR.
REFERENCES
1. Andre, Judith Bioethics as Practice, Chapel

Hill and London: University of North
Carolina Press. 2002; Pg no35-37
2. Appel, Jacob, A Supreme Cou-forrt for
Bioethics. Huffington Post. August 9, 2009;
http://huffingtonpost.com/jacob-m-appeal/asupreme-court-for-bioet_b_228967.html
903
Vedavathi et al.,
3. Aulisio, Mark; Arnold, Robert; Younger,

Stuart. Ethics Consultation; from theory to
practice, Baltimore, London: Johns Hopkins
University Press, 2003: pg 54
4. Glad Joh. Future Human Evolution: Eugenics
in the Twenty-First Century, Hermitage
Press, 2008; pg 41-44.
5. Crowley, Mary. From Birth to Death and
Bench to Clinic: The Hastings Center
Bioethics Briefing Book, Garrison, New
York: The Hastings Center. 2008 Ed; 71-75.
6. Beauchamp Tom, Childress James. Principles
of Biomedical Ethics, Oxford, New York:
Oxford University Press, 2001; pg 152-54.
7. Hyry Matti, Tuija Takala, Peter HerissoneKelly, Gardar rnason. Arguments and
Analysis in Bioethics. Amsterdam/New
York: Rodopi; 2010
8. Kochkar, S.K. Methods and Techniques of
Teaching. Sterling press New Delhi:2000; 13.
9. McCarthy P. Common Teaching Methods.
1992; Retrieved July 24, 2008, from.
http://honolulu.hawaii.edu/intranet/committe
es/FacDevCom/guidebk/teachtip/comteach.ht
m
10. Hoyt MP, Pallett WH. Appraising teaching
effectiveness: Beyond student ratings;
Kansas State University, Center for Faculty
Evaluation and Development; 1999 Pg No.
36.. Retrieved June 1, 2002, from
http://www.idea.ksu.edu/products/Papers.htm
l.
11. Centra JA. Reflective faculty evaluation. San
Francisco, CA: Jossey-Bas; 1993
12. Cohen PA. Student Ratings of Instruction and
Student Achievement: A Meta-Analysis of
Multisection Validity Studies. Review of
Educational Research. yr 1981; 51, 281-309.
13. Singer PA, Viens AM. Cambridge Textbook
of Bioethics, Cambridge: Cambridge
University Press, 2008; pg 276-78
14. Arreola RA. Developing a comprehensive
faculty evaluation system. Bolton, MA:
Anker Publishing;1995; 37-40.
15. Ory JC. Faculty thoughts and concerns about

student ratings; Techniques and strategies for
interpreting student evaluations. New
Directions for Teaching and Learning, 2001;
no. 87. Pg 3-15.
16. Doyle T. Evaluating Teachers Effectiveness.
Retrieved
July
24,
2008,
from
ferris.edu/fctl/Teaching_and_Learning_Tips/
EvalTeachEffec.htm.
17. Theall M, Franklin J. Student Ratings of
Instruction: Issues for Improving Practice.
New Directions for Teaching and Learning,
1990; 43.
18. Hamm PH. Teaching and Persuasive
Communication: Class Presentation Skills.
The Harriet W. Sheridan Center for Teaching
and Learning: Retrieved July 24, 2009, from
http://www.brown.edu
/Administration
/Sheridan_Center /publications /preskils.
Vedavathi et al.,
904
DOI:10.5958/j.2319-5886.2.4.145

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
LEVELS OF STRESS AMONGST THE SCHOOL TEACHERS IN A PUBLIC SCHOOL OF

RURAL WESTERN MAHARASHTRA
* Kunkulol Rahul R1, Rusina Karia2, Prashant Patel3, Abhinav David3
1
Associate Professor, Department of Pharmacology, Secretary, Research Cell, PIMS-DU, Loni

MBBS Student, Rural Medical College, PIMS-DU, Loni, Maharashtra
3
Resident, Department of Pharmacology, Rural Medical College, Loni, Maharashtra
2
*Corresponding author email: rahul4420@yahoo.com

ABSTRACT
Objectives: Teachers are among the professions reporting highest level of work-related stress, the study
was undertaken to evaluate the levels of stress amongst school teachers in a public school of rural
western Maharashtra Methods: Prospective survey based study was carried out amongst school teachers
of rural western Maharashtra using Copenhagen Psychosocial Questionnaire (COPSOQ).The survey was
carried out on 3 scheduled visits over a period of 2 months after the Institutional Ethical committee
approval. Total 110 Primary and secondary school teachers, satisfying inclusion and exclusion criteria
were randomly selected for the study. All the questions in the Copenhagen Psychosocial Questionnaire
(COPSOQ) were graded according to 1 (Always-0), 2 (Sometimes-25), 3 (Often-50), 4 (Seldom-75) and
5 (Never-100). The scale value was calculated as the simple average. More the average score less the
stress and vice versa Results & Conclusion: Inability to understand the meaning and importance of
work, improper clarity about the job, inability to cope with the problems were found to be the factors
always contributing to stress of teachers.
Keywords: School teacher, Job related stress, COPSOQ, Personal Stressors
INTRODUCTION
Work-related stress has been identified at

international and national levels as a concern for
both employers and workers. Occupational
stress is known as stress at work. It occurs when
there is a discrepancy between the demands of
the workplace and that of an individual. Such
individuals under occupational stress, experience
of negative emotional states such as frustration,
worry, anxiety and depression attributed to work

related factors.1 Occupational stress in the human
service professions, particularly teachers, has
been a focus of study in the last decades. Most
surprisingly, school teachers have been
considered to be under stress and undergoing the
process of burnout.2 Teaching is a physically and
mentally challenging job. The daily chores in the
Rahul et al.,
905
classroom coupled with personal and family

commitments require a lot of energy and
forwards a lot of stress to the teacher.3
Undoubtedly, teachers are among the professions
reporting the highest level of work-related stress.
The increasing workload on teachers, the role
overload, the increased class size per teacher and
an increasing number of pupils behaving in an
unacceptable way are some of the trends
identified in several countries as leading to a rise
in stress-related illnesses. 4
Teachers are exposed to a wide variety of multidimensional predisposing factors leading to
stress which can be classified as job related and
related to the personal events.5 Job related
contributory factors can be like inadequate
working conditions , role conflict and ambiguity,
pupil (student related) problems, time pressures ,
threat of redundancy, work pressure, little
participation in decision-making and distribution
of tasks , stereotypes and discrimination against
minority groups, inadequate salaries. 5
Those related to the personal events are
Marriage, Divorce, Pregnancy, Death of a loved
one, change of residence and others if any. In
addition, it has been found that job satisfaction
and teacher stress are strongly correlated.6 The
amount of stress and degree of satisfaction
experienced by teachers influences the quality of
life and may create various stress related health
problems like Hypertension, cardiac disorders,
Acid peptic diseases, psychological disorders.7,8
Work involving responsibility for other people
creates potential stress as it may heighten
expectations for job performance and emotional
availability. The complexity and diversity of
teachers work, clearly links workload and stress
not only to the quantity of hours worked, but also
to the diverse nature and demands placed on
teachers.5-8
In view of above mentioned etiological factors
and detrimental adverse effects of stress among
school teachers, it was thought prudent to
evaluate levels of stress amongst them by using
Psychosocial Questionnaire (COPSOQ) a well-
structured questionnaire developed by the

Psychosocial Department, National Institute of
Occupational Health, Copenhagen, Denmark.9
Hence a study was planned with the following
aims and objectives
Aims and objectives
1. Evaluate levels of stress amongst school
teachers in a public school of rural
western Maharashtra
2. Find
out
various
stressors
or
predisposing factors responsible for stress
among them.
3. To find out the most common stressor or
stress indicator if any amongst primary
and secondary school teachers in a public
school of rural western Maharashtra
Rahul et al.,
This was a prospective survey based study. This

survey was carried out school amongst the
teachers in a public school of rural western
Maharashtra. The School was selected on the
basis of ease and access. Consent from the school
authorities and Institutional ethical committee
approval
were
obtained
before
the
commencement of the study. The primary and
secondary school teachers were selected on the
basis of following inclusion and exclusion
criteria.
Inclusion criteria:
1. Primary and secondary school teachers of
Public School (Standard L.K.G to X)
2. Teachers willing to participate in the study
3. Ready to give written informed consent
4. Teachers completing the survey, i.e present on
the days of data collection
Exclusion criteria:
1. The teachers of XI Std. onwards.
2. The teachers who were absent on either day
during data collection.
3. The teachers suffering from debilitating
physical or psychiatric illness
4. Teachers with history of addiction, drug
history or any chronic illness
906
Study tool:
Psychosocial Questionnaire (COPSOQ): The
scales of the COPSOQ were formed by adding
the points of the individual questions of the
scales by giving equal weights to each question.
In most cases the questions had five response
options.
The Questionnaire was divided into two types:
Job related Questionnaire and Personal
stressor Questionnaire. The scale value was
calculated as the simple average from 0 to 100.
Respondent absent for any one visit were
considered as a drop out
Study conduct: Data was collected in 3
scheduled visits approximately 7 days apart
Table 1: Psychological Questionnaire
according to the convenient date and time given

by the school authorities.
Visit-1: 1. Introduction of the project 2.
Explanation of the Study Tool 3. Obtaining
consent
Visit-2: Job related questionnaire
Visit-3: Personal stressor questionnaire
Study period: 2 months from the date of
approval of the study by the Institutional Ethical
Committee
Statistical analysis: The data was collected,
pooled, subjected to appropriate statistical
analysis and conclusions were drawn
Sample size: Out of total 110 teachers enrolled
for the study effective sample was 78
Psychosocial Questionnaire (COPSOQ):9
Grade
Score
Interpretation
ALWAYS
25
SOMETIMES
50
OFTEN
75
SELDOM
100
NEVER
RESULTS
Mean Scores of Job related stressors (%)

Degree of Freedom of Work
74.49
Demands for Responsibility
52.98
Emotional Demands
37.50
34.44
Influence at Work
32.94
Predictability
Commitment to workplace
27.35
Cognitive Demands
26.81
Possibilities for Development
23.40
11.76
Meaning of Work
0
20
40
60
80
100
Fig 1: Mean scores of job related stressors
907
Rahul et al.,
Mean scores of Personal stressors (%)

SOMATIC STRESS
72.38
COGNITIVE STRESS
61.62
54.67
BEHAVIOURAL STRESS
MENTAL HEALTH
52.18
SENSE OF COHERENCE
47.65
ROLE CONFLICTS
46.50
40.03
GENERAL HEALTH
37.02
SELECTIVE COPING
JOB SATISFACTION
25.99
SOCIAL SUPPORT
23.07
PROBLEM FOCUSED COPING
22.68
16.57
ROLE CLARITY
0
20
40
60
80
100
Fig 2: Mean score of personal stressors

DISCUSSION
Among all the Job related stressors mean score

for meaning of work (11.76), possibilities of
development (23.70) were Grade I stressors
always causing stress.(Fig I)
Teachers were of the opinion that possibilities for
development were very less and was worrying
them the most. The school authorities should
give emphasis on understanding the importance,
meaning and clarity about the job and work so
that the teachers can give their best for the
school.
The personal stressors with mean score ranging
between (0-24) were Role Clarity, Problem
focused coping and social support thus were
Grade I stressors always causing stress.(Fig II)
Many of the teachers were not clear about their
own role and revealed an inability in coping day
to day problems resulting in stress. There is
consistent evidence that teachers with more
support from others experience lower strain and
burnout10 and teachers facing potentially stressful
demands, conflicts and problems in the
workplace, having support from others may
reduce the impact of the pressures on the
individuals well-being.11,12
This study reveals incorporation of measures for

coping with day to day problems.Teachers
should incorporate habbit of keeping Proper
balance between the personal, family and
professional life There is a requirement and
neccesity of analysing the system of teacher
training. Workshops on stress management,
positive attitude should be incorporated
periodically. It is necessary to provide social
support for the teachers for their betterment
through social gatherings.
A lack of appropriate professional training
specifically where teachers are required to
implement new practices with inadequate
ongoing training in order to meet the needs of an
increasingly diverse population is a particular
source of stress.
The factors that influenced the teachers mental
health status were workload. In urbanised and
modern societies, high demands by parents and
community that are constantly increasing is
becoming unrealistic with the resources that are
given to teachers 13.An study indicated that
sources of burnout and stress in the working
environment are related to role conflicts,
Rahul et al.,
908
professional isolation, lack of support, ineffective

teaching aids, student disciplinary and
behavioural problems, inadequate working
conditions and general lack of respect for the
teachers role. Our results were consistent with
with Shankar and Famuyiwa (1991)14
Stress affects the efficiency of the individual. So,
there is a need to provide a proper conducive
environment and support for teachers to maintain
individual stress at their workplace. Positive
attitude of teachers in facing their challenges will
help them in improving their functional skills and
reduce stress. Regular assessment of stress level,
direct physiological measures of stress like
diagnostic tests and consultation with medical
professionals and preventive measures should be
taken accordingly. Besides that, the institution or
management should check that, supervision,
support and relationship with the teachers is
properly taken care of and enhanced most
strongly. Most importantly, it is recommended
that principals and supervisors should investigate
the causes of stress and evaluate the
organizational climate of the school. They should
also suggest ways, like workshops and seminars
to alleviate and cope with stress.1
Limitations:
Similar studies should be done using larger
samples in different region including both
private and public schools
The accuracy of the research results should
be checked by other methods (interviews,
observations, etc.)
CONCLUSION
The factors always causing stress like job related

clarity, ability to cope with problems, inadequate
social support should be tackled by various
measures at the individual and institute level.
ACKNOWLEDGEMENT
Authors dually acknowledge the teachers,

Principal and the Director of a Public school in
rural western Maharashtra for their support and
participation in the study for the betterment of

teachers
REFERENCES
1. Mariya Aftab, Tahira Khatoon. Demographic

differences and occupational stress of
secondary school teachers. European
Scientific Journal.2012: 8(5):159-75
2. Olivier MAJ, Venter DJL. The extent and
causes of stress in Teachers in the George
region. South African Journal of Education.
2003;23(3) 186-92.
3. Surinder Kaur. Comparative Study of
Occupational Stress among Teachers of
Private and Government Schools in Relation
to their Age, Gender and Teaching
Experience.
International
Journal
of
Educational Planning & Administration.
2011;1(2):151-160
4. ETUC, UNICE/UEAPME and CEEP - the
Framework
Agreementon
work-related
stress.
8
October
2004.
www.etuc.org/IMG/pdf/Brochure_stress_EN
-3.
5. Marais JL. Faktore wat stress veroorsaak by
onderwysers in die Oranje-Vrystaat en
Kaapprovinsie. Suid Afrikaanse Tydskrif vir
Opvoedkunde. 1992:12: 305-09.
6. Hittner A. Teachers in distress: Perceptions
of stress and life satisfaction. Maryland:
Associated Press. 1981Incomplete reference
7. Liina Osila, Kirsti Nurmela. EWCO
comparative analytical report on Workrelated Stress. European Working Conditions
Survey, European Foundation for the
Improvement of Living and Working
Conditions,
on-line
database,
http://www.eurofound.europa.eu/ewco/surve
ys/index.htm
8. Constantinos M Kokkinos. Job stressors,
personality and burnout in primary school
teachers. British Journal of Educational
Psychology. 2007:77, 229243
9. Nbling M, Vomstein M, Haug A, Nbling
T, Adiwidjaja A. European-Wide Survey on
Teachers Work Related StressAssessment,
909
Rahul et al.,
Comparison and Evaluation of the Impact of

Psychosocial Hazards on Teachers at their
Workplace. FFAS:ETUCE Teacher pilot
study 2011,1-63
10. Lee R, Ashforth B. A meta-analytic
examination of the correlates of the three
dimensions of job burnout. Journal of
Applied Psychology .1996: 81,123-33.
11. Jarvis M. Teacher stress: a critical review of
recent findings and suggestionsfor future
research directions (2002). Teacher Support
Network, 14(1). Retrieved Nov.13, 2003
from
http
//www.google.com/
searc
:www.teachersupport.org.uk/index.
12. Olivier MAJ, Venter DJL. The extent and
causes of stress in Teachers in the George
region. South African Journal of Education.
2003;23(3) 186-192
13. Sveinsdottir H, Gunarsdottir H, Fridriksdottir
H. Self-Assessed Occupational Health and
Working Environmental of Female Nurses,
Cabin Crew and Teachers. Scandivian
Journal of Caring Science, 2007; 27:262-73.
14. Shankar J, Famuyiwa OO. Stress among
Factory Workers in a Developing Country.
Journal
of
Psychomotor
Research.
1991;35(2/3): 163-71.
910
Rahul et al.,
DOI:10.5958/j.2319-5886.2.4.146

&
Health Sciences
www.ijmrhs.com
th
Research article
A STUDY ON PREVALENCE OF GROUP B STREPTOCOCCI AS A COLONISER IN

WOMEN OF REPRODUCTIVE AGE GROUP
*Sobhana Surya Pradeep M 1, Vishnuvardhana Rao K 2
1
Assistant Professor, 2Associate Professor, Department of Microbiology, Dr.Pinnamaneni Siddhartha

Institute of Medical Sciences & Research Foundation Chinnaoutapalli, Gannavaram Mandal, Krishna
District, Andhra Pradesh, India
*Corresponding author email: pradeepmss7@gmail.com
ABSTRACT
The present study was undertaken to detect the presence of Group B streptococci (GBS) as a coloniser
among women of reproductive age group attending to outpatient clinic in Obstetrics and Gynaecology at
Dr.PSIMS &RF general hospital, Chinnaoutapalli. Methods: Two low vaginal swabs were collected
from 200 women in the age group of 15-45 years and the swabs were subjected to microscopy, culture,
Christie, Atkins and Munch-Peterson test (CAMP) and antibiotic susceptibility testing by Kirby-Bauer
disc diffusion method. Results: Of the total 400 vaginal swabs collected from 200 women 7 were found
to be colonized with Group B streptococci which were mostly susceptible to ceftriaxone and
erythromycin and all were resistant to penicillin except strain 1.Conclusion: Detection of colonization
with GBS and treatment helps in reducing the incidence of neonate acquiring GBS infection.
Keywords: Streptococci, colonization, CAMP test, neonatal meningitis, antibiotic sensitivity
INTRODUCTION
Women of reproductive age group are at risk of

acquiring urogenital infections. The microbes
present in the normal gastrointestinal flora are
the most common etiological agents. The
proximity between the anus and vagina facilitates
entry these microbes into urogenital tract.
Several bacteria are implicated as the common
agents causing urogenital infections among
women of reproductive age group especially
pregnant women.1 These organisms produce
urinary tract infections, bacteraemia and
endometritis and related complications such as
pre maturity and pre-term labour and even to

meningitis and pneumonia in the newborn with
high rate of mortality.1
Group B streptococcus (GBS) is a facultative
gram positive coccus known to be responsible for
bovine mastitis (1930s). It is non-pathogenic
commensal of human flora of female genital
tract. By 1970s group B streptococcus was
recognized as one of the leading causes of
neonatal mortality and morbidity. 2 It is estimated
to be responsible for neonatal infections with
case fatality ratio of 50% and at a frequency of 2-
Pradeep et al.,
911
3 per 1000 live births. 2 It is said to be the leading

cause of neonatal sepsis, meningitis and
pneumonia. Streptococcal colonization as a risk
factor for pre-term delivery is a subject of
conflicting opinions. 1 This bacterium is normally
found in vagina and rectum of 15% - 40% of all
healthy women of reproductive age group. Those
women who test positive for group B
streptococcus are said to be colonized. The vast
majority of group B streptococcal infections are
acquired during childbirth when a baby comes
into direct contact with bacteria which are carried
by mother as normal vaginal flora. 2As estimated
12000 infants in US will become infected with
group B streptococcus each year and will result
in deaths of an estimated 2000 infants yearly,
while leaving others with physical or mental
disabilities. Group B streptococcus usually
causes infant illness within first 7 days of life,
but late onset infections may occur up to 3
months of age. Performance of a caesarean
section will not eliminate the risk of infection. 3
That is why many western countries like USA,
Canada have made a national policy to screen
women of reproductive age group especially
pregnant women to detect group B streptococcus
vaginal colonization which was backed by CDC.
Few countries have also formed a national
protocol for prophylactic antibiotic treatment for
such women. Such national policies have brought
down rates of group B streptococcal infections in
reproductive age group women, pregnant women
and neonatal sepsis markedly.4 Group B
streptococcal infections are more common than
other illnesses for which pregnant women are
screened such as Rubella, Downs syndrome,
Spina bifida etc. Yet, group B streptococcus
remains generally unknown to public.
Geographical, ethnical, social, economic
conditions and rate of group B streptococcal
colonization has also been studied and also the
rate of acquisition of group B streptococci by
infants was related to the heaviness of vaginal
carriage in the mother during labour and total
acquisition rate was found to be ranging from 4%
to 48%.5 Further detailed research in this

direction would help in understanding
epidemiology of group B streptococcal
colonization.
Group B streptococcal vaginal colonization is
detected in the majority of post pubertal women.
Group B streptococcus has also been detected on
the external genitalia of men. With a degree of
colonization increasing among women of
reproductive age group there is increased
frequency of urinary tract infections. The degree
of colonization in pregnant women and rates of
neonatal sepsis are directly proportional. 6 In
women of reproductive age group it may cause
symptoms irrespective of the time of acquisition
(colonization). In pregnant women neonatal
transmission rate is less in early colonization.
But acquisition after 24 weeks of gestation, the
chances of neonatal transmission is more.
6,7
Though many western researchers have been
working on group B streptococcal colonization,
only few Indian studies are available on this
problem.
This attempt is made at DR.PSIMS & RF to find
out the incidence of group B streptococcus as a
colonizer among women of reproductive age
group.
Pradeep et al.,
MATERIALS & METHODS

Subjects: 200 women of reproductive age
attending to obstetrics and gynaecology OPD at
Dr. PSIMS and RF during the period of May
2009 to February 2011 were included in this
study.15-45 yrs of age (post-pubertal or
reproductive) group was taken as inclusion
criteria. 83 pregnant women and 117 in nonpregnant women were included in the present
study. Out of 83 pregnant women, 41 were third
trimester, 29 were in second trimester and
thirteen were in first trimester. Women having
any type of bleeding disorders like Dysfunctional
uterine bleeding (DUB) etc. were excluded.
912
METHODS
After taking informed consent from all the
participants; two vaginal swabs taken from all
subjects and the swabs were immediately
transported to the microbiology laboratory.
Direct Microscopy: One swab was used to
inoculate 5% sheep blood agar and then used for
wet mount and gram staining. Findings of
preliminary microscopic examination were
recorded. The other swab was used for
enrichment culture with Brain Heart Infusion
(BHI) broth with antibiotics (gentamicin-15
mcg/ml and Nalidixic acid-8 mcg/ml) which
after 24hrs incubation was inoculated on to 5%
sheep blood agar. 8
After overnight incubation the growth on plates
were read and suspected colonies on blood agar
were subjected to catalase test and Gram
staining. Gram positive and catalase negative
colonies were subjected to CAMP test and
confirmation was done by Latex agglutination
using latex suspension coated with anti-serum
(Bio-merieux).9 Plates which did not yield
growth of streptococci were further incubated for
24 hours, read and processed similarly for
suspected colonies. The enrichment broth was
subcultured and read and processed similarly.
Specimens yielding group B streptococcus either
on direct inoculation or on subculture of
enrichment medium were recorded as positive.
Antibiotic susceptibility of the isolated group B
streptococci was done by employing Kirby
Bauer disc diffusion method. 8
Fig 2: Antibiotic Sensitivity testing by KirbyBauer Disc diffusion technique

RESULTS
200 women in the reproductive age group were

included in the study. Out of the 200 women 83
(41.5%) women were pregnant and 117 (48.5%)
were nonpregnant women.
GBS was isolated from 7 women which indicate
an incidence of 3.5%. Out of the 7 women who
were positive for GBS, 3 were pregnant in the
age group of 23-24yrs and gestational age
between 20-37 weeks. The other four were non
pregnant and belonged to the age group of 30-35
yrs.
Antibiotic sensitivity testing was done for all the
isolated group B streptococci by Kirby Bauer
disc diffusion method (Himedia, P-SD028, ESD013, C-SD010) on 5% sheep blood agar plates
and the diameter of the clear zone around the
disc was measured under transmitted light with
measuring scale and results interpreted as
susceptible(S), intermediate (I), resistant(R) as
per the CLSI criteria.8
Fig 1: Christie, Atkins and Munch-Peterson test

(CAMP test)
913
Pradeep et al.,
Table 1: Standard zone size interpretation chart for the antibiotics tested against GBS 8, 10
Zone of inhibition (in mm)
Drug
Potency
Penicillin
10U
28
20-27
( )19
Erythromycin
15mcg
21
16-20
( ) 15
Ceftriaxone
30mcg
27
25-26
( )24
Sensitive
Intermediate
Resistant
Table 2: Antibiotic sensitivity patterns of group B streptococcal isolates (total no.7)

Strain No.
Penicillin
Erythromycin
Ceftriaxone
002
I(24)
R(14)
S(28)
003
I(25)
S(25)
S(28)
050
I(25)
S(25)
S(27)
055
I(25)
R(14)
R(24)
117
S(29)
S(22)
S(29)
131
I(27)
S(21)
S(28)
180
I(23)
S(22)
S(28)
*Figures in brackets indicate the zone of inhibition (in mm)
DISCUSSION
GBS is one of the common agents causing
urogenital infections among women of
reproductive age group especially pregnant
women and also is the leading cause of neonatal
infections in the western hemisphere. These
infections in turn lead to UTI, bacteremia,
endometritis in women of reproductive age group
and in pregnant women UTI, endometritis,
amnionitis, post-partum wound infections and
neonatal complications such as prematurity,
preterm labor GBS pneumonia and meningitis1.
The recognition that maternal colonization with
this organism is a key factor in the occurrence of
GBS infections associated with neonatal
mortality and morbidity was a milestone in the
history of perinatal health. In fact this awareness
has created a radical change in antenatal health
practice, but the spectrum of GBS disease
remains largely an under recognized problem.
The CDC advocated the prevention of GBS
infection in reproductive age group women,
especially in pregnancy by chemoprophylaxis in
women with culture evidence of recent rectal or
vaginal colonization. According to them even
women without a known GBS status but

delivering before 37 weeks of gestation with
PROM or intrapartum fever are also advised to
be given antimicrobial prophylaxis presumably
to prevent GBS infection. Even women who are
not pregnant and present with UTI, endometritis
should be screened for GBS colonization through
culture for evidence of rectal/vaginal swabs 3.
Very few Indian studies are available where an
attempt for detecting GBS colonization has been
done in women of reproductive age group. Even
the studies on pregnant women do not throw
light on the time of colonization, efficiency of
transmission and the incidence of neonatal
disease. The Indian studies available for review
have reported lower colonization and infection
rates in general. However on closer analysis
taking into consideration use of adequate culture
techniques and microbiological media some of
the GBS colonization rates reported from India
and other developing countries are similar to
those reported in the United States. In our study
out of 200 samples, 7 samples yielded the growth
of GBS which accounts for 3.5%.In the present
Pradeep et al.,
914
study, utmost care was taken for processing the

samples and standard guidelines were followed.
A further prospective study in this direction and
screening of newborn babies for GBS
colonization would help in knowing the
magnitude of GBS related problems. Our
statistics correlate with results of R Mhasker Rita
et al who have reported an incidence of 1.65%
vaginal colonization. 10 Kulkarni et al has
observed a low rate of GBS colonization
(2.52%). 11
El Kersh et al observed a rate of 2.6% GBS
vaginal colonization among 151 cases who were
negative for GBS colonization in earlier visits.
Findings of authors are correlating with that of
Mhaskar Rita et al 10 Kulkarni et al 11 and with
findings of El Kersh et al. 12
High rates of GBS colonization were detected
among Saudi women (25.7%). Similarly a very
high GBS colonization rate was identified by J
Motlova et al (29.3%) 13, Orett FA (32.9%) 14 in
their respective studies. Most of the studies
detected that GBS colonization occurred in
pregnant women more frequently during late
stages of pregnancy. These workers also opined
that early colonization of GBS has no
significance in prematurity or abortion. 13, 14
Orett FA 14 has observed a higher rate of
colonization among women of East Indian origin.
Most studies in India detected only 1.5%-2.5% of
GBS colonization among Indian women which
was correlated with the present study. But other
international
studies
revealed
vaginal
colonization rate as 21.7% and anorectal carriage
as 24.4 % 13.
In the present study author could not follow up
the positive cases, especially pregnant women to
detect whether neonatal transmission has
occurred or not. Based on the findings of the
present study and the findings of other Indian
reports it can be presumed that GBS related
problems in women of reproductive age group is
at a low rate in our country. However a
nationwide multicenter study is needed to
substantiate this finding. A nationwide screening
for GBS colonization in women of reproductive

age group, especially in pregnant women may
not be cost-effective and may not be necessary
keeping the low rates of reported colonization
rates which are confirmed.
However it is difficult to arrive at such a
conclusion based on very few studies available.
There is a need for government/non-government
organization funded projects to the screen,
especially all antenatal women for urogenital
pathogens, like Chlamydia, Mycoplasma, Urea
plasma etc. along with GBS. Screening of GBS
in 3rd trimester in pregnancy helps in detection of
colonization and also in preventing neonatal
diseases. Performance of Caesarian section will
not eliminate the risk of infection. So a national
policy to screen women of reproductive age
group especially pregnant women to detect for
GBS vaginal colonization and a protocol for
prophylactic antibiotic treatment should be
designed which would help to bring the rate of
GBS colonization and neonatal sepsis markedly.
Prophylactic immunization with Group B
streptococcal vaccines in prevention of
colonization in women of reproductive age group
and neonatal disease should be evaluated.
Pradeep et al.,
CONCLUSION
To conclude, there are very few studies in

literature which throw light on detecting GBS
colonization in women of reproductive age
group. In the present study, an attempt was made
to provide knowledge regarding prevalence of
GBS colonization in women of reproductive age
group which also included pregnant women.
Although this study was not interventional and
the positive cases were not followed, a further
study for screening of GBS colonization will be
helpful in preventing intra-partum, post- partum
and neonatal complications. Present study also
provides implications for giving prophylactic
antibiotics before caesarian sections which would
have a paramount contribution in preventing
neonatal meningitis.
915
REFERENCES
1. Maniatis AN, Palermos J, Kantzanou Ml.

Streptococcus
agalactiae:
A
vaginal
pathogen? J Med Microbial 1996; 44: 199202.
2. Gregary J locksmith, Penny Clark, Patrick
Duff. Maternal and neonatal infection rates
with three different protocols for prevention
of group B Streptococcal disease. Am J
Obstetrics Gynecology 1999; 180(2): 416422.
3. Anne Schuchat. Group B streptococcus.
Lancet 1999; 353: 51-55.
4. Sara Kenyon, Brocklehurst P, Blackburn A,
Taylor DJ. Antenatal screening and
intrapartum management of Group B
Streptococcus in the UK. BJOG 2004; 111:
226-230.
5. Ancona RJ, Ferrieri P, Williams PP. Maternal
factors that enhance the acquisition of Group
B Streptococci by newborn infants. Journal
of Medical Microbiology 1980; 13: 273-280.
6. Anitha Shet and Patricia Ferrieri. Neonatal
and maternal group B Streptococcal
infection: A comprehensive review. Indian J
Med Res 2004; 120: 141-150.
7. Regan JA, Klebanoff MA, Nugent RP,
Eschenbach DA, Blackwelder WC et al.
Colonization with Group B Streptococci in
pregnancy and adverse outcome. American
Journal of Obstetrics Gynecology 1996; 174:
1354-60.
8. Bailey and Scotts. Diagnostic microbiology,
11th ed. Andrew Allen, Mosby, Inc.2002;
167.
9. Anthony BF, Okada DM, Hobel CJ.
Epidemiology of group B Streptococcus:
Longitudinal observation during pregnancy.
Journal of infectious diseases 1978; 137:
524-530.
10. Mhaskar Rita, Sharad S, SriKanth N,

Swarnarekha B, Ranjani S. Selective risk
factor based screening of pregnant women
for group B Streptococcal colonization in a
teaching hospital in south India. Indian J
Obstetrics Gynecology 2005; 55(4): 336-38.
11. Kulkarni AA, Pawar SG, Dharmadhikari CA,
Kulkarini RD. Colonization of pregnant
women and their new born infants with group
B Streptococci. Indian Journal of Medical
Microbiology, 2001; 19(2): 1-4.
12. El-Kersh TA, Nuaim LA, Kharfy TA,
Shammary FJ, Saleh SS, Zamel FA et al.
Detection of genital colonization of group B
Streptococci during late pregnancy. Saudi
Med J 2002; 23(1): 56-61.
13. Motlova J, Strakova L, Urbaskova P,Sak P,
Server T. Vaginal and rectal carriage of
Streptococcus agalactiae in the Czech
Republic: Incidence, serotypes distribution
and susceptibility to antibiotics. Indian J Med
Res, 2004; 119: 84-87.
14. Orrett FA. Colonization with group B
Streptococci in pregnancy and outcome of
infected neonates in Trinidad. Pediatr Inf
2003; 45(3): 319-23.
916
Pradeep et al.,
DOI:10.5958/j.2319-5886.2.4.147

&
Health Sciences
Research article
Coden: IJMRHS
Copyright @2013
th
Revised: 18 Sep 2013
ISSN: 2319-5886
PREVENTIVE MEASURES NEEDED FOR LONG TERM USE OF CARBAMAZEPINE TO

LOWER THE RISK FOR CORONARY HEART DISEASE
*Paunipagar Prashant V 1, Babu Ramesh B2, Sharma Rahul P3
1
Professor and HOD, Department of Biochemistry, ESIC Medical College, Gulbarga, Karnataka, India
Associate Professor, Department of Psychiatry, Raichur Institute of Medical Sciences, Raichur
3
MBBS Student, Raichur Institute of Medical Sciences, Raichur, Karnataka, India
2
*Corresponding author email: drprashantesic@gmail.com

ABSTRACT
Present cross sectional study was carried out with a view to evaluate the Carbamazepine risk for
coronary heart disease. Lipid profile and Framingham point scores were studied in 60 Epilepsy patients
on Carbamazepine. The epileptic patients were compared with age and sex matched 60 healthy controls.
Framingham Point Scores were estimated by taking into consideration several parameters i.e. Age, Sex,
Systolic blood pressure, HDL levels, Total cholesterol, and smoking history, as per guidelines of the
Framingham Heart Study group We conclude that this drug significantly increases the risk for coronary
heart disease in patients with respect to lipid profile and other parameters as described by the
Framingham study group. Altogether, this drug may be one of the reasons for the high prevalence of
CHD, which is increasing day-by-day due to the globalization.
Keywords: Carbamazepine, Epilepsy, Lipid Profile, Coronary heart disease
INTRODUCTION
In Latin seizure means "to take possession of".

Seizure by definition is a paroxysmal event due
to abnormal, excessive, hyper synchronous
discharges from an aggregate of central nervous
system (CNS) neurons1. Epilepsy describes a
condition in which a person has recurrent
seizures due to a chronic, underlying process.
About 50 million people worldwide have
epilepsy, with almost 90% of these people being
in developing countries2. In India itself,
approximately 6 million people suffer from
Epilepsy.
Anticonvulsant
drugs
like
Carbamazepine are in use since 19623 for long

term antiepileptic therapy. This long term
treatment may be associated with various
metabolic abnormalities involving connective
tissues, endocrine system and liver.
Coronary Heart Disease is defined as
impairment of heart function due to inadequate
blood flow to the heart compared to its needs,
caused by obstructive changes in the coronary
circulation to the heart. Framingham heart study4
started during the 1950s has played a major role
in establishing the nature of CHD risk factors
917
Prashant V et al.,
and their relative importance. The major risk

factors of CHD are elevated serum cholesterol,
smoking, hypertension, and sedentary habits.
Previous studies by Framingham Heart Study
group have shown that alterations in serum lipids
predisposes to coronary heart disease4. Thus,
Influence of Carbamazepine on serum lipids has
been investigated many times leading to
contradictory reports5-9. Moreover, alterations in
lipid profile may vary in different populations
and not many studies have been done in Indian
scenario. Hence present study was carried out
with a view to determine the association between
long term use of Carbamazepine & changes in
Lipid/Cholesterol metabolism and also to find
the magnitude of risk for coronary heart disease
as an effect of alterations in Lipid/Cholesterol
metabolism by this drug, if any.
Study Design: Cross-sectional study.
Setting: Psychiatry OPD and Department of
Biochemistry of Raichur Institute of Medical
Sciences, Raichur (Karnataka)
Study Subjects: A total of 120 subjects aged
between 20 - 40 years were taken into study. 60
Epileptic patients who are exclusively on
Carbamazepine (in a dosage of 200 mg BD) were
compared with age and sex matched similar
number of Healthy Controls.
Only subjects classified as Epileptic as per ILAE
classification11 and those exclusively taking
Carbamazepine for epilepsy for a period of 6-12
months were included in the study. Whereas
subjects having co-morbid conditions like
hypertension, Diabetes, Tuberculosis, Obesity,

etc. were excluded from the study.
Before carrying forward the subject selection,
Institutional Ethics committee approval was
taken.
Diagnostic Criteria: Epilepsy: The subjects are
classified as per ILAE classification11,
Diagnosed by Psychiatry Department of Raichur
Institute of Medical Sciences, Raichur.
Estimation of Lipid Profile: Total cholesterol,
HDL-c and Triglycerides levels estimation done
using Randox kits by Daytona Randox fully
automated analyzer. LDL-c levels calculated as
per formula by Friedewald et al.10
Collection of Blood sample: 12 hour overnight
fasting blood sample in plain bulb is collected in
the morning from anticubital vein using 21 gauze
5ml disposable syringe using a tourniquet and
with all aseptic precaution.
Estimating the risk for coronary heart
disease: Framingham Point Scores were
estimated by taking into consideration several
parameters i.e. Age, Sex, Systolic blood pressure,
HDL levels, Total cholesterol, and smoking
history, as per guidelines from Framingham
Heart Study group4
Statistical Analysis: Data collected was
analyzed using student t-test and chi square test.
Values <0.05 were considered statistically
significant.
RESULTS
Estimation of Lipid profile in Epilepsy patients

on Carbamazepine and their Framingham score
and related risks are tabulated in following tables
Table 1: Lipid Profile in Epilepsy patients on Carbamazepine, compared with Controls
Parameter
HDL(mg/dl)
LDL(mg/dl)
TC/HDL
LDL/HDL
Framingham Risk %
Cases (n=60)
174.15 14.43
43.36 5.26
104.74 13.08
130.18 15.13
4.06 0.51
2.45 0.44
0.45 0.96
Controls (n=60)
164.27 13.19
45.65 6.03
94.52 15.09
120.45 10.76
3.67 0.57
2.12 0.51
0.27 0.76
P Value
<0.001
0.03
<0.001
<0.001
<0.001
<0.001
0.17
918
Prashant V et al.,
Table 2: Age & Sex wise Distribution of Epilepsy patients on Carbamazepine
Age (yr) Parameter
Male (n=15)
Female (n=24)
P Value
20-30
161.93 16.49
43.33 4.87
94.76 15.01
119.2 13.54
3.76 0.44
2.21 0.41
Male (n=9)
182.2211.78
45.89 5.08
109.27 13.35
135.33 23.50
4.02 0.58
2.41 0.47
178.29 11.52
42.83 4.94
108.5 10.60
134.79 12.52
4.20 0.45
2.56 0.40
Female (n=12)
175.089.83
42.58 6.45
106.33 8.99
130.83 5.63
4.18 0.55
2.55 0.46
0.003
0.759
0.005
0.001
0.005
0.013

HDL (mg/dl)
LDL (mg/dl)
TC/HDL
LDL/HDL
30-40
HDL (mg/dl)
LDL (mg/dl)
TC/HDL (%)
LDL/HDL (%)
Table 3: Framingham point scores depict the estimated 10-year % risk

heart disease in Epilepsy patients on Carbamazepine
10 year Males
% Risk
Total point Cases
scores
<1
<0
8
1
0-4
10
2
5-6
4
3
7
4
8
1
5
9
1
>6
>10
Total
24
(4)
0.199
0.205
0.579
0.588
0.535
0.524
for development of Coronary
Females
Controls
19
9
1
1
30
Total point
scores
<9
9-12
13-14
15
16
17
>18
Cases
Controls
36
36
30
30
Table 4: Age and Sex wise distribution of Framingham score in cases
Overall
20-30
Male
1.125 1.26
0.73 0.79
Female
0
0
p-Value
0.000225
0.003
30-40
1.77 1.64
0.011
Total cholesterol (TC), LDL and Triglycerides

level were elevated very significantly (p < 0.01)
in the cases, whereas significant (p < 0.05)
reduction in protective HDL levels were noted.
Further leading to significant elevation in TC:
HDL and LDL: HDL ratios. Overall increase in
framingham risk % is noted in the cases as

compared to controls.
In age group of 20-30 years, very significant (p <
0.01) elevation is noted in TC, LDL and
Triglycerides in Females when compared to
males of the same age group. However, changes
in levels of HDL are not in statistically
919
Prashant V et al.,
significant range. Overall, it leads to very

significant change in TC: HDL (p < 0.01), and
significant change in LDL: HDL ratios (p <
0.05).
However, in age group of 30-40 years, sex-wise
no significant changes noted in lipid profile
parameters. Very significant (p < 0.01) rise in 10
year % risk is noted in male cases. However,
when divided into subgroups of age 20-30 and
30-40 years, significant ( p < 0.05 ) elevation in
risk is observed in 30-40 years group with very
significant( p < 0.01) rise in the young age group
of 20-30 years is observed. Inspite of this
difference in significance values, the mean
increase in risk % is more in higher age group of
30-40 years.
In case of female study group, no significant
difference noted in two groups of cases and
controls,with all the females having < 1 % risk of
developing CHD in 10 year period.
Fig 1: 10 year Framingham % risk comparison in

Males
Fig 2: 10 year Framingham % risk comparison in
Females
DISCUSSION
The action of Carbamazepine and its metabolites

is now well understood with the advancement in
pharmacological field. Neurons are allowed to
communicate for long distance by the voltage
gated sodium channels which generate an action
potential. The sodium channels which opens with
generation of action potential are inactivated
essentially
by
closing
the
channels.
Carbamazepine acts by stabilizing the inactivated
state of sodium channels. Thus the neurons are
less excitable because very few channels are
available to open subsequently. GABA receptor
alpha 1, beta 2 and gamma 2 subunits are
potentiated with carbamazepine.12 The intake of
carbamazepine not only affects the neurons but
also other systems by inducing liver microsomal
enzymes leading to alteration in metabolism of
lipids, bile acids and bilirubin13
If Carbamazepine increases the risk of Coronary
Heart Disease, it might lead to increase in
patients burden which they are already having.
Hence, present study was carried out to evaluate
the safety or risk of these drugs. For this purpose,
we evaluated lipid profile in patients between age
group of 20-40 years, receiving Carbamazepine
for more than 6 months. From the study we
found, statistically highly significant increase in
Total
Cholesterol
(TC),
LDL-c,
and
Triglycerides (Tg) level. However, there was
also statistically significant fall in HDL-c levels,
leading to increase in atherogenic ratio (TC/HDL
and LDL/HDL ratio) in the study group. This can
attribute to increase in Total cholesterol to
increased levels of LDL and not because of the
HDL levels, as reported previously in many
reports5-8. This is consistent with the reports by
Zeilthoper S et al. (9) who also attributed
increased Total Cholesterol to increased LDL-c
levels.
10 year % risk for development of Coronary
heart disease by Framingham Point score reveals
a score in Epilepsy patients on Carbamazepine to
be less than 2% in the majority of the patients
920
Prashant V et al.,
(58 of 60), which reveals the safety of this drug;

if other modifiable factors are in control like
smoking habits, blood pressure.
CONCLUSION
Assessing and stratifying the risk for CHD, entire

constellation of factors needs to be considered,
not only just lipid profile. As Carbamazepine
used in the treatment of Epilepsy is significantly
raising Total cholesterol, LDL and Triglycerides
level, routine lipid profile estimation is required
in these patients. Moreover, due to various other
predisposing factors for the risk of CHD and a
significant increase in atherogenic ratios,
periodic Lipid Profile estimation should be
mandatory in the cases with presence of other
risk factors like hypertension and smoking
history, particularly in males. Other measures
like the addition of Lithium Carbonate and
Vitamin E 14 can be suggested in the treatment
regimens to decrease the Carbamazepine dosage
and hence its atherogenic effects and better
outcome for the patient, as the prevalence of
CHD is increasing day-by-day due to increased
Globalization.
REFERENCES
1. Lowenstein DH. Seizures and epilepsy. In:

