29 Lesions of the Stomach
JUSTIN A. SOBRINO and MARK WULKAN
The stomach forms from the foregut and is recognizable by
the fifth week of gestation. It then elongates, descends, and
dilates to form its familiar structure by the seventh week
of gestation. The vascular supply to the stomach is very
robust, and ischemia of the stomach is rare. The stomach is
supplied by the right and left gastric arteries along the lesser
curvature, the right and left gastroepiploic arteries along
the greater curvature, and the short gastric vessels from the
spleen. There is also contribution from the posterior gastric
artery, which is a branch of the splenic artery, as well as the
phrenic arteries.
In this chapter we discuss common and unusual con-
ditions of the stomach that are treated surgically. Some
topics relevant to the stomach, such as gastroesopha-
geal reflux disease (GERD) and obesity, are covered
elsewhere.
Hypertrophic Pyloric Stenosis
Hypertrophic pyloric stenosis (HPS) is one of the most com-
mon surgical conditions of the newborn.1–9 It occurs at a
rate of 1–4 per 1000 live births in white infants but is seen
less often in nonwhite children.1–4 Males are affected more
often with a 4:1 male-to-female ratio. Risk factors for HPS
include family history, gender, younger maternal age, being
a first-born infant, and maternal feeding patterns.4,9,10 Pre-
mature infants are diagnosed with HPS later than term or
post-term infants.4
ETIOLOGY
The cause of HPS is unknown, but genetic and environ-
mental factors appear to play a significant role in the patho-
physiology. A genetic predisposition has been inferred from
race discrepancies, the increased frequency in males, and
the association with birth order (first-born infants with a
positive family history). Variants near several loci includ-
ing MBNL1, NKX2-5, and APOA1 have been associated
with HPS.11,12 Environmental factors associated with
HPS include the method of feeding (breast vs formula),
seasonal variability, exposure to erythromycin, environ-
mental pesticides, and transpyloric feeding in premature
infants.5–7,13–18 Additionally, there has been interest in
several gastrointestinal peptides or growth factors that
may facilitate pyloric hypertrophy. Some of these include
excessive substance P, decreased neurotrophins, deficient
nitric oxide synthase, and gastrin hypersecretion.8,9 Thus,
the etiology of HPS is likely multifactorial with environ-
mental influences.  extrinsic gastric compression.
478
DIAGNOSIS
The classic presentation of HPS is nonbilious, projectile vom-
iting in a full-term neonate who is between 2 and 8 weeks
old. Initially, the emesis is infrequent and may appear to be
symptomatic of GERD. However, over a short period of time,
the emesis occurs with every feeding and becomes forceful
(i.e., projectile). The contents of the emesis are usually the
recent feedings, but signs of gastritis are not uncommon
(“coffee-ground” emesis). On physical examination, the neo-
nate usually appears well if the diagnosis is made early. How-
ever, depending on the duration of symptoms and degree of
dehydration, the neonate may be gaunt and somnolent. Vis-
ible peristaltic waves may be present in the mid to left upper
abdomen. The pylorus is palpable in 70–90% of patients.10,19
To palpate the pyloric mass (i.e., “olive”), the neonate must be
relaxed. Techniques for relaxing the patient include bending
the newborn’s knees and flexing the hips, and using a paci-
fier with sugar water. These techniques should be attempted
after the stomach has been decompressed with a 10 French
to 12 French orogastric tube. After palpating the liver edge,
the examiner’s fingertips should slide underneath the liver in
the midline. Slowly, the fingers are pulled back down, trying
to trap the “olive.” Palpating the pylorus requires patience
and an optimal examination setting. If palpated, no further
studies are needed. If the hypertrophied pylorus cannot be
palpated, ultrasound (US) is the next step.
US has become the standard technique for diagnosing
HPS and has supplanted the physical examination at most
institutions. The diagnostic criteria for pyloric stenosis is a
muscle thickness of ≥4 mm and a pyloric length of ≥16 mm
(Fig. 29.1).20 A thickness of >3 mm is considered positive if
the neonate is younger than 30 days of age.21 The study is
dependent on the expertise of the US technician and radiol-
ogist. There are reports of nonradiologists performing US for
diagnosing HPS, which would obviously reduce the need
for the US technician.22,23 If the US findings are equivocal,
then an upper gastrointestinal series can be helpful in con-
firming the diagnosis (Fig. 29.2).
