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Peptic Ulcer and Other Conditions of The Stomach: Epidemiology
Peptic Ulcer and Other Conditions of The Stomach: Epidemiology
Peptic Ulcer and Other Conditions of The Stomach: Epidemiology
Epidemiology
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of the Stomach antrum and has satisfied Koch’s postulates as a human path-
ogen causing primary ulceration and chronic-active gastritis in
children.15 The incidence of H. pylori infection is estimated to
L. R. Scherer III be 0.5% per year in industrialized countries16,17 and 3% to
10% per year in developing countries.18 The route of trans-
mission of H. pylori is postulated to be fecal-oral or oral-
oral.19,20 Risk factors associated with H. pylori infection in
children include crowded living conditions, endemic country
of origin, poor socioeconomic level, immigrant children, chil-
Acute and Chronic Peptic Ulcer dren born of recent immigrants, infected family members, and
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ethnicity.21 Pathologic conditions associated with H. pylori
Reports of peptic ulcer disease in infants and children date infection include nodular gastritis, primary duodenal ulcer,
back to 1826. A collective literature review on peptic ulcers gastric ulcers, Barrett esophagus, gastric cancer, and MALT
in 243 children was published by Bird and colleagues in lymphoma.22–25
1941.1 The series consisted of 119 patients who required sur-
gical treatment for peptic ulcer. Ulcers in infants aged 1 to 15
SECONDARY PEPTIC ULCER DISEASE
days of age characteristically presented acutely with hemor-
rhage or perforation without premonitory signs or symptoms. Secondary ulcers (stress ulcers) are acute ulcers in children
Preschool-aged children, on the other hand, frequently had a usually associated with major physical or thermal trauma, sep-
prodromal illness before the onset of hemorrhage or per- sis, shock, or other critical illness (see Table 79-1). Gastric
foration. The heterogeneity of the cause of the ulcers was stress ulcers are usually multiple superficial mucosal erosions
apparently not recognized, and these differences were found primarily in the fundus of the stomach. The cause of
ascribed to age. these ulcers has been related to one or a combination of three
The theories and etiology of peptic ulcer disease remained factors: (1) decreased mucosal blood flow, (2) disruption of
consistent for the next 45 years. Careful historical information the protective mucosal barrier, and (3) intraluminal acidity.26
regarding ulcer-like symptoms in children with no other iden- Stress ulcers account for 80% of the peptic disease seen during
tified causes and eliciting a family history of peptic ulcer dis- infancy and early childhood.27 Drug- and chemical-induced
ease were common in instances of primary gastroduodenal ulcers resemble stress ulcers in appearance and distribution.
ulceration.2,3 In 1984 Marshall and Warren4 reported a pos- The ulcer that occurs from intracranial disorders, however,
sible bacteriologic cause for primary ulcers. Secondary ulcers is usually a single, deep ulcer and prone to perforation
1029
1030 PART VII ABDOMEN
may be associated with gastritis that primarily involves the an- In the normal setting, this mucus provides an effective barrier
trum. The accumulation of clinical and laboratory studies pro- to the deleterious effects of acid.
vides strong evidence that H. pylori fulfills each of Koch’s Prostaglandins protect against the development of experi-
postulates as a cause of chronic active gastritis in humans.15 mentally induced stress ulcers.55 The mechanism is uncertain
The flagella-bearing H. pylori organisms require a microaero- but may be related to prostaglandin’s stimulation of chloride
bic environment for culture, reflecting their environmental ion transport out of the cell in exchange for bicarbonate
niche to navigate through the thick and viscous mucus layer ion, which blocks cyclic adenosine monophosphate (AMP)
to reach the apical layer of the gastric epithelium.42 All chil- generation. The available intracellular bicarbonate increases
dren infected with H. pylori appear to develop chronic-active the ability of the cell to buffer acid. Endogenous prostaglan-
gastritis. Most have asymptomatic infections that may never dins also have a role in maintaining adequate blood flow to
lead to clinically evident disease. Theories concerning the the gastric mucosa and stimulate production of mucus, im-
mechanism that causes inflammation include the bacterial proving the ability of the mucosa to withstand acid destruc-
production of urease and vacuolating cytotoxin. Urease hy- tion.56 Corticosteroids and NSAIDs have been implicated as
drolyzes urea to ammonia and bicarbonate at the gastric mu- causative agents in peptic ulcer disease. Studies have shown
cosal surface. Ammonia can be directly toxic to epithelial cells, the cytoprotective effect of prostaglandins, the development
and the concomitant increase in the mucosal surface pH may of ulcers during treatment with NSAIDs and corticosteroids,
interfere with gastric epithelial function such as production of and a decreased level of prostaglandins in the stomach during
mucus.43 This cytotoxin produces vacuoles in the cytoplasm treatment.35,57 Drugs can cause secondary ulcers by damaging
of eukaryotic cells in vitro. The gene (vacA) of this cytotoxin the mucosa and thereby allowing acid-peptic digestion. Aspi-
has two alleles and is variably expressed among isolates.44 rin is a common agent associated with medication-induced
CagA, a cytotoxic protein, has been isolated in approximately secondary ulcers. In general, drug-induced ulcers should re-
60% of H. pylori isolates, and its presence correlates strongly spond to cessation of the medication and conservative sup-
with the expression of the vacuolating cytotoxin.45 H. pylori portive treatment, unless complications develop.