Kasper DL, Fansi AS, Lango DL, Jameson
LJ, Braunwald E, Hauser SL, editors.
Harrisons Principles of Internal Medicine.
16th edn. (Vol II). United States of America:
McGraw Hill Companies; 2005.p.2357.
2. WHO Factsheets Epilepsy-1st Sept, 2010
http://www.who.int/mediacentre/factsheets/fs
999/en/
3. Murali MS. Epidemiological Study of
Prevalence of Mental Disorders in India.
Indian Journal of Community Medicine
2001; 26 (4): 10-12
4. Framingham Heart Study; a project of
National Heart, Lung and Blood Institute and
Boston University. Last updated: June
29,2010
http://www.framinghamheartstudy.org/
5. Nakken KO, Kornstad S. Do Males 30-50
Years of Age with Chronic Epilepsy and on
Long-Term Anticonvulsant Medication Have
Lower-Than-Expected Risk of Developing
Coronary Heart Disease?, Epilepsia. 1998;
39(3):326-330,
6. Aggarwal A, Kumar M, Faridi MMA. Effect
of Carbamazepine on Serum Lipids and Liver
Function Tests; Indian Pediatrics, 2005;
42:913-918.
7. Nikolaos T, Stylianos G, Chryssoula N, Irini
P,Christos M, Dimitrios T, et al. The effect of
long-term antiepileptic treatment on serum
cholesterol (TC, HDL, LDL) and triglyceride
levels in adult epileptic patients on
monotherepy. Med Sci Monit 2004; 10: 5052.
8. Mintzer S, Skidmore CT, Abidin CJ, Morales
MC, Chervoneva I, Capuzzi DM, Sperling
MR. Effects of antiepileptic drugs on lipids,
homocysteine, and C-reactive protein. Annals
of Neurology. 2009;65: 44856.
9. Zeilthoper S, Doppelbauer A, Tribl G, Leitha
T, Deecke L. Changes in serum lipid pattern
during long term anticonvulsant treatment.
Clin Invest 1993; 71: 574-78.
10. Friedwald WT, Levy RI, Frederickson DS.
Estimation of the concentration of LDL-c in
plasma without use of the preparative
ultracentrifuge. Clin Chem, 1972; 18: 49902.
11. ILAEs 1989 International Classification of
Epilepsies and Epileptic Syndromes,f rom
(1989). Proposal for revised classification of
epilepsies
and
epileptic
syndromes.
Commission
on
Classification
and
Terminology of the International League
Against Epilepsy. Epilepsia.1989;30(4); 38999
12. Granger P, Bilton B, Faure C, Vige X,
Depoortere H, Graham D. et al. Modulation
of the gamma-aminobutyric acid type A
921
Prashant V et al.,
receptor by the antiepileptic drugs

carbamazepine
and
phenytoin.
Mol.
Pharmacol. 1995; 47(6): 118996.
13. Havel RJ, Kane JP. Structure and metabolism
of plasma lipoproteins. In: Secriver CR,
Beaudet AL, Sly WS, Valle D (eds). The
Metabolic and Molecular Basis of Inherited
Disease, 7th edn, vol II. New York, McGrawHill, 1995; pp 1841-51.
14. Megrabian AA, Mkhitarian VG, Amadian
MG, Badalian GE, Avakian SL. Use of
lithium carbonate and vitamin E in the
complex treatment of epileptics. Zh
Nevropatol
Psikhiatr
Im
S
S
Korsakova. 1986; 86(9):1407-10.
922
Prashant V et al.,
DOI:10.5958/j.2319-5886.2.4.148

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
SCREENING OF ANTIBIOTIC RESISTANT GRAM NEGATIVE BACTERIA AND PLASMID

PROFILING OF MULTI-DRUG RESISTANT ISOLATES PRESENT IN SEWAGE
ASSOCIATED WITH HEALTH CARE CENTERS
Khan Md. Anik Ashfaq, Sutradhar Pijush, Islam Mohammad Majharul, Ojha Ravi Kant, Biswas Gokul
Chandra*
Department of Genetic Engineering and Biotechnology, Shahjalal University of Science and
Technology, Sylhet-3114, Bangladesh
*Corresponding author e-mail: gcbiswas1985@gmail.com
ABSTRACT
Background: Healthcare effluent acts as the store house of harmful infectious agents such as the
pathogens and microorganisms possessing multiple drug resistant genes. Potential health risk includes
spreading of diseases by these pathogens and wide dissemination of antimicrobial resistance genes.
Gram-negative bacteria are particularly important for causing most of the hospital and community
acquired infections. Aim: This study was carried out to highlight the incidence of antibiotic resistant
bacteria in hospital generated effluent discharged into municipal sewage system of Sylhet city,
Bangladesh. Methodology: Standard biochemical tests were used to isolate and identify 29 gram
negative bacteria from 6 effluent samples. Antibiotic susceptibility test was assessed by Kirby-Bauer
disc diffusion method. Plasmid isolation and gel electrophoresis were performed using standard
protocols. Results: Antibiogram study showed that the percentage of isolates resistant to amoxicillin,
ceftriaxone, ciprofloxacin, gentamicin, imipenem, azithromycin, andsulphamethoxazole-trimethoprim
were 93.10%, 55.17%, 27.6%, 24.14%, 20.7%, 13.8% and 10.34% respectively. Ten of the isolates
showed resistance to three or more commonly used antibiotics. Plasmid profiles of the multi-drug
resistant isolates showed to harbor two or more plasmids and almost all of them showed a common band
for plasmid DNA size of 24.5kb. Conclusion: Resistance to the bacterial pathogens causing community
acquired infections may, thus, exert a serious public health threat through confining the antibiotic pool.
Hospitals should follow, monitor and regulate proper sanitary measures of hospital generated effluents
to forestall the dissemination of multi drug resistant bacteria transfer from hospital waste to the
environment.
Keywords: multi-drug resistance, hospital effluents, antibiogram, plasmid profiling.
INTRODUCTION
Waste effluent from hospitals and clinics contain

high numbers of resistant bacterial strains and
residual antibiotics at a concentration to which
susceptible bacterial growth is inhibited.1 One

study by Schwartz et. al.,2 has evaluated the
microbiological content of hospital and
Khan et al.,
923
household waste quantitatively and qualitatively

and found that general hospital waste contains
bacteria with pathogenic potentials for humans
compared to household waste.2 Grabow and
Prozesky3 showed that two mechanisms,
introduction and selection for resistant bacteria
results in increased number of resistant bacteria
in the sewers where hospital effluents are
immediately discharged3. Excretion mechanism
is responsible for the addition of a significant
amount of un-metabolized antibiotics.4 Longterm exposure of microorganisms to low
concentrations of antibiotics in wastewater and
surface water has the potential for the
development of antibiotic resistance, which was
reported by Smith et. al.,5 If the hospital effluents
are not treated, concentrated forms of infectious
agents and antibiotic resistant microbes are shed
into communities resulting in water borne
diseases such as cholera, typhoid fever,
dysentery and gastroenteritis.6 Grabow and
Prozesky stated that, although, sewage treatment
reduces the number of bacteria in wastewater but
the effluent generally contains a large number of
both resistant and susceptible bacteria3.
The basic principle of underlying wastewater
management is the strict limit on the discharge of
hazardous liquids into sewers without prior
treatment so that living pathogenic organisms are
not introduced into the environment.7 In
Bangladesh, at present no government rule is
prevailing for regulating the hospital waste
management. No institutional mechanism is
working on the government side specially for
handling this kind of waste, which was reported
by Prism Bangladesh.8 Also, unfortunately,
there is no structured form of medical waste
treatment in Bangladesh, and most wastes are
dumped in open areas for natural degradation or
re-sold by scavengers9, although, hospitals
usually maintain local measures (e.g.,
incineration, chemical sterilization etc.) of waste
treatment before disposal. The sewerage network
of Sylhet city consists of many small drains
connected with some natural hilly channels,

which fall into the Surma River.10 Therefore,
even if the hospitals are discharging their health
care liquid waste into the sewerage system, it
mixes with the sewage and gets in surface water
without proper treatment.
Haque (1994) reported that some 5.2 million
people (including 4 million children) die each
year
from
waste-related
diseases
in
11
Bangladesh.
Therefore, untreated hospital
liquid waste discharges into surface water
directly or indirectly have been causing
additional problems. Gram-negative bacteria are
crucial in this aspect because they are the most
common causes of hospital and community
acquired infections and they are inherently
resistant to many hydrophobic antibiotics.12-15 In
such scenario, this study was carried out to
screen the antibiotic susceptibility pattern of
gram-negative bacterial isolates from healthcare
liquid waste generated in Sylhet metropolitan
area of Bangladesh and investigate on their role
in developing antibiotic resistance.
Khan et al.,
Sample collection, isolation and identification

of bacteria: A total of six sewage samples
associated with hospital and clinical effluents
were collected from six different spots in the
Sylhet Metropolitan area, where hospitals
effluents are immediately discharged. Sample
from each site was collected in 150 ml sterile
containers and transported to the laboratory
within an hour of collection in cold conditions.
100 ml diluted samples were spread over
MacConkey agar media that inhibits the growth
of gram positive bacteria and incubated for 24
hours at 37C. Differentiation as lactose
fermenter and non-lactose fermenter could be
made on Mackonkey agar for the isolates based
on pigmentation.16 Five colonies from each plate
were selected with different colony morphologies
by using five-colony method and further purified
twice.17 A total of twenty nine isolates thus
924
obtained were identified on the basis of

morphological characteristics, gram staining and
biochemical tests according to Bergeys Manual
of Determinative Bacteriology.18 Other media
used in this study include Eosine Methylene Blue
Agar (EMB), Salmonella Shigella (SS) Agar and
Thiosulfate Citrate Bile Salts (TCBS) agar.
Antibiotic sensitivity test: Antimicrobial
susceptibility testing of all 29 bacterial isolates
was performed following the modified KirbyBauer disk diffusion method on Muller-Hinton
against selected antibiotics namely Amoxicillin
(AMX) 10g, Ceftriaxone (CTR) 30g,
Azithromycin (AZM) 15g, Gentamycin (CN)
10g, Imipenem (IPM) 10g, Ciprofloxacin
(CIP) 5g and Sulphamethoxazole-Trimethoprim
(SXT) 10 g. Klebsiella ATCC and
Pseudomonas ATCC were the only standard
controls used to screen antibiotic resistance of
Klebsiella sp. and Pseudomonas sp. isolates
respectively. Inhibition zone size was interpreted
using standard recommendation of the National
Committee for Clinical Laboratory Standards19
now known as the Clinical Laboratory Standard
Institute (supplementary data: Table 1).
Plasmid analysis: The present study emphasized
on investigation on the correspondence between
antibiogram and plasmid profile of the multiple
drug resistant (MDR) isolates. Therefore,
plasmid DNA of MDR isolates was extracted
from cultured cells following alkaline lysis
method of plasmid preparation.20 The samples
were processed using gel electrophoresis to
identify the number of plasmid copies present in
different isolates. Agarose gel electrophoresis
was carried out in a horizontal gel apparatus (My
Run Cosmo bio co. ltd, IMR-201). After
electrophoresing of all the plasmids in 0.7%
agarose (Merck, Mumbai), the gel stained with
ethidium bromide were visualized by Ultraviolet
Transilluminator (UVP, High Performance
transilluminater; USA)and photographed by
Samsung camera. The number and molecular
sizes of the plasmid DNA were determined on

the basis of mobility through agarose gel and was
compared with the mobility of Supermix DNA
Ladder, (Genei Pvt. Ltd., Bangalore, India)
which was used to estimate the plasmid size.
Khan et al.,
RESULTS
In the present study, we collected effluent

samples from hospitals and clinics which were
immediately released into the corresponding
municipal sewerage. As gram negative bacteria
are the most common causes of hospital and
community acquired infections15, an effort was
given to isolate and identify gram negative
probable pathogens. Of the 29 isolates, eight
(27.58%) were found to be of Pseudomonassp.,
followed by seven (24.14%) of Escherichia coli,
six (20.69%) of Klebsiella sp., three (10.74%) of
Shigella sp., two (6.90%) each of Yersinia sp.
and Vibrio sp., and one (3.49%) of Serratia sp.
respectively.
Antibiogram study of the 29 isolates
(supplementary data: Table 2, 3, 4) showed that
the percentage of isolates resistant to amoxicillin,
ceftriaxone,
ciprofloxacin,
gentamicin,
imipenem, azithromycin and sulphamethoxazoletrimethoprim were 93.10%, 55.17%, 27.6%,
24.14%, 20.7%, 13.8% and 10.34% respectively.
Highest rates of sensitivity pattern were found to
imipenem (68.96%), followed by SXT (65.52%),
ciprofloxacin (62.06%) and azithromycin
(62.06%) (Fig. 2). Among the predominant
isolates (Pseudomonas sp., E. coli, and
Klebsiella sp.), The highest percentage of
resistance to ciprofloxacin and azithromycin was
shown by E. coli isolates (42.86%) whereas
66.66% of Klebsiella sp. showed resistance to
ceftriaxone and gentamycin which was highest
(supplementary data: Table 2). All of the isolates
of Pseudomonas and Klebsiella sp. expressed
resistance pattern to amoxicillin whereas in case
of E. coli it was 85.71%.
925
(A)
(B)
Fig. 1: Antibiogram of two of the isolates- (A) Klebsiella sp. and (B) Pseudomonas sp.
Although, imipenem showed highest sensitivity
pattern to the isolates, both of the two Yersinia
sp. expressed resistance to this antibiotic.
Bacterial isolates resistant to three or more of the
antimicrobial agents tested, hence multi-drug

resistant (MDR) were found to be 10 in number
(34.48%) out of 29.
100
90
% of Susceptibility
80
70
Resistant
60
50
40
Moderately
sensitive
30
Sensitive
20
10
0
CTR
AZM
GEN
IPM
CIP
SXT
AMX
Antibiotics
Fig. 2: Comparative antibiogram study of twenty nine isolated bacteria.
Plasmid profiling of ten isolates showed that
eight of the isolates show plasmid DNA of
varying sizes (1.5 kb to 24.5 kb) (Fig. 3and
Table 1). One of the isolates possessed single
band of plasmid while others had more than one
with different sizes as shown in the table. On the
other hand, only two isolates have no plasmid
even though they were resistant to antibiotics.
Almost all of the isolates that showed presence

of plasmid contained common plasmid DNA size
of 24.5kb. Earlier, antibiogram of MDR bacterial
isolates showed that all isolates were resistant to
amoxicillin. Four of the isolates were resistant to
ciprofloxacin and three of them (P-1-3, K-1-2
and K-6-4) harbored a plasmid each of size
around 2kb.
926
Khan et al.,
Fig. 3: Agarose gel eletrophoresis of plasmid DNA from ten MDR isolates.
*L= Ladder DNA, P-A=Pseudomonas ATCC, K-A= Klebsiella ATCC
Table: 1. Plasmid profiling and correlation with antibiogram.
Isolates
Antibiotics resistance No. of
pattern
bands
*P-4-5
AMX, CTR, SXT
0
P-1-3
AMX, CTR, CIP, 4
SXT
E-1-4
AMX, CTR, AZM
0
E-3-1
AMX, CTR, CIP
2
S-6-2
AMX, CTR, IPM
1
Y-4-4
AMX, CTR, IPM, CN 2
||
K-1-2
AMX, CTR, CIP, CN 2
K-3-2
AMX, SXT, CN
2
K-2-2
AMX, CTR, CN
2
K-6-4
AMX, CTR, CIP
2
ATCC-Pseudomonas AMX
0
ATCC- Klebsiella
AMX
0
Band size (kilo base pair)

7kb, 4.2kb, 2.4kb, 1.7kb
24.5kb,7kb
24.5kb
24.5kb, 14.5kb
24.5kb, 2kb
24.5kb, 2.8kb
24.5kb, 9kb
24.5kb, 2kb
-
*P=Pseudomonas sp., E= E. coli, S=Shigella sp., Y=Yersinia sp., || K=Klebsiella sp.

DISCUSSION
Both lactose fermenting and non-lactose

fermenting bacteria were isolated and identified
in which most predominant was Pseudomonas
sp. with 27.58%, followed by Escherichia coli24.14%, and Klebsiella sp.- 20.69%. One of the
hospital effluent studies carried out in India
involved isolation of gram negative bacilli, in
which E. coli (37.19%) was predominant
organisms, which is contrasted to this study
whereas percentages of Pseudomonas Sp.

(22.31%) and Klebsiella sp. (19.83%) were fairly
consistent. The study carried out in India showed
higher percentage of resistant isolates from
hospitals to ciprofloxacin (42.97%) and
gentamicin (27.27%) whereas the less percentage
of isolates was found to show resistance to
imipenem (16.66%).21 In contrast to this, less
percentage of isolates showed resistance to
Khan et al.,
927
ciprofloxacin (27.6%) whereas almost same

pattern of resistance was found in the present
study in case of gentamycin (24.14%).
Amoxicillin was the antibiotic to which highest
number of resistant bacteria (93.1%) was found,
followed by ceftriaxone (55.17%). Discharge of
antibiotic residues from hospitals and households
usage into effluent and municipal sewage
provides an indication of a selection pressure on
bacteria.22 Islam et al (2008) carried out a similar
type of study in Bangladesh and found that the
resistance development was directly related to
the use of antibiotics.23 It can be assumed that
isolated organisms in this study have been
persistently exposed to the antibiotic residues
and as a result, they might have developed
resistance mechanisms to them. Walton (1988)
pointed out that hospital environment appears to
be the origin of MDR bacterial strains and the
selective pressure responsible for expanding such
bacterial populations in hospitals must have been
through the use of drugs in humans and
veterinary and agricultural uses are not
responsible.24 Therefore, the results suggest that
the MDR bacteria containing multi drug resistant
genes present in the hospital effluent of this
particular locality may act as a possible source of
transfer of these resistant genes to the bacterial
population.
Plasmid profiling of two of the MDR isolates did
not show up any visible band. Possibly, some
resistant genes were not located on plasmid and
perhaps exist on the bacterial chromosome as it
is known that genetic origin of drug resistance
may be plasmid or chromosomal.25 Beta-lactams
are particularly important because they are the
most prevalently used antibiotics all over the
world, and because clinical crisis resulted due to
resistance to this antibiotic.26 -lactamases,
including
extended-spectrum
-lactamases
(ESBLs), AmpC -lactamases (AmpC) and
metallo--lactamases (MBLs) genes that are
responsible for prevalent emergence of antibiotic
resistance in gram-negative bacteria are most
often carried on plasmid, thus, facilitate rapid

spread between microorganisms.27 Being the
types of beta-lactam, this may be attributed to the
widely dissemination of amoxicillin, ceftriaxone
and imipenem resistant genes, because a
significant percentage of bacterial isolates tend to
show resistance to antibiotics in the present
study. It is suggested to carry out further research
including plasmid curing and transformation in
order to examine plasmid-mediated mode of
resistance to the antibiotics used in this study.
As this study was performed over limited number
of samples and isolates, studies in broad manner
are needed to fully understand the extent to
which hospitals and clinics in big cities of
Bangladesh contribute to resistance properties of
bacterial strains. In addition, the samples were
collected from the spots where the effluents
immediately discharged into municipal sewage,
with a view to isolating those bacteria which
have a better chance to come from effluents or
persist to effluent materials i.e., antibiotic
residues. In this circumstance, some other
bacterial strains that have attained resistant
properties from other sources other than hospital
effluents may be mixed. Despite the possibility
of this rare pitfall, the present observations
suggest that hospital effluents may contribute to
health hazard by adding MDR bacteria to city
sewage of this particular locality, which
ultimately falls into river.
Khan et al.,
CONCLUSION
The present study was carried out on a

preliminary basis, in order to investigate on the
development of antibiotic resistance and their
possible mode of dissemination. Finally, it can be
concluded that the isolated strains were showing
resistance mechanisms against various antibiotics
especially to beta lactams and these drug
resistant strains may cause to induce health
hazard. Hence, solution to the problem of MDR
bacteria in healthcare liquid waste is crucial.
Good safety sterilization methods should be
928
implemented before releasing of waste materials

to the environment or sewage. Proper regulation
and monitoring of an integrated health care liquid
waste management practice is essential in order
to diminish the risk of disseminating multiple
drug resistant microorganisms for the safeguard
of public health.
ACKNOWLEDGEMENTS
This research work was carried out both in the
former USDA laboratory and in the
Microbiology, Fermentation and Environmental
Biotechnology laboratory of the Department of
Genetic Engineering and Biotechnology,
Shahjalal University of Science and Technology,
Sylhet. We want to thank the personnel of both
laboratories for their support and technical help.
REFERENCES
1. Asha P, Jyothis M, Shini Z. Antibiotic

resistant Enterococci from driniking water
sources. Asian Journal of Pharmaceutical and
clinical research. 2012; 5(3):158-60.
2. Schwartz T, Kohnen W, Jansen B, Obst U.
Detection of antibiotic-resistant bacteria and
their resistance genes in wastewater, surface
water and drinking water bio films. FEMS
Microbiol Ecol. 2003; 43(3):325-35.
3. Grabow WO, Prozesky OW. Drug resistance
of coliform bacteria in hospital and city
sewage.Antimicrob Agents Chemother. 1973;
3(2):175-80.
4. Saini S, Das BK, Kapil A, Nagarajan SS,
Sarma RK. The study of bacterial flora of
different types in hospital waste, evaluation
of waste treatment at AIIMS Hospital, New
Delhi.Southeast Asian J Trop Med Public
Health. 2004; 35(4):986-9.
5. Smith KE,Besser JM, Hedberg CW, Leano
FT, Bender JB, Wicklund JH et al.
Quinolone-resistant Campylobacter jejuni
infections in Minnesota, 1992-1998. The
New England Journal of Medicine.1999;
340:1525-32.
6. Sharma DR, Pradhan B, Mishra SK. Multiple

drug resistance in bacteria isolates from
liquid wastes generated in central hospitals of
Nepal. Kathmandu University Medical
Journal. 2010; 8(29):40-4.
7. WHO [homepage on the internet]. Geneva:
World Health Organization [cited on July
2008]. Healthcare Waste Management
Manual. [http://www.who.int/topics/medical_
waste/en/]
8. A booklet HaspitalBorjo Babosthapona
Nirdeshika (Directives for Hospital Waste
Management) Prism Bangladesh, 1stEdn;
2005. p29.
9. Akter N,Acott RE, Chowdhury SA. Medical
waste disposal at BRAC health centres, an
environmental study. BRAC Research,
Research and Evaluation Division, 75
Mohakhali C/A, Dhaka 1212, 1998.
10. Alam R, Nath SK, Siddique MSM. A study
on municipal wastewater characteristics
monitoring of Sylhet city. An undergraduate
thesis, Department of Civil & Environmental
Engineering, Shahjalal University of Science
and Technology, Sylhet, 2002.
11. Haque. Waste Landfill and Hospital Waste
Incineration.Roteb-Solid Waste Consultency,
Kleinpolderplein 5, P.O.Box 10902- 3004.
Rotterdam, The Netherlands, 1994.
12. Hancock RE. Alterations in outer membrane
permeability.Annu Rev Microbiol.1984;
38:23764.
13. Nikaido H. Molecular basis of bacterial outer
membrane
permeability
revisited.
MicrobiolMolBiol Rev 2003; 67(4):593-656.
14. Vaara M. Agents that increase the
permeability of the outer membrane.
Microbiol Rev. 1992; 56(3):395411.
15. BastopcuA, Yazgi H, UyanikM H, Ayyildiz
A. Evaluation of quinolone resistance in
Gram negative bacilli isolated from
community and hospital acquired infections.
The Eurasian Journal of Medicine.2008;
40:58-61.
929
Khan et al.,
16. Levy SB, Marshall B, Schluederberq S,

Rowse D, Davis J. High frequency of
antimicrobial resistance in human fecal flora.
AntimicrobAgents
Chemother.
1988;
32(12):18016.
17. Osterblad M, Leistvuo T, Huovinen P.
Screening for antimicrobial resistance in
fecal samples by the replica plating method. J
ClinMicrobiol. 1995; 33(12):31469.
18. Holt JG, Krieg NR, Sneath PHA, Staley JT,
Williams ST. Group 11: Oxygenic
phototrophic bacteria. In: Hensyl WR (eds.),
Bergeys
Manual
of
Determinative
Bacteriology, 9th Edn., Williams & Wilkins,
Baltimore, 1994; pp. 377425.
19. National committee for clinical laboratory
stands. Methods for dilution aerobically
NCCLS Approved standard M7-A5 and
informational
supplement
M-100-S19
Wayne, PA USA, 2000.
20. Sambrook J, Russel D W 2001.Molecular
Cloning, 3rd Edn. 3 vol. Cold Spring Harbor
Laboratory Press, New York
21. Usha K, Kumar E, SaiGopalDvr. Occurrence
of various beta-lactamase producing gram
negative bacilli in the hospital effluent. Asian
J Pharm Clin Res. 2013; 6(3):42-46.
22. Kummerer K, Henninger A. Promoting
resistance by the emission of antibiotics from
hospitals and households into effluent.
ClinMicrobiol Infect. 2003; 9(12):1203-14.
23. Islam MJ, Uddin MS, Hakim MA, Das KK
and Hasan MN. Role of Untreated Liquid
Hospital Waste to the Development of
Antibiotic Resistant Bacteria. Journal of
Innovation and Development Strategy. 2008;
2(2):17-21.
24. Walton JR. The Veterinary Record.1988;
122:249-51.
25. Oktem IM, Gulay Z, Bicmen M and Gur D.
HITIT project study group qnrA prevalence
in extended spectrum beta-lactamase-positive
enterobacteriaceae isolates from Turkey. Jap
J Infect Dis.2008; 61:13-17.
26. Jean SS, Teng LJ, Hsueh PR, Ho SW, Luh

KT. Antimicrobial susceptibilities among
clinical isolates of extended-spectrum
cephalosporin-resistant
Gram-negative
bacteria in a Taiwanese University Hospital.
J AntimicrobChemother.2002; 49:69-76.
27. Gupta, V. An update on newer betalactamases. Indian J Med Res. 2007;
126(5):417-27.
Khan et al.,
930
DOI:10.5958/j.2319-5886.2.4.149

&
Health Sciences
Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
AN EVALUATION OF ORAL HEALTH IN ADOLESCENTS OF AHMEDABAD CITY

Parekh Paras A1, *Shah Ankita P2
1
2
Post Graduate student, Department of Physiology, B.J.Medical College, Ahmedabad, Gujarat, India.
Former Graduate student, Govt. Dental College & Hospital, Ahmedabad, Gujarat, India
*Corresponding Author email: ankita_shah1313@yahoo.com

ABSTRACT
Context: The present study evaluated oral hygiene & anomalies of tooth formation and eruption in
adolescents. This was a cross-sectional study, with the primary data was collected from two different
schools in Ahmedabad, Gujarat, India. Aims: Aim of the study was to evaluate oral health that includes
maintenance of oral hygiene and dental anomalies in adolescents of Ahmedabad city. Methods and
Material: In this study, total 500 healthy male and female subjects between 14-16 years of age were
selected for the study and examined for the oral hygiene in the form of cleaning of teeth after all meal,
flossing and regular visit to dentist for check-up. Also they were observed for dental anomalies which
were divided into three types viz. dentitional, occlusal and space anomalies. Comparison of outcome
parameters was calculated with significance test. Results: Awareness of oral hygiene was found
improper in more than half of all adolescents. Occlusal anomalies were found in 48.8% of males &
50.8% of females which were most common among all anomalies. Though all anomalies were more
prevalent in female than male subjects, dentitional anomalies were significantly more in female subject.
Conclusions: Awareness for oral hygiene in adolescent of Ahmedabad city is found to be less. Females
are even less aware than male. Malocclusion is the most common anomaly. All anomalies are more
common in females.
Keywords: Oral hygiene, Anomaly, Mal-occlusion
INTRODUCTION
Oral hygiene is the practice of keeping the mouth

clean and healthy by brushing and flossing to
prevent the build-up of plaque, the sticky film of
bacteria and food that forms on the teeth. Plaque
adheres to the crevices and fissures of the teeth
and generates acids that, when not removed on a
regular basis, slowly eat away, or decay, the
protective enamel surface of the teeth, causing
holes (cavities) to form.1,2 The primary and
permanent dentitions are subject to considerable
Ankita etal.,
variations in the number, size and form of teeth

and the structure of the dental tissue. These
developmental anomalies may be genetically
determined or brought about by environmentally
induced systemic or local changes or possibly by
combination of these factors. One of the
etiological factor of malocclusion is the dental
anomalies.3,4 Malocclusion is classified into three
main groups (1) Dentitional anomalies anomalies restricted to individual teeth
931
(2) Occlusion anomalies - anomalies in the

positional relationship between the dental arches,
and (3) Space anomalies.5,6 The present study
was planned out to assess oral hygiene and the
anomalies of tooth formation and eruption in
males and female of age group of 14-16 years
and to compare these anomalies in both sexes.
SUBJECTS AND METHODS
This study was carried out in two different

schools in Ahmedabad City in India.
All procedures followed were in accordance with
the ethical standards of experimentation and with
the Helsinki Declaration of 1975, as revised in
2000.7 Selection of study participant was done
randomly. Prior permission from the authority of
each school was obtained. Total number of 250
boys and 250 girls between 14 to 16 years of age.
Inclusion criteria: In whom permanent teeth
except third molar tooth be fully erupted and are
not undergone orthodontic appliance therapy,
irrespective of simultaneous extractions were
selected for dental examination. Written consent
was obtained and data collection forms were
distributed.
Then personal and family history that includes
frequency of brush and floss in a day, frequency
of visit to dentist for regular dental check-up etc.
was recorded. The boys and girls were examined
in the premises of the school during health camp.
Intra-Oral Examination:
Soft tissue: The condition of oral mucosa is
good indicator of general health. Examination of
mucosa of palate, tongue and cheeks for
inflammation, any swelling, white or red patches,
ulcers etc was done.
Periodontal tissue: Examination of periodontal
pocketing, oral hygiene, tooth mobility was done.
Teeth: The teeth present were counted and

recorded in full dental charting. The
supernumerary or missing teeth were looked for.
If any missing or supernumerary tooth was found
its location was noted. After counting teeth, oral
cavity was observed crowded teeth and their
location was noted. Oral cavity was searched for
the spacing of teeth, and if present, it was noted
whether they were in upper or lower arch. The
size and shape of the crown of teeth were
inspected. Tooth size was diagnosed as
anomalous when the norms for the sex and racial
group concerned were exceeded. The teeth were
inspected for discoloration, after taking the
history and grouped under intrinsic/extrinsic
discoloration.
Occlusion8: Inspecting the distance between the
upper and Lower incisors in the horizontal plane
identified the over jet. The Maxillary or
mandible over jet and distal medial molar
occlusions were looked for. The overbite was
identified inspecting vertical overlap of the upper
and lower incisors when viewed interiorly, The
overbite which was greater than one half was
described as being increased, and was noted as
overbite, The over bite which was less than one
third, was described as being reduced. Open bite
was identified by space vertically between the
incisors when the buckle segment teeth were in
occlusion. Cross bite was identified by buccal
cusps of the lower premolars and/or molars
occluded buccal cusp of the upper premolars
and/or molars. Scissor bite were identified by
buccal cusps of the lower Premolars and/or
molars occluded lingual to the lingual cusps of
the upper premolars or molars.5 Data was
analyzed using Graphpad prism (6.0.3) software.
RESULTS
Table 1: Number of visits to dentist for regular dental check-up
No any visit in a year

<3 visits in a year
3 or more visits in a year
Total
Male subject
Number
Percentage %
169
67.6
55
22
26
10.4
250
Female subject
Number
Percentage %
195
78
46
18.4
9
3.6
250
932
Ankita etal.,
Table 2 : Different anomalies found in Male and Female subjects.
Anomalies
Male
Number
83
122
108
P value
Female
%
33.2
48.8
43.2
Dentitional anomalies
Occlusal anomalies
Space anomalies
*Significant
Awareness of oral hygiene is less in females.
Occlusal anomalies are more predominant among
all anomalies. All anomalies are more prevalent
in females. Dentitional anomalies are
significantly more in females
DISCUSSION
Maintaining oral hygiene should be a lifelong

habit. With proper brushing and flossing, oral
hygiene may be maintained and oral health
problems may be avoided. Regular oral care
preserves speech and eating functions, thus
prolonging the quality of life. Variations of teeth
have been an enduring interest to a clinical
practitioner. No two teeth are alike. It is the odd,
peculiar, and stranger arrangement of teeth on
which we focus our attention here. They are
called anomalies. The primary and permanent
dentitions are subjected to considerable
variations in the number, size, and form of teeth
and the structure of dental tissue. These
developmental anomalies may be genetically
determined or systematic, prenatal, postnatal
environmental and may be due to local causes.3
The anomalies may be symmetrical or
asymmetrical and indifferent degrees of severity.
Variation in the morphology, number, time and
order of eruption of the teeth are important
etiologic factors in the establishment of
malocclusion.9
The prevalence of dental
anomalies observed in deciduous dentition is
lower than in the mixed and permanent
dentitions. Probably in part due to the fact that
many conditions do not develop or become
clearly apparent before the age of 7 to 8 years or
even later.3,9 This study suggested a fact that
recognition of dental anomalies is essential in
determining appropriate treatment for each
Number
103
128
112
%
41.2
50.8
44.8
< 0.05*
> 0.05
> 0.05
patient. Early diagnosis and timely intervention

could reduce or eliminate the need for
orthodontic treatment and prevent serious
complications. It also determines the type,
prevalence and relative severity of the condition
in the population. This study gives the health
authorities positive information concerning the
need for and the progress of dental health
programs. Malocclusion is variation from ideal
occlusion, which has a dental health and / or
psychosocial implications for an individual.9,10 It
is a condition where teeth do not erupt in normal
position causing unsightly appearance.11,12 An
epidemiological study done by Sven Helm
(1968)5 in Danish children showed that the
frequency of dentitional anomalies in males was
33.5% and 42.2% females. In the present study
the figure for males was 33.2% and for females
41.2%.The results are almost matching. The
occlusion anomalies that recorded by Sven Helm
were present in 50.1% males and 50.4% in
females. In the present study it was present in
48.8% of males and 50.8% females. According
to Helm the space anomalies were present in
47.1% males and 47.4% in females.
CONCLUSION
From present study it may be concluded that

awareness of oral hygiene in adolescents needs to
be increased through health check up camps and
electronic media to decrease overall burden on
their pockets in future. Occlusal anomaly is the
most common anomaly in both sex while
dentitional anomalies are signifcantly more
common in females. Though this is pilot study,
there is requiring more detail research in
response to larger sample size and statistical
analysis in India.
933
Ankita etal.,
ACKNOWLEDGEMENT
We would like to thank Principals of both

schools who have given permission to arrange
health check-up camp in their schools, and also
to all students who have actively participated in
our study.
REFERENCES
1. American Dental Association. 211 E.
Chicago Ave., Chicago, IL 60611. (312) 4402500. http://www.ada.org
2. American Dental Hygienists' Association.
444 North Michigan Ave., Chicago, IL
60611. (800) 847-6718.
3. Winter GB. Anomalies of tooth formation
and eruption, Paediatric denstistry. Oxford
University Press 1997:1st ed,;251-270.
4. Buschang PH, Thrackmork GS. Does
malocclusion affect masticatory performance.
Angle orthod. 2002:72(1): 21 27.
5. Sven H. Malocclusion in Danish children
with adolescent dentition. An epidemiologic
study. Am. J. Orthodontics 1968 , volume 54
Number 5, 40-47
6. Seipal CM. Variation of tooth position,
Svensktabdl-hdskr, 1946;39.:50-57.
7. Declaration of Helsinki. http://www.who.int
/bulletin/archives/79(4)373.pdf
8. Riolo and Avery. Essentials for Orthodontic
practice. First edition: Chapter 6: 163-178
9. Laury M. Cross bite, An introduction to
orthodontics, Oxford University Press Inc.
New York: 1996: First Edition 130-137.
10. Mills LF. 1455 School children in dental
arech. Dimensions Expressed on the basis of
tooth eruption as a measure of biologic age.
J. D. Res. 1965;44 : 120-141,
11. Munblatt MA. A statistical study of dental
occlusion in children. Dental Items of
Interest. 1943:65 : 43-63.
12. Miyosh S, Tanaka S, Kunimatsu H.: An
epidemiological study of supernumerary
primary teeth in Japanese children. A review
of racial differences in the prevalence. Oral
Dis 2000: 6 (2): 92-102.
934
Ankita etal.,
DOI:10.5958/j.2319-5886.2.4.150

&
Health Sciences
www.ijmrhs.comVolume 2 Issue 4 Oct-Dec
Research article
Coden: IJMRHS
Copyright @2013
th
ISSN: 2319-5886
PREVALENCE AND PATTERN OF ABNORMALITIES OCCURRING IN PLACENTA AND

UMBILICAL CORD
*Manikanta Reddy. V1, Senthil Kumar. S1, Sanjeeva Reddy. N2
1
Department of Anatomy,2 Department of Reproductive Medicine, Sri Ramachandra Medical College

and Research Institute, Chennai, Tamilnadu, India
*Corresponding author email: manikantareddy.v@gmail.com
ABSTRACT
A hospital based cross sectional study has been conducted in 975 cases to evaluate the prevalence and
pattern of Placental and Umbilical cord abnormalities. All the Placentas with Umbilical cords were
examined for different abnormalities immediately after delivery. Out of 975 specimens, a total of 262
(26.87%) were identified to have various types of abnormalities. Of which, 232 (23.79%) specimens
showed single abnormalities and the remaining 30 (3.07%) specimens were with multiple abnormalities
(more than one abnormalities in each specimen). Prevalence of most of the abnormalities in the present
study is in co ordinance with previous studies and all the abnormalities are distributed among the
specimens in two different forms i.e. specimens with any single abnormally and specimens with multiple
abnormalities.
Keywords: Placental abnormalities, Umbilical Cord abnormalities, IUGR, Circumvallate, Velamentous,
Battledore Placenta
INTRODUCTION
The Placenta and Umbilical cord plays an

efficient role alongside maternal health condition
and genetics of the parents in controlling the
growth and health of the developing fetus by
holding nutritive, respiratory, endocrine,
immunological and excretory functions. Any
abnormality in the Placenta and Umbilical cord
may lead to the impairment of the fetal growth
and health by disturbing the fore said functions.
The literature review of Placenta and Umbilical
cord abnormalities suggests its strong association
with different conditions of the fetus like IUGR,
Pre Term delivery, IUD, Fetal Anomalies and so

on1.
In such condition, we felt the necessity of
knowledge on the prevalence and pattern of
abnormalities among Placenta and Umbilical
cord, which will reinforce the prenatal care by
health providers in addressing the adverse
outcome caused by these abnormalities.
The current study has been designed to estimate
the prevalence and pattern of different
abnormalities occurring in Placenta and
Umbilical cord, to address the wide variations
regarding, in the existing literature.
Manikanta Reddy. V et al.,
935
A hospital based cross sectional study was

conducted in the Department of Obstetrics and
Gynaecology, Sri Ramachandra Medical College
and Research Institute, Chennai, over a period of
15 months (April 2012 June 2013).
Institutional Ethical Committee (IEC) approval
has been acquired for the study. A total of 975
patients, who met with selection criteria were
enrolled in the study after their written Informed
Consent.
Selection Criteria: All the pregnancies of > 32
weeks of Gestational Age onwards. Specimens
(Placenta with Umbilical Cord) were collected
immediately after the delivery. Chorioamniotic

Membranes were examined for the Blood
Vessels or any Placental masses. Then, all the
Placental discs were examined for the insertion
of Chorioamniotic Membranes, Umbilical Cord
Insertion and extra lobes. Then the Umbilical
Cord length (i.e. length of the Cord with Placenta
and Baby) has been measured with an Inch Tape.
All the Umbilical Cords were checked for the
presence of Knots and Coiling. Finally Umbilical
Cords were severed transversely at its Placental
end and examined for the presence of Whartons
Jelly and number of Umbilical Vessels.
DATA were recorded and analyzed. Specimens
with abnormalities were photographed.
RESULTS
Table 1: Placental and Umbilical cord abnormalities

Type of abnormality
Number
abnormalities
(292)
of Percentage (%) Percentage (%) of each

in 975 cases
abnormality among total
(29.74%)
abnormalities
(In
292
Abnormalities)
PLACENTAL [82 (8.41%)]

Bilobed
11
Accessory lobe
19
Placenta extrachorialis
Circumvallate
Circumvallate Complete
12
Circumvallate Partial
13
Circummarginate
Circummarginate
13
Complete
Circummarginate Partial
14
UMBILICAL CORD [210 (21.53%)
1.12
1.96
3.76
6.5
1.23
1.33
4.1
4.45
1.33
4.45
1.43
4.79
Marginal
Velamentous
Furcate
Single Umbilical Artery
False Knots
True Knots
Uncoiled Cords
Absent Jelly
Short Cords ( 35cm)
Long Cords (75cm)
7.4
0.9
0.7
0.7
4.3
0.2
1.84
0.7
2.46
2.25
24.65
3.08
2.39
2.39
14.38
0.68
6.16
2.39
8.21
7.53
72
9
7
7
42
2
18
7
24
22
936
Table 2: Specimens with multiple abnormalities

Number of Percentage in Percentage of each
Type of combined abnormalities
specimens 975 specimens abnormality among all
(30)
(%)(3.07)
multiple abnormalities
in 30 specimens
Marginal Insertions and Short Cord
7
0.71
23.33
Marginal
Cords
with
Complete 5
0.51
16.66
Circumvallate
Single Umbilical Artery with Uncoiled 3
0.3
10
Cords
False Knots with Uncoiling Cords
2
0.2
6.66
Marginal
with
Complete 2
0.2
6.66
Circummarginate
False Knots with Short Cords
2
0.2
6.66
Marginal Insertions with Accessory 2
0.2
6.66
Lobes
Marginal with Partial Circummarginate
1
0.1
3.33
Velamentous with Bilobed
1
0.1
3.33
False knots with Bilobed
1
0.1
3.33
Short cord with Partial Circummarginate 1
0.1
3.33
Marginal Cords with Uncoiled Cords
1
0.1
3.33
True knots with Partial Circumvallate
1
0.1
3.33
Long Cord with Bilobed
1
0.1
3.33
Fig 1: Marginal Insertion (Arrow)
Fig 3: Furcate Insertion (Arrow showing the cord

bifurcation before reaching Placenta)
Fig 2: Velamentous Insertion (Arrow showing the Umbilical

cord insertion on Chorioamniotic membranes)
Fig 4: Single Umbilical Artery Upper and Lower

(Arrows sowing Umbilical Vessels)
937
Out of 975 specimens, a total of 262 (26.87%)

were with different abnormalities, among 262
specimens with abnormalities, 232 (23.79%)
showed single abnormalities and 30 (3.07%)
specimen [Table 2] were with multiple
abnormalities (two abnormalities in each
specimen).
In the total 292 abnormalities 82 (8.41%) were
Placental and 210 (21.53%) were Umbilical Cord
abnormalities.
Fig 5a: True Knot
DISCUSSION
Fig 5b: False Knot
Fig 6: Circumvallate Placenta

circumvallation
Arrows showing the
Fig 7: Circumvallate with Marginal Insertion Upper

and Lower
(Arrows showing the Circumvallation middle arrow
showing the Marginal Insertion of Umbilical Cord)
Most of the Placental and Umbilical cord

abnormalities are quoted to have an association
with IUGR, IUD, Low Birth Weight, Small for
Gestational Age, Pre Term delivery, Congenital
anomalies and so on1.
In the review of literature, Placenta Previa,
Abruptio
placentae,
Cord
prolapse,
Malignancies, Tumors and pathology of Placenta
and Umbilical cord also included under the
heading of abnormalities2. We have omitted the
above conditions in the current study by adding
only developmentally malformed conditions
under the heading Abnormalities.
In our study all the abnormalities (29.7%) are
classified into two categories:
1. By affected organ wise:
a. Placental abnormalities
b. Umbilical cord abnormalities
2. Considering the number of abnormalities
in each specimen:
a. Specimens
with
any
single
abnormality
b. Specimens
with
multiple
abnormalities
We have not compared Placental and Umbilical
cord abnormalities as a whole with existing
literature as the reason mentioned earlier that
Placental and Cord pathology also included
under the heading - abnormalities. Instead, we
compared the individual abnormalities of
Placenta and Umbilical cord in the subsequent
text.
Different types1 of Umbilical cord abnormalities
are as follows, Short cords (<35 cm), Long Cords
938
(>75 cm), 2 Vessels cords, Multi Vessels cords,

