CASE REPORT

TETANUS
Compiled By:
Bintang Ruth Cicilia Febrina (110100153)

Supervisor :
dr. Wisman, M.Ked (Ped), Sp.A (K)

PEDIATRIC DEPARTMENT
HAJI ADAM MALIK GENERAL HOSPITAL
FACULTY OF MEDICINE UNIVERSITY OF SUMATERA UTARA
MEDAN
2015

ACKNOWLEDGEMENTS
We are greatly indebted to the Almighty One for giving us blessing to finish this
case report, Tetanus. This case report is a requirement to complete the clinical
assistance program in Paediatric Department in H. Adam Malik General Hospital,
Faculty of Medicine University of Sumatera Utara.
We are also indebted to our supervisor and adviser, dr. Wisman,
M.Ked(Ped), Sp.A(K) for much spent time to give us guidances, comments, and
suggestions. We are grateful because without him this case report wouldnt have
taken its present shape.
This case report has gone through series of developments and corrections.
There were critical but constructive comments and relevants suggestions from the
reviewers. Hopefully the content will be useful for everyone in the future.

Medan, September 2015

Presentators

TABLE OF CONTENTS
ACKNOWLEDGEMENTS......................................................................... i
TABLE OF CONTENTS............................................................................. ii
TABLE OF PICTURES............................................................................... iii
CHAPTER 1 INTRODUCTION................................................................. 1
CHAPTER 2 LITERATURE REVIEW....................................................... 3
CHAPTER 3 CASE REPORT..................................................................... 14
CHAPTER 4 DISCUSSION.....................................................................

26

CHAPTER 5 SUMMARY.........................................................................

29

REFERENCES .........................................................................................

31

TABLE OF PICTURES

Name

Page

Picture 2.1 Morphology of Clostridium tetani...........................................4

Picture 2.2 Clinical Manifestation of tetanus.............................................8

CHAPTER I
INTRODUCTION

1.1. Background
Tetanus is an acute, often fatal, disease caused by an exotoxin produced by the
bacterium Clostridium tetani. It is characterized by generalized rigidity and
convulsive spasms of skeletal muscles. The muscle stiffness usually involves the
jaw (lockjaw) and neck and then becomes generalized.1

C tetani is found worldwide in soil, on inanimate objects, in animal feces,

and, occasionally, in human feces. Tetanus is predominantly a disease of
underdeveloped countries. It is common in areas where soil is cultivated, in rural
areas, in warm climates, during summer months, and among males. In countries
without a comprehensive immunization program, tetanus predominantly develops
in neonates and young children. 5
C. tetani is a slender, gram-positive, anaerobic rod that may develop a
terminal spore, giving it a drumstick appearance. The organism is sensitive to heat
and cannot survive in the presence of oxygen. The spores, in contrast, are very
resistant to heat and the usual antiseptics. C. tetani produces two exotoxins,
tetanolysin and tetanospasmin. The function of tetanolysin is not known with
certainty. Tetanospasmin is a neurotoxin and causes the clinical manifestations of
tetanus. 1
Tetanospasmin is synthesized as a 150-kd protein consisting of a 100-kd
heavy chain and a 50-kd light chain joined by a disulfide bond 5. The heavy chain
mediates binding of tetanospasmin to the presynaptic motor neuron and also
creates a pore for the entry of the light chain into the cytosol. The light chain is a
zinc-dependent protease that cleaves synaptobrevin.5
After the light chain enters the motor neuron, it travels by retrograde
axonal transport from the contaminated site to the spinal cord in 2-14 days. When
the toxin reaches the spinal cord, it enters central inhibitory neurons. The light
chain cleaves the protein synaptobrevin, which is integral to the binding of
neurotransmitter containing vesicles to the cell membrane.
As a result, gamma-aminobutyric acid (GABA)-containing and glycinecontaining vesicles are not released, and there is a loss of inhibitory action on
motor and autonomic neurons. With this loss of central inhibition, there is
autonomic hyperactivity as well as uncontrolled muscle contractions (spasms) in
response to normal stimuli such as noises or lights.5
Tetanus diagnosis is strictly clinical; there are no confirmatory laboratory
tests. The WHO definition of adult tetanus requires at least one of the following
signs: trismus (inability to open the mouth) or risus sardonicus (sustained spasm

of the facial muscles); or painful muscular contractions. Although this definition

requires a history of injury or wound, tetanus may also occur in patients who are
unable to recall a specific wound or injury.3
Drugs used to treat muscle spasm, rigidity, and tetanic seizures include
sedative-hypnotic agents, general anesthetics, centrally acting muscle relaxants,
and neuromuscular blocking agents. Antibiotics are used to prevent multiplication
of Clostridium tetani, thus halting production and release of toxins. Antitoxins are
given to neutralize unbound toxin.5
1.2. Objective
The aim of this study is to explore more about the theoretical on Tetanus disease.
It is also to integrate the theory and application of pediatric with Tetanus in
children.
CHAPTER II
LITERATURE REVIEW
2.1. Definition
Tetanus is an acute, often fatal, disease caused by an exotoxin produced by the
bacterium Clostridium tetani. It is characterized by generalized rigidity and
convulsive spasms of skeletal muscles. The muscle stiffness usually involves the
jaw (lockjaw) and neck and then becomes generalized.1
Tetanus is a noncommunicable disease, it is not transmitted from one
person to another. Tetanus can manifest in one of four clinical forms: generalized,
local, cephalic and neonatal.2
2.2. Epidemiology
C tetani is found worldwide in soil, on inanimate objects, in animal feces, and,
occasionally, in human feces. Tetanus is predominantly a disease of
underdeveloped countries. It is common in areas where soil is cultivated, in rural
areas, in warm climates, during summer months, and among males. In countries

