C H A P T E R 2 9 
Lesions of the Stomach
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 gastroepi­
ploic 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 gastroesophageal
reflux and obesity, are covered elsewhere.
HYPERTROPHIC PYLORIC STENOSIS
Hypertrophic pyloric stenosis (HPS) is one of the most
common surgical conditions of the newborn.1–9 It occurs
at a rate of 1 to 4 per 1,000 live births in Caucasian
infants, but is seen less often in non-Caucasian 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 Premature 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 large role in the
pathophysiology. Circumstantial evidence for a genetic
predisposition includes race discrepancies, the increased
frequency in males, and the birth order (first-born infants
with a positive family history). Environmental factors
associated with HPS include the method of feeding
(breast vs formula), seasonal variability, exposure to
erythromycin, and transpyloric feeding in premature
infants.5–7 Additionally, there has been interest in several
gastrointestinal peptides or growth factors that may facil­
itate 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 environmen­
tal influences.
Diagnosis
The classic presentation of HPS is nonbilious, projectile
vomiting in a full-term neonate who is between 2 and 8
Curt S. Koontz  •  Mark L. Wulkan
weeks old. Initially, the emesis is infrequent and may
appear to be gastroesophageal reflux disease. 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 neonate usually
appears well if the diagnosis is made early. However,
depending on the duration of symptoms and degree of
dehydration, the neonate may be gaunt and somnolent.
Visible peristaltic waves may be present in the mid to left
upper abdomen. The pylorus may be palpable in 72–89%
of patients.11,12 To palpate the hypertrophied pylorus, the
baby must be relaxed. Techniques for relaxing the infant
include bending the knees and flexing the hips, and using
a pacifier 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 and down, trying to trap the ‘olive.’ Pal­
pating the hypertrophied pylorus requires patience and
an optimal examination setting. If palpated, no further
studies are needed. If the pylorus cannot be palpated,
ultrasound (US) should be performed.
Ultrasound has become the standard technique for
diagnosing HPS and has supplanted the physical exami­
nation at most institutions. The diagnostic criteria for
pyloric stenosis is a muscle thickness greater than or
equal to 4 mm and a pyloric channel length greater than
or equal to 16 mm (Fig. 29-1).12 A thickness of more than
3 mm is considered positive if the neonate is younger
than 30 days of age.13 The study is dependent on the
expertise of the ultrasound technician and radiologist.
There are reports of non-radiologists performing
ultrasound for HPS, which would obviously reduce the
need for the ultrasound technician.14,15 If the ultrasound
findings are equivocal, then an upper gastrointestinal
series can be helpful in confirming the diagnosis (Fig.
29-2).
In the past, the diagnosis was often delayed and pro­
found dehydration with metabolic derangements was
common. Today, however, primary care physicians are
more aware of the problem and the availability of ultra­
sound facilitates an earlier diagnosis and treatment.
However, the complete differential diagnosis for nonbil­
ious vomiting should be considered. This includes medical
causes such as gastroesophageal reflux, gastroenteritis,
increased intracranial pressure, and metabolic disorders.
Anatomic causes include an antral web, foregut duplica­
tion cyst, gastric tumors, or a tumor causing extrinsic
gastric compression.
403
404 SECTION IV  Abdomen

A B

FIGURE 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 greater than or equal to 4 mm on the transverse view or a length greater than or equal to 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.

necessary but occasionally may be required for extreme

FIGURE 29-2  ■  At some hospitals outside of urban centers, ultra-
sound technicians and radiologists proficient in performing an
ultrasound study for pyloric stenosis are not available. Also, in
some instances, an ultrasound study can be equivocal. An
upper gastrointestinal series can be helpful in making the diag-
nosis of pyloric stenosis or confirming an equivocal ultrasound
study. In this upper gastrointestinal study, note the ‘string sign’
indicating a markedly diminished pyloric channel (arrow) and
subsequent gastric outlet obstruction. It is important to evacu-
ate 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 therapy and are often
not effective.16–20
Once the diagnosis of HPS is made, feedings
should be withheld. Gastric decompression is usually not
cases. If a barium study was performed, it is important to
remove all of the contrast material from the stomach to
prevent aspiration and pulmonary complications.
The hallmark metabolic derangement of hypochlo­
remic, hypokalemic metabolic alkalosis is usually seen to
some degree in most patients. Profound dehydration is
rarely seen today, and correction is usually achieved in less
than 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 resuscitation. Initially, a 10–20 mL/kg bolus
of normal saline should be given if the electrolytes
are abnormal. Then, D5/1/2NS with 20–30 mEq/L of
potassium chloride is started at a rate of 1.25 to 2 times
the calculated maintenance rate. Electrolytes should be
checked every six hours until they normalize and the alka­
losis has resolved. Subsequent fluid boluses are given if
the electrolytes remain abnormal. It is important to
appreciate that HPS is not a surgical emergency and
resuscitation is the initial priority. Inadequate resuscita­
tion can lead to postoperative apnea due to a decreased
respiratory drive secondary to metabolic alkalosis.
The pyloromyotomy can be performed by the stand­
ard open technique or by the minimally invasive approach.
The anesthesiologist should pass and leave a suction cath­
eter in the stomach for decompression and for instilling
air after the pyloromyotomy to check for a mucosal leak.
The Open Approach
Several incisions have been described for the open
approach. The typical right upper quadrant transverse
incision seems to be used most commonly (Fig. 29-3).
An alternate more cosmetically pleasing incision involves

