CASE REPORT

Hypertrophic Pyloric Stenosis and

Severe Marasmic Type Malnourishment in a Month-Old Boy

INTRODUCTION
Hypertrophic pyloric stenosis (HPS), also known as infantile hypertrophic
pyloric stenosis (IHPS), is the most common cause of infant gastrointestinal
obstruction that requiring surgery in the first months of life. 1,2 It is characterized by a
marked hypertrophy of the pylorus muscle, which leads to a blockage of the gastric
outlet and provokes increasingly severe episodes of projectile vomiting. 2,3

The

incidence of IHPS is approximately two to five per 1,000 births per year in most white
populations, although it varies with the geographic area and the time period being
reviewed. Pyloric stenosis appears to be more common in infants of caucasian
descent and is less common in India and among black and Asian populations, with a
frequency that is one-third to one-fifth that in the white population. 4,5,6 There is maleto-female ratio of 4:1, with reported ratios ranging from 2,5:1 to 5,5:1. 1,4,5
Hypertrophic pyloric stenosis tends to run in families, however, the exact pattern of
inheritance is unclear. The incidence rate is 1 in 14 if the father is affected, the rate is
even higher if the mother is affected.1 First-born children have been noted to be more
likely affected, and a familial link is seen with a greater than fivefold increase in the
risk in first-degree relatives.5,6
Infants classically present at 2 to 6 weeks old with gradually progressive
vomiting that becomes projectile and remains nonbilious. Infants remain vigorous
with a ravenous appetite. They rapidly finish an entire feeding, only to regurgitate the
entire volume in a projectile fashion. In the later stages of the disease, children may
exhibit visible waves of abdominal peristalsis in response to intense contractions

against an obstruction. Children in the later stages of disease may exhibit marasmus
(protein-calorie malnutrition) as a result of impaired nutrient absorption.1,4,6
Although its etiology remains unknown, our understanding of the clinical
manifestation and treatment of HPS has undergone a remarkable evolution. In
patients in whom clinical examination is unsuccessful, modern imaging techniques
are highly accurate in facilitating the diagnosis.4 The diagnosis of HPS is ascertained
after obtaining an appropriate history and by the palpation of a pyloric called olive
sign. The diagnosis may be established by ultrasonography (USG) of the pylorus.
Children may have a palpable pylorus, commonly referred to as an olive in the right
epigastrium, on abdominal examination. Placement of a nasogastric tube and
emptying the stomach or placement of the infant in the prone position often facilitates
palpation.1,7,8
Most children probably are best managed with hospital admission for
rehydration, correction of electrolyte abnormalities and also for management of the
marasmus. Hypertrophic pyloric stenosis can be diagnosed or excluded by using
USG. Thus, infants presenting with nonbilious vomiting should be directed to undergo
USG if HPS is a consideration. Hypertrophic pyloric stenosis may be confirmed by
ultrasonography or upper gastrointestinal series. Ultrasonography is the diagnostic
modality of choice because it is simple, readily available, and without serious
complications such as aspiration. With both modalities, reported accuracy is greater
than 95%. Ultrasonography examination reveals a thickened pylorus, which is
diagnostic. A characteristic string sign, reflecting passage of contrast material
through the narrowed pyloric sphincter, can be seen in the upper gastrointestinal
tract. In advanced stages with complete obstruction at the pylorus, plain films may
reveal an enlarged body of the stomach and pylorus.

1,4,6,7

If the patient has HPS, the

appropriate surgical referral is made rapidly and accurately. If the sonogram

delineates a normal pylorus, a search for other causes, may allow identification of
preampullary duodenal stenosis or hiatal hernia. Upper gastrointestinal (UGI)
examination may be performed if further evaluation for these conditions is
warranted.1,4,7
Surgical correction of pyloric stenosis is not an emergency, and therefore the
electrolyte disturbances can and should be meticulously corrected before operation.
Infants undergoing pyloromyotomy are assumed to have a full stomach and the
anaesthesiologist should keep this in mind. Both the anaesthesiologist and surgeon
should be vigilant during the operation to prevent aspiration of gastric juice.5,8
The purpose of this report is to present a rare case of hypertrophic pyloric
stenosis and severe marasmic type malnourishment in a month-old boy.