Straight cords (Uncoiled cords), Hypo & Hyper
coiled cords, Cords without Whartons Jelly,
Velamentous, Marginal/Battledore Placenta and
Furcate cords. Among these, we have excluded
Hypo and Hyper coiled cords as there was much
fluctuation in the number of coils with time,
postnatally.
Different types of Umbilical cord abnormalities
observed in our study are Marginal (Fig. 1),
Velamentous (Fig. 2), Furcate cords (Fig. 3),
Single Umbilical Artery (Fig. 4), True Knots
(Fig. 5a) and False Knots (5b) occurred in
7.38%, 0.92%, 0.71%, 0.71%, 0.20% and 4.3%
rates respectively.
Michale K Fritsch3 and Cunningham et al4
mentioned the prevalence of Marginal cord as
7%, which is coinciding with our study.
Jason H Collins et al5 quoted the prevalence of
Velamentous as 0.5 2.7%, Furcate as 0.5 1%.
Jason H Collins et al5, Michale K Fritsch3 and
Fernando Heredia et al6 stated the prevalence of
Umbilical cords with Single Umbilical Artery as
0.2 2%. Whereas True Knots occurs in the rate
of 0.3 2.1%1,7, 8
The present study showed Uncoiled, Long and
Short cords in 1.84%, 2.25% and 2.46%. But
Jason H Collins et al3 placed the occurrence of
Uncoiled cords at 4.3% and 5%, Michale K
Fritsch5, BalkawadaNileshUnmesh et al9 found
the prevalence of Long and Short cords in 5 5.3% and 5.9% respectively. Jason H Collins, et
al1 mentioned the prevalence of Short cords at
3%.
Among the 8.41% of Placental abnormalities in
our study, Bilobed (Placenta Bilobata) were
1.28%, Accessory lobes (Placenta Succenturiata)
were 1.96% and Placenta Extrachorialis with
5.33% of prevalence. Placenta Succenturiara
have been classified into Complete and Partial
Circumvallate (Fig. 6) (occurred in 1.22% and
1.33%)
and
Complete
&
Partial
Circummarginate (occurred in 1.33% and 1.43%)
placenta. Michale K Fritsch3 quoted the
occurrence of Bilobed Placenta at 2 - 8%.
Whereas Michale K Fritsch3 and Joan M.
Mastrobattista et al10 stated the prevalence of
Accessory lobe as 5 - 6%, which are not in

correlation with the present study.
Michale K Fritsch3 mentioned the prevalence of
Complete and Partial Circumvallate Placenta in
co -ordinance with our study as 1 - 5% but his
finding of Circummarginate Placenta as 25% are
not in correlation with the present study. Robert
D. Harris et al11 found the rate of occurrence of
Complete Circumvallate Placenta at 2% and
Partial Circumvallate at 19%, in line with present
study findings.
Prevelance of Circummarginate is poorly quoted
in the literature. In the available literature it has
been coined as 25% [Michale K Fritsch3] which
is far high from the present finding.
Nevertheless in the literature, we encountered
specimens with multiple abnormalities in 3.07%
of cases. All these specimens (Table. 2) showed
the combination of two different abnormalities in
each. According to the authors opinion, the
degree of impairment of blood supply to the
developing fetus or impairment of the fetal heath
will be higher in this kind of cases.
Among all the abnormalities Umbilical cord
abnormalities occurred in higher rate (71.9%), in
which Marginal Insertion/Battledore cords were
predominant
(24.65%).
In
Placental
abnormalities, Partial Circummarginate Placentas
(4.79%) occurred in higher rate. Amides
specimens
with
multiple
abnormalities
combination of Marginal with Short cords
(23.33%) were predominant.
The limitation of this study is that it is a hospital
based study and further research on evaluating
the outcome in above abnormalities, with high
sample is recommended.
CONCLUSION
The prevalence of Placental and Umbilical cord

abnormalities in the present study is in line with
earlier studies.
Umbilical cord abnormalities are more
predominant (71.9%) among the Placental and
Cord abnormalities. Occurrence of Marginal
cords/Battledore cords (24.65%) is more among
Umbilical
cord
abnormalities.
Similarly
prevalence of Partial Circummarginate placentas
939
(4.79%) is higher among Placental abnormalities

(28.1%).
Specimens with multiple abnormalities were
found in 3.07%, which has not been reported in
the literature to the best of our knowledge.
The frequency of occurring Marginal with Short
cords (23.33%) is high among the specimens
with multiple abnormalities.
ACKNOWLEDGEMENT
I wish to thank INSPIRE division, Department of

Science and Technology for funding, All the
subjects of our study, Dr. S. MelaniRajendran
(Professor of Anatomy, Madha Dental College),
Dr. V. Sankar (Head, Department of Anatomy,
PGIBMS), Dr. Rameshkumar Subramanian
(Head, Department of Anatomy), Dr. Pushpa
Latha Barua (Professor of Obstetrics and
Gynaecology, Sri Ramachandra University) for
their support.
Conflict of interest: None declared
REFERENCES
1. Jason H Collins, Charles L. Collins, Candace

C. Collins. (2010). Umbilical cord Accidents.
Available From: http://www.preginst.com/
UmbilicalCordAccidents2.pdf .
2. Bettye Wilson. Sonography of the Placenta
and Umbilical cord. Radiologic Technology.
2008; 79(4): 333 45.
3. Michale K Fritsch. Placental Pathology.
Available
From:
http://pathology.bsd.
uchicago.edu/PedsPath/2012/Files/handouts/
Placental%20Pathology-Fritsch%202012.pdf.
4. Cunningham, Levono, Bloom, Rouse,
Sponge.
Abnormalities
of
Placenta,
Umbilical
cord,
Membranes.
In:
Cunningham, Leveno, Bloom, Hauth, Rouse,
Spomg. (23ed). Williams Obstetrics.
McGraw Hill, New Delhi. 2010: P 577 587.
5. Jason HC, Charles LC, Candace CC. Silent
Risk. Issues about Human Umbilical cord.
Available From: http://www.preginst.com/
silentrisk.pdf
6. Fernando
Heredia,
Philippee
Jeanty.
Umbilical cord Anomalies (2002). Available
From: http://sonoworld.com/fetus/page.aspx
?id=1149
7. Alain Goriely. Knotted Umbilical cords.
Available
From:
http://math.arizona.
edu/~goriely/Papers/2005-knotbook
(umbilical).pdf
8. Spellacy WN, Graven H, Fish RO. The
Umbilical cord Complications of True Knots,
Nucal coils, Cords around the Boby, Am J
Obstet Gynaecol.1966; 94(8): 1136 42.
9. Balkawade NU, Shinde MA. Study of Length
of Umbilical cord and Fetal outcome: A
Study of 1,000 of 1000 Deliveries. The
Journal of Obstetrics and Gynaecology of
India.2012; 62(5): 520 25.
10. Joan M. Mastrobattista, Eugene CT.
Placenta, Cord and membranes. In: Arthor C.
Fleischer, Eugene C. Toy, Wesley Lee. (7ed).
Sonography in Obstetrics and Gynaecology.
McGraw Hill, New Delhi. 2011:155 84.
11. Rodert D. Harris, Wendy A. Wells, William
C. Black, Jocelyn D. Chertoff, Steven C.
Poplack, Steven K. Sargent, Harte C. Crow.
Accuracy of Prenatal Sonography for
Detecting Circumvallate Placenta. American
Journal of Radiology.1997: 168: 1603-08.
940
DOI:10.5958/j.2319-5886.2.4.151

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
HYPERTENSION AS AN EMERGING HEALTH PROBLEM AMONGST SCHOOL

CHILDREN AND ADOLESCENTS
*Ravikumar V Baradol 1, Anand Ranagol 2, Patil SV 3
1
Asst Professor, 2Asst Professor, 3Professor & Head, Dept. of Pediatrics, BLDEUS S. B. M. Patil
Medical College, Bijapur, Karnataka, India
*Corresponding author email: ravikumar8901@gmail.com
ABSTRACT
Introduction: Hypertension is a common non communicable disease in developed countries. But

nowadays even in developing countries like India its prevalence is increasing in adults as well as in
childhood population. Objective: To find out the prevalence of Pre hypertension and Hypertension
amongst school children and adolescents. Study Design: Randomised, Cross-sectional, observational
multicentric School based study. Methodology: In this study 3 schools were selected by simple random
sampling method from Urban and rural region of Bijapur district which is a part of North Karnataka.
Total 2800 children were screened in the age group from 10-16 years. General data and Blood pressure
were recorded for each child. Blood pressure values are compared with reference charts given by
National High Blood Pressure Education Programme working group of American heart association 2004
and grouped as prehypertensive (PHTN) and Hypertension (HTN). Results: In Rural school children,
Prevalence of systolic PHTN was 2.2% and prevalence of systolic HTN was 1.8%. Among urban school
children prevalence of systolic PHTN was 3.92% and prevalence of systolic HTN was 3.79%.
Prevalence Diastolic PHTN in rural school children was 2% and that of Diastolic HTN was 1.5%. In
case of urban school children, the prevalence of Diastolic PHTN was 4.28% and that of Diastolic HTN
was 3.86%. In our study the prevalence of hypertension in males was more than female in both rural &
urban school children. Also the prevalence of HT was more in urban than in rural population.
Conclusions: Prevalence of hypertension in school children is increasing even in developing countries.
In feature to prevent morbidities, early intervention strategies for promoting healthy eating, physical
activities and health education should be undertaken from school age group. This primordial prevention
should be considered as an important public health issue in our developing country.
Keywords: Prehypertension, Hypertension, North Karnataka, Primordial prevention.
INTRODUCTION
Hypertension is of importance mainly as a risk

factor for cardiovascular and cerebrovascular
disease. High blood pressure in the adult
population has been shown to relate to the risk of

stroke,
renal
disease
and
occlusive
1
atherosclerotic vascular disease. Efforts have
941
Baradol etal.,
been made to reduce the blood pressure level

than to prevent their development.
Although it is obviously better to prevent than to
cure a disease, it is only recent years that interest
has been focused on primary prevention of high
blood pressure. Efforts should be made to
prevent the development of hypertension during
childhood only. This primordial prevention is of
utmost important thing that should be considered
in developed as well as in developing countries.
Systemic hypertension is an important condition
in childhood, with estimated population
prevalence of 1-2% in the developed countries.2
Data is lacking from India; small surveys in
school children suggest a prevalence ranging
from 5-10 %.3, 4
In the recent years numbers of studies of blood
pressure have appeared for the most part these
studies have attempted to establish value of
blood pressure measurement for the purpose
clinical diagnosis. Comparatively few studies
have considered blood pressure and its relation to
the increasing age or adolescent period and
etiology and incidence of hypertension in this
age group.5-7
So we carried out the study to find out the
prevalence of hypertension amongst school
children and adolescents in north Karnataka. The
findings of this study will be useful for initiation
of primordial prevention in this developing part
of India.
MATERIALS & METHODOLOGY
It was a Randomised, Cross-sectional,

multicentric study done in school children of the
age group of 10 to 16 years during 9 months of
study duration. 1400 Children were selected from
rural areas and 1400 children of same age groups
from the urban areas in and around Bijapur City
which is part of North Karnataka. Out of 10
affluent schools in Bijapur City and rural areas, 3
schools were selected based on simple random
sampling method. The total sample size was
2800. Exclusion criteria: Children with Renal
diseases, acute illness, systemic diseases,
students who are unwilling, children who are

known hypertensives and who are on
antihypertensive medication and children taking
medications which can modify blood pressure
measurement were excluded from the study.
Before initiation of the study, the study protocol
containing proforma was approved by
Institutional Ethics Committee. Data was
collected in a pretested proforma meeting the
objective of the study. Informed consent was
taken from the parents of all children, Head of
the Institution before examining school children.
The importance of the study was explained to the
school management, staff and teachers. The age
of the school children was obtained from the
school records. The name and other particulars
were entered in a pretested proforma.
Blood pressure was measured in all 10 to 16
years school children between 8AM to 11AM in
sitting position after 10 minutes of rest as per
American Heart Association Guidelines.8
Systolic blood pressure was determined as
appearance of 1st Korotkoff sounds and diastolic
blood pressure was taken at the point of muffling
of heart sounds (4th Korotkoff sounds). Three
measurements were taken at an interval of five
minutes each and mean of these readings were
taken as average systolic blood pressure and
average diastolic blood pressure. Blood pressure
values were compared to the values given by the
update of 1987 task force report of the National
high blood pressure Education Programme Coordinating Committee9. Children were classified
into three groups as follows:9
BP < 90th percentile - Normal (N) Blood
pressure (compared to age, sex and height
percentile in each age group)
BP = 90 - 95th percentile - Prehypertension
(PHTN)
BP > 95th percentile - Hypertension (HTN)
In those children whose systolic and or diastolic
BP value was found to be more than 95th
percentile for age, sex and height, two sets of BP
reading were taken at an interval of 4 weeks. If
systolic and or diastolic BP was found to be
942
Baradol etal.,
persistently more than 95th percentile for age,

sex, and height then child was classified as
having sustained hypertension. Those children
who had sustained hypertension were subjected
to further investigations with informed parental
consent. Investigations were done after taking
consent from the parents in a format, after
explaining the parents about the need for
investigations and treatment aspects. Following
investigations were done: Lipid profile, Blood
Urea/serum creatinine, Urine albumin, urine
sugar, urine microscopy, USG of abdomen.
Statistical analysis: Data were analyzed for
prevalence rate & Frequency distribution. All the
statistical operations were done through SPSS
(Statistical Presentation System Software) for

Windows, version 10.0 (SPSS, 1999. SPSS Inc:
New York). A value of P < 0.05 was considered
as statistically significant.
RESULTS
In the present study total 2800 students were

screened. Out of these 1400 were Rural & 1400
were urban school children. Out of 2800, 1514
were male children and 1286 were female
children. In male children, 731 students were
from rural school and 783 students were from
urban school. Also, in case of female students
669 students were from rural school, while 617
students were from urban school.
Table 1: Prevalence of Systolic Hypertension in Rural & Urban Children according to age*.
Rural school children

Urban school children
Age
(years) Normal PHTN HTN Total Normal PHT
HT
Total
10
407
2
1
410
338
2
2
342
11
219
1
1
221
292
4
4
300
12
128
4
2
134
222
4
7
233
13
124
6
5
135
111
9
13
133
14
198
8
8
214
89
11
9
109
15
182
4
4
190
156
9
7
172
16
85
6
5
96
84
16
11
111
Total 1343
31
26 1400 1292
55
53
1400
(*All values are in absolute numbers) PTHN: Prehypertension, HTN: Hypertension
Table 2: Prevalence of Systolic Hypertension in Rural & Urban Children according to sex (*)

Normal PHTN HTN
Total Normal PHTN
HTN
Total
Male
697
19
15
731
717
33
33
783
Female 646
12
11
669
575
22
20
617
Total
1343
31
26
1400 1292
55
53
1400
Sex
Table 3: Prevalence of diastolic hypertension in Rural & Urban Children according to age (*)

Age
(years) Normal PHTN HTN Total Normal PHT
HT
Total
10
408
1
1
410
335
4
3
342
11
215
4
2
221
295
3
2
300
12
131
2
1
134
222
5
6
233
13
126
4
5
135
103
8
12
133
14
208
5
3
214
87
12
10
109
15
178
6
6
190
154
10
8
172
16
88
5
3
96
80
18
13
111
Total 1353
27
20 1400 1286
60
54
1400
943
Baradol etal.,
Table 4: Prevalence of diastolic hypertension in Rural & Urban Children according to sex (*)
Sex

Normal PHTN HTN Total
Male
703
17
11
731
Female
650
10
9
669
Total
1353
27
20
1400
(*All values are in absolute numbers)
100 99.28
99.1
95.52
92.42
91.12
90

Normal PHTN HTN Total
716
36
31
783
570
24
23
617
1286
60
54
1400
95.8
87.5
80
prevalence (in %)
70
60
Normal
50
PHTN
40
HTN
30
20
10
0.48
0.24
0.45
0.45
10
2.98
11
4.44
4.44
1.5
12
3.74
3.74
13
Age groups (in yrs)
14
2.1 2.1
6.25
15
6.2
16
Fig1: Prevalence of Systolic Hypertension in Rural School Children according to age.

100 98.83
97.33
95.28
90.7
90
83.46
81.65
75.68
prevalence (in %)
80
70
60
Normal
50
PHTN
40
HTN
30
20
10
0
0.58
0.58
10
1.34
1.33
11
1.72
12
6.76
9.78
10.19
8.26
13 (in yrs)
Age Groups
14
5.23
4.07
15
14.41
9.91
16
Fig 2: Prevalence of systolic hypertension in urban school children according to age.
As shown in Table no. 1, Prevalence of systolic

prehypertension (PHTN) was 2.2% and
prevalence of systolic hypertension (HTN) was
1.8% in rural school children. It was also
observed that, systolic BP increases with age in
both male & female. Also, maximum number of

hypertensive and prehypertensive were seen in
above 13 years of age. Figure no.1 describes the
% prevalence of systolic hypertension in each
group.
944
Baradol etal.,
Among rural school children, it was found that

Prevalence of systolic prehypertension in males
was 2.6% compared to 1.79% in females. The
prevalence of hypertension in males was 2.05%,
while in females it was 1.64%.
Among urban school children, prevalence of
systolic PHTN was 3.92% and prevalence of
systolic HTN was 3.79%. As compared to rural,
the prevalence of prehypertension and
hypertension was more in urban population in all
age groups. The maximum numbers of
hypertensive were found in 16 years of age
group. (As shown in table no. 1 & figure no.2)
It was observed in our study that, the prevalence
of Systolic hypertension was predominantly seen
in males (4.21%) compared to females (3.24%)
in Urban school children. Also, the prevalence of
systolic prehypertension was more in males
(4.21%) as compared to females (3.56%).
In case of diastolic BP measurement, Prevalence
of Diastolic PHTN in rural school children was 2
% and that of Diastolic HTN was 1.5%. It was
also observed that, diastolic BP increases with
age in both male & female. Also, maximum
number
of
diastolic
hypertensive
and
prehypertensive were seen in above 13 years of
age.
When the difference between the prevalence
rates of different sex was examined, it was found
that the male prevalence of diastolic
hypertension was 1.5% as compared to 1.34% in
female.
In case of urban school children, the prevalence
of Diastolic PHTN was 4.28 % and that of
Diastolic HTN was 3.86 %. The maximum
numbers of prehypertensive and hypertensive
were found in 16 years of age group.
In the urban school children, the prevalence of
diastolic PHTN in male was 4.6% while the
prevalence of HTN was 3.96%. In female, the
prevalence of PHTN was 3.89% and the
prevalence of HTN was 3.72%.
DISCUSSION
Hypertension is a common non communicable

disease. It is also risk factor for various disorders
including
cardiovascular
disorders
like
myocardial
infarction,
angina
and
cerebrovascular
disorders
like
stroke,
haemorrhage etc. It is very important to diagnose
and to treat the hypertension at early stage only,
so as to decrease the morbidity and mortality
following these disorders. Therefore detection of
childhood
hypertension
carries
utmost
importance. Population changes in health-related
behaviours, including the childhood obesity
epidemic, indicate that the rates of hypertension
in the young are increasing.1 Although the
prevalence of HT is less common in children
than in adults,10, 11 there are studies which had
proven that the origin of essential HT start
childhood.11-15 But studies indicative of current
status of hypertension in north Karnataka are not
available in literature. Therefore, we decided to
undertake the present study to highlight the rising
problem, hypertension in both rural and urban
area of north Karnataka.
Considerable advances have been made in
detection, evaluation, and management of high
blood pressure (BP), or hypertension, in children
and adolescents.8 The level of normal BP varies
in different studies due to number of variables
such as the size of the rubber bladder within the
cotton cuff, type of sphygmomanometer, arm
position, whether the fourth or the fifth phase of
Korotkoff's sound is used to obtain the DBP, and
place and time of BP measurement.12-13 In the
present study, BP was recorded by mercury
sphygmomanometer using standardized method.
8, 9
In the present study, both SBP & DBP showed

increase in the value as with increase in age.
Similar findings were reported by Sharma et al15
The age-related increase in BP may be
attributable in part to increase in body mass.16 A
trend of increase in SBP and DBP with age in the
present study was observed in both sexes. An
increase in SBP and DBP with age has also been
945
Baradol etal.,
reported in Indian children by other authors.1720

Gupta et al21, observed a spurt in SBP between
1315 years in both sexes. The spurt in SBP
between 1315 years is mainly related to certain
biological and psychosocial factors, and puberty
timing.22-23 In our study, we observed that there
was increase in both SBP & DBP value above 13
years of age with maximum BP at the age of 16
years. Also, there was no significant difference in
BP measurement between male & female of
same age group. The differences in BP between
males and females of same age groups are
probably related to certain biological and
psychosocial factors.16 The appearance of
secondary sex characters together with the
menarche is associated with a high level of
anxiety resulting in higher SBP values in girls.
However, there are no appreciable differences in
the level of the BP of children, aged 514 years,
between the two sexes.24-27
We found that, the prevalence of systolic
prehypertension (PHTN) & hypertension (HTN)
in rural school children were 2.2% and 1.8%,
respectively, while in urban area, they were
3.92% & 3.79%, respectively. The prevalence of
HT in children has been reported to vary between
0.41% to 11.7%.17, 21 The prevalence of HT in
urban population was found to be more than rural
population. The contributing factors could be
dietary habits like junk foods, lack of physical
activity, and peer pressures16. Similar findings
were noted about diastolic HT.
But in our study has some limitations. All BP
measurements were taken by single observer.
This can be a bias source. Also we did not
include factors such as physical activity, diets
and salt intake. These factors significantly affect
the BP readings. In our study, we did not studied
that among the hypertensive children, how many
of children require antihypertensive medications,
do they develop any cardiovascular disease or
other morbidity. We referred these children to
hospital with all their recorded data. Further
research can be done in this aspect.
The study of childhood HT is important for

several reasons: i) sequelae of long-term HT are
irreversible and associated with significant
morbidity and mortality, ii) childhood BP is the
best predictor of adult BP. iii) helps in planning
28-31
primordial
preventive
strategies.16,
Therefore, this study can help to plan various
health care strategies to prevent hypertension
related comorbidities in developing countries like
India.
CONCLUSION
The findings of this study suggest that there is

increasing prevalence of hypertension both in
rural as well as in urban part. The prevalence of
HT in urban children is more than rural children.
Maximum number of hypertensive and
prehypertensives are present in more than 13
years of age. So there is need of further research
in large scale to raise the issue of early childhood
hypertension to start the primordial prevention as
early as possible.
REFERENCES
1. Munter P, He J, Cutler JA, Wildman RP,
Whelton BK. Trends in blood pressure
among
children
and
adolescents. JAMA. 2004; 291:210713.
2. Mohan B, Kumar N, Aslam N, Rangbulla A,
Kumbkarni S, Sood NK, et al. Prevalence of
sustained hypertension and obesity in urban
and rural school going children in
Ludhiana. Indian Heart J.2004; 56:3104.
3. Arvind Bagga. Evaluation and management
of
hypertension.
Indian
paediatrics.
2007;17:111-12.
4. Hari P, Bagga A, Srivatsava RN.
Hypertension in children. Indian pediatrics
2000; 37: 268-274.
5. Sidhu S, Kaur N, Kaur R. Overweight and
obesity in affluent school children. Ann Hum
Biol 2006;33: 255-259.
6. Chhatwal J, Verma M, Rair SK. Obesity
among pre-adolescent and adolescents of a
946
Baradol etal.,
developing country (India). Asia Pac J Clin

Nutr 2004; 13: 231-33
7. Ross JG, Pate RR, Lohman TG, Christenson
G M. Changes in the body composition of
children.J Phys Educ Rec Dance 1987;58:7477
8. National High Blood Pressure Education
Program Working Group on High Blood
Pressure in Children and Adolescents. The
Fourth Report on the diagnosis, evaluation
and treatment of high blood pressure in
children and adolescents. Pediatrics. 2004;
114:55575.
9. Update on the 1987 Task Force Report on
High Blood Pressure in Children and
Adolescents: A working group report from
the National High Blood Pressure Education
Program. National High Blood Pressure
Education Program Working Group on
Hypertension Control in Children and
Adolescents. Pediatrics.1996; 98:64958.
10. Bernstein D. Systemic hypertension. In:
Kliegman RM, Behrman RE, Jenson HB,
Stanton BF, editors. Nelson text book of
pediatric. 18th ed. Philadelphia: W.B.
Saunders Co. 2007;198896.
11. Rocchini AP. Childhood hypertension,
etiology, diagnosis and treatment. Pediatr
Clin North Am.1984;31:125973
12. Canner PL, Borhani NO, Oberman A, Cutler
J, Prineas RJ, Langford H. The hypertension
prevention trial assessment of the quality of
blood
pressure
measurements. Am
J
Epidemiol.1991; 134:37992.
13. Sinaiko AR, Gomez Marin O, Prineas RJ.
Diastolic fourth and fifth phase blood
pressure in 10-15-year-old children: The
children and adolescents blood pressure
program. Am J Epidemiol.1990;132:64755
14. Sarin D, Chaturvedi P. Normal blood
pressure and prevalence of hypertension in
school going children. J MGIMS. 1997;
1:325.
15. Sharma BK, Sagar S, Wahi PL, Talwar KK,

Singh S, Kumar L. Blood pressure in school
children in North-West India. Am J
Epidemiol. 1991; 134:141726.
16. Amar Taksande, Pushpa Chaturvedi, Krishna
Vilhekar, and Manish Jain; Distribution of
blood pressure in school going children in
rural area of Wardha district, Maharashatra,
India; Ann Pediatr Cardiol. 2008; 1(2): 101
106.
17. Anand NK, Tandon, L Prevalence of
hypertension in school going children. Indian
Pediatr.1996; 33:33781.
18. Badaruddoza, Afzal M. Age-specific
differences in blood pressure among inbred
and non-inbred north Indian children. J
Bioscience. 1999;2:17784.
19. Verma M, Chatawal J, George SM.
Biophysical profile of blood pressure in
school children. Indian Pediatr. 1995;32:749
54.
20. Chahar CK, Shekhawat V, Miglani N, Gupta
BD. A study of blood pressure in school
children
at
Bikaner. Indian
J
Pediatr. 1982;49:7914.
21. Gupta AK, Ahmad AJ. Normal blood
pressures and the evaluation of sustained
blood pressure elevation in childhood. Indian
Pediatr. 1990;27:3342
22. Shubi MD. Blood pressure profile and
hypertension in Iraqi primary school
children. Saudi Med J.2006;27:4826.
23. Nichols S, Cadogan F. Blood pressure and it's
correlates in Tobagonian Adolescents. West
Indian Med J. 2006;55:28
24. Bernstein D. Systemic hypertension. In:
Kliegman RM, Behrman RE, Jenson HB,
Stanton BF, editors. Nelson text book of
pediatric. 18th ed. Philadelphia: W.B.
Saunders Co. 2007;198896.
25. Rocchini AP. Childhood hypertension,
etiology, diagnosis and treatment. Pediatr
Clin North Am.1984;31:125973.
947
Baradol etal.,
26. Canner PL, Borhani NO, Oberman A, Cutler

J, Prineas RJ, Langford H., et al. The
hypertension prevention trial assessment of
the
quality
of
blood
pressure
measurements. Am J Epidemiol. 1991;134:
37992.
27. Sinaiko AR, Gomez Marin O, Prineas RJ.
Diastolic fourth and fifth phase blood
pressure in 10-15-year-old children: The
children and adolescents blood pressure
program. Am J Epidemiol.1990;132:64755
28. Task Force 1987 on Blood Pressure control
in children: Report of the Second Task Force
on
Blood
Pressure
Control
in
Children. Pediatrics. 1987;79:125.
29. Kochanek KD, Smith BL. Deaths:
Preliminary data for 2002. Natl Vital Stat
Rep. 2004; 52:147.
30. Inglfinger JR. Pediatric antecedents of adult
cardiovascular disease: Awareness and
interaction. N Engl J Med. 2004; 350:2123
26.
31. Atwood K, Colditz GA, Kawachi I. From
public health science to preventive policy:
Placing science in its social and political
contexts. Am
J
Public
Health. 1997;
87:16036.
948
Baradol etal.,
DOI:10.5958/j.2319-5886.2.4.152

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
THE EFFECT OF DIFFERENT BOUTS OF EXERCISE ON WEIGHT LOSS IN

OVERWEIGHT INDIAN FEMALE UNDERGRADUATES
*Kavitha U1, Navin Rajaratnam2, Suzanne Maria Dcruz3, Chandrasekhar M2
1
Department of Physiology, Sri Venkateswaraa Medical College Hospital and Research Centre, Pondicherry,
India
2
Department of Physiology, Meenakshi Medical College Hospital and Research Institute, Kanchipuram,
Tamilnadu, India
3
Department of Physiology, Sri Muthukumaran Medical College Hospital and Research Institute, Chennai,
Tamilnadu, India
*Corresponding author email: kavikrish.u@gmail.com

ABSTRACT
Background: The prevalence of obesity is increasing globally and in India with lack of sufficient time
for continuous exercise being one of the causes. Performing multiple short bouts of exercise has been
introduced as an alternative method to reduce weight gain. Aim: To determine the effects of different
bouts of supervised exercise accumulated in 30 minutes on weight loss, in overweight Indian female
undergraduate students, without dietary restriction. Methods and Material: Sixty otherwise healthy
overweight female undergraduate medical students aged 18 to 25 years, with a body mass index (BMI)
of 25 to 29.9 kg/m2 were randomly selected and divided into four groups of 15 students each as follows:
Group I: Non-exercising group (controls); Group II: Participants performed one 30 minute bout of
exercise (130 =30min/day); Group III: Participants performed two 15 minute bouts of exercise (215
=30min/day); Group IV: Participants performed three 10 minute bouts of exercise (310=30min/day).
Participants performed moderate intensity exercise using a bicycle ergometer for 16 weeks and their
weight and Body Mass Index were measured before and after the exercise programs and statistically
analyzed. Results: There was a significant weight reduction (p<0.05) in Group II, Group III and Group
IV. Conclusion: Our study revealed that there was significant weight reduction in participants who
performed single or multiple bouts of exercise. The use of accumulated short-bouts of moderate
intensity exercise can therefore be recommended to young overweight females who have difficulty
doing a single long-bout of exercise.
Key words: Exercise; overweight; short-bouts; weight loss.
INTRODUCTION
The prevalence of obesity is increasing globally.
In their review highlighting the Asian Indian
body composition with regards to obesity,

Chopra et al concluded from different studies
949
Kavitha etal.,
that women have higher prevalence of

overweight and obesity (15-61%) when
compared to men (12-54%) in India.1 They also
found that obesity was increasing in the youth.1
The Centers for Disease Control and Prevention
(CDC) and the American College of Sports
Medicine (ACSM) has provided new physical
activity recommendations for the public, that
adults should accumulate 30 minutes of
moderate-intensity physical activity with at least
four hours interval between the bouts for 5 days
in a week. 2, 3
Jakicic et al showed that short-bouts of exercise
enhance exercise adherence and may be
preferred when prescribing exercise to obese
adults.4 Schmidt et al proved that that exercise
accumulated in several short-bouts had similar
effects as one continuous bout with regard to
aerobic fitness and weight loss during caloric
restriction in overweight, young women.5 WoolfMay K et al 6 found like Ebisu 7 that there was
little difference in the effect of continuous and
accumulated exercise, although their findings on
the effect on lipid profile varied. Woolf-May K
et al 8 further investigated the effects of single
and accumulated short-bouts of walking on
aerobic fitness and lipid profile. They found that
there were similar changes in aerobic fitness
among long, intermediate and short walkers and
recommended the incorporation of accumulated
bouts of moderate intensity exercise for health
promotion since it might be easier for the
individuals than single prolonged bouts.8 Murphy
et al compared the effects of short and long-bouts
of brisk walking in sedentary females and found
that changes in anthropometric parameters did
not differ between short- and long-bout walkers.9
De Busk compared the effect of 30 minutes of
moderate exercise per day in 18 men with the
effect of three 10 minute bouts of exercise per
day and found that multiple short bouts of
exercise significantly increased peak oxygen
uptake.10
Quinn et al found that an intermittent exercise
program, which is incremental in nature,
provided comparable, and in some cases greater,

health and fitness benefits than those expected
following traditional continuous exercise
training.11 Jakicic et al, in addition, investigated
the effect of combining intermittent exercise with
the use of home exercise equipment.12 They
found that access to home exercise equipment
facilitated the maintenance of multiple short-bout
exercise, although subjects in the short-bout
group did not experience improved long-term
weight loss when compared with the long-bout
group.12 In a randomized controlled trial
involving 21 sedentary male and 19 female
subjects, Osei-Tutu proved that while both long
bout walking and short bout walking produced
similar and significant improvements in VO2
max, long bout walking was more effective at
reducing percent body fat.13 Darling et al proved
that intermittent bouts of moderate exercise in
young, healthy college-aged males result in the
same energy expenditure as continuous exercise
of the same intensity.14 Schmidt et al concluded
that current data appear to generally agree that
though the magnitude of benefit is unclear,
multiple short bouts of exercise per day appeared
to increase aerobic capacity and were effective in
decreasing weight.5
In view of the higher prevalence of obesity and
overweight in Indian women and the increased
prevalence among the youth; and in view of the
above studies, we decided to study the effect of
different bouts of exercise on weight loss in
overweight Indian female undergraduate
students. However, as Schmidt et al 5 advised, we
decided to verify both the actual time spent and
the intensity of exercise done (as it was felt that
this would be more informative than relying on
unsupervised or self monitored exercise by the
participants), and to include a non-exercising
group also. The aim of the present study was
therefore to determine the effect of different
bouts of supervised exercise accumulated in 30
minutes on weight loss, in overweight Indian
female undergraduate students, without dietary
restriction.
950
Kavitha etal.,
METHODS
This study was conducted in the Department of
Physiology of Meenakshi Medical College
Hospital and Research Institute in Kanchipuram
in South India, with the approval of the
Institutional Ethics Committee. Informed consent
was obtained from the all participants.
Sample Size: Sixty otherwise healthy overweight
female undergraduate medical students aged 18
to 25 years, with a body mass index (BMI) of 25
to 29.9 kg/m2 who satisfied the following
inclusion and exclusion criteria were selected
and divided into four groups of 15 students each
by using random sampling method.
Inclusion criteria: Female under graduate
medical students in the age group 18 to 25 years
who were overweight with a BMI of 25 to 29.9
kg/m2 who were staying in the hostel and eating
food provided from the same hostel mess.
Exclusion criteria: Students suffering from
diseases like diabetes mellitus, systemic
hypertension, heart disease, bronchial asthma or
medical problems that could influence heart rate
and/or exercise capacity were excluded from the
study. Students with history of smoking or
alcohol or nicotine intake; or current intake of
any medication; and students following regular
physical exercise or weight reduction programs
were also excluded from the study.
Screening of the participants (consisting of
detailed history including dietary history and
clinical examination) was done. The participants
height was measured by using a calibrated, wallmounted stadiometer while standing straight and
looking forward; weight was measured using a
weighing scale and body mass index was
calculated. Participants were randomly assigned
to the following four groups:
Group I: Non-exercising group (controls)
Group II: Participants performed one 30 minute
bout of exercise per day (130=30 min/day).
Group III: Participants performed two 15 minute
bouts of exercise per day (215 =30 min/day).
Group IV: Participants performed three 10

minute bouts of exercise per day (310=30
min/day).
All participants were advised to eat food
provided from the same hostel mess and not to
eat food from elsewhere. The participants
weight and body mass index were measured
before and after the 16 week period of exercise
(Group II, III and IV) and after 16 weeks in the
non-exercising group (Group I) also. Subjects
who belonged to Group II, III and IV were asked
to do moderate intensity of exercise on a bicycle
ergometer for 5 days a week for 16 weeks. The
intensity of the exercise was monitored by taking
the participants heart rate 10 seconds postexercise, at the halfway point, and at the end of
each session and comparing with the resting
heart rate. The exercise was considered as
moderate exercise if the participants heart rate at
the end of the session increased to 50-75% of
the resting heart rate. Means and standard
deviations of age, height, weight and BMI were
calculated.
Statistical analysis: Data was analyzed by using
SPSS 17. ANOVA was used to examine
differences between the four groups and the
paired Students t test was used to compare the
participants weight and BMI before (pretraining) and after the 16 week period (posttraining). Statistical significance was accepted at
the 5% level.
RESULTS
There was no significant difference (p>0.05) in

age, height , weight and Body Mass Index (BMI)
of participants measured at the start of the study,
in all four groups, which indicated homogeneity
between the groups in all parameters (Table 1).
Significant differences (p<0.05) were found on
comparison of the pre-training and post training
body weight and BMI (Table 2) of participants in
Group II, III and IV.
951
Kavitha etal.,
Table 1 - Baseline characteristics of participants in all four groups of the study

Parameter
Group I
Group II
Group III
Group IV
Age (years)
18 0.98
18 0.75
18 0.12
18 1.22
Height (cm)
158.933.45
158.922.62
158.425.24
157.685.22
Weight(kg)
71.463.09
70.364.6
70.364.6
71.325.00
BMI(kg/m2 )
28.401.08
27.341.22
28.761.02
28.911.03
Data presented as mean standard deviation

Table 2 - Comparison of the pre-training and post-training body weight of participants
BMI (kg/m2 )
Pre-training
Post-training
Group I
Weight (kg)
Pre-training
Post-training
71.463.09
73.634.82
28.41.68
29.022.33
Group II
70.364.60
66.423.4*
27.341.22
25.951.00*
Group III
70.364.60
67.424.54*
28.761.02
27.051.26*
Group IV
71.325.00
67.694.6*
Groups
28.911.09
Data presented as mean standard deviation. *Significant ( p < 0.05 ).
27.750.98*
DISCUSSION
Our study done to determine the effects of

different bouts of supervised exercise
accumulated in 30 minutes on weight loss, in
students, without dietary restriction, revealed that
significant weight reduction occurred in
participants in Group II (who performed one 30
minute bout of exercise per day), Group III (who
performed two 15 minute bouts of exercise per
day ie. 2 15 = 30 min/day) and Group IV (who
performed three 10 minute bouts of exercise per
day ie. 3 10 = 30 min/day) over a period of 16
weeks.
Schmidt et al also found that that exercise
accumulated in several short bouts in overweight,
young women had similar effects on weight loss
as one continuous bout. 5 However, their study
differed from ours in that they subjected their
participants to caloric restriction, while our
participants did not have any dietary restriction,
although uniformity in diet was maintained.
Woolf-May K et al 6 and Ebisu7 also found that
there was little difference in the effect of
continuous and accumulated exercise. Murphy et

al compared the effects of short- and long-bouts
of brisk walking in sedentary females and found
that changes in anthropometric parameters did
not differ between short- and long-bout walkers.9
The findings of our study differ however from
those of Osei-Tutu who found that long bout
walking was more effective at reducing percent
body fat 13 and Jakicic et al who found that
subjects in the short-bout exercise group did not
experience improved long-term weight loss when
compared with the long-bout group.12
Excess post-exercise oxygen consumption
(EPOC) and exercise induced anorexia could be
the reasons for the weight reduction in Group II,
III and IV of our study. There is a possibility of
equal energy expenditure in both single and
multiple bouts of exercise. Following each bout
of exercise, the slight elevation in body
temperature directly stimulates metabolism to
increase
recovery
oxygen
consumption.
Moreover, restoration of pulmonary ventilation
and circulation and redistribution of calcium,
952
Kavitha etal.,
potassium and sodium ions within muscle and

other compartments also require additional
energy.
The main effect of exercise is negative energy
balance due to both increased energy expenditure
and also decreased energy intake.14, 15, 16 Acute
moderate intensity exercise has been known to
increase the secretion of polypeptide YY (PYY),
glucagon-like peptide (GLP-1), and pancreatic
polypeptide (PP) and suppresses the hunger score
in the post exercise period.14, 18 Although it is
generally accepted that the role of exercise is
mainly to prevent weight gain,19 exercise also
causes moderate weight reduction even without
dietary restriction due to exercise induced
anorexia.18 In our study also, the weight
reduction that was achieved in the groups
performing different bouts of exercise, without
dietary restriction could be due to the exercise
induced anorexia.
In our study, as Schmidt et al 5 advised, we had
verified both the actual time spent in exercising
and the intensity of exercise done by the
participants. We had included a non-exercising
group also in whom it was found that there was
an increase in weight, which however was not
statistically significant. The results of our study
therefore assume more significance. In view of
the increased prevalence of obesity in females
and the youth in India,1 it is recommended that
short-bouts of exercise accumulated in 30
minutes can be adopted by young overweight
Indian females in order to reduce their weight.
Using accumulated bouts of moderate intensity
exercise has been recommended by others too,
since it is easier (than single prolonged bouts)
and since similar changes in aerobic fitness have
been found among long, intermediate and short
walkers,8 and since short-bouts of exercise also
increase the adherence to the exercise
programme.4 Limitations of this study include the
small sample size and duration of exercise;
failure to measure exact calorie intake, VO2 max
and lipid profile; and the fact that the results of
this study may not necessarily be applicable to
other age groups or even to males in the same

age group.
CONCLUSION
Our study done to determine the effects of

different bouts of supervised exercise
accumulated in 30 minutes on weight loss, in
students, without dietary restriction, revealed that
significant weight reduction occurred in
participants who performed a single bout of 30
minutes of exercise and those who performed
two 15 minute bouts of exercise or three 10
minute bouts of exercise per day over a period of
16 weeks. The use of accumulated bouts of
moderate intensity exercise can therefore be
recommended to young overweight females who
have difficulty doing a single long bout of
exercise.
REFERENCES
1. Chopra SM, Misra A, Gulati S, Gupta R.