A case in the French literature in 1990).21 Since then, this
B can be used to introduce the umbilical cannula. The
FIGURE 29-3  ■  These two children underwent open pyloromyo-
tomy through a right upper quadrant transverse incision. Over
time, the cosmetic appearance of their incision is not as attrac-
tive as that seen after the laparoscopic operation.
an omega-shaped incision around the superior portion of
the umbilicus followed by incising the linea alba cepha­
lad. 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
junction of the duodenum and is carried onto the anterior
gastric wall for approximately 5 mm. Blunt dissection is
used to initially 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 through­
out the entire length of the pyloromyotomy. This is con­
firmed by visualizing the circular muscle of the stomach
proximally as well as a slight protrusion of the submu­
cosa. The most common point of mucosal entry is at the
distal part of the incision at the duodenal–pyloric junc­
tion. Therefore, care must be exercised when dividing the
29  Lesions of the Stomach 405
fibers in this region. The pyloromyotomy can be evalu­
ated for completeness by rocking the superior and infe­
rior edges of the myotomy back and forth to ensure
independent 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
refinement 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 this approach argue that laparoscopic pyloro­
myotomy exposes the patient to undue risks compared
with the open technique. However, recent randomized
prospective trials have not shown any difference in com­
plication rates.22,23 Operative times can vary depending
on the experience of the surgeon. The minimally invasive
approach for pyloromyotomy is similar to laparoscopic
appendectomy in terms of acceptance and has become
the standard technique for pyloromyotomy in many
centers.
The technique involves entering the abdomen through
an umbilical incision. A Veress needle is inserted at the
base of the umbilicus between the umbilical arteries. It is
paramount 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 test. Alternatively, an open approach
abdomen is then insufflated to a pressure of 10 mmHg
and a 3 mm or 5 mm port is introduced for the telescope
and camera. Two stab incisions are made. One 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.
Local anesthesia is instilled at all incisions. An atrau­
matic bowel grasper is inserted through the patient’s right
incision, and a pylorotome or spatula cautery tip is intro­
duced through the patient’s left incision (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 falci­
form ligament is helpful to elevate the liver away from
the pylorus. A longitudinal pyloromyotomy is then made
with the knife or cautery in a similar manner as the open
technique (Fig. 29-5). Initially, a retractable arthrotomy
knife was used; however, it is no longer available in the
USA. Thus, most USA pediatric surgeons now use an
unguarded arthrotomy knife or the cautery. Once the
seromuscular layer is incised, a laparoscopic pyloric
spreader or a box-type grasper is inserted to perform the
myotomy. Completeness of the myotomy and mucosal
integrity are checked in a similar manner as the open
technique. Omentum can be placed over the myotomy to
406 SECTION IV  Abdomen

help with hemostasis. The pneumoperitoneum is evacu­

ated after the instruments are removed. The umbilicus is
closed with absorbable suture, and the stab incisions are
closed with skin adhesive (see Fig. 29-4B).

A encountered, it is suggested to ‘feed through it.’ At our
B
FIGURE 29-4  ■  Laparoscopic pyloromyotomy has become a
common approach for pyloric stenosis in infants. In the USA,
the sheathed arthrotomy knife is no longer available. Therefore,
other techniques 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.
Postoperative Care
Postoperative care is similar for both operative approaches,
assuming the mucosal integrity of the stomach is intact.
Complicated feeding regimens have been advocated in
the past. However, more recent studies support the use
of ad libitum feedings in the early postoperative period.
This results in a faster time to full feeding and earlier
discharge.24,25 In many centers, if postoperative emesis is
institution, we limit the feedings to a maximum of 3 oz
every three hours. There are data to suggest that the
degree and duration of preoperative metabolic derange­
ment affects the postoperative feeding schedule. Babies
who required more complicated resuscitation tend to
take longer to reach full feeding and discharge.26
A survey about postoperative feeding regimens in
pediatric surgery residency training centers in North
America was recently performed. Thirty-two of the 47
institutions responded to the survey. The average time
from operation to initiation of feedings was 4.3 hours.
There was a wide variability in responses, but 26 of the
32 responding programs employ a protocol-based feeding
regimen.27
A prospective randomized trial recently compared a
protocol-based feeding regimen to ad libitum feeding
after laparoscopic pyloromyotomy.28 Feeding was begun
two hours after laparoscopic pyloromyotomy in both
groups. The ad libitum group was allowed formula or
breast milk two hours after the operation and was con­
sidered ready for discharge after tolerating three
consecutive feeds without emesis. The babies who
underwent feeding via protocol were given Pedialyte two
hours after the operation followed by another round of
Pedialyte, which was followed by two rounds of half
strength formula or breast milk, followed by two rounds
of full strength formula or breast milk, followed by the
home feeding regimen. The baby was discharged on the
home feeding regimen if doing well. With a power of 0.9