that is present in a majority of patients with nodular gastritis,
gastric or duodenal ulcer, or in situ expression of cagA is
higher in duodenal ulcers (<0.05).46
Clinical Presentation
Cellular injury in the gastric and duodenal epithelium ini-
tiates the inflammatory infiltrate (see Table 79-2) in the gastric The clinical features of primary peptic ulcer disease in chil-
mucosa and includes monocytes, macrophages, and polymor- dren can easily be confused with those of many other disor-
phonuclear and plasma cells.47,48 These inflammatory ders; this similarity may inflate the actual incidence of ulcer
changes may be due to cagA expression and tumor necrosis disease in children (Table 79-3). Clinical symptoms in the
factor promoter,49 which may induce other cytokines includ-
ing interferon-g, interleukin-1 (IL-1), IL-2, IL-6, and IL-8.50
TABLE 79-3
Defensive Factors
Clinical Findings in Primary and Secondary Gastritis and Peptic
The presence of hydrochloric acid is required for ulcer forma- Ulcer Disease
tion even though hypersecretion is not usually present (except Disease Entity Signs and Symptoms
with Cushing ulcer). Most of the factors contributing to the
Primary gastritis Asymptomatic (most common)
development of stress ulcers reduce the ability of the stomach
Recurrent abdominal pain (any location)
mucosa to protect itself against acid injury.51 Investigators gen-
Epigastric pain
erally agree that mucosal ischemia is also implicated in the path-
Water brash, heartburn (gastroesophageal
ogenesis of stress ulcers (see Table 79-2).52 Normally, small reflux disease symptoms)
amounts of hydrogen ions diffuse into the mucosa but are rap- Vomiting, nausea, anorexia
idly cleared or neutralized if mucosal blood flow is adequate. Iron deficiency anemia
Ischemia reduces production of mucus and the capacity for Short stature, growth failure (?)
neutralization of acid entering the tissues, leading to an accu- Secondary gastritis Abdominal pain
mulation of hydrogen ions and subsequent mucosal ulceration. Upper gastrointestinal blood loss—
The adverse effect of ischemia on energy metabolism may be hematemesis, melena
an additional factor that reduces the ability of the mucosa to Epigastric pain localization (“crampy”)
defend itself against injury.53 Intravenous infusion of sodium Irritability, change in feeding patterns
bicarbonate administered during the experimental production Fatigue
of mucosal injury by hemorrhagic shock has a protective Iron deficiency anemia
effect.54 These findings suggest that ischemia, energy deficits, Primary peptic ulcer Chronic, recurrent abdominal pain
and systemic acidosis are important factors in the pathogenesis disease Episodic epigastric pain
of stress ulcers. In instances of medication-induced ulcers, the Vomiting, particularly recurrent
drug disrupts the mucosal permeability barrier.29 A thick Nocturnal awakening
mucous gel is secreted from the superficial epithelial cells Anemia
and mucus cells throughout the stomach. The release of mucus Secondary peptic Life-threatening gastrointestinal bleeding
is stimulated by cholinergic agonists, prostaglandins, and ulcer disease Gastric or duodenal perforation
inflammatory or immune cytokines. The layer of mucus in Shock
the stomach is approximately 20 times the thickness of the Abdominal pain (rare)
surface epithelial cells and is full of charged protein particles.