Overweight, obesity and related noncommunicable diseases in Asian Indian girls
and women. Eur J Clin Nutr. 2013:67(7):688696
2. American College of Sports Medicine
Exercise prescription In ACSMs Guidelines
for Exercise Testing and Prescription 7th Ed,
2006.
3. Report of the Surgeon General. Atlanta GA.
Centers for Disease Control and Prevention
Physical Activity and Health US Department
of Health and Human Services 1996 (S/N
017-023-00196-5)
4. Jakicic JM, Wing RR, Butler BA, Robertson
RJ. Prescribing exercise in multiple short
bouts versus one continuous bout: effects on
adherence, cardiorespiratory fitness, and
weight loss in overweight women. Int J Obes
Relat Metab Disord.1995;19(12):893-901.
5. Schmidt WD, Biwer CJ, Kalscheuer K.
Effects of long versus short bout exercise on
fitness and weight loss in overweight
females. J Am Coll Nutr 2001;20:494 501
953
Kavitha etal.,
6. Woolf-May K, Kearney EM, Jones DW,

Davidson RCR, Coleman D, Bird SR. The
effect of two different 18-week walking
programmes on aerobic fitness, selected
blood lipids and factor XIIa.Journal of Sports
Sciences 1998;16(8):701-10
7. Ebisu T. Splitting the distance of endurance
running:on cardiovascular endurance and
blood lipids. Japanese Journal of Physical
Exercise 1985;37.
8. Woolf-May K, Kearney EM, Owen A, Jones
DW, Davison RC, Bird SR. The efficacy of
accumulated short bouts versus single daily
bouts of brisk walking in improving aerobic
fitness and blood lipid profiles. Health
Educ.Res. 1999 Dec;14(6):803-15.
9. Murphy MH, Hardman AE. Training effects
of short and long bouts of brisk walking in
sedentary women. Med.Sci.Sports Exerc.
1998;30(1):152-7.
10. DeBusk RF, Stenestrand U, Sheehan M,
Haskell WL.Training effects of long versus
short bouts of exercise in healthy subjects.
Am.J.Cardiol. 1990;65(15):1010-13.
11. Quinn TJ, Klooster JR, Kenefick RW. Two
short, daily activity bouts vs. one long bout:
are health and fitness improvements similar
over twelve and twenty-four weeks?
J.Strength Cond Res. 2006;20(1):130-35.
12. Jakicic JM, Winters C, Lang W, Wing RR.
Effects of intermittent exercise and use of
home exercise equipment on adherence,
weight loss, and fitness in overweight
women: a randomized trial. JAMA 1999;
282(16):1554-60
13. Osei-Tutu KB, Campagna PD. The effects of
short- vs. long-bout exercise on mood,
VO2max, and percent body fat. Prev.Med.
2005;40(1):92-8.
14. Darling JL, Linderman JK, Laubach LL.
Energy expenditure of continuous and
intermittent exercise in college-aged males. J
Exer Physiol online 2005;8(4):1-8.
15. Quinn TJ, Vroman NB, Kertzer R. Postexercise oxygen consumption in trained
females: effect of exercise duration. Med Sci

Sports Exerc. 1994;26(7):908-13
16. King NA, Tremblay A, Blundell JE. Effects
of exercise on appetite control: implications
for energy balance. Med Sci Sports Exerc.
1997;29(8):1076-89.
17. King NA, Lluch A, Stubbs RJ, Blundell JE.
High dose exercise does not increase hunger
or energy intake in free living males.
European Journal of Clinical Nutrition
1997;51(7):478-83.
18. Martins C, Morgan LM, Bloom SR,
Robertson MD. Effects of exercise on gut
peptides, energy intake and appetite. Journal
of Endocrinology 2007;193(2):251-58.
19. Katsuura G, Asakawa A, Inui A. Roles of
pancreatic polypeptide in regulation of food
intake. Peptides 2002;23:323-29.
20. Miller WC, Koceja DM, Hamilton EJ. A
meta-analysis of the past 25 years of weight
loss research using diet, exercise or diet plus
exercise intervention. International Journal of
Obesity1997; 21(10):941-47
21. Haapanen N, Miilunpalo S, Pasanen M, Oja
P, Vuori I. Association between leisure time
physical activity and 10-year body mass
change among working-aged men and
women.International Journal of Obesity1997;
21(4): 288-96.
954
Kavitha etal.,
DOI:10.5958/j.2319-5886.2.4.153

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Research article
Copyright @2013
ISSN: 2319-5886
COMPARATIVE STUDY OF THE DERMATOGLYPHIC PATTERNS IN TYPE II DIABETES

MELLITUS PATIENTS WITH NON DIABETICS
*
Rakate NS1, Zambare BR2
Tutor, 2Professor & Head, Department of Anatomy, Padmashri Dr Vitthalrao Vikhe Patil Medical
College, Ahmednagar, Maharashtra, India
*Corresponding author email: nilesh.rakate19@gmail.com
ABSTRACT
Aim: To compare the differences in the finger print patterns viz., total finger ridge count (TFRC), a-b
ridge count and atd angle in patients with type II diabetes mellitus with non-diabetic as control group
Materials and methods: The study is conducted in 75 type II diabetic patients and 75 non-diabetic
persons as a control group. A sample of 51 male and 24 female patients suffering from type II diabetes
mellitus in the age group of 30 to 60 years has been examined and compared with 75 normal persons (47
males and 28 females) in the same age group to know the difference in fingerprint patterns. We have
also compared total finger ridge count, a-b ridge count and atd angle. For collection of palmar prints
Purvis Smith method has been used. Results: Increase in number of whorls, total finger ridge count, ab ridge count along with wider atd angle in type II diabetes mellitus patients. The result of the present
study is more or less coincides with the observations of the earlier researchers. Conclusion: This
inference may be widely applied clinically for the early diagnosis of type II diabetes mellitus mainly in a
mass screening of a population as an additional diagnostic tool.
Keywords: Type II Diabetes mellitus, Dermatoglyphic patterns, Total finger ridge count, a-b ridge
count, atd angle.
INTRODUCTION
Diabetes mellitus, or simply diabetes, is a

metabolic disorder in which a person has high
blood glucose level, either because the pancreas
does not produce enough insulin, or because cells
do not respond to the insulin that is produced.1
Type 2 Diabetes mellitus results from insulin
resistance, it is a condition in which cells fail to
utilise insulin properly, sometimes combined
with an absolute insulin deficiency.2 This form of
diabetes was previously referred to as non

insulin-dependent diabetes mellitus (NIDDM) or
"adult-onset diabetes".
Dermatoglyphics is the study of skin markings
produced by the ridges on hands and feet.
Dermatoglyphics is used as a way of measuring
gene expression determined by the early prenatal environment.3On each fingertip, the number
of dermal ridges (the ridge count) provides a
Rakate etal.,
955
measure of fingertip growth activity during the

early foetal period. These dermal ridges are
formed during gestational weeks 1219, and the
resulting fingertip ridge appearance (i.e.,
Fingerprint) is fixed permanently and because of
these reasons dermatoglyphics becomes an
identification marker for Diabetes.4 According to
Henrys6 classification the dermatoglyphic
patterns can be mainly recognised in to 3 forms,
those are named as arch, whorl and loop. Arch is
the pattern in which ridges are arranged in such a
way that the delta is absent. Whorl is the pattern
in which two deltas are present and ridges are
arranged circularly from the core. The loop is
formed when the ridges pass on the same side
from where it originate, in this pattern one delta
is present along with core. The arch is again
divided in to plain arch and tented arch. The
whorl is subdivided into five types, these are
plain whorl, meet whorl, double loop whorl,
central pocket loop whorl and accidental whorl,
likewise, the loop is having two types these are
radial loop and ulnar loop.
The present study is aimed to analyse the
dermatoglyphic patterns of the patients suffering
from type II diabetes mellitus and compare with
a random non diabetic population. The
observations of the present study may apply
clinically in the mass screening of diabetic
mellitus patients in a random population in
addition blood glucose level.
patients of age group between 30-60years out of

them 51 were males and 24 were female
compared with same age group of 75 nondiabetic persons as control the group, Out of
them 47 males and 28 females. The study was
carried out in Vikhe Patil Hospital, Ahmednagar,
Maharashtra, during the period of June 2012 to
December 2012. Informed consent was obtained
from the participants and ethical clearance was
obtained from the institutional ethics committee
prior to this study.
Exclusion criteria: Eliminated co-morbid
patients with associated cardiac, renal and other
life threatening diseases.
To collect the palmar prints black coloured
duplicating ink, rubber roller, glass, bond paper
were used. Patients were asked to wash their both
hands with soap water. Then ink was spread on
the glass with the help of roller and applied on
their hands carefully. Afterwards palmar prints
were taken on the bond paper by using PurvisSmith method.7
The ridges present on fingertip are counted from
core to delta for each finger. The Triradius
present below medial four fingers are named
a,b,c and d starts from index finger to little
finger, the Triradius present between thenar and
hypothenar eminence were named as t. From the
finger prints, the type of the pattern of the print,
TFRC, a-b ridge count along with atd angle were
find out, the results were recorded and
photographed.7
Fig1: Dermatoglyphic patterns of finger

Sample for the present study comprises palmar

prints of 75 clinically diagnosed Type II Diabetic
Fig 2: atd angle measurement.

956
Rakate etal.,
RESULT
In the sample of 75 type II Diabetes Mellitus

patients, we observed an increase in the number
of whorls of both hands in males and females of
compared with control group, while the
frequency of ulnar loop was more in control
group than diabetic patients. It has been found
that total finger ridge count increased in diabetic
patients along with a-b ridge count and atd angle
when compared with normal population.
Average of total finger ridge count measured in
males is 74.62 in Rt hand, 73.60 in Lt hand and
in females is 72.70 in Rt hand, 74.54 in Lt hand
which is more as compared to 75 non-diabetic
population, which shows average total finger
ridge count of 67.02 on Rt hand and 69.17 on Lt

hand in males while in females Rt hand 65.71
and Lt hand 61.89. The average a-b ridge count
of diabetic patients is 36.00 on Rt hand, 37.00 on
Lt hand in males and in females it is 34.66 on Rt
hand, 35.33 on Lt hand which is more as
compare to non-diabetic males counted 34.42 on
Rt hand and 35.44 on Lt hand, in females 35.85
on Rt hand, 36.78 on Lt hand. The atd angle is
wider in diabetic patients found in males 37.98
on Rt hand, 38.34 on Lt hand and in females
36.41 on Rt hand, 36.95 on Lt hand compared
with non-diabetic males 37.98 on Rt hand, 39
on Lt hand and in females 36.41 on Rt hand,
36.95 on left hand.
Table 1: Fingerprint patterns in Diabetic population, Non Diabetic population (N=75)
Pattern
Arch
Plain
Tented arch
Total
Loop
Ulnar
Radial
Total
Plain Whorl
Meet whorl
Whorls Central pocket loop
Double loop
Accidental
Total
Diabetic population
Male
Female
Right
Left
Right
hand
hand
hand
05
10
00
05
06
00
26
00
121
117
69
03
06
01
247
130
79
78
34
07
02
02
22
24
12
12
12
02
01
00
00
347
110
Left
hand
00
00
56
04
43
00
14
03
00
Non Diabetic population

Male
Female
Right Left Right Left
hand hand hand hand
03
02
05
02
09
05
00
04
19
11
164 172
89
88
03
04
02
06
343
185
40
12
22
16
03
03
01
00
16
10
13
12
10
13
08
11
00
01
00
01
108
84
Table 2: Ridge count and atd angle in Diabetic population, Non Diabetic population
Left
hand
74.54
Non Diabetic population

Male
Female
Right
Left
Right
hand
hand
hand
67.02 69.17 65.71
Left
hand
61.89
34.66
35.33
34.42
35.44
35.85
36.78
36.41
36.95
36.19
36.40
37.14
37.75
Total finger ridge count
Diabetic population
Male
Female
Right Left
Right
hand
hand
hand
74.62 73.60
72.70
a-b ridge count
36
37
atd angle
37.98
39
957
Rakate etal.,
DISCUSSION
Several authors have studied the Dermatoglyphic

patterns in type II Diabetes Mellitus patients and
their findings were matching with the
observations of the present study. Sant et al8
reported an increased number of Whorls and
decreased number of ulnar loops in type II
Diabetic mellitus patients. The findings are
similar with Knussmann et al9 and Hirsch5. Barta
et al10 found higher TFRC in type II Diabetic
patients. Vadgaonkar Rajinigandha et al11 found
increase TFRC in type II Diabetic patients. Rt
hand 53.85, Lt hand 54.73 compared with control
group Rt hand 44.73, Lt hand 44.70. She also
observed wider atd angles in diabetes 52.13 in Rt
hand and 52.51 in Lt hand which was compared
with control group 43.60 in Rt hand and 44.26 in
Lt hand. Iqbal et al12 reported increased TFRC in
non-insulin dependent diabetes mellitus patients.
Sarthak Sengupta et al13 reported increased
frequency of whorls in male type II diabetic
patients. However, Banarjee et al14 Chakravartti15
found a higher frequency of loops.
CONCLUSION
The current work emphasises increased number

of whorl, decreased number of loops and arch in
type II diabetes mellitus patients along with
increased TFRC, a-b ridge count and wider atd
angle in male while in females decreased tfrc, a-b
ridge count and narrower atd angle as compared
with non-diabetic population.
AKNOWLEDGEMENT
With a deep sense of gratitude I hereby

acknowledge the support render by Principal and
Management of Dr. Vikhe Patil Medical College.
REFERENCES
1. Gardner DG, Dolores. Greenspan's basic &

clinical endocrinology. New York. McGrawHill Medical. pp. 2011;9:17.
2. Diabetes
mellitus
type
2
http://en.wikipedia.org/wiki/Diabetes_mellitu
s_type_2
3. Ravindranath R, Joseph AM, Fluctuating
asymmetry in dermatoglyphics of noninsulin-dependent diabetes mellitus in
Bangalore-based population. Ind J Human
Genetics.2005;11:3: 149-153.
4. Kahn HS, Graff M, Stein AD and Lumey LH.
A fingerprint marker from early gestation
associated with diabetes in middle age. The
Dutch Hunger Winter Families Study.
International Journal of Epidemiology.2009;
38(1):10109.
5. Hirsch W. Dermatoglyphics and creases and
their relationship to clinical syndromes, A
diagnostic criteria in dermatoglyphics an
international perspective. J. Mavalwala
Jamshed.1978; 263282
6. Henry ER. Classification and uses of
fingerprints. London http://www.clpex.com/
Information/ Pioneers/henry-classification.
pdf. 1900.
7. Purvis-Smith SG. Finger and Palm printing
techniques for the clinician. Med J Aust
1969;2:189.
8. Sant SM, Vare AM, Fakruddin S,
Dermatoglyphics in Diabetes Mellitus. J
Anatomical society India. 1983;35(1): 29-32.
9. Knussmann R, Nach ZF, Zwisehen B.
Diabetes Mellitus and Hautleisten system In
Hautleisten and Krankheiten 1971.
10. Barta L, Vari A, Susa E, Dermatoglyphic
patterns of Diabetic children. Acta Paediatric
Acad Sci Hung 1970;11:71-74.
11. Vadgaonkar R, Pai M, Saralaya PL, Vasudha.
Digito-palmar complex in Non-insulin
dependent Diabetes mellitus. Turk J Med Sci
2006;36(6):353-55.
12. Iqbal MA, Sahay BK, Ahuja YR. Finger and
palmar ridge counts in Diabetes mellitus.
Acta Antropogenetica. 1978;2:35-38.
958
Rakate etal.,
13. Sengupta S, Boruah J. Finger dermatoglyphic

patterns in Diabetes mellitus J.Hum.Ecol.
1996;7(3):203-06.
14. Banerjee AR, Banarjee N, Sarkar NC, Pal,
Gupta M. Dermatoglyphics in disease
diabetes mellitus. Ind J Phys, Antrop Hum
Gen. 1985;11:165-70.
15. Chakravartti MR. Association between
Diabetes mellitus and dermatoglyphics.
1967;157-60.
959
Rakate etal.,
DOI:10.5958/j.2319-5886.2.4.154

&
Health Sciences
www.ijmrhs.com
th
Review article
HERPES ZOSTER: AN UPDATE

*Bansal Puja1, Bhargava Deepak2, Ali Sheeba3
1
Reader, 2Professor & Head, 3Postgraduate student, Department of Oral Pathology & Microbiology,
School of Dental Sciences, Greater Noida, India
*Corresponding author email: dr.puja.bansal.09@gmail.com
ABSTRACT
Herpes zoster (HZ) is the reactivated form of the Varicella zoster virus (VZV), the same virus
responsible for chickenpox. The condition produces a striking picture, with a blistering, crusting rash
confined to well demarcated areas of the body. Latency is typically life long, and Herpes Zoster is
caused by viral reactivation from the latent state. The survival of Varicella Zoster Virus in human for
several million years attests to its success. Present review provides an overview of the natural history,
epidemiology and possible complications of varicella zoster virus along with diagnosis, prophylaxis and
different treatment modalities.
Keywords: Varicella, Herpes, Shingles
INTRODUCTION
The term herpes comes from the ancient Greek

word meaning to creep or crawl. The human
herpes family is officially known as
Herpetoviridae.1 Eight different types of herpes
viruses are known whose primary hosts are
humans. They have been officially designated
Human herpes types 1-8.2 Human herpes
simplex viruses type 1 and type 2, both, are
cytolytic in nature and have neurons as the site of
latent infection, whereas human herpes viruses
type 4 (Epstein barr virus), type 6 and type 7
have lymphoproliferative effect. The only known
human herpes virus which is cytomegalic is type
5, commonly known as a Cytomegalo virus
(Table 1). 2,3 In 1889, Von Bokay suggested that
varicella (chickenpox) and herpes zoster (HZ)
are different manifestations of same virus

infection. 2 Varicella Zoster Virus, a neurotropic
human herpes virus causes chicken pox and then
remains latent for decades in cranial nerve,
dorsal root and autonomic nervous system
ganglia. The virus gets reactivated after a
variable period of time usually ranging from 5-40
years in 15% patients and causes herpes zoster.4
Herpes Zoster is more commonly known as
shingles, from the Latin cingulum, for girdle.
This is because a common presentation of HZ
involves a unilateral rash that can wrap around
the waist or torso like a girdle. Similarly, the
name zoster is derived from classical Greek,
referring to a belt-like binding (known as a
zoster) used by warriors to secure armor.3
960
Puja Bansal etal.,
Table.1: Classification, cytopathology, site of latent infection and common associated diseases of human
herpes virus.2,3
Species
Cytopathology
Common associated diseases
Cytolytic
Site of latent
infection
Neurons
Herpes simplex virusType I

Herpes simplex virusType 2
Herpes virus- Type 3
Varicella zoster virus
Herpes virus- Type 4
Epstein- barr virus
Cytomegalo virus
Cytolytic
Neurons
Genital herpes lesions
Cytolytic
Neurons
Chickenpox, shingles
Lymphoproliferative
Lymphoid tissues
Infectious mononucleosis
Cytomegalic
Secretory glands, CMV mononucleosis

kidneys etc
Lymphoproliferative
Lymphoid tissues
Lymphoproliferative
Lymphoid tissues
STRUCTURE
Varicella zoster virus belongs taxonomically to

the group of alpha herpes viruses. It has doublestranded, linear DNA, consisting of about 125kilobase pairs, encased within an icosahedral
protein capsid, composed of 162 capsomers. The
nucleocapsid is surrounded by a pleomorphous
outer shell (tegument with envelope membrane),
which is rich in phosphoprotein. Diameters vary
between 150 and 180 nm due to the variability of
the outer shell.5
EPIDEMIOLOGY
A systemic review published in 2004 found the

overall
incidence
of
zoster
among
immunocompetent subjects ranged from 1.2-4.8
per 1000 people; recent studies from United
Studies and France have also reported disease
incidences within this range.6 The estimated
annual incidence of HZ in Cebrin-Cuenca et al.
(2010) study was 4.1 per 1,000 persons >14 years
of age.7 The increased risk of zoster among older
individuals may be due to waning of specific
Oral herpes lesions
Roseola, mononucleosis
syndromes
Currently, no human disease
definitely linked
Suspected association with
Kaposis sarcoma
immunity with increasing time since primary

infection (varicella), or may occur as part of the
generalized decay in cell-mediated immunity that
occurs with age (immunosenescence), an
important factor in the increased susceptibility to
infections, malignancies, and autoimmune
disorders in the elderly. Little is known about the
determinants of either generalised or VZVspecific immune decay.8
CLINICAL MANIFESTATIONS
The prodromal syndrome stage presents as

sensations described as burning, tingling, itching,
boring, prickly or knife-like occurring in the skin
over the affected nerve distribution.9 Pain is the
most annoying symptom of herpes zoster. It
often precedes and generally accompanies the
rash.10 Zoster rash is a vesicular eruption on an
erythematous base in one to three dermatomes,
usually accompanied by severe, sharp,
lancinating, radicular pain, itching, and
unpleasant, abnormal sensations (dysesthesias).
Patients may also have decreased sensation in the
961
Puja Bansal etal.,
affected area, while the skin is exquisitely

sensitive to touch (allodynia).11
Within 3 to 5 days of the initial symptoms, an
erythematous maculopapular rash erupts
unilaterally in the nerves of sensory dermatomes
adjacent to the involved ganglia. Over the next 7
to 10 days, the rash progresses to pustules and
ulceration, with crusts, scabbing, or both, this can
persist for up to 30 days in the acute phase. At
the end of the healing process, altered (post
inflammatory) pigmentation may develop along
the affected dermatome. 12 Complete healing may
take more than 4 weeks.13 The cutaneous
eruption is unilateral and does not cross the
midline. Simultaneous involvement of multiple
noncontiguous dermatomes virtually never
occurs in immunocompetent patients, although
lesions overlap adjacent dermatomes in 20
percent of cases.14
DIAGNOSIS
Differential diagnosis: Definitive diagnosis
involves a process of elimination, with several
likely aetiologies in the differential diagnosis. A

differential diagnosis should include trigeminal
neuralgia, maxillary sinusitis, periodic migraines
neuralgia, myocardial pain, atypical facial pain
and Munchausens syndrome.9
Laboratory
diagnosis:
Histopathological
features; cytologic alterations are virtually
identical to those of human herpes simplex virus.
Intranuclear inclusions- lipschutz bodies may be
seen in smears prepared by scraping of the base
of the early vesicles (Tzanck smears) and stained
with toulidiene blue, Giemsa or PAP. Infected
cells exhibit acantholysis, nuclear clearing and
nuclear enlargement that is ballooning
degeneration.
Connective
tissue
shows
1,2
inflammatory cells infiltate.
On the basis of histological features one cant
rule out the definite diagnosis of herpes zoster
infection form herpes simplex. Co-relation with
clinical features is required. Table 2 enumerates
some differences between herpes zoster and
recurrent herpes simplex infection.
Table 2: Difference between herpes zoster and recurrent herpes simplex15

Characteristic
Herpes Zoster
Recurrent Herpes Simplex
Sites of latent infections
Sensory neurons in all sensory Sensory neurons in trigeminal and
ganglia
sacral sensory ganglia
Viral gene expression
Several immediate early
No HSV proteins are synthesized; only
during latency
and early VZV proteins are latency-associated transcripts
synthesized
Symptomatic reactivation of Infrequent (rarely involves the Frequent (usually involves the same
latent virus
same dermatome)
dermatome)
Asymptomatic reactivation
None
Frequent
with asymptomatic virus
shedding
Proportion of the affected
Large (sensory fields of many Small (often the sensory field of a
dermatome involved by rash neurons)
single neuron)
Consequences of
Extensive ganglionic
No obvious ganglionic pathology or
reactivation of latent virus
pathology and neuronal death neuronal death
Postherpetic neuralgia
Common
Extremely rare
Frequency of symptomatic
Increases with increasing age Decreases over time after primary
reactivation
(and time after primary
infection
infection)
962
Puja Bansal etal.,
In most cases, a diagnosis of VZV infection is

based on the characteristic prodrome of
symptoms and the pattern of skin eruptions.
Virus isolation can be attempted from the buccal
or cutaneous lesion in the early stages by
inoculating human amnion, human fibroblasts,
HeLa or Vero cells but typically viral culture
test.2 Viral culture, antigen detection test by
using modified Tzank technique. Serological test
via ELISA or latex agglutination, polymerase
chain reaction (PCR) is useful to detect VZV
DNA.16
COMPLICATIONS
Postherpetic Neuralgia (PHN): Postherpetic

neuralgia (defined as pain that persists more than
30 days after the onset of rash or after cutaneous
healing) is the most feared complication in
immunocompetent
patients.14
Clinically
significant PHN was described by R. Edgar
Hope-Simpson in 1975 as a chronic neuropathic
pain syndrome that may contribute recovery
from an acute attack of herpes zoster.17 Although
it has a high morbidity, the mechanism causing
PHN remains unknown, its occurrence cannot be
predicted at the time of zoster and its treatment is
still highly unsatisfactory and generally
ineffective.18
Cutaneous complications: Cutaneous dissemination of herpes zoster defined as more than 20
vesicles outside the area of primary or adjacent
dermatomes and occurs in approximately 10% of
immunocompromised persons.10 Acute and
chronic complications involving the skin are
frequent. The skin is predominantly affected by
bacterial secondary infections in the acute stage.
Ecthymiform ulcerations may develop. Other
cutaneous complications include: hemorrhages
(zoster hemorrhagicus), purulent gangrene
(zoster gangrenosus), and persistence of lesions
and dissemination (zoster disseminatus) in
immunocompromised patients. A manifestation
of psoriasis vulgaris (Kobners phenomenon)
may occur with chronic hypo-pigmented and
depigmented scar formation.19
Herpes zoster ophthalmicus (HZO): Herpes

zoster ophthalmicus occurs when reactivation of
the latent virus in the trigeminal ganglia involves
the ophthalmic division of the nerve.20 While
HZO does not necessarily affect the structures of
the eye, many of the acute and long-term
complications associated with the disease are the
result of direct viral toxicity to the eye or the
ensuing inflammatory response within the eye.21
Hutchinsons sign is dened as skin lesions at the
tip, side, or root of the nose and is a strong
predictor of ocular inammation and corneal
denervation in HZO, especially if both branches
of the nasociliary nerve are involved.22
Ramsay Hunt syndrome and other neurological
syndromes: Less common manifestations of
zoster include the Ramsay Hunt syndrome
(involvement of the geniculate ganglion of the
facial nerve) which manifests as vesicles in the
external auditory canal and palate associated
with loss of taste to the anterior two-thirds of the
tongue and facial weakness.23
Neurologic
symptoms
(headache,
fever,
vomiting, and altered sensorium) most often
occur about 1 week after the onset of the
varicella rash. The onset of symptoms may be
abrupt or gradual and is accompanied by seizures
in 29%52% of cases.24
Prophylaxis
The live attenuated Oka vaccine was developed
in 1974 by Takahashi in Japan. Virus from a
child with varicella was serially passaged at low
temperature (34C) in human broblasts,
followed by a passage in guinea pig embryo
broblasts and the production of a standardized
seed lot in human diploid cells. Production of the
vaccine is now standardized according to the
World
Health
Organizations'
good
25
manufacturing process.
Recommended dose for children 1-12 yrs is a
single subcutaneous dose, while in case of adults
and adolescents 2 doses (6-10weeks apart)
should be given.2
963
Puja Bansal etal.,
TREATMENT
The objectives of treating HZ are to control acute

pain, accelerate rash healing, minimize systemic
complications and reduce the risk of PHN and
other complications.26 In most cases, HZ is selflimiting and treatment with analgesics suffices.
Based on level I evidence, antiviral medication

might have some effect on the severity of acute
pain and the duration of skin lesions.27 Most
commonly used drugs used in treatment of
herpes infections are given in Table 3.
Table 3: Treatment of Acute Herpes Zoster.13

Class of agent and usual Patients in whom treatment is indicated
dose
*All who present within 72 h of rash onset.
Antivirals
*Famciclovir: 250 mg orally *Consider antivirals in those who present
3 times daily for 7 days.
>72 hrs after rash onset if they have the
*Valacyclovir: 1 g orally 3 following characteristics:
times daily for 7 days.
- Age >50 y
*Acyclovir: 800 mg orally 5
- Immunocompromised status
times daily for 7 days.
- Severe pain at presentation
*In immunocompromized
-High-risk lesions (involving tip of
patients/disseminated
nose/eye)
disease: acyclovir, 10 mg/kg
intravenously every 8 h
until resolution of cutaneous
/ visceral disease
Glucocorticoids
Those who are older and/or those with
Prednisone: 60 mg orally severe pain as long as no contraindications
for 7 d, then taper for next 2 exist.
weeks.
Comments
Antivirals reduce both
acute
symptoms
and
subsequent risk of PHN.
Corticosteroids have no
effect on the subsequent
development of PHN and
should be used with
antivirals, never alone;
significant adverse effects
are possible.
*Pain medications
Most will require some type of pain Opioids should be used
*Tramadol
medication.
with caution in elderly
*Oxycodone/acetaminophen
patients.
Prophylactic laxatives and
stool softeners should be
considered when
prescribing opioids.
CONCLUSION
Herpes zoster represents a mode of evolutionary

adaptation by the VZV which is an obligate
human parasite. Normal aging, poor nutrition,
and immunocompromised status correlate with
outbreaks of herpes zoster, and certain factors
such as physical or emotional stress and fatigue
may precipitate an episode. In small countries,

the susceptibilities are completely eliminated by
varicella infection in childhood. Therefore, the
ability of the virus to remain latent and reappear
as zoster years later confers on it a great survival
advantage.
964
Puja Bansal etal.,
REFERENCES
1. Neville BW, Damm DD, Allen CM, Bouquot.

Viral infections. Oral and Maxillofacial
Pathology. 3rd ed. Reed Elsevier India Private
Limited. Noida. 2009. p.240
2. Ananthanaryan R, Paniker CKJ. Virus-Host
interactions: Viral infections. Textbook of
Microbiology. 7th ed. Orient Longman Private
Ltd. Chennai. 2006.p.474
3. Roxas M. Herpes Zoster and Postherpetic
Neuralgia: Diagnosis and Therapeutic
Considerations.
Altern
Med
Rev.
2006;11(2):102-13.
4. Raza N, Iqbal P, Anwer J. Recurrence of
Herpes Zoster In An Immunocompetent
Adult Male. J Ayub Med Coll Abbottabad.
2005;17(3):80-81.
5. Wittek M. Advances in the diagnostics of
Varizella Zoster Virus and Importance of
Vaccination. J Lab Med. 2008;32(4). doi
10.1515/JLM.2008.041et
6. Forbes HJ, Thomas SL, Langan SM. The
Epidemiology and Prevention of Herpes
Zoster. Curr Derm Rep. 2012;1:3947
7. Cebrin-Cuenca AM, Dez-Domingo J,
Rodrguez MSM, Puig-Barber J, NavarroPrez J. Epidemiology of Herpes Zoster
Infection among Patients Treated in Primary
Care Centres in the Valencian Community
(Spain). BMC Family Practice. 2010;11:33.
8. Thomas SL, Hall AJ. What does
epidemiology tell us about risk factors for
herpes zoster? Lancet Infect Dis. 2004;4:26
33
9. Tidwell E, Hutson B, Burkhart N, Gutman
JL, Ellis CD. Herpes zoster of trigeminal
nerve third branch: a case report and review
of literature. International endodontic journal.
1999;32:61-66.
10. Kutlubay Z, Gksgr N, Engin B, Tzn Y.
Complications of Herpes Zoster. J Turk Acad
Dermatol. 2011;5(2):115-21
11. Nagel MA, Gilden DH. The protean
neurologic manifestations of varicella-zoster
virus infection. Cleveland Clinic Journal of

Medicine. 2007;74(7):489-500
12. Kenneth R. Cohen KR, Salbu RL, Frank J,
Israel I. Presentation and Management of
Herpes Zoster (Shingles) in the Geriatric
Population. P T. 2013;38(4):217-24
13. Sampathkumar P, Drage LA, Martin DP.
Herpes Zoster (Shingles) and Postherpetic
Neuralgia. Mayo Clin Proc. 2009;84(3):274
80
14. Gnann JW Jr, Whitley RJ. Herpes Zoster. N
Engl J Med. 2002;347(5):340-46.
15. Oxman MN. Herpes Zoster Pathogenesis and
Cell-Mediated
Immunity
and
Immunosenescence. J Am Osteopath Assoc.
2009;109(6):(Suppl 2):13-17
16. Srikrishna K, Prabhat MPV, Balmini PR,
Sudhar S, Ramarjun D. Herpes Zoster:
Report of a treated case with review of
literature. J Indian Aca Oral Med Radiol.
2012;24(1):51-55
17. Hempenstall K, Nurmikko TJ, Johnson RW,
A'Hern RP, Rice ASC. Analgesic Therapy in
Postherpetic Neuralgia: A Quantitative
Systematic Review. PLoS Med. 2005; 2(7)
:e164.
18. Kennedy PGE, Montague P, Scott F, Grinfeld
E, Ashrafi GH. Varicella-Zoster Viruses
Associated with Post-Herpetic Neuralgia
Induce Sodium Current Density Increases in
the ND7-23 Nav-1.8 Neuroblastoma Cell
Line. PLoS ONE. 2013;8(1):e51570.
19. Singh BS, Scholand SJ. Herpes Zoster: A
Clinical Review. J Infect Dis Antimicrob
Agents. 2011;28(3):211-21
20. Shaikh S, Christopher N, Evaluation and
Management of Herpes Zoster Ophthalmicus.
Am Fam Physician. 2002;66(9):1723-30
21. Catron T, Hern HG. Herpes Zoster
Ophthalmicus. WestJEM. 2008;9:174-176.
22. Liesegang TJ. Herpes Zoster Ophthalmicus
Natural History, Risk Factors, Clinical
Presentation, and Morbidity. Ophthalmology.
2008;115:S3S12
965
Puja Bansal etal.,
23. Wehrhahn MC, Dwyer DE, Herpes Zoster:

epidemiology, clinical features, treatment and
prevention. Aust Prescr. 2012;35:143-7.
24. John W, Gann Jr. Varicella-Zoster Virus:
Atypical
Presentations
and
Unusual
Complications.
J
Infect
Dis. 2002;186(1):S91-8.
25. Breuer J. Vaccination to prevent varicella and
shingles. J Clin Pathol. 2001;54:743-747.
26. Whitleya RJ, Volpib A, McKendrickc M,
Wijckd AV, Oaklander AL. Management of
Herpes Zoster and Post-Herpetic Neuralgia
now and in the future. Journal of Clinical
Virology. 2010;48(S1):S20S28
27. Opstelten W, Eekhof J, Neven AK, Verheij
T. Treatment of Herpes Zoster. Can Fam
Physician 2008;54:373-7.
966
Puja Bansal etal.,
DOI:10.5958/j.2319-5886.2.4.155

&
Health Sciences
www.ijmrhs.com
th
Accepted: 22nd Aug 2013
Case report
SEVERE PETER PLUS SYNDROME: A RARE CASE REPORT

Dhananjay Y Shrikhande1, *Amol Pokharkar2, Jayshree Jadhav3, Divyank Pathak2, Vivek Dholakiya2,
Amit Narkhede2
Professor and Head, 2Post graduate student, 3Associate Professor, Department of Pediatrics, Pravara
Institute of Medical Sciences, Loni, Maharashtra, India
1
*Corresponding author email: amolpokharkar87.ap@gmail.com

ABSTRACT
Severe Peter plus Syndrome is a rare autosomal recessive condition that is characterized by ocular
anomaly and associated with other systemic major or minor anomalies. Mutations of B3GALTL gene
encoding beta 1,3 glucosyltransferase have been seen in patients with Peter Plus Syndrome.1 We report
a male patient with unusually severe manifestations of Peter Plus Syndrome including prominent
forehead, long area between nose and mouth (philtrum), pronounced double curve of the upper lip,
Anterior Eye Staphyloma (Bilateral), retrognathia, widely spaced nipples and Fallots tetralogy. To our
knowledge Fallot has not been reported previously in Peter plus Syndrome and bilateral anterior
staphyloma, a most severe anterior chamber eye defect i s also apparently rare in this syndrome. Our
patient might represent a new variant of severe Peter plus syndrome w i t h anterior eye Staphyloma and
Fallots tetralogy.
Key words Severe Peter Plus syndrome, Fallots tetralogy, Anterior eye staphyloma, Retrognathia
INTRODUCTION
Severe Peter Plus syndrome is a very rare

autosomal recessive condition characterized by
ocular anolamly, disproportionate short stature,
developmental delay, cleft lip/palate and other
systemic major or minor anomalies. Peter plus
syndrome is also known as Krause-van
Schooneveld Kivlin syndrome. 1-3
We report a male patient with unusually severe
manifestations of Peter Plus Syndrome including
prominent forehead, long area between nose and
mouth (philtrum), pronounced double curve of
the upper lip,

Anterior eye staphyloma
(Bilateral), retrognathia, widely spaced nipples
and Fallots tetralogy.
CASE
A term male neonate (birth weight: 2.9Kg),

normal delivery, born to non consanguineous
parents at 7th week of gestational age was
brought to our hospital on 1st day of life with
complaints of protrusion of right eyeball.
Examination revealed prominent forehead, long
967
Dhananjay et al.,
area between nose and mouth (philtrum),

pronounced double curve of upper lip (Cupids
bow), bilateral anterior eye Staphyloma, webbed
neck, retrognathia & micrognathia, short stature.
Systemic examination revealed a single second
sound in pulmonary area, systolic murmur, no
cyanosis. 2D- ECHO findings revealed
Tetralogy of Fallot.
also noticed that intellectual disability may be

present which may be mild to severe, although
some
individuals
may
have
normal
6
intelligence . We report a male patient
(neonate) with unusually severe manifestations
of Peter plus Syndrome.7 Fallots Tetralogy has
not been reported previously in Peter Plus
Syndrome. Bilateral Anterior Staphyloma, a most
severe anterior chamber eye defect is also
relatively rare in this syndrome.8 Our patient
might represent a new variant of Severe Peter
plus Syndrome with anterior eye Staphyloma and
Fallots tetralogy.9,10
REFERENCES
Fig.1: Widely spaced nipples, depressed nasal

bridge, cupids bow
Fig.2: Large forehead, long philtrum, right eye

staphyloma
DISCUSSION
Mutations o f B 3 G A L T L g e n e e n c o d i n g
beta 1,3glucosyltransferase have been seen in
patients with Peter Plus Syndrome4. Less than 70
people with this condition have been reported
worldwide. Patients with this syndrome may also
have shortened upper limbs i.e. rhizomelia and
shortened fingers and toes (brachydactyly)5. It is
1. Aliferis K, Marsal C, Pelletier V, Doray B,

Weiss MM, Tops CMJ. A novel nonsense
B3GALTL mutation confirms Peters plus
syndrome in a patient with multiple
malformations
and
Peters
anomaly.
Ophthalmic Genetics. 2010;31(4):20508.
2. Boog G, Le Vaillant C, Joubert M. Prenatal
sonographic
findings
in
Peters-plus
syndrome. Ultrasound Obstet Gynecol.
2005;25:60206.
3. Frydman M, Weinstock AL, Cohen HA,
Savir H, Varsano I. Autosomal recessive
Peters anomaly, typical facial appearance,
failure to thrive, hydrocephalus, and other
anomalies: further delineation of the KrauseKivlin syndrome. Am J Med Genet.
1991;40:3440.
4. Kosaki R, Kamiishi A, Sugiyama R, Kawai
M, Hasegawa T, Kosaki K. Congenital
hypothyroidismin peters plus syndrome.
Ophthalmic Genet. 2006;27:675.
5. Kozma K, Keusch JJ, Hegemann B,
Luther KB, Klein D, Hess D, Haltiwanger
RS, Hofsteenge J. Identification and
characterization
of
abeta1,3glucosyltransferase that synthesizes the Glcbeta1,3-Fuc disaccharide on thrombospondi
type
1
repeats.
J
Biol
Chem.
2006;281:3674251.
968
Dhananjay et al.,
6. Krause U, Kovisto M, Rantakillio P. A case

of Peters' syndrome with spontaneous corneal
perforation. J PediatrOphthalmol. 1969;
6:1459.
7. Maclean K, Smith J, St Heaps L, Chia N,
Williams R, Peters GB, Onikul E, McCrossin
T, Lehmann OJ, Ads LC. Axenfeld-Rieger
malformation and distinctive facial features:
Clues to a recognizable 6p25 microdeletion
syndrome. Am J Med Genet A. 2005;132:381
8. Maillette de Buy Wenniger, Prick LJ,
Hennekam RC. The Peters' plus syndrome: a
review. Ann Genet. 2002;45:97103
9. Traboulsi E. Peters anomaly. In: Stevenson
RE, Hall JG, eds. Human
Malformations
and
Related Anomalies. 2nd ed. New
York, NY: Oxford University Press;
2006:313-14.
10. Yang LL, Lambert SR, Lynn MJ,
Stulting RD. Surgical management of
glaucoma in infants and children with Peters'
anomaly: long-term structural. J AAPOS.
2000;4(4):205-10.
969
Dhananjay et al.,
DOI:10.5958/j.2319-5886.2.4.156

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Case report
Copyright @2013
ISSN: 2319-5886
IDIOPATHIC NEONATAL RECTAL PERFORATION: A CASE REPORT

*Nyamannawar Babu1, Nagathan Vikram2, Vallabha Tejaswini3
1
Associate Professor of Surgery, 2 Resident in Surgery, 3Professor & Head, Department of Surgery,
Shri B.M.Patil Medical College, Bijapur, Karnataka, India
*Corresponding author email: babugouda@icloud.com
ABSTRACT
Idiopathic perforation of rectum in newborns is extremely rare. Etiology of spontaneous neonatal rectal
perforation is unknown. We report a case of idiopathic rectal perforation in a neonate who presented
with signs of perforative peritonitis. This case is reported because of its rarity.
Keywords: Rectal perforation, Spontaneous gastrointestinal perforation.
INTRODUCTION
Perforative peritonitis is one of the common

neonatal emergencies encountered. It is life
threatening condition. Such perforations are
explained by mechanical distal obstruction like
anorectal anomalies1, Hirschsprungs disease2,
mechanical injury like rectal thermometer usage,
and administration of contrast enema3.
Perforations are commonly observed in small
intestine, followed by large intestine, and
stomach4. Perforation of the rectum without a
known etiological factor such as injury,
iatrogenic cause, inflammatory disease, and
distal obstruction is defined as the idiopathic
perforation of the rectum4. We report a case of
idiopathic neonatal rectal perforation for its
rarity.
CASE REPORT
A day one, term, home delivered male baby

presented to hospital with complaints of
distension of abdomen noticed at 6 hours after

Shri B M Patil Medical College Bijapur. There
was no history of resuscitation, or rectal
instrumentation. Child had normal antenatal
history and care. It weighted 2.5 Kg. Child was
acutely ill, lethargic with cold peripheries,
hypothermia, tachycardia, tachypnea with feeble
peripheral pulses. The abdomen was distended
with signs of peritonitis. Anus was normally
sited. Hematological investigations were normal
&
radiography
revealed
massive
pneumoperitoneum
(Fig.1).
Baby
was
resuscitated with correction of fluid deficit,
inotrope support, and broad spectrum antibiotics.
Explorative
laparotomy
showed.
Pneumoperitoneum, fecal peritonitis with 0.5 cm
wide perforation on the rectum. Closure of rectal
perforation with loop sigmoid colostomy was
done. Postoperative recovery was uneventful.
Histopathology suggested benign nonspecific
970
Babu et al.,
inflammatory pathology. Colostomy closure was

done after 6 months. At follow up the baby has
normal growth development.
Fig.1: Erect x ray abdomen showing gross

pneumoperitoneum (saddle sign)
DISCUSSION
The etiology of spontaneous intestinal

perforation is still being debated. The common
identifiable etiologic factors are mechanical
distal obstruction like anorectal malformations1,
Hirschsprungs disease2, mechanical injury by
thermometer usage, and contrast enemas2.
However these factors were absent. Ischemic
necrosis, secondary to a localized vascular
accident in the wall of the affected viscus could
explain such spontaneous intestinal bowel
perforations5. They noticed six out of seven
babies had intestinal perforations on the antimesenteric aspect of the bowel, indicating
localized vascular accident as possible etiology.
Congenital segmental absence of intestinal wall
musculature is another proposed etiologic factor
to explain idiopathic neonatal intestinal
perforations 6.
Idiopathic intra-peritoneal perforation of rectum
in newborn is extremely rare. There is only one
case reported in literature 4. However there are
many reports, describing extra-peritoneal
perforation of rectum which classically presents
as spreading cellulites in perianal and buttock
regions with or without leakage of feces7. In such
a scenario diverting proximal sigmoid stoma
with drainage of perianal region is advised.
Defects in pelvic floor are noticed in such babies.