without a comprehensive immunization program, tetanus predominantly develops

in neonates and young children. Developed nations have incidences of tetanus
similar to those observed in the United States. For instance, only 126 cases of
tetanus were reported in England and Wales from 1984-1992.5
Although tetanus affects all ages, the highest prevalence is in newborns
and young people. In 1992, an estimated 578,000 infant deaths were attributed to
neonatal tetanus. In 1998, 215,000 deaths occurred, more than 50% of them in
Africa. Tetanus is a target disease of the World Health Organization (WHO)
Expanded Program on Immunization. Overall, the annual incidence of tetanus is
0.5-1 million cases. WHO estimated that in 2002, there were 213,000 tetanus
deaths, 198,000 of them in children younger than 5 years.5
Age-related demographies. Neonatal tetanus is rare, occurring most
frequently in countries without comprehensive vaccination programs. The risk for
development of tetanus and for the most severe form of the disease is highest in
the elderly population. In the United States, 59% of cases and 75% of deaths
occur in persons aged 60 years or older. From 1980 through 2000, 70% of
reported cases of tetanus in the United States were among persons aged 40 years
or older. Of all these patients, 36% are older than 59 years and only 9% are
younger than 20 years. 5
Sex-related demographies. Tetanus affects both sexes. No overall gender
predilection has been reported, except to the extent that males may have more soil
exposure in some cultures. In the United States from 1998 to 2000, the incidence
of tetanus was 2.8 times higher in males aged 59 years and younger than in
females in the same age range. A difference in the levels of tetanus immunity
exists between the sexes. Overall, men are believed to be better protected than
women, perhaps because of additional vaccinations administered during military
service or professional activities. In developing countries, women have an
increased immunity where tetanus toxoid is administered to women of
childbearing age to prevent neonatal tetanus. 5

Race-related demographies. Tetanus affects all races. From 1998 to 2000,

the incidence of tetanus in the United States was highest among Hispanics (0.38
cases per million population), followed by whites (0.13 cases per million
population) and then by African Americans (0.12 cases per million population).5

2.3. Etiology

Picture 2.1 Morphology of Clostridium tetani

C. tetani is a slender, gram-positive, anaerobic rod that may develop a terminal
spore, giving it a drumstick appearance. The organism is sensitive to heat and
cannot survive in the presence of oxygen. The spores, in contrast, are very
resistant to heat and the usual antiseptics. They can survive autoclaving at 249.8F
(121C) for 1015 minutes. The spores are also relatively resistant to phenol and
other chemical agents.1
The spores are widely distributed in soil and in the intestines and feces of
horses, sheep, cattle, dogs, cats, rats, guinea pigs, and chickens. Manure-treated
soil may contain large numbers of spores. In agricultural areas, a significant
number of human adults may harbor the organism. The spores can also be found
on skin surfaces and in contaminated heroin.1
C. tetani produces two exotoxins, tetanolysin and tetanospasmin. The
function of tetanolysin is not known with certainty. Tetanospasmin is a neurotoxin
and causes the clinical manifestations of tetanus. On the basis of weight,
tetanospasmin is one of the most potent toxins known. The estimated minimum
human lethal dose is 2.5 nanograms per kilogram of body weight (a nanogram is

one billionth of a gram), or 175 nanograms for a 70-kg (154lb) human.1

2.4. Pathophysiology
Clostridium tetani is an obligate, anaerobic, motile, gram-positive bacillus. It is
nonencapsulated and forms spores that are resistant to heat, desiccation, and
disinfectants. Since the colorless spores are located at one end of the bacillus, they
cause the organism to resemble a turkey leg. They are found in soil, house dust,
animal intestines, and human feces. Spores can persist in normal tissue for months
to years.
To germinate, the spores require specific anaerobic conditions, such as
wounds with low oxidation-reduction potential (eg, dead or devitalized tissue,
foreign body, active infection). Under these conditions, upon germination, they
may release their toxin. Infection by C tetani results in a benign appearance at the
portal of entry because of the inability of the organism to evoke an inflammatory
reaction unless coinfection with other organisms develops.5
When the proper anaerobic conditions are present, the spores germinate
and produce the following 2 toxins3:
-Tetanolysin : This substance is a hemolysin with no recognized pathologic
activity
-Tetanospasmin : This toxin is responsible for the clinical manifestations of
tetanus; by weight, it is one of the most potent toxins known, with an estimated
minimum lethal dose of 2.5 ng/kg body weight
Tetanospasmin is synthesized as a 150-kd protein consisting of a 100-kd
heavy chain and a 50-kd light chain joined by a disulfide bond 5. The heavy chain
mediates binding of tetanospasmin to the presynaptic motor neuron and also
creates a pore for the entry of the light chain into the cytosol. The light chain is a
zinc-dependent protease that cleaves synaptobrevin.5
After the light chain enters the motor neuron, it travels by retrograde
axonal transport from the contaminated site to the spinal cord in 2-14 days. When
the toxin reaches the spinal cord, it enters central inhibitory neurons. The light
chain cleaves the protein synaptobrevin, which is integral to the binding of

neurotransmitter containing vesicles to the cell membrane.