In the past, the diagnosis was often delayed and profound
dehydration with metabolic derangements was common.
Today, however, primary care physicians are more aware
of the problem and the availability of US facilitates an ear-
lier diagnosis and treatment of HPS. However, the com-
plete differential diagnosis for nonbilious vomiting should
be considered. This includes medical causes such as GERD,
gastroenteritis, increased intracranial pressure, and meta-
bolic disorders. Anatomic causes include an antral web,
foregut duplication cyst, gastric tumors, or a tumor causing
 

A B
Fig. 29.1  Ultrasonography has become the standard imaging study for diagnosing pyloric stenosis and has supplanted physical examination at most
institutions. The (A) transverse and (B) longitudinal views of hypertrophic pyloric stenosis are seen here. Muscle thickness ≥4 mm on the transverse
view or a length ≥16 mm on the longitudinal view is diagnostic of pyloric stenosis. On this study, the pyloric wall thickness was 5 mm and the length
(arrows) was 20 mm.
Fig. 29.2  At some hospitals outside of urban centers, ultrasound tech-
nicians and radiologists proficient in performing an ultrasound study
for pyloric stenosis are not available. Also, in some instances, an ultra-
sound study can be equivocal. An upper gastrointestinal series can
be helpful in making the diagnosis of pyloric stenosis or confirming
an equivocal ultrasound study. In this upper gastrointestinal study,
note the “string sign” indicating a markedly diminished pyloric chan-
nel (arrow) and subsequent gastric outlet obstruction. It is important
to evacuate the contrast material after this study to reduce the risk of
aspiration and pulmonary complications.
TREATMENT
The mainstay of therapy is typically resuscitation fol-
lowed by pyloromyotomy. There are reports of medical
treatment with atropine and pyloric dilation, but these
treatments require long periods of time and are often not
effective.24–29
Once the diagnosis of HPS is made, feedings should be
withheld. Gastric decompression is usually not necessary but
occasionally may be required in extreme cases. If a barium
29 • Lesions of the Stomach 479
study was performed, it is important to remove all of the con-
trast material from the stomach to prevent aspiration.
The hallmark metabolic derangement of hypochloremic,
hypokalemic metabolic alkalosis is usually seen to some
degree in most patients. Profound dehydration is rarely
seen today, and correction is usually achieved in <24
hours after presentation. A basic metabolic panel should
be ordered, and the resuscitation should be directed toward
correcting the abnormalities. Most surgeons use the serum
carbon dioxide (<30 mmol/L), chloride (>100 mmol/L),
and potassium (4.5–6.5 mmol/L) levels as markers of ade-
quate resuscitation. Initially, a 10- to 20-mL/kg bolus of
normal saline should be given if the electrolyte values are
abnormal. Then D5/½NS with 20–30 mEq/L of potassium
chloride is started at a rate of 1.25–2 times the calculated
maintenance rate. Electrolytes should be checked every 6
hours until they normalize and the alkalosis has resolved.
Subsequent fluid boluses are given if the electrolytes remain
abnormal. Then the patient can safely undergo anesthe-
sia and operation. It is important to appreciate that HPS is
not a surgical emergency and resuscitation is of the utmost
priority. Inadequate resuscitation can lead to postopera-
tive apnea due to decreased respiratory drive secondary to
metabolic alkalosis.30
After general anesthesia has been induced, an abdominal
examination should be performed to physically check for an
“olive” if one was not detectable preoperatively. The pylo-
romyotomy may be performed by the open technique or by
the minimally invasive approach. The laparoscopic tech-
nique has become the standard approach in the last 5–10
years. The anesthesiologist can pass and leave a suction
catheter in the stomach for decompression and for instilling
air after the pyloromyotomy to check for a leak.
The Open Approach
Historically, several different incisions have been described
for the open approach. The typical right upper quadrant
480 Holcomb and Ashcraft’s Pediatric Surgery
A case in the French literature in 1990).31 Since then, this
B test. Alternatively, an open approach can be used to intro-
Fig. 29.3 These two children underwent open pyloromyotomy
through a right upper quadrant transverse incision. Over time, the cos-
metic appearance of their incision is not as attractive as that seen after
the laparoscopic operation.
transverse incision seems to be used most commonly (Fig.