CASE REPORT

V, male, a month old was admitted to the Emergency Ward, Saiful Anwar
General Hospital on May 23rd 2015 after being referred from Ngudi Waluyo
Hospital Wlingi because of vomiting. The parents reported that vomiting had
started since a week before admission, non-bilious, non-projectile and nonbloody, frequency 8-10 times/day, it happened 5-10 minutes everytime he
finished nursing or bottle feeding, the amount is 10-30 ml each time and
sometimes vomiting the entire volume of his feeed, contains milk. After vomiting
the infant remains hungry and still eager to feed. Previously patient only had
breast feeding since he was born, but his mother gave him formula milk since ten
days before admission because he still looked

thirtsy after having breast

feeding. The breast feeding frequency was every one to two hours with the
length of breast feeding was 15-30 minutes every nursing and there was no
difficulty feeding. The mother gave extra formula milk about 3 times daily with
amount of 30 ml every bottle. There is no history of fever, upper respiratory
infection (URI) symptoms, diarrhea, seizure, jaundice, head injury and no sign of
dehydration. There is also no history of lump in the abdomen before starting had
vomiting. He is less active than normal. He is making fewer wet diapers and less
stool than usual.
Patient experienced weight loss since he had vomiting. He was born with
birth weight of 2600 grams and has weight gain of 2900 grams when he was
three weeks in age. He loss his weight of 2400 grams at the time when he was
admitted in Wlingi hospital, and when in the Saiful anwar hospital his body weight
was 2200 grams.

Patient had brought to pediatrician before by the parents when he had

vomiting for three days, but the pediatrician said there is no big problem and that
was only ordinary vomiting that happened to mostly baby, then the doctor gave
medication. Because there is no improvement after taking medication from the
pediatrician for two days then the parent took him to another pediatrician. The
second pediatrician referred him to Ngudi Waluyo Wlingi Hospital due to
suspected of Hirschprungs disease. The patient referred to Saiful Anwar Hospital
for further examination and management.
Pasien was the first child and during pregnancy there was no history of
bleeding, vaginal discharge, fever, diabetes mellitus, or hypertension of the
mother. She never smoking and also there is no history of taking drugs or herbal
medicine during pregnancy. She was routinely having ante natal care in midwife
every month and had USG once in the obstetrician at the 7 months gestational
age. He was delivered spontaneously at-term by a midwife in Annisa Hospital
Blitar, cried spontaneously,

weighed 2600 grams, no history of cyanosis,

respiratory distress and jaundice. The amniotic fluid was greenish, then he was
hospitalized for 2 days and given antibiotic.
The mother was 23 years old house wife and high school graduated. His
father was 23 years old, high school graduated and work as employees in an
welding industrial. There is no history of family with the same complain before.
Patient already had hepatitis B immunization.

Figure 1. The patients picture

The physical examination found him alert, his weight 2200 grams (65,6%
of increament body weight), body length 50 cms, head circumference 36 cms (-1
standard deviation to mean) and his weight for length was less than -3 standard
deviation (SD).
His axilary temperature was 36.8C, pulse rate 140 beats per minute
strong and regular, respiratory rate 46 times per minute and O2 saturation 99% .
His eyes were not yellowish and the skin turgor in the forehead was normal. The
chest examination found symmetrical movement, normal with clear breathing
sounds and no retractions. Heart auscultation reveals a regular rhythm and no
murmur. His abdomen is slightly distended with active bowel sounds. No
hepatosplenomegaly is noted. He looks very thin with old man face and baggy
pants. He has no inguinal hernias. Genitalia are normal. Extremities are normal.
Color, perfusion, and capillary refill are good. Neurologic examination is normal.