As a result, gamma-aminobutyric acid (GABA)-containing and glycinecontaining vesicles are not released, and there is a loss of inhibitory action on
motor and autonomic neurons. With this loss of central inhibition, there is
autonomic hyperactivity as well as uncontrolled muscle contractions (spasms) in
response to normal stimuli such as noises or lights.5
Once the toxin becomes fixed to neurons, it cannot be neutralized with
antitoxin. Recovery of nerve function from tetanus toxins requires sprouting of
new nerve terminals and formation of new synapses.
Localized tetanus develops when only the nerves supplying the affected
muscle are involved. Generalized tetanus develops when the toxin released at the
wound spreads through the lymphatics and blood to multiple nerve terminals. The
blood-brain barrier prevents direct entry of toxin to the CNS.5
2.5. Clinical Manifestations
The incubation period ranges from 3 to 21 days, usually about 8 days. In general
the further the injury site is from the central nervous system, the longer is the
incubation period. Shorter incubation periods are associated with a higher chance
of death. In neonatal tetanus, symptoms usually appear from 4 to 14 days after
birth, averaging about 7 days. 1
On the basis of clinical findings, three different forms of tetanus have been
described1 :
Local tetanus is an uncommon form of the disease, in which patients have
persistent contraction of muscles in the same anatomic area as the injury. These
contractions may persist for many weeks before gradually subsiding. Local
tetanus may precede the onset of generalized tetanus but is generally milder. Only
about 1% of cases are fatal.
Cephalic tetanus is a rare form of the disease, occasionally occurring with
otitis media (ear infections) in which C. tetani is present in the flora of the middle
ear, or following injuries to the head. There is involvement of the cranial nerves,
especially in the facial area.

The most common type (about 80%) of reported tetanus is generalized

tetanus. The disease usually presents with a descending pattern. The first sign is
trismus or lockjaw, followed by stiffness of the neck, difficulty in swallowing, and
rigidity of abdominal muscles. Other symptoms include elevated temperature,
sweating, elevated blood pressure, and episodic rapid heart rate. Spasms may
occur frequently and last for several minutes. Spasms continue for 34 weeks.
Complete recovery may take months.
Neonatal tetanus (NT) is a form of generalized tetanus that occurs in
newborn infants. Neonatal tetanus occurs in infants born without protective
passive immunity, because the mother is not immune. It usually occurs through
infection of the unhealed umbilical stump, particularly when the stump is cut with
an unsterile instrument. Neonatal tetanus is common in some developing countries
but very rare in the United States. World Health Organization (WHO) estimates
that in 2010, 58,000 newborns died from NT, a 93% reduction from the situation
in the late 1980s.

Picture

2.2 Clinical

Manifestation of tetanus

2.6. Diagnosis
Most cases of tetanus in the United States occur in patients with a history of
underimmunization, either because they were never vaccinated or because they
completed a primary series but have not had a booster in the preceding 10 years. 5
The median incubation period is 7 days, and for most cases (73%),
incubation ranges from 4 to 14 days. The incubation period is shorter than 4 days
in 15% of cases and longer than 14 days in 12% of cases. Patients with clinical
manifestations occurring within 1 week of an injury have more severe clinical
courses. 4
Patients sometimes remember an injury, but often, the injury goes
unnoticed. Patients may report a sore throat with dysphagia (early sign). The
initial manifestation may be local tetanus, in which the rigidity affects only 1 limb
or area of the body where the clostridium-containing wound is located. Patients

10

with generalized tetanus present with trismus (ie, lockjaw) in 75% of cases. Other
presenting complaints include stiffness, neck rigidity, restlessness, and reflex
spasms.
Subsequently, muscle rigidity becomes the major manifestation. Muscle
rigidity spreads in a descending pattern from the jaw and facial muscles over the
next 24-48 hours to the extensor muscles of the limbs. Dysphagia occurs in
moderately severe tetanus as a consequence of pharyngeal muscle spasms, and
onset is usually insidious over several days. Reflex spasms develop in most
patients and can be triggered by minimal external stimuli such as noise, light, or
touch. The spasms last seconds to minutes; become more intense; increase in
frequency with disease progression; and can cause apnea, fractures, dislocations,
and rhabdomyolysis. Laryngeal spasms can occur at any time and can result in
asphyxia.
Other symptoms include elevated temperature, sweating, elevated blood
pressure, and episodic rapid heart rate. Sustained contraction of facial musculature
produces a sneering grin expression known as risus sardonicus.
2.7. Differential Diagnosis
The differential diagnosis of tetanus can be extensive. Trismus (lockjaw) could
also be attributed to tooth abscess, mandibular dislocation, or peritonsilar or
rectopharyngeal abscess. Muscle spasms may be due to meningitis, dystonic
reactions, acute abdomen, and strychnine poisoning. Priorities for treatment
include airway management and cardiovascular stability. Ventilator support may
be needed to prevent asphyxia from the continuous muscle spasm. Significant
doses of Versed or Valium may be required to control tonic spasms and tetanic
seizures and to induce muscle relaxation. These patients need to be monitored in
an intensive care setting due to the rapid hemodynamic fluctuations.9
2.8. Treatment
If possible, a separate ward/location should be designated for tetanus patients.
Patients should be placed in a quiet shaded area and protected from tactile and