In intra-peritoneal perforation of rectum, early
diagnosis and prompt resuscitation cant be
overemphasized. Radiography allows earlier
diagnosis and prompt surgical treatment. The
abdominal upright film will show saddle or
football sign due to the massive pneumo peritoneum. Isolated rectal perforation can be
managed by closure of perforation, if general
condition is stable. In case of severe sepsis,
proximal diverting sigmoid stoma with closure of
perforation is a safer alternative.
In conclusion there are many factors associated
with Idiopathic neonatal rectal perforation, such
as localized ischemia, and defect in the muscular
wall of the bowel. In a given case their relative
significance is difficult to assess. Early
recognition of the perforation is of paramount
importance for a successful outcome. This case is
being reported for its rarity and to inform that
though rare, it can occur.
Conflict Of Interest: Authors do not have
conflicts of interest.
Funding Source: Nil
REFERENCES
1. Sharma
SB, Gupta
V, Sharma
V.
Gastrointestinal perforations in neonate with
anorecctal
malformations.
Indian
J
Gastroenterol. 2004;23:107-08.
2. Khan TR et al. Neonatal pnemopertoneum: a
critical appraisal of its causes and subsequent
management from a developing country.
Pediatr Surg Int. 2009;25:1093-97.
3. De Feiter PW, Soeters PB, Dejong CH.
Rectal perforations after barium enema: a
review. Dis Colon Rectum. 2006;49:261-71.
4. Prabhakar G. Spontaneous gastrointestinal
perforation in the neonate. Indian Pediatr.
1991;28:1277-80.
5. Weinberg
G, Kleinhaus
S, Boley SJ.
Ideopathic intestinal perforations in the
newborn: An increasingly common entity. J
Pediatr Surg. 1989;24:1007-08.
971
Babu et al.,
6. Husain
AN, Hong
HY, Gooneratne
S, Muraskas J, Black PR. Segmental absence
of small intestinal musculature. Pediatr
Pathol. 1992;12:407-15.
7. Davies MR, Cywes S, Rode H. Prenatal
perfotion of the extraperitoneal part of the
rectum associated with a developmental
defect
of
the
pelvic
floor.
Z
Kinderchir. 1984;39:271-3.
972
Babu et al.,
DOI:10.5958/j.2319-5886.2.4.157

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th
Case report
CASE REPORT OF A RARE FUNGAL CORNEAL ULCER

Rajvin Samuel Ponraj1, Srinivasan M2, Sundararajan D3, Senthamarai S4, Sivasankari S5, Anitha C6,
Amshavathani SK7
1
Post graduate student, 2Professor & Head, 3Associate Professor, Dept of Ophthalmology, Meenakshi
Medical College, Kanchipuram, Tamilnadu, India
4
Associate professor, 5Asst. professor, 6Tutor, 7Professor & HOD, Department of Microbiology,
Meenakshi Medical College, Kanchipuram, Tamilnadu, India
*Corresponding author email: samuelpnrj25@gmail.com
ABSTRACT
The dematiaceous fungi appear to be an increasing cause of human disease. This was a case of a patient
coming with complaints of watering and irritation of right eye following injury to her eye by a stick.
Scrappings from corneal ulcer were sent for gram stain, bacterial and fungal culture. Cladosporium
species of fungus was isolated from a patient who presented with a corneal ulcer not responding to
natamycin drops. Ointment fluconazole was prescribed along with natamycin , moxifloxacin and
atropine drops. The corneal ulcer began to respond and healed completely.
Keywords: Cladosporium, Dematiaceous, Keratomycosis, Conidiophores
INTRODUCTION
Many fungal species can invade the cornea and

result in Keratomycosis which is an infective
condition of the cornea. It is typically a slow
progressive disease. It is mandatory that this be
distinguished from its counterpart namely
bacterial keratitis. Ocular surfaces which have
been compromised or suffered trauma are likely
to be caused by fungus. The type of fungi varies
with the geographic location and the climate.
Due to the profound use of steroids and
antibiotic, its incidence has increased over the
years. Diagnosis and treatment of keratomycosis
has become a challenge to ophthalmologists
because of its resistance to treatment and

difficulty in obtaining drug sensitivity.1,2
Samuel Ponraj et al.,
CASE REPORT
A 50-year old female patient presented with a

history of a stick injury to her right eye. Her
main complaint was irritation and watering of her
right eye. On examination the affected eye had
oedema of the eye lid, injected conjunctiva, ulcer
on the cornea covered with slough and a sluggish
reaction of pupil to light. Scrapings from corneal
lesion were taken and sent for bacterial and
fungal culture. Gram stain showed few pus cells
and no bacteria was seen. Bacterial culture
showed no growth. Potassium hydroxide mount
973
showed actively branching septae and thin

hyphae.
Fungal culture on Sabourand Dextrose Agar
plate showed dark green to black coloured
flattened colonies and rapidly spreading black
coloured colonies on the reverse side.
Microscopic findings showed blastoconidia in
branching chains. The patient was on the
following medications during attending the
outpatient clinic. Moxifloxacin eye drops-1 drop
(8 times per day), Natamycin eye drops-1 drop (8
times per day), Atropine (1 drop twice a day).
The lesion did not respond to the above
mentioned treatment. She was prescribed
ointment fluconazole to be applied twice a day
along with the above mentioned medications.
The ulcer responded to treatment and healed
completely.
Fig 1: Culture growth of Cladosporium colonies
DISCUSSION
Keratomycosis is most commonly caused by

filamentous fungi which can be further classified
into two types: pigmented (dematiaceous) fungi
which produce characteristic black/brown
pigment appreciable clinically and/or on culture
media and nonpigmented (moniliaceous) fungi
which do not produce such pigments3
Cladosporium is a dematiaceous (pigmented)
mould widely distributed in air and rotten
organic material and frequently isolated as a
contaminant on foods. Some species are
predominant in tropical and subtropical regions.
The growth rate of Cladosporium colonies is
moderate on potato dextrose agar at 25C and the
texture is velvety to powdery. Similar to the
other dematiaceous fungi, the color is olivaceous
green to black from the front and black from the
reverse.4,5 Most of the Cladosporium spp. does
not grow at temperatures above 35C.
Cladosporium spp. produce septate brown
hyphae, erect and pigmented conidiophores, and
conidia. Cladosporium spp.
produce septate
brown
hyphae,
erect
and
pigmented
conidiophores, and conidia.
They have a geniculate appearance. In addition,
conidiophores of Cladosporium herbarum bear
terminal and intercalary swellings. Conidia
of Cladosporium spp. in general are elliptical to
cylindrical in shape, pale to dark brown in color
and have dark hila.6
REFERENCES
Fig 2: Microscopic appearance of Conidiophores,

Condidia
1. Ibrahim MM, Vanini R, Ibrahim FM, Fioriti

LS, Furlan EM, Provinzano LM, etal.,
Epidemiologic aspects and clinical outcome
of fungal keratitis in southeastern Brazil. Eur
J Ophthalmol. 2009; 19(3):355-61
2. Foster CS. Fungal keratitis. Massachusetts
Eye and Ear Infirmary, Harvard Medical
School, Boston.
Infect Dis Clin North
Am. 1992;6(4):851-57
3. Comparative study on the incidence and
outcomes of pigmented versus non
974
pigmented keratomycosis. Ind J Opthalmol

2011 ;59:291-6
4. Dixon DM, Polak-Wyss A. The medically
important dematiaceous fungi and their
identification. Mycoses. 1991;34:1-18.
5. Collier L, Balows A, Sussman M. Topley &
wilsons Microbiology and Microbial
Infections, 1998;9th ed, vol .4. Arnold,
London ,Sydney , Auckland , New York.
6. Sutton DA, Fothergill AW, Rinaldi MG.
Guide to Clinically Significant Fungi,.1998;
1st ed. Williams & Wilkins, Baltimore
975
DOI:10.5958/j.2319-5886.2.4.158

&
Health Sciences
Coden: IJMRHS
rd
nd
Accepted: 3rd Sep 2013
Case report
CASE REPORT OF GIANT CONGENITAL MELANOCYTIC NAEVUS
*Shilpa Reddy, Archana S, Shefali Singhal, Muruganandam TV, Hamedullah A.
Department of Dermatology, Meenakshi Medical College Hospital and Research Institute, Enathur,
Kanchipuram, Tamilnadu, India
*Corresponding author email: shilpa29reddy@gmail.com
ABSTRACT
This is a case of giant congenital melanocytic nevus, associated with a single lipoma & multiple satellite
lesions. Biopsy report showed skin with groups of nevoid cells extending into underlying fat, intimately
associated with the lobules & surrounding many blood vessels. The systemic examination was normal.
This is a typical case of a giant congenital melanocytic nevus with satellite lesions and a lipoma
association. As the surface area is greater than 40cm in diameter; the risk of developing melanoma is
higher.
Keywords: Bathing trunk nevus, Satellite lesions, Lipoma
INTRODUCTION
Congenital melanocytic nevi are benign

proliferation of melanocytes located in different
skin levels that have existed since one's birth.
However, the same lesion can also appear within
the first 2 years of life, in this case its called
nevus tardive1 Congenital melanocytic nevi are
more common in Asian and Black children.2 The
incidence is between 1-2% of newborns3. A giant
congenital melanocytic nevus has a diameter of
20cm or more & is very rare. One study
including over 5000,000 newborns has shown
that only one baby in 20,000 has a nevus with a
diameter larger than 10cm.4 It is reported to be
associated with leptomeningeal melanocytosis,
meningomyelocoele and spina bifida, ocular
malformations
and
glaucoma,
auricular
malformation,angiomatous lesions,bone atrophy,
musculoskeletal deformities, neurofibromatosis,
Shilpa et al.,
diffuse lipomatosis, vitiligo etc5 there are other

case reports of association of garment nevus with
lipoma, neurofibroma & spina bifida occulta.6,7,8
A case of giant naevi with hydrocephalus was
reported in mexico.9 It is said to occur in the
epidermal
naevus
syndrome.10A
well
substantiated association with neurofibromatosis
is documented.1
CASE REPORT
A 5-year-old girl second born by normal vaginal

delivery (birth weight was 2.8kgs & cried
immediately after birth) to non consanguineous
parents hailing from Papum Pare in Arunachal
Pradesh, India, presented with a large
asymptomatic
hyper
pigmented
lesion
encompassing the entire trunk involving the
chest, abdomen, back, buttocks and genitalia
976
covering more than 40% of the body surface

area, present since birth [figure 1]. It has been
growing in size with age. The lesion was flat
initially and gradually started becoming thicker.
Distant to the giant nevus, multiple satellite nevi
[figure 2] started developing gradually on the
upper and lower limbs, that was not present at
the time of birth. Hypertrichosis was seen all
over the large pigmented lesion converging
toward the midline [figure 3]. Scalp, mucosa,
palms, soles and nails were normal. There was
no significant family history. The patients cause
of worry was the cosmetic disfigurement caused
by the large hyper pigmented lesion & the
swelling in the left loin which has been gradually
increasing in size. [Figure 1] The swelling was
first noted by the patients mother approximately
4 years ago, on examination it was 86 cm in
size, soft in consistency, non tender, mobile&
skin pinches able over the swelling. The
diagnosis was made clinically. General,
systemic, ophthalmologic & Musculoskeletal
examinations were normal. The X-Ray spine &
MRI Brain were both normal. Basic blood work
& urine routine were normal .The USG of the
swelling in the posterior left flank was done
using a linear transducer & showed a diffuse well
defined thickening of the skin and subcutaneous
plane at the site of swelling, no obvious
vascularity was noted within, the underlying
muscular plane appears normal. Under GA, the
swelling in the left loin was sent for excisional
biopsy.
Histopathology of the swelling showed, skin with
underlying groups of cells with pigmentation
[figure 4], which extends into the underlying fat
[figure 5]. The nevoid cells are seen surrounding
blood vessels in the subcutaneous fat. The cells
extend into the fat intimately associated within
the lobules & surround many blood vessels. The
patient was advised to report immediately if
changes in symmetry, color, border, diameter of
the lesion or any symptoms of itching, oozing or
swellings from the lesion were noted. We
recorded all the pigmented moles on her body
and are following them up periodically to
Shilpa et al.,
identify malignant change by the mole-mapping

technique11,12. She was advised to undergo a
series of diode laser treatments to treat the
hypertrichosis. Patient is under Psychiatric
counseling to deal with the cons of this
disfiguring disease.
Fig 1:Giant congenital naevus(>40%

involvement) Associated lipoma.
BSA
Fig 2:Satellite lesions distant to giant naevus.
Fig 3:Hypertrichosis showing midline

convergence.
977
Fig 4: Histopathology skin with underlying groups

of pigmented cells extending into underlying
subcutaneous fat. (10x)
Fig 5: The nevoid cells are seen surrounding blood

vessels in the subcutaneous tissue, extending into
the fat intimately associated within the lobules &
surround many blood vessels. (40x)
DISCUSSION
Synonyms: Giant garment nevi, bathing trunk

nevi, Giant hairy nevus
Incidence/prevalence: Giant congenital nevi are
very rare. One study including over 5000,000
newborns has shown that only one baby in
20,000 has a nevus with a diameter larger than
10cm.4
Classification: The American national institutes
of health (NIH) are used to categorize naevi
according to size small are under 1.5cm in
diameter, large between 1.5 and 20 cm and giant
naevi having a diameter of 20cm or more.13
Association with lipoma: The central nervous
melanocortin system regulates peripheral lipid
metabolism via the beta adrenergic receptors of
the sympathetic nervous system. This autonomic
outflow shifts substrate metabolism to modulate
Shilpa et al.,
energy storage and adiposity. This mechanism

explains the occurrence of lipoma in giant
congenital melanocytic nevus14.
Clinical features: Congenital nevi are usually
intensely pigmented macules with hypertrichosis
(terminal hair which is darker and more coarse
than normal hair with a tendency to be
concentrated in the central midline) at birth .As
the child grows the nevus grows in proportion
and the surface may become warty or get thrown
into folds & nodules can develop within a large
nevus.
The bathing trunk nevus is very rare but poses a
definite cosmetic problem for the patient.
Commonest site is the lower back and thigh area
& a surface area of a diameter greater than 20cm
is involved. This may be accompanied by large
numbers of smaller congenital nevi present in
areas distant to the giant nevus. An increase in
number may develop over time. They are called
satellite nevi.
The hairy component, which occurs in 95% of
the lesions, tends to become more prominent in
late childhood & seems to be more centered and
dense toward the midline, but at this stage the
nevus ceases to thicken and may become paler.
The hair growth pattern usually has a vortex
distribution, often centered on the midline in the
giant nevus in the back. It is crucial to rule out
CNS, ocular and musculoskeletal deformities.
Histopathology: In congenital nevi, melanocytes
are typically located on the lower two-thirds of
the dermis. Occasionally they extend into
subcutaneous tissue, with isolated cells or groups
of cells within the reticular dermis collagen
fibres, with a tendency to be located around
cutaneous appendages. 5
Prognosis & complications: Sometimes there is
spontaneous regression during childhood or
adolescence. This premature regression is
commonly due to immunological mechanisms
.Rarely, it may result in complications like
Superficial spreading melanoma, neurocutaneous
melanosis , raised intracranial pressure,
hydrocephalus, or space occupying lesions,
rapidly growing ulcerative tumor called nodular
978
proliferative
neurocristic
hamartoma
(neuroectodermal & ectomesenchymal origin15 .
Genetic counseling: It is very important to
reassure the parents of a child with a giant
melanocytic naevus that, the risk of recurrence is
very low in subsequent pregnancies but a few
rare cases have occurred which suggest an
inherited tendency.
Diagnosis &Treatment: MRI scans should be
done in babies with nevi over the cranium or
spine to exclude significant leptomeningeal
melanocytosis.16
Regular
neurological
examination is crucial. The treatment aims at
improving the cosmetic aspect and balancing the
risk of melanoma by excision which may not be
possible in giant melanocytic nevi & periodic
check up to keep an eye out for changes of
malignant transformation. Dermabrasion may
help with a mild reduction in pigmentation.
REFERENCES
1. Marghoob AA, kopf AW, Rigel DS. Risk of

cutaneous malignant melanoma in patients
with classic atypical-mole syndrome:a
case-control study . Arch Dermatol 1994;
130:993-8.
2. Castilla E, Da Graca Dutra M, OrioliParreiras I. Epidemiology of congenital
pigmented naevi: risk factors. Br J Dermatol
1981;104:421-7.
3. Osburn K, Schosser RH, Everett MA.
Congenital pigmented & vascular lesions in
newborn infants. J Am Acad Dermatol
1987;16:788-92.
4. Castilla EE, Da Graca DM, Orioli-Parreiras
IM.Epidemiology of congenital pigmented
naevi, 1: incidence rates and relative
frequencies. Br J Dermatol 1981; 104:30715.
5. Zaal LH, Mooi WJ, Sillevis Smitt JH, Van
der Horst CMAM. Classification of
congenital melanocytic naevi and malignant
melanoma transformation:a review of the
literature. Br J Plast Surg 2004;57:707-19.
Shilpa et al.,
6. Mc Kie RM. Disorders of the cutaneous

melanocyte . In:Burns T, Breatnach S,Cox N,
Griffiths C,editors.Rooks Textbook of
Dermatology.7 th ed.London:Blackwell
Science 2004; 18-38.20.
7. Habib A,Razieh SA,Darius M,Nasrin
S,Payam S.Giant congenital melanocytic
nevus with neurofibroma-like changes and
spina bifida occulta. Int J Dermatol 2006
;45:1347-50.
8. Bhagwat PV, Tophakhane RS, Shashikumar
BM, Noronha TM, Naidu V. Giant congenital
melanocytic nevus (bathing trunk nevus)
associated with lipoma and neurofibroma:
Report of two cases. Indian J Dermatol
Venereol Leprol 2009;75:495-8
9. Ruiz-Maldonado R, Tamayo L, Laerza AM,
Duran C. Giant pigmented nevi: clinical,
histopathologic,
&
therapeutic
considerations. J Pediatr 1992; 120:906-11.
10. Carney J, Gordon H, Carpenter P. The
complex of myxomas, spotty pigmentation
and endocrine overactivity. Medicine
1985;64:270-83.
11. Carli P, De Giorgi V,Chiarugi A,et
al.Addition of dermoscopy to conventional
naked eye examination in melanoma
screening : A randomized study .Jam Acad
Dermatol 2004;50:683-9.
12. Kittler H, Binder M. Risks and benefits of
sequential imaging of melanocytic skin
lesions in patients with multiple atypical
nevi. Arch Dermatol 2001;137:1590-5.
13. Anon. Consensus conference: Precursors to
malignant melanoma. JAMA 1984; 251:
1864-6.
14. Nogueiras R, Wiedmer P, Perez-Tilve D,
Veyrat-Durebex C, Keogh JM, Sutton GM, et
al. The central melanocortin system directly
controls peripheral lipid metabolism. J Clin
Invest 2007; 117:3475-8.
15. Mancianti M-L, Clark WH, Hayes FA,
Herlyn M. Malignant melanoma simulants
arising in congenital melanocytic nevi do not
show experimental evidence for a malignant
phenotype. Am J Pathol 1990;136:817-29.
979
16. Foster RD, Williams ML, Barkovich AJ.

Giant congenital melanocytic nevi: The
significance of neurocutaneous melanosis in
neurologically asymptomatic children. Plast
Reconstr Surg 2001:107:933-41
Shilpa et al.,
980
DOI: 10.5958/j.2319-5886.2.4.159

&
Health Sciences
Copyright @2013
ISSN: 2319-5886
Case report
TUBERCULOUS MENINGITIS: PRESENTING AS ISOLATED COMPLETE III NERVE

PALSY
* Laul Rohit S 1, Avhad Vinod2, Laul Abhishek S3, Laul Subodh S4
1
Chief resident, Department of Ophthalmology, 2Chief resident Department of Medicine, Annasaheb

Chudaman Patil Memorial Medical College and Hospital, Dhule, Maharashtra, India.
3 Chief Resident, Pad.Dr Vithalrao Vikhe Patil Medical College, Ahmednagar, Maharshtra, India
4
Chief Resident, Dhoot Hosptial, Aurnagabad, Maharasthra, India.
*Corresponding author email: drlaulrs@rediffmail.com
ABSTRACT
Tuberculous meningitis (TBM) is the most common form of central nervous system tuberculosis (TB)
and has very high morbidity and mortality. TBM is a subacute disease with symptoms that may persist
for weeks before diagnosis. Based on the clinical features alone, the diagnosis of TBM can neither be
made nor excluded with certainty. A high clinical suspicion and vigilance is required for early diagnosis
of TBM. The present case report demonstrates a patient with TB meningitis, who presented with clinical
manifestation of isolated left III nerve palsy. Case: A 32 years female was hospitalized with acute onset
of left sided ptosis, diplopia and mild generalized headache. Neurological examination at admission
revealed isolated left III nerve palsy. CT scan and MRI of Brain showed no specific finding. Lumbar
puncture was performed four days later due severe headache, low grade fever and neck rigidity.
Cerebrospinal fluid (CSF) study, raised ESR and positive Montoux Test confirmed the diagnosis of TB
meningitis. Since TB meningitis is a chronic disease, cranial nerve palsies are common manifestations.
This case report suggests that TB meningitis should be considered as a disease of differential diagnosis
for isolated III nerve palsy.
Keywords : III nerve palsy, Tuberculous meningitis, Oculomotor nerve palsy
INTRODUCTION
India has approximately one fifth of the global

incidence of tuberculosis with an estimated
prevalence of 3million cases annually as per
WHO1. 9.1% of extra pulmonary TB cases in the
adult population are of Tubercular Meningitis
(TBM). The diagnosis of TBM can be difficult
early in its course, often be a diagnostic
challenge. Because of unusual presentation and
delay in diagnosis and seeking care, TBM causes

an increase in morbidity of the treatable
condition. Early diagnosis and prompt treatment
of TB is important to minimize complications
and reduce morbidity and mortality.
The outcome of TBM depends on the degree of
neurological deterioration that has occurred by
the time antitubercular therapy (AKT) is started.
Laul et al.,
981
Age is an important determinant of the risk of

disease after infection. So in this typical case
report the woman patient adds the landmark to
the rare event in a rural health care sector of
Maharashtra.
CASE REPORT
We report this case of Tuberculous meningitis:

Presenting as isolated complete III nerve palsy
after taking a written valid informed consent
from the patient.
A 32 years female was hospitalized with a
history of acute onset of left sided ptosis,
diplopia and mild headache. No other CNS
symptoms were present. She had a past history of
being operated for swelling in the upper quadrant
of the right sided neck region a year before. She
had no history of any other significant medical
illness in the past. On the 4th day of admission
she developed low grade fever, severe headache
and neck rigidity following which L.P. was
performed. Cerebro-spinal fluid examination
confirmed the diagnosis of tuberculous
meningitis. On examination she was found to be
conscious, cooperative and well oriented to time,
place and person. Initial observations recorded a
temperature of 98.2 0 F, a regular pulse of 76
beats/min, Blood Pressure of 104/72 mm of Hg
and Respiratory rate of 18 breaths/min with no
lymphadenopathy.
Cardiorespiratory
examination
was
normal.
Abdominal
examination was also within normal limits. CNS
examination revealed signs of complete left sided
third nerve palsy (head deviated to right side,
reduced interpalpebral fissure, drooping of upper
eyelid covering upper half of the cornea,

ipsilateral pupil dilatation of 7mm, loss light
reflex. In primary position, left eyeball appeared
to be in an outward & downward gaze with
normal abduction but restricted adduction,
supraduction, and infraduction) with intact
higher, sensory & motor functions. There was no
neck stiffness or no involvement of any other
cranial nerve.
Laboratory Investigations: Blood tests reported
Hb of 9.6g%, 4200/cu.mm Leucocytes,
180000/cu.mm platelets, ESR of 80mm at the
end of the first hour, urea 16.0mg/dl, Serum
creatine 1.2 mg/dl, Serum sodium 135.2 mEq/L
and Serum potassium 3.6 mEq/L. All other blood
tests including liver function tests were normal.
Urine analysis was negative. Montoux test was
positive. CT brain and MRI performed on day 1
showed no any significant abnormal finding.
Repeat CT brain was performed on day 4, this
time with contrast & revealed no abnormality.
CSF examination on day 5 showed cloudy
appearance, elevated opening pressure, high
protein levels (264mg/dl), low sugar levels
(37mg/dl). Cytological examination of CSF
revealed lymphocyte predominance, total cell
count 424cells/micro.litre, (polymorphs 20%,
lymphocytes 20% & RBCs few). Gram stain &
Ziehl Neelsen stain revealed no any organism.
This confirmed the diagnosis of TBM in addition
CSF culture yielded growth of TB bacilli at 7th
week.
Diagnosis: The initial impression was Isolated
III Nerve palsy under evaluation.
Table.1: Cerebro- spinal fluid analysis
CSF study
5th Day
th
14 Day
Cell
count
Protein
Sugar
P/M %
mg/dl
Cloudy
424
Clear
168
Appearance
Initial Pressure
mg/dl
Blood
Sugar
mg/dl
264
16
84
280
112
40
105
146
mm of H2O
21st Day
Clear
46
58
46
108
68
CSF: cerebro-spinal fluid; P: polymorphonuclear leukocytes; M: mononuclear leukocytes.
982
Laul et al.,
Fig.1:Showing isolated IIIrd nerve involvement in a case of tuberculous meningitis.
Final diagnosis: TB Meningitis presenting as

isolated III Nerve palsy.
Management: The patient was initially treated
with i.v. antibiotics & conservative treatment
with a lack of response. After the confirmation of
diagnosis on 4th day, she was started with four
drug AKT and i.v. dexamethasone in tapering
doses. The patient was discharged on 21st day
with improvement in her clinical symptoms. CSF
examination at the time of discharge was within
normal limits On discharge patient was advised
to continue AKT4 and was shifted on Tab.
Prednisolone 40 mg in tapering doses.
DISCUSSION
According to an earlier studies, Chotmongkol

and colleagues found that initial clinical
presentations of TBM include headache (95.6%),
fever (91.1%), stiff-neck (77.8%), mental
impairment (40.0%), motor weakness (11.1%)
and cranial nerve palsies (11.1%). Unilateral
oculomotor nerve palsy has been found to be
quite uncommon (2.2%). Other atypical
Manifestations
include
inter-nuclear
ophthalmoplegia, psychosis and hemianopia. The
presence of focal neuro-logical deficits often
indicates that the neurological sequale may
persist in the survivors2-6. Another study showed
that cranial nerve palsies occur in 2030% of
patients and may be the presenting manifestation
of TBM. The sixth cranial nerve is most
commonly affected7.
In the present case, acute drooping left eyelid
with dilated pupil suggests the initial diagnosis of
isolated III nerve palsy. No abnormalities in CT

scan and MRI along with persistent low grade
fever, headache and neck rigidity which
developed after admission made CSF study
necessary. The present case serves a good
example of the diversity and rarity of the initial
manifestations in TB meningitis. Therefore, it is
always necessary to take TBM into consideration
whenever there is an abrupt deficit of 3rd cranial
nerve 8-10.
Many diseases can present with acute or subacute
unilateral III nerve palsy like aneurysm, temporal
lobe herniation, infection, cavernous sinus
thrombosis, diabetes, brainstem vascular disease,
multiple sclerosis, tumor, mellitus, arteriovenous
malformations,
Tolosa-Hunt
syndrome,
migraine, myasthenia gravis and carotidcavernous fistula11 and can be excluded by
obtaining detailed history and thorough clinical
examination, brain imaging studies, including
cerebral arteriography.
The prognosis of TB meningitis is related to
early initiation of treatment any delay may
results in poor prognosis with neurological
sequelae. However, early diagnosis of TBM is
often difficult and the discrimination of cases
from those of bacterial meningitis or other
meningo-encephalitis are sometimes difficult, if
not impossible, by clinical features alone. Thus,
empiric anti-tuberculosis therapy may be
necessary when TBM was suspected 8-10,12
If unrecognized TBM is uniformly fatal. This
case report shows that Tuberculous Meningitis
should be considered as a differential diagnosis
983
Laul et al.,
in a case of Isolated III Nerve palsy. The

diagnosis was made on the basis of positive CSF
findings in favour of TBM with supportive
evidence of raised ESR, positive Montoux test
and response to Anti-tubercular Therapy.
The patient recovered rapidly with a resolution of
palsy at the time of discharge. No any
neurological deficit was found after 2 weeks at
the time of follow up.
To summarize for every patient presenting with
sudden onset of unilateral III nerve palsy, TB
meningitis should be in the list of differential
diagnosis since the timing of initiation of
treatment is an important factor in the prognosis.
REFERENCES
report of twelve cases and a literature review.

Neurosurgery 1986;18:604-10.
9. Thwaites GE, Chau TT, Stepniewska K. .
Diagnosis of adult tuberculous meningitis by
use of clinical and laboratory features. Lancet
2002;360:1287-92.
10. Holdiness MR. Management of tuberculosis
meningitis Drugs 1990;39:224-33.
11. Brown RB, Lau SK. A 59-year-old diabetic
man with unilateral visual loss and
oculomotor-nerve palsy. N Engl Med
2001;344:286-93.
12. Harris PJ, Saper CB, Anderson C, et al.
Clinical problem solving: diagnosis of
tuberculous meningitis. N Engl J Med
1999;340:1047-9.
1. TB INDIA 2011. Revised National TB

Control Programme. Annual Status Report.
Government of India. Central TB Division.
http://planningcommission.nic.in/reports/genr
ep/health/RNTCP_2011.pdf
2. Chotmongkol V, Panthavasit J, Tiamkao S.
Tuberculous meningitis in adults: a four-year
review during 1997-2000. Southeast Asian J
Trop Med Public Health 2003;34:869-71.
3. Mak W, Cheung RT, Ho SL. Tuberculosis
meningitis in Hong Kong: experience in a
regional hospital. Int J Tuberc Lung Dis
1998;2:1040-3.
4. Souza RD. Franklin D, Simpson J. Atypical
presentation of tuberculosis meningitis: a
case report. Scott Med J 2002;47:14-5.
5. Thwaites GE, Simmons CP, Than Ha Quyen
N. Pathophysiology and prognosis in
vietnamese
adults
with
tuberculous
meningitis. J Infect Dis 2003;188:1105-15.
6. Daif A, Obeid T, Yaqub B, et al. Unusual
presentation of tuberculous meningitis. Clin
Neurol Neurosurg 1992;94:1-5.
7. Berger JR. Tuberculous meningitis. Curr
Opin Neurol. 1994;7:191200.
8. Clark WC, Metcalf JC Jr, Muhlbauer MS.
Mycobacterium tuberculosis meningitis: a
984
Laul et al.,
DOI:10.5958/j.2319-5886.2.4.160

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Health Sciences
www.ijmrhs.com
Volume 2 Issue 4 Oct - Dec Coden: IJMRHS
th
Case report

SURGICAL RECONSTRUCTION OF CLOACAL MALFORMATION: A CASE REPORT

*Mehul Vikani1, Dattatray Bhusare2, Aniruddha Bhagwat3, Sagar Shetty4, Renu Bakshi4, Sheetal
Aggarwal6.
1
Resident, Department of General Surgery, MGM Hospital, Navi Mumbai

Professor and Head of Department, 3Assistant Professor, Department of Pediatric Surgery, MGM
Hospital, Navi Mumbai
4
Resident, Department of Radiodiagnosis, MGM Hospital, Navi Mumbai
5
Resident, Department of Pediatrics, MGM Hospital, Navi Mumbai
2
* Corresponding author email: mehulvikani@gmail.com

ABSTRACT
It is a surgical challenge to repair a cloacal malformation. We are reporting a case of cloacal

malformation in which we performed a reconstructive surgery. We performed a reconstructive surgery
in a 5 yr old patient who had got a colostomy done in the neonatal period. The surgical management
included purely a posterior sagittal anorectovaginourethroplasty without an abdominal approach.
Keywords: Cloaca, Anorectal malformations, Posterior sagittal anorectovaginourethroplasty.
INTRODUCTION
Persistent cloaca has a wide spectrum of

anomalies including those of urogenital and hind
gut. It is comes under rare malformations in the
Krickenbecks classification of anorectal
malformations1. Clinical presentation consists of
imperforate anus with a single perineal opening
through which urine and meconium are passed.
The surgical correction is very tough and
challenging and urinary and fecal incontinence
are frequent complications following operation.
The ultimate goal of treatment includes
achieving satisfactory bowel and urinary control
as well as normal sexual functions at
maturity1,2,3.
CASE REPORT
Mehul et al.,
A five year old female child, with a full term

normal hospital delivery, colostomised on 2nd
day of life for imperforate anus with single
perineal opening was referred to us for definitive
treatment. Past history and family history was
not relevant.
On local examination A single opening in the
perineum was present. The labial folds were
fused and the clitoris was well developed. Anal
pigmentation was present. Gluteal cleft was not
well developed. All sacral pieces could be felt.
Per abdomen, a healthy right transverse
colostomy was present.
985
A diagnostic pan endoscopy was performed

which showed a short channel cloaca with
common channel of about 2.5 cms. Posterior
urethra, bladder neck and urinary bladder were
normal. A short channel communicating with

cloaca and ending with two visible openings
separated by a septum was visualized. Another
third tiny opening was also visualized however
the scope could not be negotiated into this
opening.
Operative findings: The patient was in
jackknife position. A posterior sagittal approach
was used. The incision was taken from
midsacrum upto the single perineal opening. All
the structures were divided in midline. The
coccyx was split. The endopelvic fascia was
incised. The rectal pouch was visualized and the
rectum was opened posteriorly; however no
fistulous communication could be seen. Rectum
was separated off vagina so that it could reach
the perineal skin. The common channel was
incised. Per-urethral catheter had entered into the
vagina. The urethra was visualized and bladder
was catheterized. Entire anomaly was laid open
and all openings into the common channel were
seen. Vagina was septate. The vaginal septum
was excised and the septate vagina was
disconnected from the common channel.
Common channel was repaired over a 10F
Foleys catheter to create a new urethra. Vagina
was quite high and was sharing a paper thin wall
with the urethra. Hence decision was made to
create a vaginal substitute. Various options were
available like using bowel segments, pedicle
graft, split thickness skin graft etc. But the
surgery was performed by perineal route alone
and abdomen was not opened. Surgery was
completed by doing an ano-rectoplasty which
could accommodate a 12 no Hegars dilator.
Rectum was placed in the middle of the sphincter
muscle complex which was identified by muscle
stimulator. The perineal body was reconstructed
anteriorly. The child was turned supine and a YV plasty was performed using labial skin flaps
which were sutured to the native vagina to create
a new vagina over a 10F red rubber catheter. Post
operatively, feeds were started after 6 hours. Post
operative period was uneventful.
Mehul et al.,
Single perineal opening
Fig. 1: Pre-operative picture showing single

perineal opening.
Investigations CBC, Coagulation profile, Renal

function tests, Liver function tests were normal
with normal routine urine analysis. Ultrasound
of abdomen was normal except for small sized
left kidney. Intravenous Urogram was also
normal except for small sized left kidney. CT
scan and MRI scan pelvis showed atretic
vagina. Uterus was normal for age. Both ovaries
were normal. Genitogram showed that bladder
was filled with contrast and was normal. Contrast
entered the rectum and entire distal colon was
opacified. Internal genitalia could not be
visualized. Recto-urinary fistula with common
channel opening in the perineum was seen.
Distal cologram did not reveal a recto-urinary
fistula. Rectal ectasia was present.
Fig. 2: Genitogram
986
Rectum
Septate Vagina
Urethra
Fig. 3: Intra-operative findings
Fig. 4: Post-operative reconstruction

DISCUSSION
A persistent cloaca is a complex anorectal

and genitourinary malformation, in which
the rectum, vagina, and urinary tract meet and
fuse, creating a cloaca, a single common
channel4. Cloacas probably occur in 1 in 20,000
live births5,6. This defect has been considered one
of the most formidable challenges in pediatric
surgery. The goals of treatment include achieving
bowel and urinary control, as well as normal
sexual function, intercourse, menstruation and
obstetric issues. The repair of persistent cloaca
represents a serious technical challenge and
should be performed in specialized centers.
History of the procedure. Hendren has published
the most comprehensive and authoritative reports
on the subject of cloacal malformation repair.
Hendren has described the posterior sagittal
anorectovaginourethroplasty (PSARVUP). For
more complex anomalies, an abdominal
approach is added to mobilize a very high vagina

or rectum.
The etiology of persistent cloaca is unknown.
More than 80% of all patients with a cloaca
experience an associated urogenital anomaly.
Rich et al report the following associated
urogenital anomalies9 - Cloaca, Rectovesical
fistula, Rectoprostatic fistula, Rectovestibular
fistula, Rectobulbar fistula, Rectoperineal fistula
and all malformations.
In most centers, a single stage reconstruction is
the definitive treatment though some surgeons
prefer a two staged approach where they opt for
repairing the anorectal anomaly initially and
perform urogenital sinus repair at a later date.
The planning of surgical management includes
carefully identifying the anatomy specially
measuring length of common channel, level of
insertions of urinary channel, vagina and rectum,
and associated urogenital anomalies. Depending
upon the length of the common channel, cloacal
malformations are categorized into two groups.
Patients having common channel lesser than 3
cm (more than 60% of entire group) can be
repaired by posterior sagittal approach. In
patients having a length of the common channel
more than 3 cm, it would be difficult to perform
total urogenital mobilization from perineum to
repair the malformation, so the common channel
is left intact to be used as urethra, and
colovaginoplasty along with anorectoplasty is
performed. The major complication is fecal and
urinary incontinence. The incidence is usually
higher in cases of higher confluence where an
abdomino-perineal approach is used1,2,3,7,8.
Prognostic factors include quality of the sacrum,
quality of the muscles, and length of the common
channel. Total urogenital mobilization is a
technique devised by Alberto Pena; it allows
mobilization of the urethra and vagina as one
structure. This is possible in patients with the
more benign types of cloacae. If total urogenital
mobilization does adequately lengthen the
vagina, the vagina and urethra must be separated,
987
Mehul et al.,
which is a technically challenging maneuver.

Vaginourethral fistulae are more likely after this
plane is dissected. Approximately 50% of
patients have various degrees of vaginal or
uterine septation. These can be totally or partially
repaired during the main operation or deferred
for definitive repair until puberty. Approximately
one third of the patients have obstructed
Mllerian structures, which can lead to severe
problems due to retrograde menstruation,
amenorrhea in patients with atretic uteri or
hydrometrocolpos.
ACKNOWLEDGEMENT
Philadelphia: Elsevier Saunders, pp. 496

517.
7. Malik A, Iqbal Z, Hameed S, Khalid C,
Iftikhar A, Hussain M. Persistent cloaca with
complete duplex ectopic ureters: A rare
presentation. J Med Rehabilit 2007;1:7-9.
8. Levitt MA, Pena A. Pitfalls in the
management of newborn cloacas. Pediatr
Surg Int 2005;21:264-9.
9. Rich MA, Brock WA, Pena A. Spectrum of
genitourinary malformations in patients with
imperforate anus. Pediatric Surg Intl.
1988;(3):110-113.
We would like to extend our heartfelt gratitude to

the Dept of Pediatric Surgery, Dept of General
Surgery, Dept of Pediatrics and Dept of
Radiology.
REFERRENCES
1. Buhilla P, Torres PC, Bruned BJ, Emparan

G, DeSalazar C, Castro LC. Total
mobilization of the urogenital sinus in the
treatment of cloaca. An Esp Pediatr 2001;55:
573-5.
2. Kay R, Tank ES. Principles of management
of persistent cloaca in the female newborn. J
Urol 1977;117:102-4.
3. Masuko T, Higashimoto Y, Iwai J. Singlestage operation without temporary colostomy
for persistent cloaca with short common
channel. Pediatr Surg Int 2005;21:922-4.
4. Jenkins D, Bitner-Glindzicz M, Thomasson
L. Mutational analyses of UPIIIA, SHH,
EFNB2 and HNF1 in persistent cloaca and
associated kidney malformations. J Pediatr
Urol. 2007;3 (1): 29,
5. Spitz Lewis, Coran, Arnold G. Operative
Pediatric Surgery (6th ed.), London: Hodder
Arnold, pp. 2006;503519.
6. Ashcroft, Keith; Holcomb, George; Murphy,
J Patrick, Pediatric Surgery. 2005; 4th ed.
988
Mehul et al.,
DOI:10.5958/j.2319-5886.2.4.161

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Case report
PRIMARY MALIGNANT MELANOMA OF UTERINE CERVIX: A RARE OCCURRENCE
*Hemalatha AL1, Umarani MK2, Shashikumar SD3
1
Professor & Head, 2Associate Professor, 3Post-graduate student, Department of Pathology, Mysore
Medical College and Research Institute, Irwin Road, Mysore, Karnataka, India
*Corresponding author email: halingappa@gmail.com
ABSTRACT
Primary malignant melanoma of uterine cervix is a rare and aggressive neoplasm. In women, genital
tract is the site of approximately 3%-7%of malignant melanomas. Majority of these occur in vulva or
vagina, but cervix is a rare site. Cervical melanoma is reported in the age range of 19 to 83 years with
peak incidence between 60 to 70years. Malignant melanoma presents with vaginal bleeding or discharge
and appears as exophytic, polypoid, pigmented or colorless cervical mass. Diagnosis is by histopathology which should be confirmed by immunohistochemical staining with S100 protein and HMB45.
Primary cervical melanoma must be differentiated from secondary metastasis of melanoma to the cervix
from other sites in the body. In general, prognosis of primary cervical melanoma is poor, because it is
diagnosed at an advanced stage. No consensus has been established regarding treatment of primary
malignant melanoma of cervix, because of its rarity. Cervical melanoma is incurable in totality with the
currently available therapies and hence it has to be diagnosed early.
A 60 year old woman presented with white discharge per vagina. On examination, there was a bluish
black colored mass arising from the anterior lip of cervix. Following histopathology and other investigations, a diagnosis of primary malignant melanoma of uterine cervix was made. The case is reported for
its rarity.
Keywords: Malignant melanoma, primary, uterine cervix
INTRODUCTION
In 1959, Cid reported the presence of melanocytes in the cervical epithelium of 3.5% of women1 .Since then, in the literature, about 78 cases
of primary malignant melanoma of the uterine
cervix have been reported 2. Primary malignant
melanoma of the cervix is a rare neoplasm. It
constitutes less than 2% of cases of malignant
melanoma of the genital tract3. The diagnosis
may be missed or delayed as it often presents in
an amelanotic form4. Majority of the patients are

in advanced stage of the disease on presentation
and respond poorly to therapy4. Diagnosis is by
histopathology and immunohistochemistry and
by exclusion of primary melanoma at other sites.
We report for its rarity, a case of a 60 year old
female with primary malignant melanoma of the
uterine cervix and describe its clinical and histological features.
989
Hemalatha et al.,
CASE REPORT
A 60 year old post menopausal woman presented

to the gynaecology department with a history of
white discharge per vagina since 2 months.
On per speculum examination a 4*5centimeter
bluish black colored mass was seen arising from
the anterior lip of the cervix. The clinical diagnosis was endometriosis or endometrial polyp.
A punch biopsy of the cervix was done and the
specimen was submitted for histopathological
examination which revealed a diffusely infiltrative malignant neoplasm composed of highly
pleomorphic, round, polygonal to spindle shaped
cells with atypical large irregular nuclei and
prominent nucleoli. Intra and extra cellular fine
brown granules of pigment which were Masson
Fontana positive was present. Junctional activity
was
seen
in
the
epithelium.
Immunohistochemical staining for HMB 45 was
positive. The histopathological diagnosis was
pigmented malignant melanoma of the cervix.
No melanotic lesions were found in the skin, eye
and other mucosal sites. Abdominal ultra
sonography and chest radiograph were normal.
Considering the absence of malignant melanoma
at any other site and presence of Junctional activity, the diagnosis was given as primary malignant
melanoma of uterine cervix. The patient was referred to the regional cancer institute for further
management.
Fig.1: Stratified squamous epithelium of cervix

with pigmented cells beneath the epithelium (10X)
Fig.2: Intracellular fine granules of brown pigment (40X).
Fig.3: Pleomorphic cells

eosinophilic nucleolus (100X).
with
prominent
DISCUSSION
Malignant melanomas are generally found in areas of skin exposed to the sun but may also present in nonexposed sites, such as genital tract and
esophagus, among other sites 3. Approximately,
3-7% of malignant melanomas in women develop within genital tract.6 Majority of them occur
in vulva and vagina. Primary cervical melanoma
is a rare entity.
Cervical melanoma arises from melanocytes in
the cervix. The complete spectrum of melanocytic lesions, from benign lentigenes to blue nevi
to melanoma can be seen in the cervical epithelium 3, 4.
Primary malignant melanoma of cervix is very
rare4. A cervical melanoma may be either
melanotic or amelanotic .Diagnosis of
amelanotic melanoma may be missed due to the
990
Hemalatha et al.,
absence of pigment and thereby needs caution.