1032 PART VII ABDOMEN
infant include refusal of feedings, persistent crying, and early diagnosis of acid-peptic disease are gastrointestinal
vomiting.6 The risk of a child developing an ulcer may be bleeding, dysphagia, persistent vomiting, and the abdominal
higher with a positive family history. Several studies present pain characterized earlier.65 Gastric analysis is not a useful
evidence that in an endemic population of infected parents, diagnostic test. Secondary ulcer was previously diagnosed
mothers in particular may play a key role in transmission of by contrast radiologic studies, angiography, laparotomy, and
H. pylori to the child.11 The diagnosis is often elusive until autopsy. The known occurrence of secondary ulcers in associ-
such complications as perforation or bleeding occur. Vomiting ation with physiologic stress should lead to the diagnosis
is common in preschool-aged and school-aged children with before signs and symptoms become catastrophic. Radiologic
peptic ulcers. Abdominal pain is recognized with increasing diagnosis can be difficult in the presence of hemorrhage
frequency as the child becomes older. The pain is often vague because blood clots can mask the ulcer; therefore endoscopy
and difficult to describe and may be related to meals or re- has become the standard for the diagnosis of the acute bleed-
lieved by eating, as is seen in adults.34,58 In older children ing ulcer. In one report, endoscopy provided a diagnosis
and adolescents, the clinical presentation and natural history in 85% of children with upper gastrointestinal bleeding
of peptic ulcers are more comparable with those observed in compared with 62% using radiologic studies.66 Angiography
adults.59–61 The ulcers present with epigastric and nocturnal can be useful in locating a bleeding ulcer if the rate of
abdominal pain in teenagers with a positive family history of bleeding is at least 0.5 mL/min.67,68
peptic ulceration. In this setting, despite healing of the acute
ulceration, the natural history of this disease process is for H. pylori Invasive Methods: Endoscopy is the method of
the ulcer to recur. It is now clear that such ulcers are not choice to accurately diagnose peptic ulceration in children.
related to a genetic predisposition to hyperpepsinogenemia Nodularity in the antrum of the stomach is a specific (but
but are associated with H. pylori infection.14 Almost all patients not sensitive) feature indicative of active H. pylori infection
with primary peptic ulcer disease present with abdominal pain. in children. Biopsy specimens should be taken from the stom-
Unfortunately, psychogenic, recurrent abdominal pain of child- ach and tested for the presence of H. pylori by a variety of tech-
hood, the most common pediatric intestinal disorder, causes niques including staining of biopsy sections (silver, Giemsa,
nearly identical symptoms.62 Nocturnal awakening caused by Genta, acridine orange) and microscopic evaluation, culture,
episodes of abdominal pain may differentiate organic from and testing for the presence of urease activity. In children and
psychogenic origin. Gremse and Shakoor63 evaluated the pre- teenagers receiving concurrent therapy with a proton pump
dictive values of signs and symptoms of acid-peptic disease in inhibitor, biopsies should be performed on the body and
children in whom endoscopy confirmed the diagnosis. Six cardia (and, possibly, transition zones) of the stomach, as well
symptoms correlated significantly with acid-peptic disease: as from the antrum to reduce the chances of false-negative
epigastric pain, nocturnal pain, postprandial pain, water brash, results.69 Follow-up endoscopy is rarely necessary in pediatric
weight loss, and a family history of peptic ulcer disease. Only 7% populations, except in the setting of peptic ulceration asso-
of children with psychogenic recurrent abdominal pain report ciated with complications (e.g., massive hemorrhage or
pain occurring at night compared with 60% of children with perforation).