11

auditory stimulation as much as possible. All wounds should be cleaned and

debrided as indicated.3
The goals of pharmacotherapy are to stop toxin production within the
wound, to neutralize unbound toxin, and to control disease manifestations. Drugs
used to treat muscle spasm, rigidity, and tetanic seizures include sedative-hypnotic
agents, general anesthetics, centrally acting muscle relaxants, and neuromuscular
blocking agents. Antibiotics are used to prevent multiplication of Clostridium
tetani, thus halting production and release of toxins. Antitoxins are given to
neutralize unbound toxin.5
Antibiotics are used to eradicate clostridial organisms in the wound, which
may produce tetanus toxin. They are administered to patients with clinical tetanus;
however, their efficacy is questioned. Penicillin G was long considered the drug of
choice, but metronidazole is now considered the antibiotic of choice. Although
tetracyclines are an alternative in patients who have a history of serious allergic
reactions to penicillin or metronidazole (eg, urticaria, anaphylaxis), strong
consideration should be given to desensitizing the patient to penicillin before
resorting to alternative agents. Large doses of antibiotic are recommended to favor
diffusion into the devitalized tissue. In infants and children, for anaerobic
infection, we use metronidazole 30 mg/kg/day PO/IV divided q6hr; not to exceed
4 g/day. And for Penicillin G, in moderate infection we use 25,000-50,000
units/kg/day IV/IM divided q6hr, but if severe Infection, we use 250,000-400,000
units/kg/day IV/IM divided q4-6hr, not to exceed 24 million units/day.6
Anticonvulsants (Sedative-hypnotic) agents are the mainstays of tetanus
treatment. Benzodiazepines are the most effective primary agents for muscle
spasm prevention and work by enhancing gamma-aminobutyric acid (GABA)
inhibition. Diazepam is the most frequently studied and used drug. Lorazepam is
an effective alternative. Phenobarbital is another anticonvulsant that may be used
to prolong the effects of diazepam. Other agents used for spasm control include
baclofen, dantrolene, short-acting barbiturates, and chlorpromazine. For pediatric
the dosage of diazepam are : Less than 1 month: 0.83 to 1.67 mg/kg/hour by

12

continuous IV infusion, or 1.67 to 3.33 mg/kg IV, slowly, every 2 hours (20 to 40
mg/kg/day). 1 month to 5 years: 1 to 2 mg IM or IV, slowly, repeated every 3 to 4
hours as necessary, or 15 mg/kg/day in divided doses every 2 hours. Greater than
5 years: 5 to 10 mg IM or IV, slowly, repeated every 3 to 4 hours as necessary.5
Antitoxins are used to neutralize any toxin that has not reached the CNS.
They are used for passive immunization of any person with a wound that might be
contaminated with tetanus spores. (Tetanus Immune Globulin) TIG is used to
prevent tetanus and to treat patients with circulating tetanus toxin. It provides
passive immunity. TIG should be used to treat all patients with active tetanus, in
combination with other supportive and therapeutic treatments. Should also be
used to prevent tetanus in patients with inadequate or unknown immunization
status after an acute injury. Administration should begin as soon as the clinical
diagnosis of tetanus is made. 5 The dosage for Human tetanus immunoglobulin
(TIGH) is 3000-6000 U/IM or Tetanus antitoxiin (TAT) from animal 50.000100.000 U, half IV and half IM.8
Active immunization increases resistance to infection. Vaccines consist of
microorganisms or cellular components that act as antigens. Administration of the
vaccine stimulates the production of antibodies with specific protective properties.
Administer tetanus toxoid vaccine for wound prophylaxis if the vaccine history is
unknown or if fewer than 3 tetanus toxoid immunizations have been administered.
DTaP may be administered into the deltoid or midlateral thigh muscles in children
and adults. In infants, the preferred site of administration is the midlateral thigh
muscles. DTaP (Diphtheria & Tetanus toxoids/acellular Perussis) vaccine
promotes active immunity to diphtheria, tetanus, and pertussis by inducing the
production of specific neutralizing antibodies and antitoxins. It is indicated for
active booster immunization for tetanus, diphtheria, and pertussis prevention for
persons aged 10-64 years. It is the preferred vaccine for adolescents scheduled for
booster. For 6 weeks-7 years, use 0.5 mL IM x 3 at 2, 4, 6 months of age; may
administer as early as six weeks of age and repeated every 4-8 weeks; then 4th
dose at 15-20 months of age but at least 6 months after the third dose & 5th dose

13

at 4-6 years of age, prior to starting school or kindergarten; if fourth dose given at
>4 years of age, may omit fifth dose; For children <7 years who didn't receive
DTaP at early infancy, give first 3 doses q1Month, then 4th dose at least 6 months
later, but if the children >7 years, its not approved for use; use tetanus and
diphtheria toxoids vaccine instead.5

2.9. Complication
In severe cases of tetanus, life-threatening respiratory and cardiovascular
complications can present with troubling rapidity following the initial diagnosis
and admission to the hospital. One half of mortality associated with tetanus can be
attributed to the respiratory complication of the disease. Respiratory failure may
occur as a result of muscle rigidity and reflex muscle spasm that characterizes the
disease or secondary to hypoxia following atelectasis and pneumonia.7
The cardiovascular complications are the most serious complications of
tetanus once the airway has been secured. The pathogenesis of cardiovascular
disturbances is postulated to result from the effect of tetanus exotoxin with: (a)
brain stem damage resulting in fatal cardiac and respiratory failure, (b) myocardial
depression, or toxic myocarditis, believed to be due to excessively high levels of
circulating catecholamines or (c) widespread disinhibition of autonomic nervous
system in the CNS, which may lead to the syndrome of sympathetic nervous
hyperactivity and/or parasympathetic overactivity.7
The syndrome of sympathetic nervous hyperactivity "sustained but labile
hypertension and tachycardia, irregularities of cardiac rhythm, peripheral vascular
constriction, profuse sweating, pyrexia, increased carbon dioxide output,
increased catecholamine excretion, and in some cases, the late development of
hypotension." These signs and symptoms, if they occur, usually develop toward
the end of the first week. They may occur spontaneously or in response to minor
stimuli, as in the case with tetanus spasms, and cannot be alleviated through pain
control or sedation. Most such patients manifest elevated plasma catecholamine