A B C D

FIGURE 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 hyper-
trophied 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.
 29  Lesions of the Stomach 407

and an alpha of 0.05, a sample size of 150 patients was
calculated. There were no differences in patient charac­
teristics at presentation. The ad libitum group reached
goal feeding sooner than the group who were fed via
protocol (Table 29-1). However, this did not translate
into a difference in length of postoperative hospitaliza­
tion. There were more patients with emesis in the ad
libitum group after reaching goal feedings. There was no
difference in readmission rates, as two patients in each
group were readmitted after discharge.28
Postoperatively, pain is usually controlled with aceta­
minophen. Most infants are ready for discharge on the
first postoperative day.
Complications
The major complications of pyloromyotomy include
mucosal perforation, wound infection, incisional hernia,
prolonged postoperative emesis, incomplete myotomy,
and duodenal injury. There are prospective randomized
trials that do not show any difference in complication
rates between the laparoscopic and open techniques.22,23
Mucosal perforation occurs in 1–2% of cases.22,23 If the
disruption occurs at the duodenopyloric junction, a
simple interrupted absorbable suture can be used to close
the defect and a patch of omentum can be positioned over
the closure. This can be accomplished laparoscopically
depending on the surgeon’s experience. Otherwise, the
laparoscopic procedure 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 new myotomy can then be made 90–180° from
the original incision. 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 lapar­
oscopic 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 devel­
oped after the operation.29
Wound infections also occur in 1–2% of cases.22,23
There are no data to support the use of prophylactic
perioperative antibiotics because a pyloromyotomy is
considered a clean procedure. Local wound care is usually
sufficient to treat these infections.
Incisional hernias and wound dehiscence occurs in
approximately 1% of cases.22 Most hernias 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, ligating and trimming the
extracorporeal omentum, elevating the abdominal wall to
get the omentum back into the peritoneal cavity, and
using fine absorbable suture to close the skin.
Postoperative emesis is common, occurring in most
infants to some degree. Prolonged emesis is less common
and ranges in incidence from 2–26%. Most commonly,
this is due to gastroesophageal reflux but can occur sec­
ondary to an incomplete myotomy. It has been suggested
that the laparoscopic approach may be a risk factor for
inadequate myotomy, but this is likely related to the sur­
geon’s experience with this technique.24
Outcomes
In the past, the mortality from pyloric stenosis was con­
siderable and approached 50%. Today, however, mortal­
ity 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 1–2%. Additionally,
with more pyloromyotomies being performed laparo­
scopically, the cosmetic advantage of the minimally inva­
sive technique cannot be overemphasized.
PYLORIC ATRESIA
Pyloric atresia is a rare disease (1 : 100,000 live births) and
presents with symptoms of gastric outlet obstruction. The
disease is difficult to characterize because it is so rare.
However, several generalizations can be made from looking

TABLE 29-1 Preoperative and Postoperative Data from a Prospective Randomized Trial Comparing Ad
Libitum Feeding to Feeding Using a Standardized Protocol after Laparoscopic
Pyloromyotomy28
Ad lib fed (n = 75; Mean Protocol fed (n = 75; Mean
Variable ± Standard Deviation) ± Standard Deviation) P value
Age (days) 39.9 ± 19.08 39.75 ± 14.90 0.93
Pre-op pyloric thickness (mm) 4.44 ± 0.84 4.43± 0.89 0.93
Pre-op pyloric length (mm) 19.56 ± 3.44 19.97 ± 3.64 0.48
Operating time (minutes) 20.63 ± 10.64 18.19 ± 7.99 0.11
Postoperative emesis pre-goal feed (number) 1.04 ± 2.16 0.57 ± 0.99 0.09
Number of patients with pre-goal feed emesis 45 (60%) 51 (68%) 0.40
Post-goal feed emesis (number) 1.05 ± 2.26 0.47± 2.79 0.16
Number of patients with post-goal feed emesis 31 (41%) 11 (14.6%) 0.0000
Doses of analgesia (number) 1.47 ± 1.38 1.56 ± 1.40 0.68
Time to goal feeds (hours) 9.15 ± 7.02 16.58± 7.86 0.0000
Length of stay after goal (hours) 16.18 ± 14.65 9.20 ± 6.15 0.0002
Length of stay after operation (hours) 25.39 ± 15.41 25.78 ± 10.05 0.85
Readmission for emesis 2 (2.6%) 2 (2.6%) 1.0