peptic ulcer disease. In a study of 110 children with duodenal Noninvasive Methods: Infection with H. pylori induces a vig-
ulcers, the mean age at diagnosis was 11.3 years; in 46% of orous immune response resulting in the presence of local and
children, some symptom of peptic ulcer disease manifested systemic antibodies. H. pylori-specific IgG antibodies are pre-
before 10 years of age.2 sent in serum, plasma, whole blood, saliva, gastric juice, and
Secondary ulcers are acute. Although the age of patients urine. The humoral immune response is less vigorous in chil-
with secondary ulcers ranges from 1 day to 18 years, most dren. Therefore the cutoff values established for use in adults
patients are younger than 6 years of age. Secondary peptic to determine the presence or absence of H. pylori infection are
ulcers are usually due to noxious agents (e.g., corticosteroids not appropriate in young children. Increasing concerns have
and NSAIDs) or after major stresses (e.g., burns, head injury, been raised about the utility of testing for antibodies in low-
systemic illness).21 In these settings, upper gastrointestinal prevalence settings, such as is the case for children and ado-
tract hemorrhage, vomiting, and perforation are frequent pre- lescents living in developed nations. Although immunoassays
senting features. Diagnosis is therefore more difficult and are relatively inexpensive and technically easy to perform,
usually made when a catastrophic event such as hemorrhage those used in children must first be validated in each country
or perforation occurs. Gastrointestinal bleeding, the predom- or region, using serum samples obtained from relevant popu-
inant presenting symptom of secondary ulcers, occurs in 92% lations.12 Breath testing using the stable isotope 13C- or radi-
of patients younger than 6 years of age.64 The ulcers tend not olabeled 14C-urea as substrate shows great promise as an
to recur after healing if either the offending agent or underly- alternative approach to noninvasively diagnose H. pylori infec-
ing disease predisposing to mucosal ulceration is successfully tion in adults. However, 14C-labeled substrates should not be
treated. used in children and women during their reproductive years.
Urea breath testing is accurate in children older than 2 years of
Diagnosis
age.70,71 A commercially available stool antigen test has been
Endoscopic diagnosis followed by treatment with histamine-2 reported to be highly accurate as a diagnostic test in adults. In
(H2)-receptor antagonists has changed the presentation and contrast to serology, in which antibody titers may remain ele-
course of acute ulcer disease in children. Before the use of vated for months after successful eradication of the organism,
endoscopy in children, patients with peptic ulcer disease the stool antigen test is reported to turn negative within a week
frequently presented with an acute surgical abdomen, massive after elimination of H. pylori. The accuracy of the stool antigen
hemorrhage, or perforation; the diagnosis was made at the test when used in pediatric populations in a variety of clinical
time of operation or autopsy. The present indications for the settings validates its usefulness.71,72
CHAPTER 79 PEPTIC ULCER AND OTHER CONDITIONS OF THE STOMACH 1033
Treatment
imidazole ring, is six to eight times more potent and is equally
The treatment of peptic ulcer disease in children is similar to effective (85% to 95%) in healing ulcers in 8 weeks. However,
that used in adults. Antacids and H2 receptor antagonists a relapse rate of 20% has been reported. Famotidine and niza-
(e.g., cimetidine) are the mainstays of medical therapy. Other tidine are other potent antagonists used in adults, but little in-
therapeutic agents include selective anticholinergic agents, formation regarding their use in children has been reported.
proton-pump inhibitors, cytoprotective agents, and anti- The cytoprotective effect of sucralfate results from a coating
infective agents (Table 79-4). action due to the negative charge of the sulfated disaccharide alu-
Omeprazole and lansoprazole, proton-pump inhibitors, minum salt that adheres to the positive protein charge of the in-
inhibit the stimulation of gastric acid secretion at the final jured mucosa. The compound also seems to stimulate mucus
common pathway (cyclic AMP-adenylate cyclase, Hþ-Kþ production and prostaglandin synthesis, bind bile salts, and
adenosine triphosphatase inhibition). Therefore all forms of neutralize pepsin and acid. The adult dosage is 1 g (1 g/10 mL
secretion (histaminergic, gastrinergic, and cholinergic) are slurry) four times per day; the childhood dose is 40 to 80 mg/
blocked. A pediatric dosage of omeprazole, 1 mg/kg/day up kg/day. Constipation is the only clinically significant side effect.
to 20 mg/day; or lansoprazole, 0.5 mg/kg/day up to 30 kg The E-type prostaglandins including misoprostol, en-
and then 30 mg daily in children greater than 30 kg, is effec- prostil, and arbaprostil are cytoprotective.35 The mechanism
tive in 95% of patients within 4 weeks.21,73 Although omep- of action that provides protection to the mucosa is related to
razole is well tolerated, side effects include headache, nausea, blocking production of cyclic AMP, stimulation of HCO3 ,
and abdominal pain. and an increase in mucosal blood flow. The adult dose
In children with documented H. pylori gastritis or duodenal is 200 mg four times daily, but there is little documented
ulcer, eradication of this microorganism requires the use information concerning experience in children.