The present case exhibited classic features of
melanotic melanoma and hence posed no diagnostic dilemma.
Patients with malignant melanoma of the cervix
may range between 19 to 83 years, although the
majority of them occur between 60 to 70 years.5,
6
In most cases, vaginal bleeding or discharge is
the usual presenting complaint.4 Some patients
may remain asymptomatic. Physical examination
usually reveals a polypoidal exophytic mass
which may be grey, brown, black, blue or red in
color or it may be colorless in amelanotic melanoma ,which constitute up to 55% of cases in the
cervix.7 Recently the morphological features of
primary cervical malignant melanoma in pap
smear have been reported as, bizarre and abnormal cells containing pigment, raising the hope
for an early diagnosis. 4
Histologically, malignant melanoma in the uterine cervix is similar to malignant melanoma at
other sites and is composed of cells with varying degree of pleomorphism and prominent
eosinophilic nucleoli. In the melanocytic type,
dark brown intracellular pigments which stain
positive with Massons Fontana stain are seen.
In the absence of pigment, the differential diagnosis includes anaplastic carcinoma, poorly differentiated squamous cell carcinoma, adenocarcinoma, rhabdomyosarcoma, leiomyosarcoma,
stromal sarcoma and high grade lymphoma. Melanoma cells are positive for S100 protein (more
sensitive) and HMB45 (more specific).8 They
also stain positively with Melan A, Vimentin,
Tyrosinase and MITF (Microphthalmic Transcription Factor). They are usually negative for
epithelial markers Cytokeratin and EMA and
also Desmin. Primary melanoma of cervix must
be differentiated from metastatic melanoma from
other sites of the body including skin and eye 6.
Norris and Taylor have suggested the following
criteria to diagnose primary malignant melanoma
of the cervix (a) presence of melanin in the
normal cervical epithelium (b) absence of melanoma in another site of the body (c) presence of
junctional activity in the cervical epithelium near

the lesion (d) if metastasis is found, it should be
according to the cervical carcinoma patern3, 6.
Instead of Clark and Breslow scales, the International Federation of Gynecology and Obstetrics
(FIGO) staging system for cervical cancer is used
for staging of cervical malignant melanoma as
cervix is an unusual site for malignant melanoma
and, the FIGO staging system has better correlation with prognosis.3
There is no consensus on optimal management of
primary malignant melanoma of cervix, because
of its rarity6. Radical hysterectomy with pelvic
and paraarotic lymphadenectomy is the most
common procedure which may be followed by
radiotherapy or chemotherapy.
Malignant melanoma of the cervix is a rare and
aggressive neoplasm 9. The prognosis of primary
malignant melanoma is generally poor because
diagnosis is usually made at an advanced stage
and the tumor is highly aggressive in both local
recurrence and wide spread metastases 6, 10. These
patients have an average survival ranging from
6 months to 14years according to world literature 7.
Hemalatha et al.,
CONCLUSION
Primary malignant melanoma of the cervix is a

rare neoplasm. However, it should be included in
the differential diagnosis of cervical malignancies. Special staining and immunohistochemistry
should be used to confirm the diagnosis. Treatment of primary malignant melanoma of cervix
is not yet standardized because of its rarity .In
general, prognosis of primary cervical melanoma
is poor, because it is diagnosed at an advanced
stage. Hence early diagnosis of cervical melanoma is essential.
REFERENCES
1. Cid JM. Melanoid pigmentation of the

endocervix: a neurogenic visceral argument.
Ann Anat Pathol (Paris) 1959;4:617-28.
2. Pusceddu S, Bajetta E, Carcangiu ML,
Formisano B, Ducceschi. A literature review
991
of primary cervical malignant melanoma: an

exceedingly rare cancer. Crit Rev Onccol
Hematol. 2012:81(2) 185-95.
3. Calderon Salazar L, de Leon DC , Montiel
DP, Almogabar-Villagran E, Villavicencio V.
Primary malignant melanoma of the uerine
cervix treated with ultraradical surgery : A
case report. ISRN Obstetrics and gynecology
2011 Article ID68 3020
4. Gupta R, Singh S, Mandal AK. Primary malignant melanoma of cervix - a case report.
Indian J Cancer 2005;42:201-04
5. Clark KC, Butz WR, Hapke MR. Primary
malignant melanoma of the uterine cervix:
case report with world literature review. International Journal of Gynecological Pathology1999; 18(3): 265-73.
6. Yun NR, Park JW, Park JH, Choi SJ, Hwang
SO. Primary malignant melanoma of the uterine cervix: A case report. Korean J Obstet
Gynecol 2012;55(5):343-47.
7. Hinde E F, Amal B, Hannane S, Cherhazade
B, Abdelaziz B. Unusual primary location of
the malignant melanoma, the cervico-vaginal
region: 3 cases and literature review. Open
Journal of Obstetrics & Gynecology 2012(2)
279-282
8. Santoso JT, Kkucera PR and Ray J. Primary
malignant melanoma of the uterine cervix:
Two case reports and a centurys review
.Obstetrical and Gyecolological Survey
1990:45(11)733-39.
9. Teixeira JC, Salina JR, Teixeira LC, Andrade
LA. Primary melanoma of the uterine cervix
figo stage III B. Sao Paulo Med J
1998;116:1778-80.
10. Khurana A, Jalpota Y. Primary malignant
melanoma of the uterine cervix. Indian J
Pathol Microbiol 2009;52:575-6
992
Hemalatha et al.,
DOI:10.5958/j.2319-5886.2.4.162

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Case report
CORTICAL BLINDNESS FOLLOWING TWO STAB WOUNDS TO THE SCALP IN AN

ADULT: A CASE REPORT
*Azonobi IR1, Odogu V2
1
2
Niger Delta University Teaching Hospital, Okolobiri, Bayelsa State, Nigeria

Diete Koki Memorial Hospital, Opolo-Yenagoa, Bayelsa State, Nigeria
*Corresponding author email: doctorazonobi2002@ymail.com

ABSTRACT
Visual disturbances have been reported as a consequence of acute severe blood loss. They are related to
hypoperfusion related watershed infarcts in the posterior visual pathway apparatus.
In this case report, we report the clinical course of a young male adult who suffered transient blindness
following an assault in which he sustained deep cuts to the temporal and parietal regions of the scalp. He
was managed in our hospital with copious infusion of intravenous fluid (normal saline) and subsequent
transfusion of 2 pints of whole blood. Blindness persisted from less than one hour following assaut to 96
hours post admission. Blindness resolved completely by the 9th day of admission but was associated
with a homonymous visual field defect.
Keywords: Blindness, cortical, stab wound, blood loss
INTRODUCTION
Sudden onset of bilateral visual loss

characterized by normal pupillary responses and
normal appearances of the ocular fundus is
considered as blindness of cortical origin until
proven otherwise.
Cortical blindness has been found to be
associated with a host of clinical states and
procedures (Table 1).
They are due to lesions of the geniculocalcrine
visual pathway in the posterior hemisphere1. The

geniculocalcrine visual pathway is known to
occupy a delicately supplied vascular border
zone. Thus, most cases of cortical blindness is
associated with hypo-perfusion related watershed
infarcts2-4.
We report the case of a young man who suffered
severe blood loss following an assault and
subsequently developed a reversible visual loss.
993
Azonobi et al.,
Table 1: Causes of Cortical Blindness

Vascular
Preeclampsia/ecclampsia
Stroke
Hypertensive encephalopathy
Cerebral venous thrombosis
Severe hypotensive states
Infections
Bacteria meningitis
Mumps encephalitis
Cerebral malaria
Toxic
Iodinated contrast agents
Metrizamide
Amphetamine
Chemotherapy
Heroin
FK 506
CASE REPORT
A 25 year old undergraduate of a Nigerian

university had previously enjoyed good vision in
both eyes until that fateful day when he was
assaulted by a known assailant. He sustained
matchet cuts on both sides of his scalp. He was
said to have bled profusely with an estimated
blood loss of about 1.5 liters. He became
disoriented shortly after the assault as he lost
orientation in space. There was no associated
blunt trauma to the head and no bleeding from
any of the craniofacial orifices.
He was rushed to the Niger Delta University
Teaching Hospital (NDUTH) where he was
attended to and admitted. On examination, he
was noticed to be drowsy but rousable,
disoriented and mentally confused. He was very
pale, anicteric and not dehydrated. His cranial
nerves were grossly intact.
He had deep lacerations at the left temporal
region (6cm long) and at the right parietal region
(10cm long). His pulse rate was 140/min,
regular, poor volume. Blood pressure was
Trauma
Head trauma
Cervical trauma
Iatrogenic
Post cardiac catheterization
Cardiac surgery
Metabolic
Hypoglycemia
Uraemia / Haemodialysis
Acute intermittent porphyria
Miscellaneous
Status epilepticus
Status asthmaticus
Intracranial haemorrhage
Brain tumour
Liver cirrhosis and encephalopathy
90/46mmHg (supine) and Heart sounds were

normal.
Chest and Abdominal examination was normal.
Ocular examination revealed a visual acuity of
no light perception (NPL) in both eyes and
external eye and anterior segment examination
were normal. Both pupils were round and
reactive. Fundoscopy revealed a pink disc (C/D
ratio of 0.3), round with well defined edges in
both eyes. Both retinea were flat and normal. A
provisional diagnosis of cortical blindness
secondary to severe hypovolaemia was made. He
was resuscitated with I.V Normal Saline and
thereafter transfused with 2 pints of whole blood.
The two stab wounds were repaired with
appropriate sutures.
Investigation ordered included urgent PCV
(23%), Electrolyte and urea (normal), random
blood sugar (normal) and cranial CT Scan (not
done as a result of absence of equipment in our
centre).By the fourth day on admission following
normalization of his cardiovascular status (PR
70bpm, BP 128/80mmHg), visual recovery was
noticed with a visual acuity of hand motion
(H.M) in both eyes. Visual recovery became full
994
Azonobi et al.,
on the 9th day of hospital admission (6/6{OD},

6/6+ 4 {OS}). He was then discharged for follow
up at the ophthalmic outpatient.
A visual field analysis requested at this stage
confirmed a homonymous hemianopia first
detected clinically on the 9th day of admission.
DISCUSSION
Cortical blindness is a hallmark of posterior

cerebral arterial border zone infarcts1. It is
caused by hypoxia of the visual pathways at the
territories supplied by the distal posterior
cerebral arteries. The possibility that vascular
factors (a limited capability of the posterior
vascular system to autoregulate blood flow) and
cortical tissue vulnerability to hypoxia as being
responsible for the hypoxic damage has been
suggested5.
The dog electromagnetic flow metre study during
hypoxia and hypercapnia has demonstrated a
decrease in the compensatory dilatation response
of the basilar arterial system to occlusion of the
carotid system5. Loss of the normal protective
autoregulation of blood flow was suggested as
one of the pathomechanism of pre-ecclampsia /
ecclampsia induced cortical blindness6. A
sparing effect of chronic hypoxia on the anterior
cerebral artery has been suggested by an
ultrasonic study on fetal brain circulation7.Thus
under chronic hypoxia the frontal lobes are
spared longer than the lateral and occipital lobes.
It has also been shown that the parieto occipital
border
zone
is
most
susceptible
to
haemodynamic ischaemic damage as it is the
most peripheral region of the distribution of the
anterior, middle and posterior cerebral
circulation8. Posterior cerebral arterial border
zone infarction has been shown to be a
consequence of profound systemic hypotension
and has been found to be associated with cortical
blindness9-12.
The patient in our case report developed cortical
blindness following an episode of severe blood
loss. Ischaemia and infarction secondary to
hypoperfusion in severe systemic hypotension is

known to lead to cytotoxic oedema in border
zone infarcts. Radiological evidence of neuronal
oedema in hypotension related watershed infarcts
manifests as hypodense lesion on CT images
and hyperintense lesions on T2 weighted MRI
images in very specific distal field territories of
the middle and posterior cerebral arteries13.
Although, it was not possible to obtain a CT or
MRI images in our patient, clinical evidence
suggests that the above radiologic changes are
not unlikely. The clinical and radiologic changes
in posterior border zone infarcts may be
reversible. Clinical recovery is known to precede
normalization of radiologic abnormalities14,15. In
our patient visual recovery was noticed on the
fourth day post admission earlier than what was
reported in most studies. This may be due to
aggressive effort in normalization and sustenance
of the patients cardiovascular status.
In hypoperfusion related posterior border zone
infarcts, prompt re-establishment of normal
perfusion pressure may be associated with
resolution of the cytotoxic oedema and visual
recovery. In such cases prompt arrest of blood
loss and restoration of normal cardiovascular
functions may improve the prognosis of visual
recovery.
CONCLUSION
Acute severe blood loss could result in cortical

blindness. Prompt restoration of normal
cardiovascular status is a key step that must be
undertaken in such cases in order to ensure or
optimize visual recovery.
REFERENCES
1. Aldrich MS, Alessi AG, Beck RW, Gilman

S. Cortical Blindness: Aetiology, Diagnosis
and Prognosis. Ann Neurol 1987; 21: 149
58.
2. Argenta PA, Morgan MA. Cortical blindness
and Anton Syndrome in a Patient with
995
Azonobi et al.,
Obstetric Haemorrhage. Obstet Gynaecol

1998; 91: 810 12.
3. Belden JR, Caplan LR, Pessin MS, Kwan E.
Mechanisms and clinical features of posterior
border zone infarcts. Neurology 1999; 53:
1312 18.
4. Boromeo CJ, Blike GT, Wiley CW, Hirsch
JA. Cortical blindness in a Pre-ecclamptic
patient after a caesarean section delivery
complicated by hypotension. Anaesth
Analog 2006; 9: 609 11.
5. Shima T, Ishikawa S, Sasaki U, Miyazaki M,
Hibino H. Quantitative measurement of the
basilar
arterial
flow
in
the
dog
electromagnetic flow metre study of the extra
and intracranial arterial occlusion. No
Shinkei Geka 1976; 4: 451 57.
6. Schwartz RB, Jones KM, Kalina P et al.
Hypertensive encephalopathy: findings on
CT, MR Imaging and SPECT Imaging in 14
Cases. Am J R Roeentgenol 1992; 159: 379
83.
7. Dubiel M, Gunnarsson GO, Gudmundsson S.
Blood redistribution in the fetal brain during
chronic hypoxia. Ultrasound Obstet Gynaecol
2002; 20: 117 21.
8. Torrik A. Pathogenesis of watershed
infarction in the brain. Stroke 1984; 15(2) :
221 23.
9. Adams JH, Brierley JB, Connor RCR, Treip
CS. The Effect of systemic hypotension upon
the
human
brain:
Clinical
and
neuropathologic observations in 11 cases.
Brain 1966 ; 89(2) : 235 68.
10. Brierley JB, Excel BJ. The effects of
prolonged systemic hypotension upon the
Brain of M Rhesus: Physiologic and
pathologic observations. Brain 1966: 89(2) :
269 298.
11. Mofred A, Curan D, dArondel C, Larib K,
Courtarel P, Cassaz C et al. Blindness
following gastrointestinal haemorrhage. Eur J
Gastrointestinal Hepatol 2000; 12(12): 1339
41.
12. Argenta PA, Morgan MA, Cortical blindness

and Anton Syndrome in a Patient with
Obstetric Haemorrhage. Obstet Gynaecol
1998; 91: 810 2.
13. Golberg HI, Lee SH, Stroke IN, Rao KC,
Zimmerman RA, eds. Cranial MRI and CT.
New York: MC Graw-Hill, 1992: 623 99.
14. Sharma JA, Bhatt S. Reversible blindness in
severe Pre-ecclampsia and Ecclampsia. JK
Science 2004; 6(1): 43 45.
15.Gaurav S, Bhatia R, Sanjiv B, Ajay KW. MR
Findings of Cortical Blindness Following
Cerebral Angiography:Is This Entity Related
to Posterior Reversible Leucoencephalo
pathy? Am J.Neuroradiol.2005;26:193-94.
996
Azonobi et al.,
DOI:10.5958/j.2319-5886.2.4.163

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Coden: IJMRHS
th
Case report
Copyright @2013
ISSN: 2319-5886
Accepted: 22nd Sep 2013
REGAUDS TUMOUR INVOLVING THE TONSILS: A CASE REPORT

*Muthubabu K, Srinivasan MK, Sakthivel
Department of ENT, Meenakshi Medical College and Research Institute, Kanchipuram, Tamilnadu,
India
*Corresponding author: muthubabu67@gmail.com
ABSTRACT
Regauds tumour is a lymphoepithelioma which usually arises in the nasopharynx. Outside the
nasopharynx such lymphoepithelioma like carcinomas are exceedingly rare. Such tumours in the tonsil
are rare. Here we report a 35 year old lady, a case of Regauds tumour involving the Rt. Tonsil.
Tonsillectomy was performed and the patient was subjected to radiotherapy. 2 years follow up showed
no recurrence of tumour.
Keywords: Regauds tumour, Schminkes tumour, Lymphoepithelioma
INTRODUCTION
Non nasopharyngeal Lymphoepithelioma is rare

and when it occurs in the tonsil it is typically
unilateral. Three fourths of the patients have
nodal involvement. Non nasopharyngeal
Lymphoepithelioma
affects
the
younger
population.
Histopathology
and
Immunohistochemistry is valuable in the
diagnosis.
These
tumours
are
highly
radiosensitive. This characteristic along with the
classical histological structure and clinical
typicality made it justifiable for a separate group
and name for the neoplasm.1
A 35 year old lady presented with complains of

swelling in the right tonsillar region of 4 months
duration, swelling on the right side of the neck
20 days duration. She had uneasiness in the
throat and difficulty in swallowing. There was no

difficulty in breathing. No pain and no change in
voice.
On Examination there was a unilateral
enlargement of the right tonsil. Surface of the
tonsil was smooth and not ulcerated
macroscopically. Left tonsil was absolutely
normal. On palpation the mass was firm in
consistency. Induration was felt. Ear and Nose
were clinically normal. Indirect laryngoscopy
showed normal posterior third of tongue,
vallecula, epiglottis, arytenoids, aryepiglottic
folds, ventricular bands, vocal folds and piriform
fossa. Examination of the neck revealed Right
sided Jugulodigastric node enlargement, Non
tender, mobile and firm in consistency.
Routine blood investigations were normal. CT
scan showed enlargement of the Right side
Muthubabu K et al.,
CASE REPORT
997
tonsil. Under General anaesthesia, Tonsillectomy

was performed. Whole tonsil was removed in
toto and the specimen was sent for
histopathology and immunohistochemistry. Post
operative period was uneventful.
Histopathology confirmed the diagnosis the
photomicrograph showing epithelial islands
surrounded by lymphocytes. Immunohisto
chemistry showed cytokeratin showing positivity
for the epithelial cell nests. After confirmation
patient was referred for radiotherapy and
followed up every 6 months for the past 2 years.
2 years follow up showed no evidence of
recurrence or residual tumour.
Fig.1:
Epithelial
lymphocytes.
islands
surrounded
by
Fig.3: Macroscopic appearance of dissected Tonsil

DISCUSSION
Non nasopharyngeal lymphoepitheliomas are

rare. Such lesions have been reported in the base
of tongue2 In 1921 Reverchan and coutard
reported from Regauds clinic tumours of
hypopharynx to which Regaud had given the
name lymphoepithelioma. In the Same year
Schminke also reported a series with the same
name. The name was applied by Regaud and
Schminke apparently independently in view of
the probable origin from the structure described
as
lymphoepithelial
organs3.
Tracheal
lymphoepithelioma like carcinoma has also been
reported.4 Relationship with Ebstein Bar virus is
less in Non nasopharyngeal Lymphoepithelioma.
Even if it is related it does not affect the mode of
treatment.
CONCLUSION
Fig.2: Immunohistochemistry shows cytokeratin

showing positivity for the epithelial cell nests
Regauds tumour involving the Tonsil is rare. It

affects the younger age group. Lymphnode
involvement is common. Diagnosis is made by
CT scan and clinical examination. Confirmed by
Histopathology and Immunohistochemistry.
Tumour is radiosensitive. Removal of the tonsil
and subjecting the patient to radiotherapy is
helpful.
REFERENCES
1. Munro Black JL. The lymphoepitheliomata.

The journal of laryngology And Otology.
1938;53 (4) 225 -245.
998
Muthubabu K et al.,
2. Merz H, Marnitz S, Erbersdobler A, Goektas

O. Schminckes tumour, Carcinoma of the
base of the tongue, a case report. Case rep
oncol. 2010;3(1):77 82
3. Cappel DF. On lymphoepithelioma of
nasopharynx and tonsils. The journal of
pathology and Bacteriology. 1934;39(1):49
64
4. Sathyanarayana
Pathak.
Tracheal
lymphoepithelioma like carcinoma A case
report. Indian journal of cancer. 2002; 39 (3)
112 -1
999
Muthubabu K et al.,
DOI:10.5958/j.2319-5886.2.4.164

&
Health Sciences
Coden: IJMRHS
rd
Case report
Copyright @2013
ISSN: 2319-5886
th
INCOMPLETE FORMATION OF POSTERIOR CORD OF BRACHIAL PLEXUS: A CASE

REPORT
*Rajeshwari MS1,Vijay Kumar S2
1
Associate Professor, 2Post Graduate, Department of Anatomy, Bangalore Medical College and
Research Institute, Bangalore, Karnataka, India.
*Corresponding author email: rajeshwari.roshan8@gmail.com
ABSTRACT
Brachial plexus is a network of nerves formed at the root of the neck to provide motor and sensory
branches to the upper limb. The major contribution for this plexus is by the anterior primary rami of
C5,6,7,8 and T1. The roots join to form the trunks which in turn divide into anterior and posterior
divisions to form the cords. The knowledge of brachial plexus is important for the anaesthetists while
administering brachial blocks. During routine dissection in a female cadaver aged 65years, the posterior
division of upper trunk fails to fuse with the posterior divisions of the middle and lower trunk and gives
out four branches independently.
Keywords: Brachial plexus, Posterior cord, Radial nerve, Axillary artery.
INTRODUCTION
Brachial Plexus is a complicated network of

nerves where the ventral primary rami of
C5,6,7,8,T1 confluence at the root of the neck and
then ramify to provide sensory and motor
branches to the upper limb. The roots join to
form the trunks, namely the upper trunk formed
by the union of C5 &C6, the middle trunk
formed by the continuation of C7 root and lower
trunk formed by the union of C8 &T1. This
formation takes place in the interscalene space
in the posterior triangle. 1 Each trunk gives off
anterior and posterior divisions behind the
clavicle to form three cords viz.., the lateral,
medial and posterior cords. The three cords
enter the axilla and are named according to their
relation with second part of axillary artery. The
Rajeshwari et al.,
lateral cord is formed by the union of anterior

division of upper and middle trunk, the medial
cord is formed by the anterior division of lower
trunk and the posterior cord is formed by the
union of posterior divisions of all the three
trunks.2 The cords branch out to supply the
flexor and the extensor compartments of upper
limb. The branches which arise from the roots
and the trunks are seen above the clavicle and
these are called as supraclavicular and the
branches which arise mainly from the cords are
seen below the clavicle hence these are infraclavicular branches. The posterior cord provides
the upper subscapular nerve, thoraco-dorsal
nerve, lower subscapular nerve, axillary nerve
and the continuation of the cord is the Radial
1000
nerve. The upper subscapular, lower

subscapular and axillary nerves convey fibers
from C5,6 the thoraco-dorsal nerve conveys
fibers from C6,7,8 and radial nerve conveys fibers
from C5,6,7,8,&T11
CASE REPORT
During routine dissection for I year MBBS in

the department of Anatomy at Bangalore
Medical College and Research Institute,
Bangalore, during the exposure of axilla in a
female cadaver aged 65years, it was noted on
the left side that the posterior cord of brachial
plexus was not formed completely and the
branches originated independently from the
posterior division of the upper trunk, the
branches were traced and photographed.
The Posterior division of upper trunk conveying
fibers from C5 &C6, failed to unite with the
posterior division of middle and lower trunk.
The posterior division of upper trunk provided
four branches directly -upper subscapular, lower
subscapular and axillary nerve, thus carrying
fibers from C5 & C6, it also provided an
additional branch which lies lateral to axillary
nerve course downwards behind the subscapular
artery which is called here, as the inferior
division of radial nerve (fig1).The posterior
divisions of middle trunk and lower trunk unite
and immediately gives out the thoraco-dorsal
nerve. Close to its origin it receives a
communicating branch from the posterior
division of upper trunk (fig2), the rest of the
nerve then courses downwards in front of the
subscapular artery to form the superior division
of radial nerve. At the lower border of
subscapularis muscle the two divisions of radial
nerve unite to continue as the radial nerve thus
comprising of fibers from C5, 6,7,8, &T1. The
two divisions of radial nerve form a loop around
the subscapular artery which is branch of third
part of axillary artery. (fig2)
Rajeshwari et al.,
Fig 1: Four branches from the posterior division

of upper trunk
Fig2: Showing thoraco-dorsal nerve (TDN) and

superior division of radial nerve derived from the
union of posterior divisions of middle and lower
trunk.
Also seen is the thoraco-dorsal nerve receiving
communicating branch (COM.Br) from the posterior
division of upper trunk. (coloured yellow are the
two divisions of radial nerve, pierced by the

subscapular artery)
Abbreviations: Upper subscapular nerve
(USN), Lower subscapular nerve (LSN),
Axillary nerve (AN), and inferior division of
radial nerve (RN) deep to subscapualar artery
DISCUSSION
Posterior cord is formed by the union of the

posterior divisions of upper, middle and lower
trunks. The variations in the formation and
branching patterns of brachial plexus are quite
common and have been reported time and again
by several authors. The variations can occur in
the formation of trunks, divisions, cords, at the
1001
level of branching or its relationship with the

axillary artery; however the make-up of terminal
branches remains unchanged.2 The unusual
formation may be attributed embryologically
where the axons of the spinal nerve grow
distally in different directions to reach the limb
bud mesenchyme. Once these developmental
variations are formed they persist post-natally
and appear as variations in adulthood.2 The
radial nerve was formed by the posterior
divisions of middle and lower trunk without any
contribution from the upper trunk3. The
posterior cord divided into two roots enclosing
the subscapular artery and the roots fused to
continue as radial nerve4. The radial nerve has
two roots arising from the posterior cord the two
roots unite to continue as radial nerve after
clasping the subscapular artery5. Posterior cord
is formed by the union of posterior division of
upper and middle trunk without any
contribution from lower trunk6.
3.
4.
5.
6.
Lippincott, Williams and Wilkins :2006,

pg774-75.
Aktan. A cadaveric study of the anatomic
variations of the brachial plexus nerves in
the axillary region and arm, Turkish Journal
of Medical sciences. 2001;31(2);147-50.
Bhat KMR. Variation in the branching
pattern of posterior cord of brachial plexus;
Neuroanatomy. 2003;7:10-11.
Jamuna M. A rare variation of the branching
pattern of radial nerve; International Journal
of Anatomic Variation 2011;4:22-24.
Fazan. Brachial plexus variations in its
formation and main branches; Acta
Cirurgica Brasiliera; 2003;18(5):14-18.
CONCLUSION
The variations usually occur at the junction or

separation of individual parts. Variations in
nerves in their course or branching are prone for
entrapment neuropathies. The close relationship
of the variant nerves with the axillary artery
may result in arterial compression leading to
ischemic pain. The knowledge of these
variations is useful for the neurosurgeons while
managing axillary tumors, for orthopedic
surgeons in treating upper limb fractures or for
anesthetists in proper planning of brachial
plexus blocks.
REFERENCES
1. Dutta
AK.
Essentials
of
human
Anatomy,superior
and
inferior
Extremities,2nd edition;1995;51-52.
2. Moore KL, Dally AF. Upper limb in
clinically Oriented Anatomy, 5thedition,
Rajeshwari et al.,
1002
DOI:10.5958/j.2319-5886.2.4.165

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Health Sciences
www.ijmrhs.com
rd
Case report
HYPERSENSITIVITY TO LIGNOCAINE: A CASE REPORT

*
Rupankar Nath1, Sanju Sharma1, Anshuman Dutta2, Joydeep Roy3, Tulika Singh4
Department of Anaesthesiology, 2Department of Orthopaedics, 3Department of Dermatology, Silchar

Medical College, Assam, India
4
Department of Community Medicine, Lady Hardinge Medical College, New Delhi, India
*Corresponding author email: rupankarnath05@gmail.com
ABSTRACT
Local anaesthetics are a very important group of drugs in the anaesthetists armamentarium. They have
very widespread use in many branches like surgery, Orthopaedics, ENT, Obstetrics & Gynaecology.
Most popular amide group representative lignocaine is used as its hydrochloride salt at a
concentration of 1 or 2% with or without epinephrine. Though hypersensitivity reactions are rare, they
may occur and varies from life threatening anaphylaxis to less severe delayed type reactions. Here we
are reporting a case of delayed type 4 reaction to lignocaine after supraclavicular brachial plexus block
which was managed conservatively.
Keywords: Lignocaine, Local anaesthetics, Type 4 hypersensitivity, Supraclavicular brachial plexus
block
INTRODUCTION
Local anaesthetics have been very widely used

since the discovery of the anaesthetic effect of
cocaine in 1884. In spite of their widespread use,
true hypersensitivity appears to be infrequent.
Most of the adverse reactions are due to
pharmacologic or toxic effects of local
anaesthetics. While type 1 hypersensitivity
reactions to lignocaine are uncommon, type 4
hypersensitivity is reported even less frequently1.
Here we report a case of a patient with no history
of allergy to local anaesthetics, which developed
an allergic reaction after exposure to preservative
free lignocaine.
CASE REPORT
Rupankar et al.,
A 45 year-old male presented for implant

removal from lower third of humerus. He
underwent surgery for fracture lower third of
humerus about a year back under GA which was
uneventful. This time as it was decided for a day
care surgery anaesthetic plan was supraclavicular
brachial plexus block. He had no previous
history of allergic reactions to food or drugs and
was not on any medications. After obtaining
informed written consent supraclavicular
brachial plexus block was administered with 1%
30 ml lignocaine with 1:2,00,000 adrenaline.
1003
That formulation was preservative free. After the

block was established surgery was allowed to
proceed. Intra operatively he did not receive any
other medication and the surgery was uneventful.
Though the procedure was planned as day -care
but he was not discharged on-request and
admitted. Next day he complained of itching and
rashes in the neck. On examination we found
severe urticarial rashes in the neck and chest
extending to sternum on the side where block
was administered (Fig 1). He was treated
conservatively with anti histaminics and was
discharged on symptomatic relief.
Fig 1: Urticarial rashes on the neck and chest

after supraclavicular brachial plexus block with
lignocaine
DISCUSSION
Local anaesthetics have traditionally been

divided into 2 groups according to their chemical
structure: esters and amides2. Allergic reactions
of local anaesthetics are extremely rare (less than
1%) 3. Aminoesters such as procaine may
produce allergic-type reactions more commonly
than aminoamides. Even with aminoesters, the
vast majority of reactions are not allergic.
Aminoesters,
unlike
aminoamides,
are
derivatives of p-aminobenzoic acid (PABA),
which is known to be allergenic. Allergy to local
anaesthetics may be type 1 immediate
hypersensitivity reaction mediated by IgE
antibodies or type 4 delayed hypersensitivity
mediated by lymphocytes.
Lignocaine (Lidocaine, Xylocaine) is an

aminoamide type of local anaesthetic agent. It is
probably the most widely used local anaesthetic
agent not only as a topical and injectable
anaesthetic, but also intravenously in the
treatment of cardiac arrhythmias. Despite its
widespread use adverse reactions to lignocaine
are uncommon. Most reactions are type 1
immediate hypersensitivity1. There are few
published
cases
of
type
4
delayed
hypersensitivity. It is likely that many cases are
not recognized. On January 1, 2001, the North
American Contact Dermatitis Group (NACDG)
added this antigen to their standard tray to assess
the frequency of sensitivity to lignocaine1.
Adverse reactions to lidocaine and others LAs
are extremely rare and less than 1% of adverse
reactions caused by local anaesthetic drugs are
due to be true allergy. There are a few cases
reported in literature in which the patient had
developed a type 4 hypersensitivity reaction to
injection of lignocaine.
Bircher et al4reported a patient with localized
swelling 24 hours after dental surgery with patch
test showing lignocaine sensitivity.
Whalen5 reported a patient with localized,
pruritic,
vesiculobullous
delayed
type
hypersensitivity reaction on the dorsum of the
hand 12 hrs after lignocaine injection. Patch test
confirmed it.
Briet et al6 described a man who developed
pruritus, swelling erythema at lignocaine
injection sites. Results from prick and
intradermal tests were negative at 20 minutes,
but intradermal test results were positive at 48
hours; thus indicating type 4 hypersensitivity.
Downs AMR et al7 described one patient having
immediate hypersensitivity to lignocaine during
an injection for a dental procedure, but patch test
revealed delayed type of hypersensitivity.
Christine L. Mackley et al1 patch tested 183
patients and all those who were positive to
lignocaine were challenged with 0.1 ml
preservative free 1% lignocaine intradermally.
Four cases had positive reaction to lignocaine.
1004
Rupankar et al.,
They
concluded
that
delayed
type
hypersensitivity to lignocaine may occur more
frequently than previously thought and given its
frequent use, may become widespread.
Duque et al8 described a woman who suffered
eczematous eruption on her face after the
administration of lignocaine and mepivacaine for
dental surgery. Patch test showed delayed type
hypersensitivity to amide local anaesthetics
lignocaine and mepivacaine.
In our case the patient received preservative free
1% lignocaine with adrenaline (1:2, 00,000) for
supraclavicular brachial plexus block.
The
intraoperative and immediate postoperative
period was uneventful. The patient developed
itching and subsequently skin rashes about 16 to
20 hours after administration of Local
anaesthetic. It was diagnosed as urticarial rashes
and the patient was treated conservatively with
anti allergic medications as soon as the rashes
were reported. Patient was advised patch test for
lignocaine for further evaluation; which he
refused. So we could not proceed for further
testing. On clinical grounds it is assumed to be
because of hypersensitivity to lignocaine. We
suspected lignocaine to be the cause because the
preparation was preservative free and no other
drug or sedative were used to supplement the
block. Adrenaline as causative agent was ruled
out because the reaction was localized and also
delayed. On further enquiring it was found that
the patient had no history of exposure to Local
anaesthetics or allergy to any drug or substance.
Moreover he underwent surgery for once only
before this, for putting the implant which he
underwent under general anaesthesia without the
use of local anaesthetic.
After ruling out other probable causes of allergy
we came to conclusion that the reaction was a
true hypersensitivity to lignocaine as the
formulation we used was preservative free. We
finally conclude with a note that allergic
reactions to local anaesthetics though rare can
occur in clinical situations in our day to day

practice to anyone of us and given its widespread
use the incidence is likely to increase. So it is
better to be aware of these adverse reactions and
be prepared for any untoward incident that may
occur during simplest of procedures.
Rupankar et al.,
REFRENCES
1. Mackley CL, Marks JG, Jr, Anderson BE.
Delayed-Type Hypersensitivity to Lidocaine.
Arch Dermatol. 2003;139(3):343-346.
2. Miller RD, Ed. 7th edn, Anesthesia, Churchill
Livingstone Publisher: 2009; 913-15
3. Giovannitti J, Bennett CR. Assessment of
allergy to local anaesthetics. Journal of
American Dental
Association.
1979;98:701-76.
4. Bircher AJ, Messmer SL, Surber C, Rufli T.
Delayed-type
hypersensitivity
to
subcutaneous lidocaine with tolerance to
articaine: confirmation by in vivo and in vitro
tests. Contact Dermatitis.1996;34:387-89.
5. Whalen JD. Delayed-type hypersensitivity
after subcutaneous administration of amide
anesthetic. Arch Dermatol. 1996;132:125657.
6. Breit S, Rueff F, Przybilla B. Deep impact
contact allergy after subcutaneous injection
of local anesthetics. Contact Dermatitis.
2001;45:296-97.
7. Downs AMR, Lear JT, Wallington TB,
Sansom JE. Contact sensitivity and systemic
reaction to pseudoephedrine and lignocaine.
Contact Dermatitis. 1998;39:33.
8. Duque S, Fernndez L. Delayed-type
hypersensitivity to amide local anesthetics.
Allergol et Immunopathol 2004;32(4):23334.
1005
DOI:10.5958/j.2319-5886.2.4.166

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Health Sciences
Coden: IJMRHS
rd
Copyright @2013
ISSN: 2319-5886
Case report
A RARE CASE OF FAMILIAL ADENOMATOUS POLYPOSIS
Saxena D, Akhtar M, *Kundra DN, Zaki M, Rangwala M
Department of Surgery, NKPSIMS & LMH, Nagpur, Maharashtra, India
* Corresponding author email - drdhruvkundra@gmail.com
ABSTRACT
FAP is an autosomal dominant disease characterized by numerous polyps, numbering from hundreds to
thousands, in intestine. It is a very rare condition with incidence ranging from 1 in 6000 to 1 in 12000
births. In absence of surgical intervention, their malignant transformation is inevitable. We report this
case because of its rarity.
Keywords: Familial adenomatous polyposis, Colonoscopy, Adenomatous polyposis coli gene, Ileal
pouch-anal anastomosis
INTRODUCTION
Colorectal carcinoma is one of the leading cause

of deaths due to malignancy globally. FAP is a
type of inherited colorectal carcinoma which is
autosomal dominant and characteried by
numerous polyps in the epithelium of intestine.
These polyps are benign in beginning and their
malignant transformation is inevitable around the
age of 34-43 years, if no surgical intervention is
done.1,2
CASE REPORT
A 24 years old male presented with complaints

of tenesmus and passing watery stools since 2 yrs
and passing blood with stools since 4 months.
There was no significant family history .His
vitals were normal and on per-rectal
examination, multiple polyps were palpable
around 2cms from anal verge. On proctoscopy
there was mucoid discharge with multiple polyps
all around. His routine blood investigations were

normal and USG abdomen also did not reveal
any abnormality. On Colonoscopy there were
multiple polyps in rectum, 1-4cms in size, which
were both pedunculated and sessile. There were
more than 100 polyps throughout the colon till
caecum (Fig.1). Their density decreased
proximally. The biopsy report was suggestive of
adenomatous polyps. A diagnosis of FAP was
kept and decision to perform exploratory
laparotomy with total proctocolectomy with ileal
pouch anal anastmosis was planned. Surgery
was performed by midline incision, specimen
was dissected from terminal ileum up to anal
canal, around 2cms from anal verge .Colon was
studded with polyps throughout its length (figure
2,3). Ileal J pouch was created (figure 3) and
anastmosed with anal canal using circular
staplers. A diverting loop ileostomy was done
1006
Saxena D et al.,
before closure. The histopathologic findings

were consistent with multiple adenomatous
polyps with mild to moderate dysplasia (figure4).
Patient was regularly followed up and 6 months
later ileostomy closure was planned. A distal
loopogram was done which was within normal
limits. Anal continence was checked and
ileostomy closure was done. The immediate
family members of patient could not be screened
as they lived in a different city. Patient has been
followed up to date and no complications have
been detected so far.
Fig 1: Colonoscopic image showing numerous polyps

throughout colon
Fig 4: Creating ileal j-pouch
Fig 5: Histological appearance of specimen

(magnification x200)
DISCUSSION
Fig 2: Photograph of colon after resection
Fig 3: The opened section of specimen showing

numerous sessile and pedunculated polyps
FAP is one of the familial causes for colorectal

carcinoma. Sklifasowski published the first
verified case of FAP in 1881 in Russia. Over the
years, with discovery of APC gene FAP has
become a separate entity.3 FAP results from
mutation in the APC (adenomatous polyposis
gene) gene. APC is a tumor suppressor gene
located on the long arm of chromosome 5 in
band q21.4
Symptoms may not present until the adenomas
are large and numerous so as to cause intestinal
bleeding. Patient may complain of change in
bowel habits, constipation/diarrhea, abdominal
pain or weight loss.5
Extraintestinal manifestations may include
Osteomas, which can be identified as occult
radio-opaque
jaw
lesions,
Congenital
hypertrophy of the retinal pigment epithelium
and cutaneous lesions such as fibromas, lipomas,
1007
Saxena D et al.,
sebaceous cysts, epidermoid

cysts
and
3
nasopharyngeal angiofibromas. Association of
gastro-intestinal polyps with other extra intestinal
manifestations is known as Gardners
syndrome. 6
Surveillance examination in patients with family
history or suspected cases, is recommended
beginning at age 10-12 years .Sigmoidoscopy is
recommended every year. Once colon polyps are
found, or by age 20-25 years, colonoscopy
should be done. Multiple colonic polyps, usually
more than 100 are diagnostic for FAP. Genetic
testing is useful in confirming a diagnosis of
FAP in those cases where there is some doubt
about the diagnosis. 7
The aim of the surgical treatment of FAP is to
remove the polyps before the transformation to
malignancy occurs. The surgical options are
1. Colectomy
and
ileo-rectal
anastomosis(IRA)
2. Proctocolectomy with ileal pouch-anal
anastomosis (IPAA)
3. Proctocolectomy and ileostomy
Choice of surgery depends upon extent of rectal
involvement. IRA is a simple operation with
quick recovery, low complication rates and
minimal lifestyle interference; however the risk
of cancer in rectum mandates yearly surveillance.
IPAA minimizes this risk but adenomas develop
in the ileal pouch so surveillance is still
necessary. A hand sewn IPAA has more
complications and poorer function than a stapled
IPAA. Laparoscopic surgery can be attempted in
cases which are detected early and with less
extensive intestinal involvement.8
Medical management of FAP is also under
research. Sulindac, a non-steroidal antiinflammatory drug, has been shown in studies to
achieve prolonged remission of polyps. However
it is still under investigation and not a routine
treatment replacing surgery. Aptosyn, a
derivative of sulindac and Celecoxib, a COX-2
specific antagonist have also been tried but are
not as effective as Sulindac.9
Genetic counseling should be offered to family

members of a diagnosed patient.
REFERENCES
1. Boia ES, Mejdi R. Familial adenomatous

polyposis (FAP); What must be known and
what should be done-case report. Pediatr J
2008;11:46-9.
2. Srinivasamurthy M, Geethamala K, Kumar
BD, Sudhrao M . Familial adenomatous
polyposis coli and adenocarcinoma of the
colon: A silent synchronous presentation.
Arch Int Surg 2012;2:101-4.
3. Steffen Bulow, Terri Berk, Kay Neale. The
history of Familial Adenomatous Polyposis.
Familial Cancer 2006;5:213-220.
4. Groden J, Thliveris A, Samowitz W, Carlson
M, Gelbert L, Albertsen H, Joslyn G, Stevens
J, Spirio L, Robertson M: Identification and
characterization of the familial adenomatous
polyposis coli gene. Cell 1991, 66:589-600.
5. Elizabeth Half, Dani Bercovich, Paul Rozen;
Review of Familial adenomatous polyposis.
Orphanet Journal of Rare Diseases.
2009, 4:22
6. Polymnia Galiatsatos, William D. Foulkes;
Familial Adenomatous Polyposis, American
Journal of Gastroenterology. 2006;101:385
98
7. Familial Adenomatous Polyposis (FAP)
2002, 2008 The University of Texas MD
Anderson Cancer Center 10/01/08
8. Ambroze WL, Dozois RR, Pemberton JH.
Familial adenomatous polyposis: results
following ileal pouch-anal anastomosis and
ileorectostomy. Dis
Colon
Rectum.1992;35:12-15
9. Giardello FM, Hamilton SR, Krush AJ.
Treatment of colonic and rectal adenomas
with sulindac in familial adenomatous
polyposis. N Engl J Med. 1993;328:1313-16.
1008
Saxena D et al.,
DOI:10.5958/j.2319-5886.2.4.167

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Case report
KETOTIC HYPOGLYCEMIA IN CHILDREN NOT AN UNCOMMON ENTITY BUT IS

RARELY THOUGHT OF: CASE SERIES
*Santosh Yadav1, Prashant Nigwekar2, Dhananjay Y Shrikhande3, Amit Patil1, Amit Yadav1, Nilesh
Maniya1
1
Resident, 2Assoc. Professor, 3Professor and Head, Department of Pediatrics, Rural Medical College,
Paravara Institute of Medical Sciences, Loni, Maharashtra.
*Corresponding author email: santoshyadav117@gmail.com
ABSTRACT
Ketotic hypoglycemia is the most common form of childhood hypoglycemia. Periods of Hypoglycemic
episodes typically occur during early morning, especially during intercurrent illness when food intake is
limited. The symptoms and signs of hypoglycemia are often overlooked .Because hypoglycemia is a life
threatening event can lead to severe neurological sequel, intravenous administration of glucose is
necessary. These children respond promptly to glucose. We share our experience of four cases of
Ketotic hypoglycemia admitted during last 2 years.
Key words: Hypoglycemia, Ketosis, Ketotic hypoglycemia, Methylcrotonyl-CoAcarboxylase.
INTRODUCTION
Ketotic hypoglycemia (KH) is a good example of

what eyes dont see that mind doesnt know.
KH should be suspected in every child who
present with early morning drowsiness and/ or
convulsions especially after poor intake on the
previous day. So any child presenting with such
symptoms and hypoglycemia proved by
glucometer, urine should be immediately sent for
ketone bodies. If urine ketones are positive the
most likely cause is KH.1
With such an approach we were able to detect
more cases of Ketotic hypoglycemia during the
last few months. This has now become a routine
PICU protocol for children presenting with
morning seizures, drowsiness altered sensorium.
Blood glucose estimation and urine for ketone
bodies as a bedside test are done and confirmed

by laboratory. It is considered as a benign
condition as neurological damage and other
sequels are rare 2. The inform consent taken from
parents in the study.
CASE SERIES
Case1. A 6 years old female presented with

complaints of early morning generalized tonicclonic convulsions. She had similar episodes 6
times in the past; all occurred early in the
morning. She had been diagnosed as epilepsy
and had been put on anticonvulsants. Seizure
episodes continued. Each episode was associated
with skipping dinner the previous night.
1009
Santosh et al.,
Case2. A 7 years old female presented with

drowsiness since morning, difficulty in arousing
her from sleep and mild grade fever since one
day. History of skipped dinner the previous
night. There was a past history of similar episode
3 months ago. She had been admitted in private
hospital we had low blood sugar was
documented. She improved with IV dextrose and
was discharged. Ketotic hypoglycemia was
neither thought of nor investigated during the
previous episode. We also documented marked
hypoglycemia during this episode.
Case 3. A 4 years male came with the history of
loose motions since previous evening and history
of poor oral intake since previous afternoon. The
child has been drowsy since morning. There
were no signs of dehydration. No history of
convulsions.
Case 4. A 2 years old female admitted with
altered sensorium and generalized tonic-clonic
convulsions early in the morning. There was no
history of fever.
As per protocols blood sugar was obtained in all
the patients, who showed severe hypoglycemia in
the range of 20- 35mg/dl on glucometer (Model
no.Abbott 0088,Abbott Diabetes care ltd, ART
16648,Rev.B05/10)
Hypoglycemia
was
confirmed by laboratory method (Glucose
Oxidase Peroxidase) also. Urine ketones were
positive in all patients 3+ to 4+,
Anthropometry,
general
and
systemic
examination was normal in all cases.
Biochemical parameters like serum calcium,
serum magnesium, Liver function test, Renal
function test, Ceribro spinal fluid, CT scan head
and EEG done in all patients, were within normal
limits.
All the four cases were managed according to
routine emergency management. IV 10 %
dextrose bolus was given, followed by
appropriate IV fluid infusion. Blood glucose
level was monitored until condition was
stabilized.
Out of four, only three patients case 1,2,3 were
investigated for metabolic disorders by tandem
mass spectrometry (TMS) due to financial
constraints these could not be done in case 4.