14

levels. Prolonged sympathetic overactivity may end with profound and

preterminal hypotension and bradycardia; it often indicates imminent death.
Parasympathetic overactivity may lead to preterminal bradycardia and sinus
arrest, salivation and increased bronchial secretions. Direct damage to the vagal
nucleus has been implicated, as well as local damage to the sinus node, and to
reflex excessive vagal tone.7

15

CHAPTER III
CASE REPORT
3.1 Objective
The objective of this paper is to report a case of a 5 years 0 months old
boy with a diagnosis of tetanus.
3.2 Case
NH, a 5 years 0 months old boy, with 15kg of BW and 100cm of BH,
came to Haji Adam Malik General Hospital on September 30th 2015 at 12.00. His
main complaint was seizure.
History of disease:
NH, a 5 years 0 months old boy, with 15kg of BW and 100cm of BH, came to
Haji Adam Malik General Hospital on September 30th 2015 at 12.00. His main
complaint was seizure. It has been experienced by the patient since since 5 days
ago, seizure was found in whole body, the arms and legs were stiff, eyes staring
upwards, the teeth clenched and it occurred about 2-3 minutes long, the frequency
is more than 10 times a day. After the seizure patient fall asleep. Seizure was
happened if patient hear the sound and touch. Patient didnt have a fever.
Patient also complained that he couldnt open his mouth. This happened since 4
days ago, his ability to open his mouth is only about 1cm. Patient also complained
that he walk like a robot since 3 days ago. And his family didnt recognize that his
stomach was rigid. Patient have a history that he impaled on the barbed wire on
his right foot sole one month ago, the wound has been closed as deep as 1 cm.
According to the mother, the wound is not treated.
Patient is a referral patient from Eparina Etaham Hospital by a pediatrician and
has been diagnosed pediatric tetanus had been given diazepam and metronidazole.

16

History of medication: Inj. Diazepam maintenance 5,5mg/3hrs

Inj. Metronidazole 100mg/6hrs
TT 0,5cc IM
History of family: None
History of parents medication: None
History of pregnancy: Unclear
History of birth: Birth was assisted by his familys friend. Baby was born by
normal delivery and cried spontaneously. Bluish was not
found. Body weight, body length and head circumference was
not known.
History of feeding: 3 months of breast feeding and then continued with formula
milk until age 2. Family food was given from 24 months
onwards.
History of immunization: None
History of growth and development: Patients mother explained that he grew
normally. He was able to talk, crawl and
walk appropriately based on his age.
Physical Examination:
Present status: Sensorium : compos mentis, body temperature: 36.8C, HR:
108x/I, RR: 28 x/i, BW: 15 kg, BH: 100 cm, BW/A: 83%, BL/A: 91%,
BW/BL: 94%, anemic (-), icteric (-), dyspnea (-), cyanosis (-), edema (-),
bruise (-).
Localized status:

Head:

Eyes: Pale on inferior palpebral conjunctiva(-/-), scleral icterus (-/-),

light reflex (+/+), isochoric pupil.

Ears: within normal range

17

Nose: within normal range

Mouth : trismus, open mouth width 1cm

Neck : JVP: R-2 cmH2O, Lymph node enlargement (-)

Thorax : Symmetrical fusiform, retraction (-)

HR: 108 bpm, regular, murmur (-)
RR: 28 x/i, regular, ronchi (-/-)

Abdomen: muscular rigidity (+), normal peristaltic, liver and spleen:

undeterminable

Extremities : pulse 108 bpm, regular, adequate p/v, felt warm, CRT < 3,
closed wound 1cm.

Differential diagnosis : Tetanus

Working diagnosis

: Tetanus

Laboratory finding: (Eparina Hospital)

Complete blood analysis (Sept 29th 2010)
Test
Hemoglobin
Erythrocyte
Leucocyte
Thrombocyte
Hematocrite
Eosinophil
Basophil
Neutrophil : band
Neutrophil :
segment
Lymphocyte
Monocyte
MCV
MCH
MCHC

Result
12,6
4,2
11,7
238
38
2
0
2
85

Unit
g%
6
10 /mm3
103/mm3
103/mm3
%
%
%
%
%

References
14-18
4,5-6
4-10
140-400
40-50
1-3
<1
2-6
50-70

10
1
89
29
33

%
%
fL
Pg
g%

25-40
2-8
80-97
27-34
32-36

18

Therapy: - NGT insertion

- IVFD D5% NaCl 0,45% 50gtt/I micro
- Inj. Diazepam 5,6mg/iv/3hrs = 1,1cc/3hrs
- Inj. ATS : 20.000 IU/IM
20.000 IU in 250cc NaCl 0,9% (30-45 minutes)
- Inj. Metronidazole 100 mg./6hrs
- SV diet 1200 kcal + 20gr protein + 900cc water divided to 6
portions 150cc/hrs via NGT

FOLLOW UP
Aug 30st 2015
S

19

Inability

to

Sens

Compos

open

the

Mentis

mouth

(+),

BW: 15 kg, BH: 100

seizure

(+),

cm, T: 37C

opisthotonus

(+), fever (-)

Face

Tetanus

IVFD

D5%

NaCl

0,45% 50gtt/i micro

Inj.