of standard antimicrobial agents and bismuth preparations
(see Table 79-4). The current standard treatment consists of
Surgical Treatment
two antibiotics (choosing two of the following): amoxicillin
(50 mg/kg/day), clarithromycin (15 mg/kg/day), or metronida- Historically and presently, surgical management of peptic ul-
zole (20 mg/kg/day) and a proton pump inhibitor. Treatment cer disease has been reserved for complications such as perfo-
regimens include twice-daily dosing of antibiotics for 2 weeks ration, bleeding, obstruction, and intractable pain.59–61
and a proton-pump inhibitor for 4 weeks. The use of this triple Follow-up studies of children with primary ulcer disease trea-
therapy results in eradication of the infection in more than 80% ted medically revealed a high rate of recurrence after cessation
to 90% of patients.21,73 of treatment throughout childhood and into adult life.2,74
Antacids effectively neutralize acid secretion and heal Increasing numbers of these patients eventually required sur-
peptic ulcer disease compared with placebo (75% compared gical treatment. Because of the prolonged morbidity reported
with 40%). Unfortunately, compliance is disappointing, and in medically treated patients, earlier surgical intervention
the complications of the medications including diarrhea had been recommended.75 Vagotomy and pyloroplasty rather
and constipation are bothersome. Therapy requires antacid than gastric resection are recommended as effective treatment,
administration (0.5 mL/kg) 1 hour before meals, 3 hours after with a minimal effect on subsequent growth and develop-
meals, and at bedtime. ment.76 In the past decade, highly selective or parietal cell va-
Histamine is a stimulant of gastric secretion. H2 receptors gotomy has been used extensively in several centers to treat
are present on the gastric acid–producing parietal cells of the adult patients with peptic disease, but no series has been
stomach; H2 receptor antagonists inhibit responses to all se- reported in children. The high recurrence rate observed with
cretagogues and thus are effective in suppressing gastric this approach (10% to 15%) may be an issue; however, some
acid secretion. Cimetidine (20 to 40 mg/kg/day) was the first consider this rate to be acceptable in children because it may
commercially available antagonist. The antiandrogen side cause only minimal disturbance of growth and development
effects and the effects on the central nervous system are likely while providing a reasonably good long-term outcome.77
due to the imidazole ring of the compound, which inhibits the Bleeding or perforated ulcer that occurs in the first 1 to 2
cytochrome P450 system of the liver. Ranitidine (6 to 9 mg/kg/ weeks of life (unassociated with other illness or stress) appears
day PO or 2 to 4 mg/kg/day IV), an H2 antagonist that lacks an to be an acute ulcer resulting from hypersecretion of acid
caused by maternal gastrin. These ulcers are usually compli-
TABLE 79-4 cated by bleeding and often respond to orogastric decompres-
Three Recommended Combination Eradication Therapies sion, accompanied by careful saline lavage to keep blood clots
for Helicobacter pylori–associated Disease in Children evacuated from the stomach and appropriate volume replace-
ment. Perforation requires prompt surgical intervention with
Duration of Medications Dose Treatment
the simplest method (i.e., a Graham patch) to safely close the
Amoxicillin 50 mg/kg/day 14 days bid defect.60 If the operation is performed for hemorrhage, simple
Clarithromycin 15 mg/kg/day 14 days bid suture ligation of the ulcer bed should suffice.61 No evidence
Proton pump inhibitor 1 mg/kg/day 1 month bid suggests that these ulcers recur. Although the incidence of
Amoxicillin 50 mg/kg/day 14 days bid bleeding and perforation has diminished over the past 2 de-
Metronidazole 20 mg/kg/day 14 days bid cades, the complication of chronic obstruction from peptic ul-
Proton pump inhibitor 1 mg/kg/day 1 month bid cer disease is unchanged. In a recent 45-year review, Azarow78
Clarithromycin 15 mg/kg/day 14 days bid and colleagues described a persistently high incidence of
Metronidazole 20 mg/kg/day 14 days bid gastric outlet obstruction requiring surgical intervention.
Proton pump inhibitor 1 mg/kg/day 1 month bid Vagotomy and pyloroplasty or gastroenterostomy were used
1034 PART VII ABDOMEN
to relieve the obstructions. Chronic, partial gastric outlet ob- hemorrhage and be immediately available for surgical inter-
struction secondary to a congenital problem such as a duode- vention if necessary.