29.3). An alternate, more cosmetically pleasing incision
involves an omega-shaped incision around the superior
portion of the umbilicus followed by incising the linea alba
cephalad. With either incision, the pylorus is exteriorized
through the incision. A longitudinal serosal incision is made
in the pylorus approximately 2 mm proximal to the junc-
tion of the duodenum and is carried onto the anterior gas-
tric wall for approximately 5 mm. Blunt dissection is used to
divide the firm pyloric fibers. This can be performed using
the handle of a scalpel. Once a good edge of fibers has been
developed, a pyloric spreader or hemostat can be used to
spread the fibers until the pyloric submucosal layer is seen.
The pyloromyotomy is then completed by ensuring that all
fibers are divided throughout the entire length of the inci-
sion. This is confirmed by visualizing the circular muscle
of the stomach proximally as well as a slight protrusion of
the submucosa. The most common point of mucosal entry
is at the distal part of the incision at the duodenal-pyloric
junction. Therefore, care must be exercised when divid-
ing the fibers in this region. The pyloromyotomy can be
checked for completeness by rocking the superior and infe-
rior edges of the myotomy back and forth to ensure inde-
pendent movement. The mucosal integrity can be checked
by instilling air through the previously placed suction
catheter. If there are no leaks, the air should be suctioned.
Minor bleeding is common and should be ignored because it
will cease after the venous congestion is reduced when the
pylorus is returned to the abdominal cavity. The abdominal
incision is then closed in layers. 
The Laparoscopic Operation
Neonatal laparoscopy has grown in popularity with the
refinements in technique and smaller instruments. The
first reported laparoscopic pyloromyotomy in the English
language was in 1991 (the authors had reported the first
procedure has been accepted by most pediatric surgeons.
Critics of the procedure argue that laparoscopic pyloromy-
otomy exposes the patient to undue risks compared with
the open technique. However, randomized prospective tri-
als and subsequent meta-analyses have not shown any
difference in complication rates.32–37 More recent analysis
of the NSQIP database shows that open pyloromyotomy
is associated with in increased length of stay compared to
laparoscopic pyloromyotomy.38 The minimally invasive
approach is similar to laparoscopic appendectomy in terms
of acceptance and has become the standard technique for
pyloromyotomy in most centers.
The technique involves entering the abdomen through
an umbilical incision. A Veress needle is placed at the base
of the umbilicus between the umbilical arteries. It is impor-
tant to ensure proper placement of the Veress needle before
insufflation. This can be done by several simple methods,
including the “blind man’s cane” sweep and the water drop
duce the umbilical cannula. The abdomen is then insuf-
flated to a pressure of 10 mmHg and a 3- or 5-mm port is
introduced for the telescope and camera. Two stab incisions
are made. One stab incision is in the right paramedian side
of the abdomen at the level of the umbilicus, and the other
is in the left paramedian side of the abdomen just superior to
the umbilicus (Fig. 29.4).
Local anesthesia is used at all incisions. An atraumatic
bowel grasper is placed through the left incision, and a knife
or long cautery tip is introduced through the right inci-
sion (see Fig. 29.4). The duodenum is grasped firmly just
distal to the pylorus, and the pylorus is maneuvered into
view. Occasionally, a transabdominal stay suture wrapping
around the falciform ligament is helpful to elevate the liver
away from the pylorus. A longitudinal pyloromyotomy is
then made with either the knife or the electrocautery in a
manner similar to the open technique (Fig. 29.5). Initially,
a retractable arthrotomy knife was used. However, this is
no longer on the market in the United States. Most surgeons
now use an unguarded arthrotomy knife or the spatula
tip electrocautery blade (see Fig. 29.5A,B), which appear
equivalent in operative time and complications.39 A lapa-
roscopic pyloric spreader or a box-type grasper can be used
to complete the myotomy (see Fig. 29.5C). Completeness of
the myotomy and mucosal integrity is checked in a similar
 29 • Lesions of the Stomach 481

manner as the open technique. Omentum can be placed
over the myotomy to help with hemostasis, if necessary.