Figure 2. The patients growth chart

Initial laboratory findings at the time of presentation at Saiful Anwar

Hospital are shown in table 1.
Table 1. Initial laboratory tests results (23-3-2015)
Hemoglobin
Leukocytes
Thrombocytes
Hematocrits
Differential count

14.4 gms/dl
16.290/mm3
444,000/mm3
39 %
0.6/0.4/47.9/41.2/9.9

CRP
PPT
APTT
Albumin
Sodium/Potasi

Eosinofil/Basofil/

um/Chloridel/

Neutrophil/Lymfosit

Calsium/

/Monosit

Phosfor
SGOT/SGPT

0.06 mg/dL
11.3 seconds
39.8 seconds
4.66 gms/dl
126/3.48/99/10.7/4.3

46/14 mU/dl

A plain abdominal X-ray on May 24th 2015 showed the dilatation of gaster.

Figure 3. Chest X-ray and plain abdominal X-ray , May 23th 2015
Based on the anamnesis, clinical signs and radiological findings, the initial
diagnosis was vomiting due to diffrential diagnosis with hypertrophy pyloric
stenosis (HPS), gastro esophagal reflux disease (GERD), pylorospasm, pyloric
atresia, and severe marasmic type malnourishment. An abdominal USG was
planned to confirm the diagnosis. Initial treatment of the patient was oxigenation,
fluid and nutritional support,

antibiotics, and micronutrient. Those are nasal

canule oxigen 2 liters per minutes if clinicaly there were dyspneau due to
displacement by enlarged stomach, semifowler position 30, intravenous fluid
drip Dextrose 12,5 0,18 NaCl 0,9% 232 ml/day, lipid 20% 20 ml (2,5 gms/kg body
weight/day), aminosteril infant 6% 86 ml (1,5 gms/kg body weight/day), ampicillin
3x75mg (100mg/kg body weight/day), vitamin A 1x2500 IU, vitamin E 1x50 IU,
vitamin K 1x1mg, vitamin C 1x25mg, vitamin B complex 1x 1/4 tablet, zinc
8

1x10mg, folic acid 1x1mg and breast feeding 60 ml given intermitten. Patient also
consulted to surgery departement. The conclusion from surgery department was
high level bowel obstruction due to suspected hypertrophic pyloric stenosis and
planned to have abdominal USG.
The Abdominal USG on May 25th 2015, found thickening of the walls of
the pylorus with the thickness of 0.65 cms along the 1.69 cms, with the patient
postion tilted to the right, there were still a little liquid that passes through the
pylorus. The conclusion of abdominal USG was hypertrophic pyloric stenosis.
From surgery departement patient planned to have pylorotomy.

Figure 4. Abdominal USG, May 25th 2015

On June 3rd 2015 the surgery department performed pyloromyotomy to

patient. Operation report showed there were thickeness of pylorus along 1.6
cms and thickeness of serous muscularis length 0.6 cms.

DISCUSSION

10

Vomiting is forceful oral expulsion of gastric contents associated with

contraction of the abdominal and chest wall musculature. Vomiting is a complex
process that involves various systems that influence the vomiting. Center vomiting is
a complex process that involves various systems that influence the vomiting center.
The act of vomiting has multiple phases: a preejection phase, a retching phase, and
an ejection phase. In the preejection phase, gastric relaxation and retroperistalsis
occur. In the retching phase, rhythmic contractions of respiratory, abdominal wall,
intercostal, and diaphragm muscles occur against a closed glottis. In the final phase,
intense contraction of the abdominal muscles combined with relaxation of the
pharyngoesophageal sphincter results in ejection. Vomiting can also occur abruptly
without the preejection and retching phases; such vomiting is often forceful and is
referred to as projectile vomiting, which is seen in cases of gastric outlet obstruction.
Vomiting is often characterized as nonbilious, bilious, or bloody based on the content.
Vomiting could happened by multifactor, so we have to make a differential diagnosis
of vomiting based on the patient complain and characteristic.9