Reports of case1,3 patients were within normal
limits.
TMS report of one patient case 2 came positive
for acylcarnitine profile showing increased levels
of 3-OH isovalerylcarnitine (C5OH). Urinary
organic acid profile showed increased levels of
3-methylcrotonyl glycine. Above findings were
suggestive of inborn error of metabolism of
leucine metabolism due to deficiency of enzyme
3-methylcrotonyl-CoA carboxylase (MCC)3.
This child was kept on oral carnitine, restricted
protein diet and asked for regular follow-up.
All patients were discharged with an advice of
frequent feedings of a high-carbohydrate,
balance protein diet and no skipping dinner at
night especially during intercurrent illnesses.
Parents were asked to monitor urine ketones
during intercurrent illness by ketosticks. They
were also told that an improvement and a marked
reduction in the occurrence of these episodes can
be expected as the child grows and attains
puberty and adolescence, with an increase in
muscle mass.
Santosh et al.,
DISCUSSION
KH is most commonly seen in early childhood
between 1.5-5years of age. Condition remits
spontaneously by the age of 89 years.
Hypoglycemic episodes typically occur during
periods of intercurrent illness when food intake is
limited. The classic history is of a child, who eats
poorly or completely avoids the evening meal,
who is difficult to arouse from sleep the
following morning, and may have a seizure or be
comatose by early or mid morning. Infants with
this condition do not manifest hypoglycemia due
to frequent breastfeeding.
The etiology of ketotic hypoglycemia may be a
defect in any of the complex steps involved in
protein catabolism, oxidative deamination of
amino acids, transamination, alanine synthesis,
or alanine efflux from muscle. Rarely, inborn
errors of fatty acid metabolism present as ketotic
hypoglycemia, although, typically, fatty acid
1010
oxidation
defects
produce
hypoketotic
1
hypoglycemia . Diet rich in Carbohydrates and
Protein with more frequent feeding is the
recommended
treatment
for
ketotic
hypoglycemia. The appearance of ketone in
urine precedes hypoglycemia by several hours.
Parents are advised to test the child's urine for the
presence of ketones. In the presence of ketonuria,
liquids of high carbohydrate content should be
given. Patient requires hospitalization in case if
oral feeding is not tolerated. During the
intercurrent illness, if frequent estimations and
early detection of urinary ketones done at home,
hypoglycemia can be prevented (as ketones are
detected in urine much before hypoglycemia).
Other causes of hypoglycemia with ketosis
Adrenal insufficiency, Hypopituitarism, Glucose6-phosphatase debrancher defect, Fructose-1, 6diphosphatase defect, Galactosemia, glycogen
storage disease, fatty acid oxidation defects.
Adrenal
insufficiency,
Hypopituitarism,
glycogen storage disease, galactosemia could be
the other cause in children and infants with
seizures, drowinessor coma in the morning.
Glucose-6-phosphatase
debrancher
defect,
Fructose-1,6-diphosphatase defect have moderate
hepatomegaly. Fatty acid oxidation defects
usually do not manifest as ketosis. More
advanced investigations like estimation serum
levels of alanine, insulin, and lactate before and
after deliberate fasting for 24-36 hours are not
done in our cases due to non availability and
economic reasons.
3-Methylcrotonyl-CoA Carboxylase (3-MCC)
Deficiency: 3-Methylcrotonyl-CoA Carboxylase
(3-MCC) deficiency has been recognized since
19847.It is a defect in the degradation of the
amino
acid
leucine
which
is
glucogenicaminoacid7. The clinical presentations
of 3-MCC deficiency range from mild to severe
illness. The age of onset of 3-MethylcrotonylCoA
Carboxylase
(3-MCC)
deficiency
symptoms is between 1-5 years. Clinical
presentation is often with infection, illness, or
after fasting. Most common symptoms are
vomiting, lethargy, hypotonia, apnea, or
hyperreflexia and seizures8. Patients may have

profound hypoglycemia, mild metabolic acidosis,
hyperammonemia, elevated liver transaminases,
and ketonuria8. Plasma free carnitine may be
low. Newborn Screening using tandem mass
spectrometry reveals an elevation of C5-hydroxy
acylcarnitine from the dried blood spot of an
affected patient. Diagnosis of 3-MCC deficiency
then requires further testing. Urine organic acid
analysis finds elevation of 3- hydroxyisovaleric
acid and usually 3-methylcrotonylglycine3.
The condition is inherited as an autosomal
recessive trait. The gene for subunit (MCC1) is
located on chromosome 3q2527 and that for the
subunit (MCC2) is mapped to chromosome
5q1213. Mutation in either of these genes may
result in the deficiency of the enzyme activity5.
Tandem mass spectrometry have identified an
unexpectedly high number of infants with 3methylcrotonyl CoA carboxylase deficiency
(1:50,000), suggesting that this condition may be
one of the most common organic acidemias in
certain populations4.
Assay of 3-MCC in fibroblasts or leukocytes can
be used for confirmation of deficiency, along
with at least one other carboxylase having
normal enzyme activity must also be
assayed.3This assay was not possible in our case.
Santosh et al.,
CONCLUSION
KH though not uncommon, require a high index

of suspicion and should be suspected in any child
with early morning seizure, drowsiness and / or
altered sensorium and confirmed by glucometer.
Urinary ketones should be done routinely in such
patients. Further metabolic screening and other
advanced investigations may be done after
inquiry of consanguinity, proper history and
clinical examination. Early recognition of the
condition will prevent further hypoglycemic
episodes and unnecessary anticonvulsants. TMS
should be done in every patient to find a rare
metabolic disorder.
1011
REFERENCES
1. Mark A.Sperling. Nelson text book of
pediatrics, Elsevier, 19th edition 2012 ; 52830.
2. Mitchell GA, Fu Kao T. Inborn error of
ketone metabolism.In: Scriver CR, Baudet
AL. The Metabolic and Molecular Bases of
Inherited Disease..New York: McGraw-hill
Co. Inc.;2001;2(Chap. 102):2327-35
3. http://www.perkinelmer.com/Industries/Healt
hcare/NewbornTestingServices/ClinicianInformation /3-Methylcrotonyl-CoACarboxylase-Deficiency-(3MCCDeficiency).xhtml
4. Koeberl DD, Millington DS, Smith WE.
Evaluation of 3methylcrotonyl-CoA
carboxylase deficiency detected by tandem
mass spectrometry newborn screening. J
Inherit Metab Dis 2003; 26:25-35.
5. Baumgatner, Baumgatner MR. Molecular
mechanism of dominant expression in 3methylcrotonyl CoA carboxylase deficiency.
J Inherit Metab Dis 2005; 28:301-09
6. Dantas, Dantas MF, Suormala T, Randolph
A. 3-Methylcrotonyl-CoA
carboxylase
deficiency: Mutation analysis in 28 probands,
9 symptomatic and 19 detected by newborn
screening. Hum Mutat 2005; 26:164.
7. Satyanarayan U. Metabolism of amnoacids.
Biochemistry. 2010;15;364-66.
8. William L Nyhan. Abnormalities in
aminoacid metabolism in clinical medicine ;
Appleton-Century-Crofts 1984;chapter 5; 6578
1012
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DOI:10.5958/j.2319-5886.2.4.168

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Case report
KIKUCHI-FUJIMOTO DISEASE (HISTIOCYTIC NECROTIZING LYMPHADENITIS):

CASE REPORT
Saleem Nasir1, Mubbasher Ameer Syed2
1
2
Training Medical officer (Resident), Medicine, Hayatabad Medical Complex, Peshawar, Pakistan
Medical officer, Peshawar Health Clinic, Peshawar, Pakistan
*Corresponding author email: nasirsaleems@hotmail.com

ABSTRACT
Kikuchi-Fujimoto disease (KFD) is a self-limited pathological entity that is benign in its course. The
main features of this disease are tender regional cervical lymphadenopathy, usually accompanied by
low-grade fever and night sweats. Less frequently patients may report weight loss, nausea, vomiting, and
sore throat. Often referred to as KFD; Kikuchi-Fujimoto disease has a global prevalence with high report
rates from Japan and other Asian regions. That said, it is a very uncommon case to encounter due to its
rare occurrence. A viral causation is suggested keeping in view the clinical presentation, the histology
and immunohistochemical pattern. The recommended procedure to diagnose this disease is an excisional
biopsy of an affected lymph node. This histopathologic analysis is essential for the clinician to
differentiate it from similarly presenting conditions like tuberculous lymphadenitis (scrofula), lupus
(SLE) or malignant lymphoma to state a few. This is especially pertinent in regions where there is a high
index of suspicion for tuberculosis given its high prevalence, like Pakistan and India for example. It is
also essential to inculcate an understanding of this clinically and histopathologically challenging disease
amongst physicians and pathologists alike to decrease the risk of misdiagnosis. Steps to increase
awareness will also help curb the excessive costs and unnecessary interventions that go with wrong
diagnoses. In young patients who present with lymph node enlargement in the posterior cervical chain; a
biopsied node showing cellular and nuclear fragmentation along with features of necrosis should incite
the consideration of KFD amongst other differentials. Once diagnosed; symptomatic treatment with
NSAIDs, analgesics, antipyretics and in some cases corticosteroids is sufficient as the self limited
disease resolves by itself within a period of 1 month in most cases. It is unlikely to stretch beyond 4
months. Patients with KFD are followed for many years nonetheless, since these patients are at a slightly
increased risk of developing systemic lupus erythmatosus later in life than the general population.
The case we report is that of an 18 year old female patient who presented with a month history of low
grade fever, night sweats and cervical lymphadenopathy, which was minimally tender. She was initially
labeled as a case of tuberculous lymphadenitis and put on antituberculous therapy. However, she did not
respond and further diagnostic studies revealed the presence of KFD.
Keywords: Cervical lymphadenopathy, Kikuchi-Fujimoto disease, Self-limiting
1013
Saleem et al.,
CASE REPORT
An 18 year old female college student presented

to the outpatient department of Medical B unit of
Hayatabad Medical Complex, Peshawar,
Pakistan, in February of 2012, with a one month
history of low grade fever, spiking mostly in the
evening and night, and associated with nausea,
malaise and sweating. The fever was intermittent
in character. There were no aggravating factors,
however it was relieved to some extent with
Mefenamic acid but not with Paracetamol. She
also complained of a few lumps in the cervical
and left axillary area for the same duration. There
was no history of any chronic medical illness in
the past. She had no family history of
tuberculosis, no contact history to an active case
of TB, no family history of rheumatological
disorders like rheumatoid arthritis or systemic
lupus erythematosus and no family history of any
blood disorders. Her vitals on presentation were,
Pulse: 105/min, BP: 130/80, and temperature of
100.5oF. On examination she had pale
conjunctivae, and had left cervical and axillary
lymphadenopathy. The rest of her general
physical and systemic examinations were
unremarkable with no pertinent positive findings.
Notably she had no visceromegaly on abdominal
examination.
Lab Investigations:
CBC: Hb: 9.6mg/dl, TLC: 3600/cmm, Plt:
305000/cmm, ESR:
12mm/1st hr, LDH:
625U/L, RFTs: Urea: 20mg/dl, S.Creat: 0.7
mg/dl, LFTs: Serum total bilirubin: 0.7 mg/dl,
ALT: 64U/L, ANA and anti-dsDNA: Negative,
Mantoux showed an induration of 6mm, which
was reported as borderline positive, HBsAg by
ELISA: non-reactive, Anti-HCV antibodies by
ELISA: non-reactive, Monospot Test: Negative,
Urine R/E: Normal, Chest X-ray: Normal, U/S
of the neck showed cervical lymphadenopathy
involving the left mid cervical nodes, U/S
Abdomen: Normal Study, with no evidence of
hepatosplenomegaly.
During a previous admission in another medical

unit two weeks back an FNAC from a lymph
node is the left cervical region was done with an
impression
of
"chronic
granulomatous
inflamation most likely due to Tuberculosis. As
the FNAC report was inconclusive, a excisional
lymph node biopsy was taken and the patient was
empirically started on anti-tuberculous therapy
while awaiting the biopsy result. She was asked
to report back with the same. The biopsy report
confirmed findings consistent with "Kikuchi
Fujimoto Lympahadenitis."
Treatment: Following the biopsy report the antituberculous medications were stopped. She was
started on oral Prednisone (1mg/kg/day), for a
period of 06 weeks followed by a rapid taper.
She responded dramatically to this treatment and
became asymptomatic over the next 4-5 days.
She was counseled about the benign nature of
this disease and advised a 6 week follow-up in
the OPD. On follow up in the OPD six weeks
later she was asymptomatic with complete
regression of her lymph nodes and abatement of
her symptoms. She has remained in remission
after one and a half years of follow up.
DISCUSSION
A disease that most often presents with cervical

lymphadenopathy in young women; histiocytic
Necrotizing Lymphadenitis or more frequently
known as KFD, has now been established as a
pathologic entity with global prevalence. It was
an entity unheard of until the first case was
reported and recorded in 1972 from Japan.1,2 In
as much as half the patients, the clinical picture
includes fever and low leucocyte counts.3
When a clinician has the job to draw differentials
for a patient presenting with cervical
lymphadenopathy and fever; he has a lot on his
plate all the way from the most obvious entities
like infectious mononucleosis and bacterial
pharyngitis to the more ominous ones like
1014
Saleem et al.,
tuberculosis and lymphoma. Other considerations

might
be
cytomegalovirus
infection,
toxoplasmosis, syphilis and even HIV. With so
much to work out, it is often a taxing diagnostic
workup that ensues. If the culture and stains for
the various organisms are negative and the
presence of unifocal or multifocal necrosis and
histiocytic infiltrate in the backdrop of capsular
invasion and inflammation around the nodes4 is
detected under a microscope; it is strongly
suggestive of KFD.
Some authors have described an association
between systemic lupus erythmatosus and
histiocytic necrotizing lymphadenitis (KFD).5
Others have even gone on to propose the notion
that KFD is merely an unusual presentation of
SLE itself. In 2003 a Medline/LILACS (Latin
American and Caribbean Health Sciences) search
was performed by Santana et al.; that discovered
35 instances where KFD and SLE were reported
in the same patients. As per their findings; most
of the cases of SLE were either found after the
diagnosis of KFD or at the time of labeling.6 Our
patient was tested serologically for SLE but all
her results returned negative.
Since KFD is a disease that has a self-limited
course and is deemed benign to add to its rarity
in presentation; not much has been achieved in
the way of creating a targeted treatment for it. It
is recommended that symptomatic measures to
relieve localized and systemic distress associated
with the disease be employed. To counter
tenderness in the enlarged lymph nodes and the
fever that accompanies it; most clinicians rely on
NSAIDs, analgesics and antipyretics. Although
the efficacy of their use is not established
epidemiologically, corticosteroids have been
prescribed in cases with systemic involvement
outside the nodal region or a more severe
presentation of KFD. Neurological involvement
that often presents with aseptic meningitis or
cerebellar ataxia and/or a fulminant lupus like
presentation with positive serologic titers for
ANA have been cited by some authors as
indications for steroid use in KFD patients.
Another similar indication for steroid use is
involvement of the liver with high LDH levels.

This latter finding was positive in our patient.
Although the evidence for these widely accepted
indications for steroid use is insufficient itself;
some have gone on to suggest inclusion of a less
severe presentation amongst the indication for
steroid usage. Jang and colleagues suggested
Prednisolone prescription in patients with
recurrent disease, refractory patients who remain
symptomatic despite two weeks or more of
treatment with NSAIDs and for those who desire
a quicker recovery. The monitoring must not be
ignored though since there is always a risk of
developing SLE and/or, much rarely, a
recurrence of KFD later in life.7
Kikuchi's disease is an entity with an unclear
etiology. However, several hypotheses have been
put forth with regards to its etiology and
pathogenesis. A number of organisms like human
herpes virus 6, Epstein-Barr virus, HTLV-1
(human T-cell leukemia virus type 1),
cytomegalovirus, parvovirus B19, Yersinia
enterocolitica and parainfluenza virus have been
suggested as organisms that might be implicated
in the etiology of KFD.8
Since it has been observed and reported in
association with SLE; autoimmune processes
contributing to the etiological picture of KFD
have also been suggested. One of the theories in
regards to its causation cites the concept of
molecular mimicry. It proposes that an antigen of
an infectious agent that is similar to a selfantigen leads to an attack against self by the
activated T-cells.9 This concept can be
exemplified by quoting Lyme disease where such
cross-reaction between LFA-1 (human leucocyte
function associated antigen type 1) and Borrelia
burgdorferi antigen results in chronically
inflamed joints.10 Yet another proposal puts forth
a theory based on apoptotic cells that express
nuclear antigens on their surface, a process very
strongly implicated in the pathogenesis of SLE.
If such apoptotic cells are not adequately and
promptly cleared (i.e. due to complement
deficiency), these can act as a nidus for an
1015
Saleem et al.,
autoimmune process culminating in severe

damage to self tissues.11
5.
CONCLUSION
In view of the lingering fever and fatigue that

often accompany Kilkuchis disease, it can
become quite distressing and frustrating for both
the patient and caring physician whilst running
its course. Stating that observation, we are of the
opinion that clinicians should be reminded to
always consider it on the list of differentials for
young patients who present with cervical
lymphadenopathy. We also suggest an effort to
inculcate awareness amongst the pathologists to
look for the characteristic histopathologic
findings of KFD when deciding on specimen
from patients with the aforementioned features.
These steps are bound to culminate in a decrease
in the number of opinions sought, unrequired
interventions performed and valuable resources
expended. It deserves mention here that in our
review of literature of the disease, we concluded
that whilst associations of KFD with systemic
lupus erythmatosus and other autoimmune
diseases are cited12,13; these claims are yet to be
adequately verified.
6.
7.
8.
9.
10.
REFERENCES
1.
2.
3.
4.
Lopez C, Oliver M, Olavarria R, Sarabia

MA,
Chopite
M.
Kikuchi-Fujimoto
necrotizing lymphadenitis associated with
cutaneous lupus erythematosus: a case
report. Am J Dermatopathol. 2000;22
(4):32833
Kaur S, Thami GP, Kanwar AJ. Kikuchi's
disease,
skin
and
systemic
lupus
erythematosus. Br J Dermatol. 2002;146(1):
16768
Norris AH, Krasinskas AM, Salhany KE,
Gluckman SJ. Kikuchi-Fujimoto disease: a
benign cause of fever and lymphadenopathy.
Am J Med. 1996;101(4):40105
Loachim HL, Ratech H. Loachim's Lymph
Node Pathology. 3rd ed. New York:
Lippincott Williams & Wilkins; 2002.
11.
12.
13.
Mahajan T, Merriman RC, Stone MJ.

Kikuchi-Fujimoto
disease
(histiocytic
necrotizing lymphadenitis): report of a case
with other autoimmune manifestations .Proc
(Bayl Univ Med Cent). 2007 April; 20(2):
14951
Santana A, Lessa B, Galrao L, Lima I,
Santiago M. Kikuchi-Fujimoto's disease
associated
with
systemic
lupus
erythematosus: case report and review of the
literature. Clin Rheumatol. 2005;24(1):60
63
Litwin MD, Kirkham B, Henderson DR,
Milazzo SC. Histiocytic necrotising
lymphadenitis
in
systemic
lupus
erythematosus.
Ann
Rheum
Dis.
1992;51(6):80507
Menasce LP, Banerjee SS, Edmondson D,
Harris
M.
Histiocytic
necrotizing
lymphadenitis (Kikuchi-Fujimoto disease):
continuing
diagnostic
difficulties.
Histopathology. 1998;33(3):24854
Marrack P, Kappler J, Kotzin BL.
Autoimmune disease: why and where it
occurs. Nat Med. 2001;7(8):89905
Gross DM, Forsthuber T, Tary-Lehmann M,
Etling C, Ito K, Nagy ZA, Field JA, Steere
AC, Huber BT. Identification of LFA-1 as a
candidate auto-antigen in treatment-resistant
Lyme
arthritis.
Science.
1998;281(5377):70306.
Botto M. Links between complement
deficiency and apoptosis. Arthritis Res.
2001;3(4):20710.
Bosch X, Guilabert A, Miquel R, Campo E.
Enigmatic Kikuchi-Fujimoto disease: a
comprehensive review. Am J Clin Pathol.
2004;122:14152.
13.Martinez-Vazquez C, Hughes G, Bordon
J, Alonso-Alonso J, Anibarro-Garcia A,
Redondo-Martinez E, Touza-Rey F.
Histiocytic
necrotizing
lymphadenitis,
Kikuchi-Fujimoto's disease, associated with
systemic lupus erythemotosus. QJM.
1997;90:53133.
1016
Saleem et al.,
DOI:10.5958/j.2319-5886.2.4.169

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Case report
Coden: IJMRHS Copyright @2013 ISSN: 2319-5886

MECKEL'S DIVERTICULUM SIX CASE REPORTS OUR EXPERIENCE AND REVIEW OF

LITERATURE
*Meena H. Shaikh, Khilchand Bhangale, Swapnil Kadam, Shantanu Pawar, Tanmay Bhavthankar
Department of General Surgery, Rural Medical College, Pravara Institute of Medical Sciences (DU),
Loni, Ahmednagar, Maharashtra, India
*Corresponding author email: drmeena15@yahoo.com
ABSTRACT
A Meckel's diverticulum, a true congenital diverticulum, a vestigial remnant .It connects the yolk sac to
the small intestine in the early embryonic life. It remains without symptoms. In the children symptoms
occur below 2 years. It may contain heterotopic gastric, pancreatic tissue. Presentation can include
gastrointestinal bleeding, obstruction, perforation, and volvulus. Because of this wide range of clinical
scenarios it is important for a clinician to have a high index of suspicion to prevent significant
complications. Investigations like Ultrasonography, Computed tomography (CT scans) and Technetium
99m pertechnate scan helps in diagnosis Treatment is surgical. We are presenting the management of the
six cases supported by a review of the literature. The five patients presented with complications and
needed emergency operation. This is from the rural set up where the advance facilities are limited. The
knowledge of its anatomical and patho-physiological properties is essential to deal with such
complications.
Keywords: Meckel's Diverticulum, Volvulus, Perforation, Gangreen.
INTRODUCTION
According to Dr Charles Mayo, a Meckel's
diverticulum is frequently suspected, often
sought for and seldom found. 1 An accepted
incident of Meckels diverticulum is 1 to 3
percent. There are many complications related to
Meckel's diverticula . It is difficult to diagnose
Meckels diverticulum clinically and by modern
imaging technique. Depending on the type of the
anomaly patients may be completely symptom
free or may present with the complications with
the chronic abdominal pain. The presentation in
six patients in the present case report is different

and created diagnostic dilemma. Meckels
diverticulum have no specific signs so difficult to
diagnose High index of possibility of the
Meckels diverticulum is essential to manage it
properly. The aim of presenting these case
reports is to share our experience in these cases
and to make clinicians aware of the Meckel's
diverticulum.
Meena H et al.,
1017
Case report
Case 1: A five year old boy diagnosed as acute
appendicitis. He was taken for emergency
operation. Laparotomy reveled inflamed and
obstructed Meckel's diverticulum. The obstructed
part resected and ileoileal anastomosis was
done. Histopathology confirmed the diagnosis.
Case 2: A 6 years old boy Presented with
chronic pain in abdomen. His ultrasonography
showed inflamed Meckel's diverticulum. He
underwent elective laparotomy. There was a
band extending from the ileum to the umbilicus.
At the umbilicus there was cystic swelling. (Fig.
1) There was no communication between the cyst
and the umbilicus. Resection and anastomosis
with excision of the band and cyst was done. The
postoperative
course
was
uneventful.
Histopathology confirmed the diagnosis.
Case 3: Ten years old boy presented in the
emergency with the signs suggestive peritonitis.
He underwent emergency laparotomy. There was
perforation of Meckel's diverticulum at its base.
(Image no2) .Resection and anastomosis was
done. The postoperative course was uneventful.
Histopathology confirmed the diagnosis. [Fig 2]
Case 4: Thirteen-year-old boy was presented
with intestinal obstruction. Plain x-ray abdomenerect and USG abdomen confirmed the
diagnosis. Except leucocytosis all other blood
report
were
normal.
The laparotomy showed
gangrenous small
bowel around the constricting band of Meckel's
diverticulum. The affected part excised and
anastomosis
was
done.
Histopathology
confirmed the diagnosis.
Case 5: Eighteen year-old boy was presented
with signs and symptoms of intestinal
obstruction in shock. He was operated for acute
appendicitis six months back by the Mac
Burneys incision. He had leucocytosis, decreased
platelet count, Raised blood urea and creatinine.
He was taken for emergency surgery. On
exploring the abdomen, we found the small
bowel volvulus with extensive gangrene due the
band extending from small intestine to the
umbilicus. Resection and anastomosis was
performed. Postoperatively the patient went into

the renal failure. He received two hemodialysis.
He expired, gave the message that every effort
must be taken to exclude the Meckel's
diverticulum and to treat it properly.
Histopathology confirmed the diagnosis.
Case 6- Seventy five year-old male patient
admitted with generalized abdominal pain,
vomiting and absolute constipation since two
days before admission. He gave the history of
operation two years back for blunt abdominal
trauma. He was taken for emergency laparotomy
for intestinal obstruction. On exploration, a
Meckel's diverticulum with a length of seventeen
cm was found, with adhesions extending from
Meckel's diverticulum to the umbilicus. Meckel's
diverticulum showed gangrene. (Fig 3).
Adhesinolysis and resection- anastomosis was
performed. The post-operative course was
unremarkable. Histopathology confirmed the
diagnosis.
Meena H et al.,
Fig.1: Resceted small intestine with Meckels

diverticulum and cyst.
Fig.2: Arrow shows perforation of Meckels

diverticulum at its base.
1018
Fig.3: Arrow
sdiverticulum
shows
gangrene
of
meckel
DISCUSSION
German surgeon Wilhelm Fabricius Hildanus

was first described the diverticulum in 1598, the
entity was not named until 1809, when Johann
Friedrich Meckel reported diverticulum's
anatomy and embryology in his research.2,3
Furthermore, Meckel also showed that the
incomplete obliteration of the vitelline duct can
result in not only Meckel diverticulum but also
enterocysts,
mesodiverticular
bands
and
intestinal-umbilical fistulas. Salzer became the
first to identify ectopic mucosa within the
diverticulum in 1904.4 Meckels diverticulum is
located on the antimesentric border of ileum
around 45 to 60 cm proximal to ileocecal valve.
It is usually 3-5 cm 2% are in length.Its walls
are made up of three layers and are similar to the
intestinal wall.It derives its arterial blood supply
from superior mesenteric artery.5-7 It is present in
2% of population. 2 feet from the ileocecal valve.
2 inches in length.symptomatic. 2 types of
common ectopic tissues are present. 2 times
more boys are affected. In the present case report
all the patients are male. Furthermore, it can be
attached to the umbilical region by the vitelline
ligament, with the possibility of vitelline cysts, or
even a patent vitelline canal forming a vitelline
fistula when the umbilical cord is cut. Torsions
of intestine around the intestinal stalk may also
occur, leading to obstruction, ischemia, and
necrosis. A six years old boy in the case report
five presented with cyst at the umbilical side.
The male patient in the case reports one, two,
three, four and five were asymptomatic and

presented as intestinal obstruction with gangrene.
One patient expired in the immediate
postoperative period.7 The majority of people
with Meckel's diverticulum are asymptomatic. If
symptoms occur, they typically appear before
two years of age. Meckel's diverticulitis
occasionally may present with all the features of
acute appendicitis .The presence of ectopic
gastric cells lead to acid-peptic disease .
Bleeding, strangulation of bowel, bowel
perforation or bowel obstruction are known
complications, treatment involves surgical
resection of the Meckel's diverticulum itself
along with the adjacent bowel segment. In
patients without any complications, treatment
involves surgical resection of the Meckel's
diverticulum
only.8 In every
case
of
appendicectomy / laparotomy a search for
Meckel's diverticulum must be done and if
found Meckel's diverticulectomy or resection
should be performed to avoid secondary
complications arising from it
CONCLUSION
Meckels diverticulum is a rare entity. It may

remain asymptomatic. It may present with life
threatening complications. Every effort should be
taken to exclude Meckel's diverticulum in every
case of abdominal pain.
ACKNOWLEDGEMENT
The authors gratefully acknowledge the support

from the management of Pravara Medical Trust,
PIMS and Principal Rural Medical College,
Loni. We appreciate the help of colleagues in the
surgery department. We are grateful to the
patients for their cooperation consent.
REFERENCES
1. Neil J. McC, Mortensen. The small and large

intestines.IN Bailey & Loves short practice
of surgery. 23rd Edition. chapter 57, 1033.
1019
Meena H et al.,
2. Jay GD III, Margulis RR, McGraw AB.

Meckel's diverticulum: a survey of 103 cases.
Arch Surg. 1950;61:158169
3. Haber JJ. Meckel's diverticulum: review of
literature and analytical study of 23 cases
with particular emphasis on bowel
obstruction. Am J Surg. 1947;73:46885.
4. Mortensen NJ, Jones O. The Small and Large
Intestines. In Bailey & Love's Short Practice
of Surgery 24th edition. Edited by Russell
RCG, Williams NS, Bulstrode CJK Arnold.
2004, 1159-60.
5. Evers BM. Small Intestine. In Sabiston
Textbook of Surgery. 17th edition. Edited by
Townsend CM. Elsevier; 2004:1366-1368.
6. Whang EE, Ashley SW, Zinner MJ. Small
intestine. In Schwartz's Principles of Surgery.
Eighth edition. Edited by Brunicardi FC.
McGraw-Hill; 2005:1043-1044.
7. Yamaguchi M, Takeuchi S, Awazu S:
Meckel's diverticulum: investigation of 600
patients in Japanese literature. Am J Surg
1978, 136:247-49.
8. Horn F, Trnka J, Simickova M, Duchaj B,
Makaiova
I.
Symptomatic
Meckel's
diverticulum in children. Rozhl Chir 2007,
86(9):480-2
1020
Meena H et al.,
DOI:10.5958/j.2319-5886.2.4.170

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Health Sciences
Copyright @2013
th
th
Case report
ISSN: 2319-5886
LATE ONSET HEMORRHAGIC DISEASE OF NEWBORN DUE TO CMV HEPATITIS

PRESENTING AS SCALP HEMATOMA
*Amit Yadav1,Shrikhande DY2, Rajib Chatterjee3, Amit Narkhede1, Amol pokharkar1, Santosh Yadav1
1
PG student, 2Professor & Head, 3Professor, Department of Pediatrics, Rural Medical College, PIMS,
Loni, Maharashtra
*Corresponding author email: amityadav1985.ay@gmail.com
ABSTRACT
Vitamin K deficiency bleeding (VKDB) according to recent studies is the preferred term for
hemorrhagic disease of the newborn (HDN). This is due to deficiency of clotting factors as a result of
vitamin K deficiency. VKDB was first described over a hundred years ago but its relationship to vitamin
K was not released until 40 years later. Vitamin K is required for the production of clotting factors II,
VII, IX and X. It is involved in the normal clotting of blood, is present in some plants and is also
synthesized by some E. coli in the gut. Due to low levels of vitamin K all newborn infants are at risk of
developing hemorrhagic disease of the newborn. The body has very limited ability to store the vitamin.
We present an unusual case of Neonatal Hepatitis due to CMV as a rare cause of late onset vitamin kdeficiency bleeding.
Keywords: Cholestatic liver disease, Vitamin K, Vitamin K deficiency bleeding.
INTRODUCTION
Hemorrhagic disease of the newborn (HDN) is a

coagulation disturbance in newborns due to
Vitamin K deficiency. As a consequence of
vitamin K deficiency there is an impaired
production of coagulation factors II, VII, IX, X
by the liver.1,2 Newborns are relatively vitamin K
deficient for a variety of reasons. They have low
vitamin K stores at birth, Vitamin K passes the
placenta poorly, the levels of vitamin K in breast
milk are low and the gut flora have not yet been
developed (Vitamin K is normally produced by
bacteria in the intestines). HDN causes an
increased risk of bleeding. The common sites of
bleeding are the gastrointestinal tract, Mucous
membranes, umbilicus, injection sites and

circumcision.3
A number of review articles provide useful
overviews of vitamin K and its importance to
human beings. Bleeding disorders in newly born
infants were first described over 100 years ago
when Townsend reported 50 cases in 1894.1
Vitamin K, however, was only discussed about
40 years later, by Dam, in a study of bleeding
disorder in chickens.1
CASE REPORT
A term male baby appropriate for gestational age

(AGA) with birth weight 2400grms was
1021
AmitYadav et al.,
delivered vaginally to a primigravida mother at a

private hospital without any antenatal or
postnatal complications, baby was discharged on
breast feeding on 3rd day of life. The baby was
asymptomatic till 1month 5days and was on
exclusive breast feeding brought to our hospital
with c/o convulsion and swelling over scalp on
left side (7 x 8 cm), there being no h/o drug
intake during pregnancy.
On physical examination baby had severe pallor,
icterus, hepatomegaly, one oval shaped (7x8cm)
swelling present over left fronto-temporoparietal region, admission weight was 3400grms,
head circumference was 34.5cm.
Investigations revealed Hb 5.9 %, TLC
18400/cumm, DLC (N 56%, L40%,M4%),
platelet count 4.9 Lacks/cumm, prothrombin
time(PT)>2 min, partial thromboplastintime
(APTT)>2 min, LFT (Total Bilirubin 9.3gm/dl,
Direct Bilirubin 5.6gm/dl, SGOT 290IU/L,
SGPT235IU/L) , CSF study reaveled 2 cells, all
lymphocytes with normal protein and sugar, CT
scan suggestive of hemorrhagic contusions in
left temporal-parietal region, generalized cerebral
oedema, scalp hematoma ,USG
abdomen
showed Liver parenchymal disease. Torch study
of baby CMV (cytomegalovirus) IgG & IgM
Both positive also mother CMV reports shows
IgG +ve, IgM -ve
Fig 2: Contrast CT of brain

In treatment IV vit k 1mg, inj phenobarbitone,
inj Gancyclovir (6mg/kg/day, 12 hrly) for 21
days with monitoring complete blood count
every alternative day. Patient recovered
completely.
On follow up patient showed complete recovery
with normal hematological parameter and with
normal growth and development.
DISCUSSION
In 1894, Townsend described a self-limited

bleeding condition that usually occurs 1-5 days
after birth in patients with nonclassic
hemophilia.1,4,5The term vitamin K originated
from coagulations-vitamin in German.5 Henrik
Dam and Edward Doisy won the 1943 Nobel
Prize for the discovery and functions of vitamin
K. Subsequent research has provided significant
contributions to current knowledge of vitamin K
and its association with coagulation factors,
namely the vitamin Kdependent coagulation
factors VII, IX, and X.6
Fig 1: Plain CT scan of brain

Respectively showing hemorrhagic contusion in
left temero-perital region, generalized cerebral
oedema, scalp hematoma
Early VKDB occurs within 24 hours of

birth.
Classic VKDB happens between day 1 and
day 7 of life.
Late VKDB occurs between week 2 and
week 12 of life.
Late VKDB can result in significant morbidity
and mortality due to intracranial hemorrhage and
has resulted in most developed countries having
in place a protocol for giving supplemental
vitamin K to all newborn babies.
1022
AmitYadav et al.,
Late VKDB most commonly occurs at 2-12 week

of age, although cases can occur up to 6 months
after birth. All cases are in breast-fed infants due
to low vitamin k content of breast milk. An
additional risk factors are occult malabsorption
of vitamin k (cystic fibrosis), cholestatic liver
disease, pancreatic disease, intestinal disorders
(celiac sprue, inflammatory bowel disease, short
bowel syndrome). Cholestatasis in newborns can
be due to infectious, genetic, metabolic or
abnormalities giving rise to mechanical
obstruction of bile flow or to functional
impairment of hepatic excretion function and bile
secretion3
Human cytomegalovirus (CMV) is widely
distributed. Most CMV infections inapparent, but
virus can cause a variety of clinical illness that
range from mild to fatal. The incidence of
congenital CMV infection ranges from 0.2% to
2.2% (average 1%) of all live births, with the
higher rates among populations with a lower
economic standard of living. The risk for fetal
infection is greatest with maternal primary CMV
infection (30%) and much less likely with
recurrent infection (<1%).In infants and young
children, primary CMV infection occasionally
causes pneumonitis, hepatomegaly, hepatitis
(cholestatic liver disease) and petechial rashes.3
In our case, patient had swelling over scalp with
convulsion due to intra-cerebral contusion which
was present with late VKDB due to unusual
causes of hepatitis due to CMV infection.A
randomized controlled study with ganciclovir (6
mg/kg/dose every 12 hrly for 2-4 weeks)
concluded as a treatment for hepatitis due to
CMV infection.
CONCLUSION
We suspected late VKDB due to its presentation

at age of 4 weeks, PT/APTT had been improved
after giving single dose vitamin k, reduction in
swelling over scalp and also recovered from
neonatal cholestasis(hepatitis) after giving inj
Gancyclovir. CMV induced hepatitis is an
unusual presentation of late VKDB. On follow
up patient showed complete recovery with
normal hematological parameter and with normal

growth and development.
REFERENCES
1. Townsend CV. The Hemorrhagic Disease of

the Newborn. Arch Pediatr. 1894, 11:559-62.
2. Hubbard D, Tobias JD. Intracerebral
hemorrhage due to hemorrhagic disease of
the newborn and failure to administer vitamin
K at birth. South Med J 1999; 11: 1216-20.
3. Stoll BJ, Kliegman RM, Behrmann RE,
Kliegman RIV, Jenson HB. Nelsons
Textbook ofPediatrics. 18th Ed. Philadelphia:
W.B Saunders; 2007. p. 773-5.
4. McNinch AW, Tripp JH. Hemorrhagic
disease of the newborn in the British Isles:
two year prospective study. BMJ.
1991;303(6810):1105-9.
5. Chaou WT, Chou ML, Eitzman DV.
Intracranial hemorrhage and vitamin K
deficiency in early infancy. J Pediatr.
1984;105(6):880-4.
6. Van Winckel M, De Bruyne R, Van De
Velde S. Vitamin K, an update for the
pediatrician. Eur J Pediatr. 2009;168(2):12734.
7. Puckett RM, Offringa M. Prophylactic
vitamin K for vitamin K deficiency bleeding
in neonates. Cochrane Database Syst Rev.
2000;Issue4. Art. No.:CD002776.
8. Costakos DT, Greer FR, Love LA. Vitamin
K prophylaxis for premature infants: 1 mg
versus 0.5 mg. Am J Perinatal.
2003;20(8):485-90.
9. Loughnan
PM,
McDougall
PN.
Epidemiology of late onset hemorrhagic
disease: a pooled data analysis. J Pediatric
Child Health. 1993;29(3):177-81.
10. No authors listed; Controversies concerning
vitamin K and the newborn. American
Academy of Pediatrics Committee on Fetus
and Newborn. Pediatrics. 2003;112(1 Pt
1):191-2.
11. Zipursky A. Prevention of vitamin K
deficiency bleeding in newborns. Br J
Haematol. 1999;104(3):430-7.
1023
AmitYadav et al.,
DOI:10.5958/j.2319-5886.2.4.171

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Case report
AN UNUSUAL FINDING OF EPIDIDYMAL

ORCHIDECTOMY SPECIMEN: A CASE REPORT
Copyright @2013
ISSN: 2319-5886
SPERM
GRANULOMA
IN
AN
*Vandana Gangadharan1, Geetha Prakash 2, Hema Maheshwari 3, Shaffy Tukkral4, Archana S4

1&3
Assistant Professor, 2 Professor& HOD, 4Post Graduates, Department of Pathology, Meenakshi

Medical College & Research Institute, Enathur , Tamilnadu, India
*Corresponding author email: vandanagangadharan@gmail.com
ABSTRACT
Epididymal sperm granuloma as a cause of granulomatous epididymitis is rare. Most of the cases are
found post vasectomy as part of the late vasectomy syndrome. These lesions are known to mimic other
conditions including testicular malignancies. We report this interesting case of an epididymal sperm
granuloma which was not only an incidental finding in an orchidectomy specimen of a 55 year old male
with no antecedent history of surgery, trauma or clinical infection but also mimicked a testicular tumor.
Keywords Epididymitis, Sperm granuloma,Vasectomy
INTRODUCTION
Epididymitis is defined as the inflammatory

condition of the epididymis. It may be acute or
chronic depending on the inciting agent as well
as the duration. Specific causes of chronic
epididymitis include a) Tuberculosis b) Leprosy
c) sarcoidosis and d) Sperm granuloma 1 .
Sperm granuloma is an exuberant foreign body
reaction to extravasated sperm and occurs in 42%
of patients after vasectomy 2 and 2.5% of routine
autopsies 1 .This lesion is thought to result from
damage to the epithelium and basement
membrane of epididymal ducts by inflammation
or trauma 3 with subsequent spillage of sperm
into interstitium. The granulomatous reaction is
probably induced by an acid fast fraction of lipid
from the sperm; a hypothesis supported by the
fact that this material has been found to provoke
a granulomatous reaction when injected

subcutaneously in hamsters 4. Epididymal sperm
granuloma may account for late vasectomy
syndrome in which patients complain of pain
many months or years after vasectomy. Ligation
vasectomy accounts for most cases whereas
cauterization vasectomy rarely results in
granuloma 1.
Vandana et al.,
CASE REPORT
55 year old male reported with h/o pain abdomen

since 10 days with inguinoscrotal swelling on left
side since 1 month. He also complained of pain
in the scrotal region on and off since 10 days. No
other positive history or co morbidities noted. On
examination vitals were normal and a left direct
inguinal hernia with scrotal swelling measuring
1024
2x1 cm was felt. On ultra sound the inguinal

hernia was confirmed and the scrotal swelling
was hypoechoic with calcification of testis. With
a suspicion of carcinoma testis (L) meshplasty
with (L) orchidectomy was planned.
For histopathological examination we received
an orchidectomy specimen measuring 6x4x3cm
with spermatic cord measuring 9cm. A nodule
measuring 2 cmx1cm was felt in the epididymal
area. On microscopic examination testicular
tubules with both normal and arrested
spermatogenesis were seen. The epididymal
tubules showed extravasated sperms along with a
granulomatous
reaction
composed
of
lymphocytes, lipid laden and sperm laden
macrophages (Spermiophages). Some of the
epididymal tubules showed haemorrhage,
necrosis and cholesterol clefts. Focal areas of
calcification were also seen. A diagnosis of
Epididymal Sperm granuloma was given.
Fig 1: Focal areas of calcification. H & E 10x
Fig 2: Sperm granuloma H & E 40x
Fig 3: Sperm granuloma with spermiophages. H &

E 40x
DISCUSSION
Sperm granuloma was first described by

Grunberg in 1926 5. They have been reported in
upto 42% of men who have undergone
vasectomy and 2.5% of general population 1.
They can range in size from microscopic upto
4cm but most are less than 1 cm 1. Although
most sperm granulomas are asymptomatic, some
manifest as painful nodules. They are generally
well defined, hypoechoic, solid masses at ultra
sonography. On histopathology foreign body
granulomas may be present with necrosis and
later progressive fibrosis. Extravasated sperms
are plenty with many engulfed by macrophages
(referred to as spermiophages).Yellow brown
ceroid pigment; a lipid degradation product of
sperm may persist. Vasitis nodosa occurs in
about one third of cases of sperm granuloma
1
.Although they can occur anywhere in the ductal
system, they are most common at the cut ends of
the vas deferens and can be multiple 6. It is also
known to occur in the epididymis. However the
incidence in the testis is exceptional. It is
probably the microenvironment of the testicular
interstitium rather than the extravasated
components from the ruptured seminiferous
tubules, which is the main factor determining the
limited formation of spermatic granuloma in the
testis 7.The incidence of sperm granuloma in our
knowledge is limited. In his study of 228 cases of
epididymal nodule in india Gupta et al found an
incidence of 5.3% 8.In another study by Shah et
1025
Vandana et al.,
al the incidence was found to be 7.5%9.