The stomach can be inflated with air through an orogastric
tube to evaluate for perforation. However, in one study in
which there were two perforations, inflating the stomach
did not detect the leak.38 The leaks were detected by careful
inspection of the pyloromyotomy. The pneumoperitoneum
is evacuated after the instruments are removed. The umbi-
licus is closed with absorbable suture, and the stab incisions
are closed with skin adhesive. 

POSTOPERATIVE CARE
Postoperative care is similar for both surgical techniques,
assuming the submucosa is intact. Complicated feeding
regimens have been advocated in the past. However, recent
studies support the use of ad libitum feeds in the early post-
operative period. This results in a faster time to full feeds
and quicker discharge.34,40–43 If postoperative emesis is
encountered, it is suggested to “feed through it.” At our
institution, we limit the feedings to a maximum of 3 ounces
every 3 hours. There are data to suggest that the degree and
duration of metabolic derangement affects postoperative
A feeding. Patients who required more complicated resuscita-
tion tend to take longer to reach full feeds and discharge.44
Pain is usually controlled with acetaminophen. Intrave-
nous fluids are discontinued when the patient tolerates a
2-oz feeding twice. The infant can be discharged when tol-
erating full feeds, which is usually on the first postoperative
day. 

B techniques.32,33,35–37
Fig. 29.4 Laparoscopic pyloromyotomy has become a common
approach for pyloric stenosis in infants. In the United States, the
sheathed arthrotomy knife is no longer available. Therefore, other tech-
niques are now utilized. (A) The atraumatic grasper that is holding the
duodenum is seen on the patient’s right (solid arrow). In the patient’s
left upper abdomen, a spatula tipped cautery (dotted arrow) has been
introduced to incise the serosa of the stomach. The 5-mm cannula has
been placed in the umbilicus through which an angled telescope is
introduced for visualization. (B) The stab incisions have been closed
with steri-strips.
COMPLICATIONS/OUTCOMES
The major complications of pyloromyotomy include
mucosal perforation, wound infection, incisional hernia,
prolonged postoperative emesis, incomplete myotomy,
and duodenal injury. There have been prospective and
retrospective studies that do not show any difference in
complication rates between the laparoscopic and open
In pooled analyses, perforation occurs in approximately
1%.45–47 If the disruption occurs at the duodenopyloric
junction, a simple interrupted absorbable suture can be
placed to close the defect and a patch of omentum can be
used to bolster the repair. This can be accomplished lapa-
roscopically depending on the experience of the surgeon.
Otherwise, the operation should be converted to open. If
the perforation is large or in the middle of the myotomy,
then the myotomy should be closed with absorbable suture.

A B C D

Fig. 29.5  These intraoperative photographs depict a laparoscopic pyloromyotomy. (A) The spatula-tipped cautery is being used to incise the serosa
and outer muscular layer of the hypertrophied pylorus. (B) The tip of the cautery is introduced into the hypertrophied muscle and twisted to break up
the muscle fibers and create a space for insertion of the pyloric spreader. (C) The pyloric spreader is introduced into the muscle and gently opened to
split the hypertrophied muscle fibers. The submucosa is visualized through the myotomy. (D) Air is introduced into the stomach to assess the integrity
of the mucosa.
482 Holcomb and Ashcraft’s Pediatric Surgery
A new myotomy can then be made 90–180° from the origi-
nal incision. Repairing this injury is difficult to perform lap-
aroscopically, so conversion is usually necessary. Feedings
should be held for 24 hours and then restarted. A water-
soluble contrast study can be performed if desired.
Duodenal injuries also can occur with either the laparo-
scopic or open approach. In a 25-year retrospective review
of 901 open pyloromyotomies performed between 1969
and 1994, there were 39 duodenal perforations that were
recognized intraoperatively and repaired. There were no
unrecognized duodenal perforations that developed after
the operation.36
Incisional hernias and wound dehiscence occurs in
approximately 1% of cases.32 Most hernia defects require
repair at some point. Laparoscopically, port site hernias
usually involve omentum protruding through the incision.