Table 2. Age-Related Differential Diagnosis of Emesis9

11

Hypertrophic pyloric stenosis is the most common cause of infantile

gastrointestinal obstruction beyond the first month of life. The first clinical description
of HPS was by Fabricious Hildanus in 1627, but Harald Hirschsprungs seminal
article in 1888 led to our modern understanding of the condition. Although HPS is the
most common surgical condition producing emesis in infancy, its etiology is unknown.
Whether the condition is congenital or acquired is debated. 6 Infants classically
present at 2 to 6 weeks old with gradually progressive emesis that becomes
projectile and remains nonbilious. In general, vomiting in IHPS is projectile, but in
these patients was not found. Research by Sandra et al found only 89% of infants
with HPS showed manifestation projectile vomiting.10
Infants remain vigorous with a ravenous appetite.1,5 Infants classically present
at 2 to 6 weeks old with gradually progressive vomiting that becomes projectile and
remains nonbilious.The cause of pyloric stenosis is unknown. Genetic, familial,
gender, and ethnic origin can influence the incidence rates of HPS. 8,11,12 There is
12

evidence both for and against an increased incidence in the first-born child, and there
is familial clustering of HPS, but not in a Mendelian pattern.5,6 There is male-tofemale ratio of 4:1, with reported ratios ranging from 2,5:1 to 5,5:1.1,4,5
Bottle-feeding has been suggested to increase the risk of HPS. Research by
Krogh et al and Mc.Ateer et al showed that bottle-fed infants experienced a 4.6-fold
higher risk of pyloric stenosis (PS) compared with infants who were not bottle-fed.
The result adds to the evidence supporting the advantage of exclusive breastfeeding
in the first months after birth.3,14
This is a case that occurred in infants aged 1 month with onset at age 2
weeks, present with non bilious and projectile vomiting. In epidemiology in
accordance with an average age IHPS is 2-6 weeks. Patient is male and was the
first born child but there is no history of HPS in his parents. In these patients from
birth to age 2 weeks does not indicate an abnormality. He started having complain of
vomiting since 2 weeks of age. This complain noted by her mother since she gave
extra bottle feeding instead of giving breast feeding. Based on the research about
bottle feeding is associated with an increased risk of HPS, this patient had only
breast feeding before he starting vomiting. The mother started giving bottle feeding
instead of breast feeding because she felt that his baby still look thirsty after having
nursed on her. That could happened because she didint know how to give correctly
breast feeding since this is the first child.
One of differential diagnosis of this this patient is GERD as the vomiting of
this patient was not projectile. The results of abdominal plain X-ray shows there is
stomach widened, meaning there is probablitiy of obstruction in the stomach.
The diagnosis of HPS is initially suggested by the typical clinical presentation.
Palpation of the hard muscle mass, or olive, is diagnostic but is often challenging and
time consuming. In experienced hands and with adequate time and preparation,