Commonest cause of these granulomas is thought
to be vasectomy. However, trauma , epididymitis
and orchitis have also been described 1, 8. Silch et
al describes sperm granuloma in a patient 4 years
after inguinal hernia repair 10 and Deane et al
describes sperm granuloma presenting as a
recurrent inguinal hernia11. However as in our
patient, case reports without any antecedent
history of surgery trauma or clinical infection
have been seen 3, 8. Another important feature is
the rare confusion it can cause with testicular
tumor 12, 13. As seen in our case the testicular
tumor is thought of because of proximity to the
testes, solid nature and calcification.
CONCLUSION
We present this rare case of sperm granuloma

which was an incidental finding with no
antecedent history of vasectomy, trauma or
clinical infection and mimicked a testicular
tumor. The patient also had a concurrent direct
inguinal hernia on the same side. The possible
etiology of sperm granuloma in our patient may
be an unnoticed trauma or subclinical epididymal
infection.
REFERENCES
1. Bostwick DG, Eble JN .Urologic surgical

pathology. St Louis Mosby 2000.
2. Mc Donald SW. Cellular responses to
vasectomy. Int Rev Cytol 2000; 199:295-339.
3. Glassy FJ, Mostofi FK. Spermatic
granulomas of the epididymis. Am J Clin
Pathol 1956; 26:1303-13.
4. Berg JW. An acid fast lipid from
spermatozoa. Arch Pathol. 1954; 57; 115-20.
5. JBL Taylor. Spermatic granuloma. British
Journal of Urology 1959; 31 (2):196-200.
6. Holden A, List A.Extratesticular lesions: A

radiological and pathological correlation.
Australas Radiol 1994; 38:99-105.
7. Itoh M, Xieq, Miyamoto K. Major
differences between the testis and epididymis
in the induction of granulomas in response to
extravasated
germ
cells.
A
light
microscopical study in mice. Int J Androl
1999;22(5):316-23.
8. Gupta N, Rajwanshi A, Srinivasan . Fine
needle aspiration of epididymal nodules in
Chandigarh, North India : An audit of 228
cases. Cytopathology 2006;17(4):195-8.
9. Shah VB, Shet MT, Lad KS. Fine needle
aspiration cytology of epididymal nodule. J
cytol 2011; 28(3) : 103-07.
10. Silch RC, McSherry CK. Spermatic
granuloma an uncommon complication of
tension free hernia repair. Surgical
endoscopy.1996;10(5):537-39.
11. Deane LA, Suding PN, Lekawa ME, Narula
N, McDougall EM. Sperm granuloma of the
inguinal vas deferens mimicking recurrent
incarcerated inguinal hernia. Urology.
2007;69(6):1-3.
12. Oliva E, Young RH. Paratesticular tumorlike
lesions.
Semin
Diagn
Pathol
2000;17(4):340-58.
13. Wada N, Kato Y, Iwats T. A case of
spermatic granuloma difficult to differentiate
from malignant tumour. Hinyokika Kiyo
2002;48(9):549-5
1026
Vandana et al.,
DOI:10.5958/j.2319-5886.2.4.172

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Case report
Copyright @2013
ISSN: 2319-5886
CASE OF KIKUCHI S DISEASE AND SYSTEMIC LUPUS ERYTHEMATOSUS ASSOCIATED

WITH ANTIPHOSPHOLIPID ANTIBODY SYNDROME AND COMPLICATED BY
HEMOPHAGOCYTIC SYNDROME (HPS)
*Koushik Pan, Subrata Chakrabarti, Rajdip Choudhury, Anup Sarkar
Department of General Medicine, SSKM, IPGME& R, Kolkata, West Bengal, India
*Corresponding author e-mail: panjoy86@gmail.com
ABSTRACT
Kikuchi disease is a rare benign self limited lymphadenopathy. It is often associated with Systemic
Lupus Erythematosus which can be diagnosed before; at the same time or after a diagnosis of Kikuchi
disease is made. Again SLE is usually associated with APLA syndrome. Furthermore both SLE and
Kikuchi disease can be complicated by HPS. We present a unique case in which Kikuchi disease and
SLE were diagnosed together and disease course was complicated by Hemophagocytic syndrome (HPS).
SLE was also associated with Anti Phospholipid Antibody Syndrome (APS) in this patient.
Keywords: Kikuchi, SLE, APLA, Hemophagocytic syndrome
INTRODUCTION
Kikuchi disease or histiocytic necrotizing
lymphadenitis a rare, benign, self limiting
cervical lymphadenitis of unknown etiology1
mainly affecting young adults with females
outnumbering males.2 Sometimes association
with SLE
has led to the probability of
autoimmune etiology being one of factors
leading to Kikuchi disease. SLE is probably the
most common underlying diseases of APLA
syndrome.3 Hemophagocytic syndrome is a rare
but potentially fatal disease of normal but
overactive histiocytes and lymphocytes often
complicating connective tissue disorder &
haematological malignancies. Kikuchi disease
can independently lead to hemophagocytic
syndrome in rare instances. Kikuchi disease and
SLE with APLA syndrome can coexist rarely &
may be complicated
syndrome.
by
hemophagocytic
Koushik et al.,
Int J Med Res Health Sci. 2013;2(4):1027- 1031
CASE REPORT
A 16 year Hindu Male from rural Bengal, student

by profession, presented with fever, joint pain
and glandular swelling in neck and axilla for last
1 month. Fever was high grade reaching upto
104F; continuous; chill and rigor; intense
constitutional
symptoms,
no
localising
symptoms; relieved partly on medications. Joint
pain involved mainly small joints of both upper
limb and lower limbs [metacarpophalangeal joint
(MCP), Proximal interphalangeal joint (PIP),
distal
interphalangeal
joint(DIP),
metatarsophalangeal
joint
(MTP),
Interphalangeal joints (IP)] ; simultaneous onset;
1027
additive; pain, Restriction of movement present

but no swelling or redness. Painless glandular
swelling in the neck and axilla started for last 15
days; gradually increasing in size but no
discharge. No history of bleeding manifestations,
purpuric rash, bone pain. No history of morning
stiffness, pain in large joints or spine, oral or
genital ulcers, facial rash, erythematous,
evanescent rash over the trunk during spikes of
fever. No history of prior tuberculosis, malaria,
kalaazar. No history of chronic intake of any
drug or any family history of arthritis. A
significant history of spontaneous development
of painful swelling in Right thigh 1 year ago
which was documented as deep vein thrombosis
involving iliofemoral veins. On clinical
examination, patient had significant pallor, mild
icterus. Lymph nodes palpable in right
supraclavicular middle group, bilateral axillary
central group and posterior triangle; all were soft,
mobile, nontender with no fixity; mediastinal
percussion resonant. No sternal tenderness. Chest
-Bilateral Vesicular breath sounds heard normally
with normal S1, S2. Abdomen was soft,
nontender; spleen palpable 2cm below Left
costal margin, nontender, no rub; liver not
palpable; no free fluid. Musculoskeletal exam
reveals pain, slight swelling, range of movement
restricted in bilateral MCP, PIP, DIP joints in
upper limb; MTP, IP joints in lower limb;
tenderness at bilateral Achilles tendon insertion;
Axial system uninvolved. Routine blood tests
show Hb-7.2 gm/dl,
PCV-22.3%,
TLC2300/cmm; N-69%; L-25%; M-5% ; E-1% ,
Platelet-41000/cmm , Reticulocyte-2%, MCV72.4fl; MCH-23.3pg; MCHC-32.2%, RDW16%;
Peripheral blood smear shows
hypochromic, microcytic RBCs; anisocytosis,
elliptocytes, tear drop cells but no abnormal
cells, ESR- 84mm/1st hr, Ur-19mg/dl; Cr1mg/dl; LDH-1890U/L, Bil-0.7mg/dl; SGOT39U/L; SGPT-56U/L; Alkaline phosphatase-112;
Albumin-3.2gm/dl; Gloulinb-2.8gm/dl; A:G
ratio:1.1, Na+-137.3meq/l; K+-3.89meq/l; Ca++-
8.9mg/dl; TG-360mg/dl, PT-13s; INR-1.03;

APTT-70s
HBsAg, Anti HCV, ICTC were all negative;
Chest X Ray-within normal limit; USG Whole
abdomen showed mild splenomegaly; ECHO
Cardiography: Normal; Malaria parasite Dual
Antigen-Negative; Malaria Parasite on slide-not
found. Dengue serology was Negative. Blood
and urine Cultures were sent on day of
admission; Sputum AFB-Not found; Mantouxnegative; urine routine & microscopic
examination -normal. Patient was started on
empirical IV antibiotics after sending blood and
urine cultures; Bone marrow aspiration and
Lymph node excision biopsy done. In the
background of history of spontaneous DVT and
isolated APTT rise, testing for Antiphospholipid
antibody syndrome was done. PTT-A(test)161.3s( N--35-42s)
PTT-A(control)-39s(N35-42s)
PTT-A1:1 Mixing test-108.9s
Interpretation- NOT CORRECTED
DRVV(diluted russel viper venom)(test)155.2s (N35-42s)
DRVV(control)-38.3s (N35-42s)
DRVV ratio: 4.05 (N-0.85-1.12), Cardiolipin AbIgG-Positive 57.53 GPL U/ml
(N<10 U/ml)
antiphospholipid Ab IgG-POSITIVE
35.11
GPL U/ml (N<10 U/ml); lupus anticoagulant was
positive. A diagnosis of possible APLA syndrome
was made based on the presence of 1 episode of
venous thrombosis; anticardiolipin Ab >40 GPL
U/ml and lupus anticoagulant positivity. Patient
was started on inj.LMWH (given for 5 days with
target INR 2-3) with oral Warfarin to be given
lifelong.Blood culture & sensitivity, Urine
culture & sensitivity reports reached our hands
which revealed no growth; Bone marrow
aspiration showed reactive hyperplasia; no
leukemic cells; Hemophagocytosis noted;
Ferritin -1480mcg/l ; serum Fe-28mg/dl;
Transferrinsaturation36%.
Koushik et al.,
1028
phospholipid antibody and anti cardiolipin

antibody was positive in significant titre.
Fig 1: Bone marrow showing hemophagocytosis

(40 x)
Area of necrosis surrounded

by infiltrated histiocytes
Fig 2: Lymph node histopathology (40X)
X ray both hands- No erosive features. A

diagnosis of HPS was made due to presence of
fever, pancytopenia, splenomegaly, raised ferritin
(>500ng/ml), raised Triglyceride (>250mg/dl)
and evidence of hemophagocytosis on
BMAspiration. Patient continued to have high
fever and on 11th day of admission became
disoriented with irrelevant words. CT brain was
normal; CSF Study revealed no features of acute
CNS infection. Psychiatry referral done; a
diagnosis of psychosis was made. Now workup
for collagen vascular diseases was done- ANA2+ homogeneously at 1:200 dil; C3
50.9mg/dl(N90-180mg/dl) C47.3mg/dl (N10-40mg/dl). Anti ds-DNA-negative; A diagnosis
of SLE was made based on the presence of
clinical features (non erosive arthritis involving
more
than
2
peripheral
joints
with
tenderness,swelling; psychosis without other
causes)and lab features (an abnormal titre of
ANA in the absence of drugs known to induce
ANAs
and
leucopenia
(<4000/cmm),
lymphopenia(<1500/cmm), thrombocytopenia(
<100000/cmm)in the absence of offending
drugs). Patient was treated accordingly. Fever
gradually abated and patient became conscious
and responsive. He was put on oral steroids
1mg/kg/day with gradual tapering. LN HPE
report reached our hands which revealed
Necrotizing
Histiocytic
Lymphadenitis
compatible with Kikuchis disease. Patient was
followed up at 6 weeks & repeat anti
CT thorax and abdomen was done which

revealed no malignancy. So the complete
diagnosis was SLE associated with Kikuchi
disease
and
APLA
syndrome
and
hemophagocytic syndrome.
DISCUSSION
Kikuchi-Fujimoto disease (KFD) is a unique
disease which was first described in 1972 in
Japan. KFD is a very rare disease and mainly
seen in Japan although occasional cases are
reported in America and Europe. It is also known
as Kikuchi disease1, histiocytic necrotizing
lymphadenitis,
phagocytic
necrotizing
lymphadenitis,
subacute
necrotizing
lymphadenitis.KFD generally affects the cervical
lymph nodes. Cause of disease is unknown
although infectious and autoimmune etiologies
have been discussed as probable etiologies. A
genetic predisposition to the proposed
autoimmune response cannot be ruled out.
Several infectious candidates have been proposed
like Mycobacterium szulgai, Yersinia and
Toxoplasma. Role of Epstein-Barr virus, as well
as other viruses (HHV6, HHV8, Parvovirus B19,
HIV- and HTLV-1) in the pathogenesis cannot
be ruled out. Serologic tests including antibodies
to viruses have not been proven fruitful and viral
particles cannot be identified in electron
microscopy. KFD generally affects the cervical
lymph nodes. It can be confused with
1029
Koushik et al.,
tuberculosis, lymphoma which can have similar

presentation it mainly affects young adults (20
30 years), with females outnumbering males2.
Course of the disease is generally benign and
self-limiting. Lymphadenopathy usually resolves
within several weeks to months. Recurrence rate
is about 4-5%. Mortality is very rare and usually
results from hepatic, respiratory, or cardiac
failure. SLE is the single most disease associated
with this disorder.3,4 Similar autoimmune states
such as polymyositis, juvenile idiopathic
arthritis, antiphospholipid syndrome can be
associated with KFD. KFD may be an aberrant
T-cell mediated immune disoeder in a genetically
susceptible individual in response to appropriate
stimuli. The exact relationships between SLE and
KFD are not known as SLE can coincide,
proceed, or follow KFD. Clinical features of
SLE and KFD can be identical; fever,
lymphadenopathy, fatigue, and joint pain are
noted in both. These two diseases are separated
by histopathological features; the presence of
hematoxylin, plasma cells, and deposition of
DNA is seen in SLE only.SLE is probably the
most common underlying diseases of APLA
syndrome. Kikuchi disease and SLE with APLA
syndrome can coexist as documented in
literature.5
SLE is often complicated by hemphagocytosis
syndrome6 which is also called as Macrophage
Activation Syndrome (MAS). Now MAS is
called hemophagocytic lymphohistiocytosis
(HLH).Criteria
for
hemophagocytic
lymphohistiocytosis (HLH) , which include
fever, splenomegaly, cytopenias affecting at least
two of three lineages in the peripheral blood,
hypertriglyceridemia and/or hypofibrinogenemia,
hemophagocytosis in bone marrow, spleen or
lymph nodes, low or absent natural killer cell
activity, hyperferritinemia, and high levels of
sIL-2 receptor. Five of the eight criteria should
be fulfilled to make this diagnosis. Patients with
a molecular diagnosis of HLH are exempted
from fulfilling all the diagnostic criteria. The
prevalence of HPS among patients with
autoimmune diseases varies but around

3%4.Incidence is highest in patients with adult
onset Stills disease, followed by Sjogrens
Syndrome and SLE. Increased mortality is noted
in age above 50 years, the presence of coexistent
infection, leucocyte count < 5000/mcl, platelet
count < 50000/mcl and CRP level < 50 mg/L at
the onset of HPS5 .Current treatment strategy is
induction therapy over an eight-week period with
dexamethasone,
etoposide
(VP-16),
and
intrathecal
methotrexate, followed by
cyclosporine started at 9 th week . Pulses of
dexamethasone and etoposide to be given for one
year.7 This case presents an extremely rare
coexistence of SLE, Kikuchi disease, APLA
syndrome and finally HPS & highlights the fact
that patient may manifest with APLA at earlier
stage & later turn into florid SLE in the
subsequent disease course, even after years.
Whether the HPS in this case was a complication
of kikuchis disease or SLE per se cannot be
determined with certainty as both of them are
established predisposing factor for HPS.
Koushik et al.,
REFERENCES
1. Kikuchi M. Lymphadenitis showing focal
reticulum cell hyperplasia with nuclear debris
and
phagocytes. Acta
haematologica
Japonica. 1972;35:37980.
2. Fujimoto Y, Kojima Y,. Yamaguchi K.
Cervical
Subacute
necrotizing
lymphadenitits. Naika.1972, 20:92027.
3. Khanna D, Shrivastava A, Malur PR, Kangle
R. Necrotizing lymphadenitis in systemic
lupus erythematosus: is it kikuchi-fujimoto
disease? Journal of Clinical Rheumatology.
2010;16(3):12324
4. Londhey VA, Buche AS, Kini SH,
Rajadhyaksha GC. Kikuchi fujimoto disease
and systemic lupus erythematosusa rare
association, Journal of Association of
Physicians of India. 2010;58(10):64243.
5. Chen HC, Lai JH, Huang GS. Systemic lupus
erythematosus with simultaneous onset of
1030
Kikuchi-Fujimoto's disease complicated with

antiphospholipid antibody syndrome: a case
report and review of the literature.
Rheumatology International. 2005;25(4): 303
06.
6. Kampitak T. Fatal Kikuchi-Fujimoto disease
associated with SLE and hemophagocytic
syndrome:
a
case
report, Clinical
Rheumatology. 2008;27(8):1073
7. Fukaya S, Yasuda S, Hashimoto T, Oku K,
Kataoka H, Horita T, Atsumi T, et al.
Clinical features of haemophagocytic
syndrome in patients with systemic
autoimmune diseases: analysis of 30 cases.
Rheumatology (Oxford). 2008;47(11):168691
1031
Koushik et al.,
DOI:10.5958/j.2319-5886.2.4.173

&
Health Sciences
www.ijmrhs.com
Coden: IJMRHS
th
Case report
Copyright @2013
ISSN: 2319-5886
URINARY TRACT ENDOMETRIOSIS: A CASE REPORT

*Radha Bai Prabhu T, Velayudam DA, Manjula P, Niharika S, Cynthia S
Department of Obstetrics & Gynaecology, Meenakshi
Kancheepuram, Tamilnadu, India
Medical college and Research Institute,
*Corresponding author email: radhaprabhu54@ymail.com.

ABSTRACT
Endometriosis affecting the urinary tract is rare and when involved it predominantly affects the bladder,
followed by the ureter. The diagnosis of bladder endometriosis is difficult because of its varied clinical
presentation. Here we report a case of bladder endometriosis, which was suspected pre-operatively and
was confirmed after the histo pathological examination of the excised tissue.
Key words: Extra genital Endometriosis, Bladder Endometriosis, Vesical Endometriosis
INTRODUCTION
Endometriosis is the presence of functioning

endometrial glands and stroma outside the
uterine cavity and musculature. It is a well
recognised gynaecological condition affecting 510% of women of reproductive age and up to
50% of infertile women. Though endometriosis
is a disease of the genital tract, literature review
shows that endometriosis can be found in almost
any tissue in the body 1. Here we describe a case
of
bladder
endometriosis,
its
clinical
presentation, diagnosis and management.
44 years old, Para 2, presented to the

Gynaecological outpatient department with a
history of constant lower abdominal pain for 8
years and cyclical heavy periods of six months
duration. In detailed questioning, she described
the pain to be worse during the premenstrual and
menstrual period. She also complained of urinary

symptoms such as increased frequency and
painful micturition for the last four years which
was worse during the premenstrual period. There
was no history of haematuria. She was married
for 25 years, delivered two children by caesarean
section and the last childbirth was 21 years ago.
In the past, she has had regular menstrual cycles
lasting for 3-4 days. However, in the last six
months her periods became very heavy and
prolonged, occurring once in 30 days, lasting for
10-15 days and changing 10-15 pads per day.
She
also
complained
of
congestive
dysmenorrhoea and deep dyspareunia. There was
no history suggestive of pelvic inflammatory
disease (PID) and her bowel habits were normal.
In her past history she was treated by many
doctors for PID and was not relieved of her
symptoms. Because of her recurrent urinary
Radha Bai et al.,
CASE REPORT
1032
symptoms, she was also evaluated and treated by

Urologists many times. In the last four years only
once her urine culture showed evidence of
infection and was treated. She has had a
cystoscopy two years ago which showed a raised
lesion in the trigone close to the left ureteric
orifice. The biopsy of the lesion was reported as
inflammatory lesion.
On examination, the patient was thin made, very
pale, thyroid and breasts were normal. She had
two vertical scars in the abdomen, there was
suprapubic tenderness and the uterus was
palpable 3 centimeters above the symphysis
pubis. By speculum examination, the cervix was
eroded. Bimanual pelvic examination showed the
uterus to be uniformly enlarged to 16 weeks size
and was tender. There was also tender nodularity
in the midvaginal region in the anterior fornix.
Rectal examination did not reveal any nodules in
the pouch of douglas. Her investigation results
were as follows: Haemoglobin 6.1gms. %,
PCV 18, bleeding time, clotting time were
normal, TSH 2.1, and other investigations were
within normal limits. Pap smear was negative for
intra epithelial lesion. Combined transvaginal
and transabdominal ultrasound of the pelvis
showed an enlarged uterus with asymmetrically
thickened myometrium with heterogenous echo
texture. The endometrial thickness was 18 mm.
The left ovary showed a clear cyst measuring
6cm. in size. Some irregularity was noted near
the bladder base. Because of the long duration of
her symptoms, MRI of the pelvis was also taken.
MRI confirmed the USG findings and showed
the bladder wall to be thickened to 8mms. near
the trigone.
Her anaemia was corrected with three units of
packed cells and she was taken up for a
diagnostic curettage. Under anaesthesia, the
irregularity in the anterior fornix was well
appreciated. The HPE of the endometrial
curetting showed severe complex hyperplasia
without atypia.
With her history, examination findings and the
results of imaging studies, a diagnosis of
adenomyosis with endometrial hyperplasia was

made and the possibility of endometriosis of
bladder was strongly suspected.
She was prepared for Total abdominal
hysterectomy
with
bilateral
salpingooophorectomy (TAH with BSO). Because of her
previous two caesarean sections and the strong
possibility of bladder endometriosis, it was
decided to proceed with the surgery with a
preliminary cystoscopy.
The patient was
adequately counselled as to the possibility of
opening into the bladder and extensive bladder
surgery may be required.
At cystoscopy, there were bluish nodules bulging
into but not eroding through the mucosa around
the left ureteric orifice. (Fig. 1) Other areas of the
bladder mucosa were normal. Ureteric stenting
was done on the left side and was not possible on
the right side. On opening the abdomen, there
were dense omental adhesions and were released.
The bladder was densely adherent to the cervix
and was freed by sharp dissection. On the left
side there was a firm bluish nodule between the
bladder and the cervix. (Fig.2) In order to avoid
injury to the bladder, sharp dissection was
carried out close to the cervix and a wedge of
tissue was excised from the nodular area for
HPE. The remaining nodular area over the
bladder was ablated with bipolar diathermy and
TAH with BSO was carried out. Her
postoperative period was uneventful except for
the haematuria which cleared after one week.
She was kept on continuous bladder drainage for
10 days and the ureteric stent was removed after
15 days.
The HPE was reported as follows:
Endometrium showing complex cystoglandular
hyperplasia without atypia, and the myometrium
showing
adenomyosis
with
marked
myohyperplasia. The left ovary showed a simple
ovarian cyst and the excised nodule was reported
as endometriosis.
At one year follow up, patient did not have any
urinary symptoms or lower abdominal pain. On
Radha Bai et al.,
1033
examination, the anterior vaginal fornix was

smooth without any nodularity.
Ureteric orifice
Fig1: Picture showing bluish nodules around the
ureteric orifice at cystoscopy
Bluish area between the bladder and

the cervix
Fig 2: Picture showing bluish area between the
bladder and the cervix
DISCUSSION
Involvement of the urinary tract by

endometriosis is rare, and it predominantly
affects the bladder, followed by the ureter and
the kidney in a ratio of 40:5:1.2
Endometriosis affecting the bladder could be
primary or secondary. The primary form is a
spontaneous
disease.
The
secondary
manifestation results following pelvic surgery
such as caesarean section.3 The primary form is
commonly seen in association with severe pelvic
endometriosis. Tohic et al reported that in a
series of 24 patients with bladder endometriosis
concomitant deep nodules were seen in the
rectovaginal septum and uterosacral ligaments in
66% of patients.4 Bladder endometriosis can be
intrinsic or extrinsic and the extrinsic disease is

more common, where the disease involves the
serosa and the peritoneal surface. The lesions are
generally found in the trigone, dorsal wall or at
the ureterovesical junction.
In nearly 50% of cases, there are catamenial
frequency, urgency and dysuria. (Symptoms
presenting around the time of menstruation).
Most of them present with features of recurrent
cystitis but, without evidence of bacteriuria.
They can also present with dyspareunia with the
involvement of the anterior vaginal wall.
Occasionally gross haematuria is encountered
where there is an intrinsic bladder disease.5
Our case was more of an extrinsic disease,
because, though she had suffered from
catamenial urinary symptoms for many years,
she has never had haematuria. As well as at
cystoscopy , endometriotic implants were not
eroding through the bladder mucosa.
Endometriosis of the bladder, especially the
extrinsic type is very difficult to diagnose and
relies heavily on clinical suspicion. When young
women present with urinary symptoms around
the time of menstruation, with or without a
possible diagnosis of pelvic endometriosis one
should suspect bladder involvement and
investigations should be initiated. In our case,
endometriosis of the bladder was suspected preoperatively as the patient presented with
catamenial urinary symptoms and the presence of
nodularity in the anterior vaginal fornix.
The occurrence of bladder endometriosis has
been explained by various theories such as a
development from the Mullerian remnants in the
vesico-uterine/ vesico- vaginal septum, extension
of an adenomyotic nodule of the anterior uterine
wall or it results from implantation of
regurgitated endometrium. Vercellini et al has
looked at the association between the bladder
endometriosis and adenomyosis and they have
concluded that vesical endometriosis seems to
originate from the implantation of regurgitated
endometrial cells in the anterior cul-de-sac and
not to be associated with uterine adenomyosis. 6
1034
Radha Bai et al.,
In our case the involvement of bladder with

endometriosis could be due to the direct
implantation of the endometrial cells on to the
bladder because of the previous two uterine
surgeries.
Imaging modalities such as USG, CT and MRI
may facilitate diagnosis.. Cystoscopy is able to
visualize the endometriosis foci only when
present on bladder mucosal surface.7 In our case,
cystoscopy which was done 2 years ago was
reported normal. However, with increasing
severity of the symptoms and further progression
of the disease, repeat cystoscopy revealed the
presence of endometriotic areas around the left
ureteric orifice in the trigone.
Majority of bladder lesions are superficial and
can be vaporized or ablated with bipolar or co2
laser.
In our case, after the bladder was
separated from the cervix, the bladder lesion was
fulgurated with bipolar diathermy.
When
endometriosis invades the mucosa of the bladder,
segmental resection of the bladder is the
treatment of choice. 8
Some authors have suggested hysterectomy with
bilateral salpingo-oophorectomy to prevent
relapses. Namnoum et al9 concluded that
compared with women who had oophorectomy
for endometriosis, patients who underwent
hysterectomy with ovarian conservation had 6.1
times greater risk of developing recurrent pain
and 8.1 times greater risk of reoperation. 9 Others
claim no specific advantages and suggest that
hysterectomy with BSO should not be carried out
for the sole purposes of prevention of relapses.5
In our case, we had to proceed with TAH with
BSO because of the adenomyosis of the uterus
and the complex hyperplasia of the endometrium.
CONCLUSION
Endometriosis involving the bladder is rare. One
should have a high degree of clinical suspicion to
diagnose
the
condition.
Urinary
tract
involvement with endometriosis should be
considered in all women who present with
recurrent urinary symptoms not responding to
medical management, especially in those who

have undergone caesarean deliveries or other
pelvic surgeries.
REFERENCES
1. Douglas C, Rotimi O. Extragenital
endometriosis: a clinicopathological review
of a Glasgow hospital experience with case
illustrations. J Obstet Gynaecol. 2004; 24:
804-08.
2. Nezhat CH, Malik S, Osias J, Nezhat F,
Nezhat C. Laparoscopic management of 15
patients with infiltrating endometriosis of the
bladder and a case of primary intravesical
endometroid adenosarcoma. Fertil steril.
2002; 78:872-75.
3. Agarwal N, Kriplani A, Parul, Nabi G.
Intramural bladder endometriosis after
caesarean section: diagnostic and therapeutic
aspects. J Gynecol Sur. 2002; 18: 69-73
4. Le Tohic A, Chis C, Yazbeck C, Koskas M,
Madelenat P, Panel P. Bladder endometriosis:
diagnosis and treatment: A series of 24
patients. Gynecologie, Obstetrique & Fertilite
DOI: 10.1016/j.gyobfe. 2009.01.018.
5. Veeraswamy A, Lewis M, Mann A, Kotikela
S. Extra genital endometriosis: In clinical
obstetrics and gynecology. Lippincott
Williams and Wilkins. 2010;53:449-66
6. Vercellini P, Frontino G, Pisacreta A, De
Giorgio, Cattaneo M, Crosignani PG. The
pathogenesis of bladder endometriosis. Am J
Obstet Gynecol. 2002; 187: 538-42.
7. Liselotte Mettler, Vidya Gaikwad, Bastian
Riebe and Thoralf Schollmeyer. Bladder
endometriosis: Possibility of treatment by
Laparoscopy. JSLS. 2008; 12 (2): 162-65.
8. Nezhat CR, Nezhat FR. Laparoscopic
segmental
bladder
resection
for
endometriosis: a report of two cases. Obstet
Gynecol , 1993;81: 882-84.
9. Namnoum AB, Hickman TN, Goodman SB,
Gehlbach DL, Rock GA. Incidence of
symptom recurrence after hysterectomy for
endometriosis. Fertil Steril.1995;64:898 -902.
1035
Radha Bai et al.,

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www.ijmrhs.com Volume 2 Issue 4 Oct - Dec Coden: IJMRHS Copyright @2013 ISSN: 2319-5886
Case report
LIMB SALVAGE IN RECURRENT GIANT CELL TUMOUR PROXIMAL END RADIUS
*Ravishanker R
Professor, Reconstructive & Burns Unit, Rural Medical College, Pravara Institute of Medical Sciences,
Loni, Maharashtra, India
*Corresponding author email: reconsravi@gmail.com
ABSTRACT
An 18years old male patient had undergone surgery for a giant cell tumour upper end of the right radius
in Jan 2007. The tumour recurred within two months. Patient took alternative methods of treatment
including indigenous medicines for the condition; all these failed and the patient was advised an above
elbow amputation. By Sep 2008 the tumour had grown to a 14x11x11 swelling in the forearm
extending to the distal arm with neurovascular involvement. A total resection of the tumour was done;
vascular continuity of the brachial to the ulnar artery was done with a vein graft to salvage the limb. In
2012 tendon transfer was done to restore function to the wrist. Now there is no recurrence of the tumour
and the patient has a fully functional limb.
Keywords: Giant cell tumour; proximal end radius; recurrent; salvage of limb; functional limb
INTRODUCTION
Giant cell tumours represent 5% of all bone

neoplasms.1,2 A benign but locally aggressive
tumour it typically occurs in patients between 30
to 40 years, with a female predominance. 75% to
90% of all tumours are found in the long tubular
bones especially the distal femur (30%),
proximal tibia (25%), distal radius (10%) and the
humerus (6%). The spine in 7% and the
inominate bone in 4% cases are other common
sites.3
The upper end of the radius is very rarely
involved and in literature there are just about a
dozen cases reported.4,5
This case report is not only a giant cell tumour in
the upper end of the radius, but one which has
occurred in a young adolescent male. The tumour
was surgically removed after a local recurrence;
Ravishanker etal.,
vascular continuity of the brachial artery to the

ulnar artery with a vein graft restored viability to
the limb. Tendon transfers have given a good
functional recovery. There is no recurrence after
five years of follow up.
The case is unusual in the rarity of the lesion; a
recurrence which occurred within months of the
original resection; and the fact that the limb
could not only be saved but also made fully
functional; there is no evidence of recurrence
five years post surgery.
CASE HISTORY
An 18y old male patient had reported to a

surgeon with a painful swelling upper end of the
right forearm in Jan 2007. He was diagnosed as a
case of a Giant Cell Tumour and resection of the
1036
upper end of the radius was done in Feb 2007.

The patient however noticed a recurrence of
swelling at the same site in the forearm within
two months of the surgery. For reasons
unexplained he did not go in for a redo surgery,
but took a series of treatment of indigenous
medicine including Ayurveda, Homeopathy etc.
After all these failed he was advised an above
elbow amputation of the limb.
By Sep 2008 the tumour had grown to a
14x11x11 painful lobulated swelling at the
site of the previous surgical scar. (Fig 1, 2).
taken to salvage the limb by an enbloc resection

and necessary reconstruction.
The patient and relatives were however
explained about the real possibility of having to
do an above elbow amputation and a preoperative consent for the same was taken.
The patient was operated on 6 Sep 2008. During
surgery an enbloc removal of the recurrence
along with the tissues enveloped by the tumour
along with the scar over the tumour was done.
The resection included the encompassed radial,
ulnar and brachial arteries, the radial nerve, and
involved muscles with a 2 inch segment of the
radius and the previous scar. (Fig 3,4).
Fig: 1: Recurrent giant cell tumour upper end radius
Fig 3: Resected tumour with 2 inches of radius
Fig 2 : Lobulated swelling with the scar of previous

surgery
The tumour had extended into the distal arm. The

skin over the swelling was warm, adherent to the
growth over the scar. There were dilated veins
over the swelling. There was evidence of radial
palsy and the distal radial pulsation was not
palpable. An MRI scan revealed a soft tissue
recurrence of the GCT encompassing the radioulnar neurovascular bundle, the brachial artery
and the muscles in the proximal forearm.
In view of the young age of the patient and the
limb being a dominant one, a calculated risk was
Ravishanker etal.,
Fig 4: Bridging of brachial artery to ulnar artery

with a vein graft
Further specimens were taken from deeper

tissues including the joint capsule, forearm soft
tissue, from over the ulna and bone marrow from
the distal radius.
Vascular reconstruction was done by bridging
the brachial and ulnar arteries with a vein graft.
(Fig 4).
1037
Fig 5: Well healed transposition flap over vessel

repair
Fig 7: Return of function in the hand with a good

grip and extension of the thumb, fingers and wrist
The repaired vessels and exposed joint capsule

were covered with a local transposition flap.
Other raw areas were split skin grafted. All these
healed well. (Fig 5)
The histopathology report confirmed soft tissue
recurrence of the giant cell tumour with all
margins including the bone marrow, and deeper
soft tissues free of tumour.
The patient did well and despite a wrist drop with
the help of a radial palsy splint could carry out
all his normal functions of life.
In August 2011 a tendon transfer to correct the
wrist drop was done. As most of the major flexor
and extensor tendons of the forearm had been
removed at the time of the tumour resection, only
the Flexor Carpi Ulnaris could be spared. (Fig 6).
A follow up done five years after the recurrence

and resection have shown no evidence of local
recurrence. There are no pulmonary metastases.
DISCUSSION
The tendon was split into two and used to power

both the Extensor. Digitorum Communis and the
Extensor Pollicis Longus.
The patient has good wrist and thumb extension
following the tendon transfer and is able to carry
out all functions with the hand. (Fig 7)
Though giant cell tumours represent 5% of bone

neoplasms (as reported in a study from the Mayo
clinic)1,2, the proximal end of the radius is an
extremely uncommon site of the lesion, Lewis et
al having reported only seven cases in their
extensive study.4-7 The lesion mainly affects
patients between the third and fourth decades of
life (60% to 70% of cases) with the frequency
being more in women than men.1- 6 The lesion in
the order of predominance affects the distal
femur (30%) the proximal tibia (25%) and the
distal radius (10%). Other sites affected are the
humerus (6%), the spine (7%) and the inominate
bone (4%). The proximal radius is affected in
only about 0.5% cases.3-6
Treatment ranges from simple curettage for
Stage 1 lesions to resection and reconstruction
for Stage 3 lesions. The recurrence rate after
simple curettage however ranges from 10% to 50
%.1-3,7,10,11 With adjuvant therapy like
radiotherapy, cryosurgery, argon therapy the
recurrence rate can be brought down. However
nearly one third of the long term survivors of
bone tumours require an amputation.6-11
Limb saving surgery after an extensive soft tissue
recurrence has not been reported in literature, the
mainstay of treatment recommended being in
these cases being an amputation, as the risk of
Ravishanker etal.,
1038
Fig 6: FCU being tunneled for transfer
recurrence after resection and reconstruction is

considered very high.1-3,5-11.
CONCLUSION
The aim of publishing this case report is the
rarity of the case itself, as a giant cell tumour of
the proximal end of the radius has been reported
in literature less than a dozen times with
successful treatment of a recurrent lesion never
so. In this case the lesion has affected an
adolescent male; and despite the recurrence of
the tumour within two months of the first
surgery, and the advice of three surgeons to go in
for an amputation, salvage and reconstruction of
an apparently hopeless limb was possible as the
resection was complete; requisite reconstruction
restored vascularity to the limb. A suitable
tendon transfer restored effective function.
The message is that with advances in imaging
techniques, radiotherapy, and aggressive surgical
techniques, salvage of a limb should be the first
option.
Key Message: Even an extensive recurrence of a
giant cell tumour can be effectively operated
upon and with adequate reconstruction not only
can the limb be saved, it can be made fully
functional.
4. Lewis MM, Kaplan H, Klein MJ, Ferrirer PJ,

Legouri RA. Giant cell tumor of the proximal
radius. Clin Orthop Relat Res 1985; 201:
186-89.
5. Singh AP, Mahajan S, Singh AP. Giant cell
tumour of the proximal radius. Singapore
Med J. 2009; 50(11): 308-10.
6. Campanacci M, Giunti A, Olmi R. Giant cell
tumours of bone. A study of 209 cases with
long term follow-up in 130. J Orthop Trauma
1975; I :249-77.
7. Dahlin Dc, Cuppa RE, Johnson EW Jr. Giant
cell tumour. A study of 195 cases. Cancer.
1970; 25: 1062-70.
8. Turcotte RE. Giant cell tumor of bone.
Orthop Clin of North Am.2006; 37:35-51.
9. Heck Jr RK. General principles of tumors. In:
Canale TS, Beaty TH, eds. Campbells
Operative
Orthopaedics.
11th
ed.
Philadelphia; Mosby Elsiever; 2007: 775-54.
10. Laba K, Perka C, Schmidt R : Treatment of
stages 2 and 3 giant cell tumours. Arch
Orthop Trauma Surg. 2001; 121:83
11. Mc Gough R, Rutledge J, Lewis. Impact
severity of local recurrence in giant cell
tumour of the bone, Clin Orthop,Relat
res2005;438:116
REFERENCES
1. Robert K, Heck, Jr. Benign (Occasionally

Aggressive) Tumors of Bone.In: S Terry
Canale, James H Beaty, ed. Campbells
Operative Orthopedics. Philadelphia: Mosby
Elsiever; 2012: Vol I, 12th ed. 887-88.
2. Robert K Heck, Jr. Benign (Occasionally
Aggressive) Tumors of Bone.In:S Terry
Canale,
ed.
Campbells
Operative
Orthopedics. Philadelphia: Mosby Elsiever;
2003: Vol I, 10th ed. 813-26.
3. Donald S Resnick MD. Tumors and Tumor
like lesions of Bone. In. Diagnosis of Bone
and Joint Disorders. 4th ed. WB Saunders and
Company. 2002: 3939-62.
Ravishanker etal.,
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DOI: 10.5958/j.2319-5886.2.4.

International Journal of Medical Research

Asso. Prof, Dept. of Pharmacology, Dr. V.P.M.C. Nashik, Maharashtra, India

*Corresponding author email: rahulbraje@gmail.com, vasantjamdhade@gmail.com

Anemia is associated with higher perinatal

which 95% of cases are having iron deficiency

Int J Med Res Health Sci. 2013;2(4):719-723

gastrointestinal absorption, late pregnancy, and

After the approval of

received intravenous iron sucrose, Group B: 50

Mean age (years)

Int J Med Res Health Sci. 2013;2(4):719-723

Table 2: Hemoglobin level before starting therapy

Table 3: Hemoglobin level 2 and 4 weeks after starting therapy

After 4 weeks of therapy

Table 4: Time period taken to achieve target hemoglobin level (>11g/dl)

Table 5: Adverse effects in both the groups

Adverse effects (all grade I)

Int J Med Res Health Sci. 2013;2(4):719-723

The mean pre therapy hemoglobin level in group

The current study was undertaken to evaluate the

which were given intravenous iron sucrose

Int J Med Res Health Sci. 2013;2(4):719-723

relieved of their symptoms. The difference was

Intravenous iron sucrose therapy is safe,

1. Fernando Arias, Shirish ND. Anemia in

anemia. Ann Pak Inst Med Sci. 2006;2;18891.

Int J Med Res Health Sci. 2013;2(4):719-723

International Journal of Medical Research

IMMEDIATE EFFECT OF SURYANADI PRANAYAMA ON PULMONARY FUNCTION

Yoga is the best lifestyle, which aims to attain

Int J Med Res Helath Sci. 2013;2(4):724-729

yoga is an important component of yoga

migraine, peptic ulcer, dysmenorrhoea, lack of

Int J Med Res Helath Sci. 2013;2(4):724-729

min. of right nostril breathing have any

Subject selection: This is a cross-sectional study

counting 1to 6 over a period of 6 seconds and

The data were expressed as mean SD, were

Int J Med Res Helath Sci. 2013;2(4):724-729

variables like ventilatory capacities, volumes and

FEF25-75% (p<0.0001), MVV (p<0.0001), SVC

Table 1. Anthropometric parameters

Table 2. Comparison of respiratory variables before and after suryanadi pranayama

Yoga is the ancient science which makes use of

Each cycle of suryanadi pranayama is a complex

Int J Med Res Helath Sci. 2013;2(4):724-729

the respiratory system and fills the lungs with

positive impact of suryanadi pranayama on

Int J Med Res Helath Sci. 2013;2(4):724-729

The immediate effect of suryanadi pranayama

breathing, and whether the effects are greater if

We kindly acknowledge Mr. Sukumar BV,

11. Shankarappa V, Prasanth P, Nachal

Int J Med Res Helath Sci. 2013;2(4):724-729

International Journal of Medical Research

Copyright @2013 ISSN: 2319-5886

RELATIONSHIP BETWEEN THE RETINAL NERVE FIBRE LAYER (RNFL) PARAMETERS

Glaucoma is a disease which is associated with

by automated perimetry . However, the results of

Int J Med Res Health Sci. 2013;2(4):730-736

Various studies have shown that structural

This was a cross sectional study, prospectively

>21 mm Hg now on medical control and