This can sometimes be managed at the bedside by cleansing
the area with povidone-iodine (Betadine), ligating and trim-
ming the extracorporeal omentum, elevating the abdomi-
nal wall to get the omentum back into the peritoneal cavity,
and using a fine absorbable suture to close the skin. Lapa-
roscopic pyloromyotomy also appears to have less wound
complications.36 When the open approach through a right
upper quadrant incision is used, the incision usually heals
nicely and looks cosmetically pleasing in the early postoper-
ative period. However, later in infancy and into adulthood,
these incisions enlarge and often contract, leading to a less
cosmetically pleasing appearance (see Figs. 29.3 and 29.6).
Postoperative emesis is common, occurring in most
patients at some point.44,48 Prolonged emesis is less com-
mon and ranges in incidence from 2–26%. Most commonly,
this is due to gastroesophageal reflux (25%) but can be sec-
ondary to incomplete myotomy (0–6%).33,48,49 It has been
suggested that the laparoscopic approach may be a risk fac-
tor for inadequate myotomy, but this is likely related to the
surgeon’s experience with this technique.32
In the past, the mortality from pyloric stenosis was con-
siderable and approached 50%. Today, however, mortality
is nearly zero with improvement in neonatal resuscitation
and anesthesia as well as surgical techniques. Morbidity
is also significantly lower than in the past, with an overall
complication rate between 1% and 2%. In addition, with
more pyloromyotomies being performed laparoscopically,
the cosmetic advantage of the minimally invasive tech-
niques cannot be overemphasized (see Fig. 29.6).50 
Pyloric Atresia
Pyloric atresia is a rare disease (1 in 100,000 live births)
and presents as symptoms of gastric outlet obstruction. The
disease is difficult to characterize because it is so rare. How-
ever, several generalizations can be made from looking at
larger series. Pyloric atresia may be associated with epider-
molysis bullosa and other gastrointestinal anomalies, such
as duplications.51–58 Pyloric atresia is diagnosed with a “sin-
gle bubble” on the abdominal radiograph (Fig. 29.7). The
diagnosis may be confirmed with a contrast study. Pyloric
atresia may occur as a web, a cord, or a gap between the
antrum of the stomach and the first portion of the duode-
num. Repair is performed after resuscitation. These infants
may have similar electrolyte abnormalities to infants with
HPS. Repair is usually with a Billroth type I (gastroduode-
nostomy) anastomosis. Morbidity and mortality are usually
related to the associated anomalies. 
Gastric Perforation
The causes of gastric perforation are spontaneous perfora-
tion of the newborn, iatrogenic perforation from instrumen-
tation, peptic ulcer disease, and trauma. Gastric perforation
usually presents as abdominal distention and signs of sepsis
or shock related to the perforation. The diagnosis is sus-
pected when a large amount of extraluminal gas is seen on
an abdominal radiograph.
Neonatal gastric perforations most commonly occur in
premature infants. About half of neonatal perforations are
spontaneous, and the other half are iatrogenic from instru-
mentation.59,60 Prematurity is associated with an increased
mortality.60 The perforations are usually managed with
laparotomy or laparoscopy. The perforation can usually be
closed primarily with or without an omental patch.59 Gas-
tric perforation due to peptic ulcer disease in infants and
children is very rare. Typically, perforation occurs at the
site of a prepyloric ulcer. Again, this may be repaired pri-
marily via laparotomy or laparoscopy with or without an
omental patch.59 
Peptic Ulcer Disease
Peptic ulcer disease and its complications are rarely seen in
children. However, there have been reports of neonatal and
pediatric bleeding ulcers, perforated ulcers, and gastric out-
let obstruction in children due to peptic ulcer disease.59–62
Peptic ulcer disease appears to be associated with Helico-
bacter pylori in the majority of pediatric cases. Treatment is
primarily directed at acid reduction and eradication of H.
pylori. Triple therapy with a proton pump inhibitor, amoxi-
cillin, and clarithromycin is typically used initially.63 For
strains that are resistant to clarithromycin, metronidazole
Fig. 29.6  The cosmetic advantage of the laparoscopic approach can-
not be overemphasized. This father of a baby with pyloric stenosis
underwent pyloromyotomy as an infant through a right upper abdomi-
nal incision.