13

abdominal palpation can be successful in 85%100% of infants.4 Children may have

a palpable pylorus, commonly referred to as an olive in the right epigastrium, on
abdominal examination. Placement of a nasogastric tube and emptying the stomach
or placement of the infant in the prone position often facilitates palpation. 1 If the
pylorus is palpated by an experienced clinician, no further imaging is necessary.
Gastric distension or visible gastric peristalsis, seen as a wave of contraction from
the left upper quadrant to the epigastrum, may be seen in some cases. The inability
of a clinician to palpate an olive does not rule out the diagnosis of HPS.5,6,8
From the patients physical examination we didnt find olive sign, so that we
need further examination to make the correct diagnosis. Fluoroscopic upper
gastrointestinal contrast study was first proposed in 1918, and is performed with the
child drinking from a bottle. In patients with HPS, there is failure of relaxation of the
prepyloric antrum and the pyloric canal is outlined by a string of contrast material.
The thickened muscle causes an external impression on the gastric antrum, termed
the shoulder sign. Fluoroscopy can be time consuming and involves radiation.
Sensitivity as high as 95% is reported but depends on experience and skill of the
examiner. Ultrasonography is noninvasive, can be performed quickly and there is no
radiation exposure. Accuracy approaches 100% in experienced hands,20 with 99.5%
sensitivity and 100% specificity.5,6 This would normally confirm the presence of a
pyloric tumour. The characteristic appearance of pyloric stenosis on ultrasound is
that of a doughnut or bulls eye on cross section of the pyloric channel. The
hypertrophied pyloric canal may range from 14 mm to more than 20 mm in length
and the muscle thickness is variable (from 3 to 5 mm). Real time observation of
failure of relaxation of the pyloric canal is important. These limits may be lower in
infants younger than 30 days of age. An experienced sonographer will recognize
periods of relaxation in infants with pylorospasm, commonly confused with pyloric

14

stenosis at examination.5,6,8 The USG examination of this patient we found that there
is thickening of the walls of the pylorus with the thickness of 0.65 cms along the
1.69 cms. This abdominal USG result retained HPS.
Before surgery we have to keep the patient's general condition to remain
stable. Because the patient was also suffering from severe marasmic type
malnourishment which is one of the complications of HPS, then we did treatment of
malnutrition. Malnutrition is a pathologic state of varying severity with clinical features
caused by deficiency, excess, or imbalance of essential nutrients. The cause may be
primary (involving the quantity or quality of food consumed) or secondary (involving
alterations in nutrient requirements, utilization, or excretion). Historically, malnutrition
in children has been defined using the terms marasmus and kwashiorkor. Marasmus
develops after severe deprivation of calories and is characterized by weight loss and
wasting of fat and muscle tissue. Low weight-for-height and a reduced height-for age
are commonly observed. In the child with kwashiorkor, protein deficits outweigh
calorie deficits. Edema due to visceral protein depletion occurs along with muscle
wasting. Although some degree of growth failure may be present, weight-forheight
may not be notably low secondary to retention of fluid in the extravascular
compartment. Irritability, apathy, anorexia, and fatigue may be seen in both
marasmus

and

kwashiorkor.15

The

diagnosis

of

severe

marasmic

type

malnourishment from this patient based on clinical finding and anthropometric

evaluation. From the anthropometric we found that his weight for length was less
than -3 SD with percentage of increament body weight was 59,9%. From the physical
examination patient looks like old man face with very thin body and there was baggy
pants. 16,17
In the stabilisation phase a cautious approach is required because of the
childs fragile physiological state and reduced homeostatic capacity. Feeding should

15

be started as soon as possible after admission and should be designed to provide

just sufficient energy and protein to maintain basic physiological processes. Based
on WHO the essential features of feeding in the stabilisation phase are:17
small, frequent feeds of low osmolarity and low lactose
oral or nasogastric (NG) feeds (never parenteral preparations)
100 kcal/kgs/day
1-1.5 grams protein/kgs/day
130 ml/kgs/day of fluid (100 ml/kgs/day if the child has severe oedema)
if the child is breastfed, encourage to continue breastfeeding but give the
prescribed amounts of starter formula to make sure the childs needs are met.
This patient had problem profuse vomiting due to HPS made the enteral
nutrition will barely difficult to give, so we gave parenteral nutrition (PN) for this
patient. The time when PN should be initiated will depend both on individual
circumstances and the age and size of the infant or child. In the small preterm infant
starvation for just one day may be detrimental and where it is clear that enteral feeds
will not be tolerated soon PN must be instituted shortly after birth. However in older
children and in adolescence longer periods of inadequate nutrition up to about seven
days may be tolerated, depending on age, nutritional status, and the disease, surgery
or medical intervention.18
Carbohydrates are the main source of energy in nutrition and usually provide
4060% of the energy supply in western diets. The majority of the carbohydrate
derived from a normal diet reaches the bodys peripheral tissues as glucose. Glucose
is utilised by all cells and serves as metabolic fuel for muscle, liver, heart, kidneys
and gut and as the obligate energy source for brain, renal medulla and erythrocytes.
Glucose is the main carbohydrate utilised during foetal life; about 7 gms/kgs per day
(approximately 5 mgs/kgs per minute) of glucose crosses the placenta in the last