nal web79,80 or hypertrophic pyloric stenosis also can result in If massive hemorrhage continues or recurs despite drug
peptic ulcers in infants and children. It is important to identify and endoscopic therapy, surgical control is indicated. Massive
the cause in these instances because the ulcer can be completely hemorrhage has been defined as blood loss in a 24-hour pe-
eradicated by treatment of the distal obstruction. riod equal to the total estimated blood volume in infants youn-
ger than 2 years of age and as loss equal to half of the estimated
blood volume in older children (with 80 mL/kg used as an
ZOLLINGER-ELLISON SYNDROME
estimation of total blood volume). This definition correlates
The Zollinger-Ellison syndrome is relatively rare in children.81 with the report of Williams and colleagues,32 in which no
The diagnosis may be suggested by the presence of large gastric child recovered without surgical management if the rate of
rugal folds, duodenal dilatation, and edema of the small-bowel blood loss was more than 60% of the estimated total blood vol-
mucosa and can be confirmed by an elevated serum gastrin ume in 24 hours. The successful use of selective intraarterial
level. The calcium infusion test, reliable in both adults and chil- vasopressin to manage bleeding stress ulcer in a child has been
dren, has been used to confirm the diagnosis of hyper- reported,86 but others have not found this to be useful.33,87
gastrinemia. Treatment of the Zollinger-Ellison syndrome has Although bleeding often precedes perforation of a secondary
traditionally been total gastrectomy unless the primary pancre- ulcer, perforation can be the initial presentation and requires
atic tumor can be completely resected. Some reports suggest immediate operation.
that H2 receptor antagonists or proton-pump inhibitors can The surgical procedures used to treat stress ulcers have
eliminate the need for gastrectomy in children.82 The fact that ranged from simple closure of a perforation to oversewing
many of these endocrine tumors may be malignant suggests that of the base of a bleeding ulcer to gastrectomy.88 As a general
a careful evaluation of each case to determine its nature and rule, these ulcers are not associated with an ulcer diathesis and
long-term follow-up after treatment with H2 receptor antago- therefore should respond to the simplest procedure that effec-
nists or proton-pump inhibitors is necessary before reliable tively treats the presenting problem. Because stress ulcers are
conclusions about management can be drawn. In addition, oc- the result of an underlying disease, recurrence of the ulcer is
casionally the gastrin-producing tumors may occur in the wall possible if the underlying problem is unresolved; this fact
of the duodenum and require resection. The multiple endo- must therefore be considered when the appropriate operation
crine neoplasia type 1 syndrome may be present in 25% of is being selected. The simplest procedure, plication of the site
the cases. Somatostatin receptor scintigraphy is useful in detect- of perforation or oversewing of the bleeding point, is usually
ing primary and metastatic gastrinomas. effective. On the other hand, when it is apparent that the un-
derlying problem will remain unresolved for an extended pe-
riod, a more definitive ulcer procedure may be appropriate.
STRESS ULCER
Vagotomy and pyloroplasty are recommended most frequently
Prevention is the preferred treatment goal for stress ulcers. It because they rarely interfere with subsequent growth. Vagot-
has been shown experimentally that, under simulated clinical omy and antrectomy may occasionally be necessary to control
conditions, development of stress ulcers requires a low gastric the bleeding ulcer in patients with extensive burns and intra-
pH. The use of prophylactic antacids to maintain the gastric cranial problems.89 Antrectomy also may be necessary for
intraluminal pH at a value of 6 or greater is effective. Support- large perforations that cannot be managed by pyloroplasty, al-
ive care with improved ventilatory support, maintenance of though the possibility of serosal patching to close such large
vascular volume, correction of acid-base imbalance, and nutri- defects should be kept in mind. In adults, even total gastrec-
tional support may also contribute to the ability of the gastric tomy has been infrequently recommended for treating massive
mucosa to withstand acid-peptic injury. hemorrhage from multiple gastric ulcers. Such a procedure is
The effectiveness of H2 receptor antagonists and proton- rarely indicated in children. The surgeon who operates on a
pump inhibitors for the prevention of stress ulcers is ex- child for ulcer disease must remember that the patient must
tremely effective.83,84 An H2 receptor antagonist is probably continue to grow and develop; therefore the simplest, least
indicated in the prevention and treatment of Cushing ulcers, disruptive procedure should be selected. Evidence suggests
which are associated with gastric hypersecretion. that these children do have problems such as low hemoglobin
When a secondary ulcer presents as bleeding, immediate levels.90 Experimental evidence comparing the effects of gas-
supportive treatment with balanced salt solution and blood trectomy with vagotomy and pyloroplasty on growth and
transfusion is frequently adequate. Children who have expe- development in miniature swine91 suggests that vagotomy
rienced a major episode of upper gastrointestinal hemorrhage with pyloroplasty results in less growth disturbance. Follow-
or recurrent bleeding require endoscopy.85 Endoscopy for up data indicate that vagotomy with pyloroplasty is an
bleeding requires greater skill and greater technical demands effective method of treatment unassociated with substantial
than do other endoscopic procedures. The endoscopist long-term problems.76 In view of the reports of osteoporosis,
should have the knowledge and experience not only to iden- iron deficiency, and dumping noted in adults who have had
tify the source of bleeding but also to control it. Potential in- various operations for peptic ulcer disease,92,93 long-term
terventions include therapeutic injections (of hypertonic follow-up is essential. There are rare reports of adenocarcinoma
NaCl, epinephrine, or absolute ethanol) and cauterization occurring in gastric remnants after subtotal gastrectomy.94 The
with heater probe, bipolar coagulation, or laser (Nd:YAG or risk is higher after a Billroth II (gastrojejunostomy) anastomosis.