Diazepam

5,6mg/iv/3hrs

Head:

1,1cc/3hrs
:

Risus

sardonicus (+)
Eyes:

Pale

inferior

Inj. ATS :

20.000

IU/IM, 20.000 IU in
on

200 cc NaCl 0,9%

(30-45minutes)

palpebral

conjunctiva(-/-),

already been given in

scleral icterus (-/-),

ER

light reflex (+/+),

isochoric pupil.

Inj.

Metronidazole

150 mg/6hrs

E/N/M:

within

normal

range/

20gr protein + 900cc

within

normal

water divided to 6

range/

trismus

portions 150cc/hrs

1cm
Neck

JVP:R-2

cmH2O,

Lymph

enlargement

(-)

Thorax

opisthotonus

(+),

symmetrical
fusiform, retraction
(-), HR: 100 bpm,
regular,

SV diet 1200 kcal +

via NGT
:

node

murmur

(-/-), RR: 24 x/i,

regular, ronchi (-/-)

20

Abdomen: muscular
rigidity (+), normal
peristaltic, liver and
spleen:
undeterminable

Extremities : pulse
100 bpm, regular,
adequate p/v, felt
warm, CRT < 3,
closed wound 1cm

st

Sep 1 2015 (06.00)

S
Spontaneous
Sens

O
:

seizure (+)

Mentis

04.30

&

T : 37,3 C

05.00,

fever

(-)

Compos

A
Tetanus

IVFD

D5%

NaCl

0,45% 50gtt/i micro

Head:

Face : Risus sardonicus

Inj.

Diazepam

5,6mg /3hrs /iv

(+)

dose 10% 6,18

Eyes: Pale on inferior

mg/3hrs

palpebral

1,2cc/3hrs/iv

conjunctiva(-/-), scleral

Inj. ATS :

20.000

icterus (-/-), light reflex

IU/IM, 20.000 IU in

(+/+), isochoric pupil.

200 cc NaCl 0,9%

E/N/M: within normal

range/ within normal

(30-45minutes)

range/ trismus 1cm

Neck :

P
Isolation ward

JVP:

R-2

Inj.

Metronidazole

150 mg/6hrs (D-2)

SV diet 1200 kcal +

cmH2O, Lymph node

20gr protein + 900cc

enlargement (-)

water divided to 6

Thorax : opisthotonus

portions 150cc/hrs

(+),

via NGT

symmetrical

21

fusiform,

retraction

For attack seizure,

(-), HR: 110 bpm,

inj. Diazepam 5mg/iv

regular, murmur (-/-),

= 1cc/iv (slow bolus)

RR: 28 x/i, regular,

Planning :

ronchi (-/-)

o Consult to plastic

Abdomen:

muscular

rigidity (+), normal

surgery division
o If

patient

have

peristaltic, liver and

seizure

spleen:

diazepam dose 10-

undeterminable

15%

Extremities : pulse
110

bpm,

adequate

regular,
p/v,

felt

warm, CRT < 3,

closed wound 1cm
Sep 1 2015 (16.00)
S
O
A
Seizure (+)
Sens
:
Compos Tetanus
st

Mentis

Planning :

T : 37,3 C
HR

P
Stesolid 5mg supp

120x/i,

reg,

Inj.

Diazepam

maintenance

murmur (-)

dose 15% 7

RR : 28x/I, reg, ronchi

mg/3hrs/iv

(-/-)

1,4cc/3hrs/iv

16.30 Plastic surgery

division
Physical exam :
- Laceration wound on
dorsum pedis dextra,
1 month ago, after
impaled

on

barbed

wire, pain (-), size

22

1x0,5cm,

active

hemorrhage (-)
- Advice therapy :
Wound toilet with
NaCl 0,9% +
antiseptic,
Wound management
Sep 2nd 2015
S
Attack

Sens

seizure (+),

Mentis

spontaneous

T : 36,3 C

O
:

A
Compos Tetanus

rigidity (+)

Face

06.30,
14.15, 16.00,
17.00

Head:

inferior

D5%

NaCl

Inj. Diazepam 7mg /

3hrs

Risus

sardonicus (+)
Eyes:

IVFD

0,45% 50gtt/i micro

seizure (+),
muscular

P
Isolation ward

Pale

/iv

1,4cc/3hrs/iv

Inj. ATS :

20.000

on

IU/IM, 20.000 IU in

palpebral

200 cc NaCl 0,9%

conjunctiva(-/-),
scleral icterus (-/-),

(30-45minutes)

light reflex (+/+),

isochoric pupil.

Inj.

Metronidazole

150 mg/6hrs (D-3)

SV diet 1200 kcal +

E/N/M:

within

20gr protein + 900cc

normal

range/

water divided to 6

within

normal

portions 150cc/hrs

range/

trismus

via NGT

1,5cm
Neck

For attack seizure,

: JVP: R-

inj. Diazepam 5mg/iv

2 cmH2O, Lymph

= 1cc/iv (slow bolus)

node
(-)

enlargement

23

Thorax

opisthotonus

(+),

symmetrical
fusiform, retraction
(-), HR: 90 bpm,
regular,

murmur

(-/-), RR: 22 x/i,

regular, ronchi (-/-)

Abdomen: muscular
rigidity (+), normal
peristaltic, liver and
spleen:
undeterminable

Extremities : pulse
90 bpm, regular,
adequate p/v, felt
warm, CRT < 3

14.15

Spontaneous

14.15

seizure (+)

Sens : GCS 12

5mg/iv = 1cc/iv to

(E3V4M5)

attack seizure

Inj.