16

trimester of pregnancy. The major source of non-protein calories in PN is D-Glucose

(dextrose), which is provided in the monohydrate form for intravenous use. Dextrose
usually contributes most of the osmolality of the PN solution. Proteins are the major
structural and functional components of all cells in the body. They consist of chains of
amino acid subun, its joined together by peptide bonds. The chain length ranges from
two amino acids to thousands, with molecular weights subsequently ranging from
hundreds to hundreds of thousands of Daltons. From a nutritional perspective, an
important aspect of a protein is its amino acid composition. WHO recommended
giving lipid emulsions are used in paediatric PN as a non-carbohydrate source of
energy in a low volume and with low osmolarity. Lipid intake should usually provide
2540% of non-protein calories in fully parenterally fed patients.18
Based on WHO recommedation we gave parenteral nutrition with dextrosa
12,5% 0,18 NaCl 0.9% combined with lipid 20% and aminosteril infant 6%. We still
gave breest feeding as enteral nutrition given by intermitten feeding. The enteral
nutrition given as the patient complient. And for the severe malnutrition we also gave
antibiotic and micronutrient.
This patient have had operation using methode of pyloromyotomy by FredetRamstedt. During operation the surgeon found pylorus muscle thickening over 6 mm
and a length of more than 16 mm pylorus. The surgeon did incision exstramukosal of
serous towards mucous without injuring the mucosa. Surgery remains an option with
a success rate of almost 100%. Therapy with this operation has a mortality rate of
less than 0.5%, morbidity between 1-5%, and 1-3% recurrence rate.19,20

17

Figure 5 Diagnostic Algorithm for Hypertrophic Pyloric Stenosis8

18

SUMMARY

V, male, a months old was admitted to the Emergency Ward, Saiful Anwar
General Hospital on May 23rd , 2015 after being referred from Ngudi Waluyo Wlingi
Hospital because of vomiting since a week before admission, non bilious and non
projectile, frequency 8-10 times/day. Previously patient only had breast feeding
since he was born, then his mother gave him formula milk since ten days before
admission. There is no history of fever, upper respiratory infection (URI) symptoms,
diarrhea, seizure, jaundice, head injury and no sign of dehydration. There is also no
history of lump in the abdomen before starting had vomiting. He is less active than
normal. He is making fewer wet diapers and less stool than usual.
Physical examination found him alert, looks very tiny with old man face and
baggy pants. From the anthropometric we found that his weight for length was less
than -3 SD with percentage of increament body weight was 59,9%. His temperature
was 36.8 C, pulse rate 140 beats per minute strong and regular, respiratory rate 46
times per minute. There was no liver and spleen enlargement. Plain abdominal X-ray
showed the dilatation of gaster. From physical examination there were no olive sign,
so that we perform USG to make the correct diagnosis as USG is noninvasive, can
be performed quickly and there is no radiation exposure. The USG examination of
this patient we found that there is thickening of the walls of the pylorus with the
thickness of 0.65 cms along the 1.69 cms. This abdominal USG result retained
HPS.
This patient have had surgery using methode of pyloromyotomy by
Fredet-Ramstedt. During operation the surgeon found pylorus muscle thickening
over 6 mm and a length of pylorus more than 16 mm. The diagnosis was
hypertrophic pyloric stenosis (HPS) and severe marasmic type malnourishment.

19

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