argon). If the endoscopist is not a surgeon, a pediatric surgeon One of our patients developed cancer in the gastric remnant at
should evaluate the child before emergency endoscopy. The age 23 years—12 years after a vagotomy and antrectomy for
surgeon may then be available to observe the source of a chronic obstructing duodenal ulcer. Other tumors may arise
CHAPTER 79 PEPTIC ULCER AND OTHER CONDITIONS OF THE STOMACH 1035
in the stomach and present with bleeding due to erosion. These is delayed, excessive distention of the stomach may lead to
include rare cases of gastric teratoma and instances of leiomyo- perforation. Because the obstruction is proximal to the am-
sarcoma and gastrointestinal stromal tumors (GIST). pulla of Vater, the passage of a meconium stool may mislead
the casual observer.
TABLE 79-5
Classification of Antral and Supraampullary Atresias
I. Pyloric
A. Membrane
B. Atresia
FIGURE 79-2 Incomplete antral diaphragm in a newborn. This infant had
II. Antral (1 cm or more proximal to pylorus) non-bile-stained vomitus shortly after birth. A dilute barium contrast swal-
A. Membrane low established the diagnosis of an incomplete obstruction. Treatment
B. Atresia with a Heineke-Mikulicz pyloroplasty and with excision of the web was
successful.
1036 PART VII ABDOMEN
Treatment Pyloric atresia can usually be recognized at the Outcomes Survival should be anticipated if diagnosis and
time of operation; a fibrous cord may join two blind ends surgical intervention occur early and if adequate supportive
(Fig. 79-3). Gastrotomy and distal passage of a catheter may care is provided. Death has been associated with delayed
be required to detect membranous obstructions (Fig. 79-4). diagnosis80,98,108 and associated conditions.109 Fifty-nine
Excision of a complete or partial diaphragm with Heineke- cases of congenital pyloric atresia have been reported. A famil-
Mikulicz or Finney pyloroplasty is the most straightforward ial occurrence was described in 13 infants in six families; an
corrective procedure. Haller and Cahill106 warn against miss- unexplained high-mortality rate was seen in this familial
ing a pyloric web in association with a duodenal atresia. They group. Some familial cases are associated with epidermolysis
recommend a wide gastrotomy and distal passage of a catheter bullosa.98,110 Junctional epidermolysis bullosa/pyloric atresia
after excision of the prepyloric diaphragm to identify an asso- syndrome is associated with extremely adverse outcomes due
ciated duodenal diaphragm. In the presence of pyloric atresia to the risk of sepsis, malabsorption, renal disease, and failure
with the atretic ends separated by a cordlike or discontinuous to thrive. Of the 70 cases presented in the medical literature,
segment, gastroduodenostomy is necessary. Dessanti107 and death occurred in 54 patients by 11 months of age. Of the 16
colleagues described an anatomic pyloric sphincter recon- survivors, all are plagued with complications of epidermal
struction procedure using the atretic cul-de-sac to perform disease ranging from 30 days to 16 years.100 Pyloric atresia
an end-to-end anastomosis. This procedure replaces the resec- associated with junctional epidermolysis bullosa results from
tion of the atretic segment and a side-to-side or end-to-oblique mutations in the PLEC1 gene. The lethal form is associated
anastomosis because of the size disparity between the stomach with intracellular degradation of beta-4 integrin.
and duodenum. A temporary decompression gastrostomy and
insertion of a transgastric feeding tube may be useful. Recent
Pyloric Duplication
advances in endoscopy have stimulated development of alter-
nate treatment strategies including balloon dilatation, laser Duplications of the stomach and pylorus are uncommon,
web excision, and laser radial incisions of a type I membrane. representing less than 3% of alimentary tract duplications.