Diazepam

T : 36,6C

Planning :

HR: 98x/i, reg, murmur

(-)

maintenance

RR : 30x/i, reg, ronchi

7mg/3hrs/iv Inj.

(-/-), stridor (+/+)

Diazepam

Inj.

Diazepam
dose
7mg/2hrs/iv

(slow bolus)
16.00

Planning :

Spontanous

seizure (+)

7mg/2hrs/iv

Inj.

Diazepam

dose

24

10% 7,7mg/2hrs/iv
1,54cc/2hrs/iv
rd

Sep 3 2015
S
Spontaneous

Sens

seizure (+),

Mentis

fever (-)

T : 36,7 C

A
Compos

IVFD

Risus

inferior

NaCl

Pale

Inj.

Diazepam

7,7mg/3hrs/iv

sardonicus (+)
Eyes:

D5%

0,45% 50gtt/i micro

Head:

Face

P
Isolation ward

1,54cc/3hrs/iv
on

palpebral

Inj. ATS :

20.000

IU/IM, 20.000 IU in

conjunctiva(-/-),

200 cc NaCl 0,9%

scleral icterus (-/-),

(30-45minutes)

light reflex (+/+),

isochoric pupil.

Inj.

Metronidazole

150 mg/6hrs (D-4)

E/N/M:

within

normal

range/

20gr protein + 900cc

within

normal

water divided to 6

range/

trismus

portions 150cc/hrs

1,5cm
Neck

via NGT
: JVP: R-

For attack seizure,

2 cmH2O, Lymph

inj. Diazepam 5mg/iv

node

= 1cc/iv (slow bolus)

enlargement

(-)

SV diet 1200 kcal +

Thorax

opisthotonus

(+),

symmetrical
fusiform, retraction
(-), HR: 90 bpm,
regular,

murmur

25

(-/-), RR: 24 x/i,

regular, ronchi (-/-)

Abdomen: muscular
rigidity (+), normal
peristaltic, liver and
spleen:
undeterminable

Extremities : pulse
90 bpm, regular,
adequate p/v, felt
warm, CRT < 3

th

th

Sep 4 5 2015
S
Spontaneous
Sens

O
:

seizure (+),

Mentis

fever (-)

T : 37,1C

A
Compos Tetanus

Risus

inferior

D5%

NaCl

Pale

Inj.

Diazepam

7mg/3hrs/iv

sardonicus (+)
Eyes:

IVFD

0,45% 50gtt/i micro

Head:

Face

P
Isolation ward

1,4cc/3hrs/iv
on

palpebral

Inj. ATS :

20.000

IU/IM, 20.000 IU in

conjunctiva(-/-),

200 cc NaCl 0,9%

scleral icterus (-/-),

(30-45minutes)

light reflex (+/+),

isochoric pupil.

Inj.

Metronidazole

150 mg/6hrs (D-5)

E/N/M:

within

normal

range/

20gr protein + 900cc

within

normal

water divided to 6

range/

trismus

portions 150cc/hrs

1,5cm
Neck

SV diet 1200 kcal +

via NGT
: JVP: R-

For attack seizure,

26

2 cmH2O, Lymph

inj. Diazepam 5mg/iv

node enlargement -

= 1cc/iv (slow bolus)

Thorax

opisthotonus

(+),

symmetrical
fusiform, retraction
(-), HR: 96 bpm,
regular,

murmur

(-/-), RR: 24 x/i,

regular, ronchi (-/-)

Abdomen: muscular
rigidity (+), normal
peristaltic, liver and
spleen:
undeterminable

Extremities : pulse
96 bpm, regular,
adequate p/v, felt

warm, CRT < 3

Sep 6 2015 : OUT PATIENT
th

CHAPTER IV
DISCUSSION

THEORY
Epidemiology

CASE
Epidemiology

- Tetanus is predominantly a disease - NH, is a patient in Haji Adam Malik

of

underdeveloped

countries.

General Hospital Medan, where

Developed nations have incidences of

placed in developing countries.

tetanus similar to those observed in - NH, is a 5 years 0 months old boy.

the United States. For instance, only

27

126 cases of tetanus were reported in

England and Wales from 1984-1992
- Age-related demographies. Although
tetanus affects all ages, the highest
prevalence is in newborns and young
people.WHO estimated that in 2002,
there were 213,000 tetanus deaths,
198,000 of them in children younger
than 5 years.
- Sex-related demographies. Tetanus
affects both sexes. No overall gender
predilection has been reported, except
to the extent that males may have
more soil exposure in some cultures.
- Race-related demographies. Tetanus
affects all races. From 1998 to 2000,
the incidence of tetanus in the United
States was highest among Hispanics ,
followed by whites and then by
African Americans
Etiology

Etiology

- C. tetani is a slender, gram-positive, - This patient is diagnosed with

anaerobic rod that may develop a tetanus which is caused by C.tetani
terminal spore, giving it a drumstick
appearance. The organism is sensitive
to heat and cannot survive in the
presence of oxygen.
Clinical Manifestations

Clinical Manifestation

- Patients with generalized tetanus - NH, came to Haji Adam Malik

present with trismus (ie, lockjaw) in General Hospital with chief complaint
75%

of

cases.