The number of these cases is few, and long-term follow-up Pyloric duplications are slightly more frequent in girls. They
data are limited. share a common wall with the stomach or pylorus and rarely
communicate. Infants present with nonbilious vomiting and
weight loss in the first 2 to 3 weeks of life.111,112 The condition
may be mistaken for hypertrophic pyloric stenosis. Occasion-
ally, pyloric duplications present with a palpable mass, further
confusing this occurrence with hypertrophic pyloric stenosis.
The diagnosis is suggested by ultrasound studies that show a
cystic extraluminal mass compressing the gastric outlet.113
The condition may not be recognized until the time of oper-
ation. The procedure of choice is extramucosal excision.
Occasionally cyst-gastrostomy may be necessary. Postopera-
tive survival is expected and complications are few. Dupli-
FIGURE 79-3 Pyloric atresia. The seromuscular layers are uninterrupted. cation cysts affecting the stomach usually present later in
The tissue between the gastric and duodenal mucosa was of two types: life. Duplications are covered extensively in Chapter 90.
fibrous and areolar.
Radiologic Features B
Radiographic examination confirms the diagnosis of gastric FIGURE 79-5 Gastric volvulus. A, Organoaxial. The greater curvature
volvulus and often identifies underlying associated congenital usually passes forward, as depicted, but may rotate posteriorly. B, Mesen-
anomalies or defects. The radiographic features of acute vol- teroaxial. The pylorus or the cardia commonly rotates anteriorly, but the
vulus of the stomach include (1) localized massive distention opposite may occur. (With permission from Cole BC, Dickinson SJ: Acute
volvulus of the stomach in infants and children. Surgery 1971;70:707.)
TABLE 79-6
of the upper abdomen; (2) high greater curvature of the stom-
Anatomic Etiology of Gastric Volvulus
ach (87%); (3) greater curvature crossing the stomach (83%);
(4) fixation of the loop regardless of the position of the patient;
I. Absence, Failure of Attachment, or Elongation of Gastric Fixation (5) delimitation of ingested barium at the tapered extremity of
A. Gastrosplenic the esophagus, the so-called “bird’s beak”; (6) possible evi-
B. Gastrocolic dence of a hiatal sacculation or other diaphragmatic hernia-
C. Gastrohepatic tion; and (7) deviation of the position of the spleen.
D. Greater omentum
II. Disorders of Gastric Anatomy or Function Treatment
A. Acute or chronic distention
1. Gastric outlet obstruction Gastric volvulus may present acutely and require acute surgi-
2. Gastric hypomotility cal intervention to prevent or limit vascular compromise. Sim-
3. Massive aerophagia ple decompression with a nasogastric tube may temporize the
B. Peptic ulcer disease situation but is inadequate as a long-term treatment. At oper-
C. Neoplasm of the stomach ation, gastric decompression facilitates reduction. Once nor-
D. Hourglass stomach mal anatomic relationships have been restored, the site is
E. Gastric ptosis carefully inspected to identify possible areas of perforation
III. Abnormalities of Adjacent Organs or gangrene. The remainder of the procedure is focused on
A. Diaphragm preventing a recurrence of volvulus and correcting any dia-
1. Hiatal hernia, sliding or paraesophageal phragmatic defects (hiatal and Bochdalek hernias). In infants
2. Bochdalek’s hernia or other congenital defect and children, gastrostomy or anterior gastropexy is then per-
3. Diaphragmatic rupture formed. Several cases of successful outcomes using each of
4. Eventration of the diaphragm these techniques by open or endoscopic repair have been
5. Phrenic nerve palsy reported.114,115,118,121 Follow-up of these patients ranges
B. Splenomegaly, polysplenia from 1 to 10 years without recurrence. Recurrence despite
C. Volvulus of transverse colon fixation has also been reported.122 Outside of North America
D. Malrotation and midgut volvulus nonoperative treatment strategies are emerging in the manage-
E. Dislocation or hypoplasia of the left lobe of the liver ment of chronic volvulus. In Africa, Asia, and Europe, 36%
to 60% of infants and children are treated successfully
1038 PART VII ABDOMEN