Other

presenting seizure. seizure was found in whole

28

complaints include stiffness, neck body, the arms and legs were stiff,
rigidity,

restlessness,

and

reflex eyes

spasms.
-

staring

upwards,

the

teeth

clenched and it occurred about 2-3

Subsequently,

muscle

rigidity minutes long, the frequency is more

becomes the major manifestation. than 10 times a day. After the seizure
Muscle

rigidity

spreads

in

a patient

fall

asleep.

Seizure

was

descending pattern from the jaw and happened if patient hear the sound and
facial muscles over the next 24-48 touch. Patient didnt have a fever.
hours to the extensor muscles of the - Patient also complained that he
limbs.

Dysphagia

moderately

severe

occurs
tetanus

in couldnt
as

open

his

mouth.

This

a happened since 4 days ago, his ability

consequence of pharyngeal muscle to open his mouth is only about 1cm

spasms, and onset is usually insidious - Patient also complained that he walk
over several days. Reflex spasms like a robot since 3 days ago. And his
develop in most patients and can be family

didnt

recognize

that

his

triggered by minimal external stimuli stomach was rigid.

such as noise, light, or touch. The - Patient have a history that he impaled
spasms last seconds to minutes; on the barbed wire on his right foot
become more intense; increase in sole one month ago, the wound has
frequency with disease progression; been closed as deep as 1 cm.
and

can

cause

dislocations,

and

apnea,

fractures,

rhabdomyolysis.

Laryngeal spasms can occur at any

time and can result in asphyxia.
- Other symptoms include elevated
temperature, sweating, elevated blood
pressure, and episodic rapid heart rate.
Sustained

contraction

of

facial

musculature produces a sneering grin

expression known as risus sardonicus.
Diagnosis

Diagnosis

29

- Tetanus diagnosis is strictly clinical; - NH, came with trismus, risus

there are no confirmatory laboratory sardonicus, painful muscle contraction,
tests. The WHO definition of adult seizure, and history of injury or wound
tetanus requires at least one of the
following signs: trismus (inability to
open the mouth) or risus sardonicus
(sustained

spasm

muscles);

or

of

the

painful

facial

muscular

contractions. Although this definition

requires a history of injury or wound,
tetanus may also occur in patients who
are unable to recall a specific wound
or injury.
Treatment

Treatment

- The goals of pharmacotherapy are to - NGT insertion

stop toxin production within the

-IVFD D5% NaCl 0,45% 50gtt/I

wound, to neutralize unbound toxin,

micro

and to control disease manifestations.

-Inj.

Drugs used to treat muscle spasm,

1,1cc/3hrs

Diazepam

5,6mg/iv/3hrs

rigidity, and tetanic seizures include - Inj. ATS : 20.000 IU/IM

sedative-hypnotic

agents,

general

anesthetics, centrally acting muscle

20.000 IU in 250cc NaCl

0,9% (30-45 minutes)

relaxants, and neuromuscular blocking - Inj. Metronidazole 100 mg./6hrs

agents. Antibiotics are used to prevent - SV diet 1200 kcal + 20gr protein +
multiplication

of Clostridium

tetani, thus halting production and

release of toxins. Antitoxins are given
to neutralize unbound toxin

900cc water divided to 6

portions 150cc/hrs via NGT

30

CHAPTER V
SUMMARY
NH, a 5 years 0 month old boy, came to Haji Adam Malik General
Hospital on August 31st

2015 with chief complaint of seizure. Based on

anamnesis, physical examination, and laboratory assesment, he was diagnosed

with tetanus and was given treatment of the followings ; IVFD D5% NaCl 0,45%
50gtt/I micro, Inj. Diazepam 5,6mg/iv/3hrs = 1,1cc/3hrs, Inj. ATS :

20.000

IU/IM + 20.000 IU in 250cc NaCl 0,9% (30-45 minutes), Inj. Metronidazole 100
mg/6hrs, SV diet 1200 kcal + 20gr protein + 900cc water divided to 6 portions
150cc/hrs via NGT

REFERENCES
1. Center of Disease Control and Prevention. Epidemiology and prevention of
vaccine-preventable diseases. The pink book. 13th edition chp. 2015. 21: 341352. (Available at : http://www.cdc.gov/nip/publications/pink).
2. Missouri Department of Health and Senior Services. Tetanus. Communicable
Disease Investigation Reference Manual. 2013. Page : 1-7. (Available at :
http://health.mo.gov/living/healthcondiseases/communicable/communicabledi
sease/cdmanual/pdf/Tetanus.pdf).
3. World Health Organization. WHO Technical Note: Current recommendations
for treatment of tetanus during humanitarian emergencies. January 2010
4. Sanford JP. Tetanus--forgotten but not gone. N Engl J Med. 1995 Mar 23.
332(12):812-3.
5. Hinfey

PB.

Tetanus.

Medscape.

2010.

(Available

at

http://emedicine.medscape.com/article/229594-overview#a3)
6. Ahmadsyah I, Salim A. Treatment of tetanus: an open study to compare the
efficacy of procaine penicillin and metronidazole. Br Med J (Clin Res Ed).
1985 Sep 7. 291(6496):648-50.
7. Abdelmoneim, T. DeNicola LK, Hasan Yousuf. Tetanus : Complications and
Management in a Pediatric Intensive Care Unit. The Division of Prediatric
Critical Care, University of Florida-Jacksonville. PCCMeds.
8. Ikatan Dokter Anak Indonesia. Tetanus. Buku Ajar Infeksi & Pediatri Tropis.
2008. 28 : 322-330.
9. Quackenbush,P. Tuorinsky, S. Rabb, R. Tetanus Diagnosis Sometimes

Elusive. The Nurse Practitioner. 2003. 28(11) : 50-53