Esophagitis is responsible for 15% to 19% of upper GI hemorrhage found in childhood (1). In infancy, esophagitis
often results from gastroesophageal reflux (GER). Although biopsy evidence of esophagitis is present in 61% to 83% of infants with GER, clinically apparent bleeding is unusual (2). Esophagitis usually causes occult blood loss and anemia. Acute bleeding from esophagitis is treated with nasogastric decompression, histamine-2 (H₂) antagonists, proton pump inhibitors, or oral antacids, and positional therapy. If nonoperative therapy is successful, reflux is documented, and medical management is instituted. If medical management does not control reflux, an antireflux operation is performed. Severity of esophagitis has not been shown to correlate with the need for antireflux surgery (3).

Variceal hemorrhage is an important cause of 7% to 10% of upper GI hemorrhage in children and adolescents (4). Most children with portal hypertension and variceal hemorrhage present before 5 years of age. Portal hypertension in children results from both extrahepatic and intrahepatic causes. Among the known causes of extrahepatic portal hypertension are neonatal omphalitis, umbilical vein catheterization, and portal vein hypoplasia associated with Klippel-Trenaunay syndrome. Intrahepatic portal hypertension most commonly results from cirrhosis secondary to biliary atresia. Nonoperative management includes endoscopic variceal ligation or injection, placement of a Sengkstaken-Blakemore tube, and use of intravenous octreotide or vasopressin (5). Operative management includes portosystemic shunts, variceal ligation, esophageal division, and esophageal devascularization.

Gastritis is responsible for 13% to 22% of pediatric upper GI hemorrhage and may be defined as primary or secondary. Primary gastritis in children is most often due to Helicobacter pylori infection. This rarely results in symptomatic gastritis (6). Its importance lies in its relation to peptic ulcer disease in children. Secondary gastritis resulting in GI hemorrhage can occur secondary to mechanical injury to the gastric mucosa as occurs with long-term nasogastric suction, or due to stress ulceration of the stomach. Premature infants and children sustaining trauma, burns, or serious medical illnesses are at risk for developing stress ulcers. Stress ulceration has been found to be responsible for approximately 10% of GI hemorrhage in pediatric intensive care patients (7). The pathophysiology of stress ulceration of the stomach is not fully defined. Important concepts include loss of mucosal barrier function, alterations in gastric microcirculation, back diffusion of hydrogen ion, and duodenogastric bile reflux. Neonates and children present with either “coffee ground” emesis or frank hematemesis. Children with significant ongoing bleeding should undergo prompt diagnostic endoscopy. Initial nonoperative management includes transfusion, correction of any coagulopathy, and the use of antacids, H₂-antagonists, proton pump inhibitors, or sucralfate. If correctable causes of stress exist, such as burn wound infection or intraabdominal abscess, they should be treated concurrently. If initial management does not succeed,
operative exploration should be performed, although this is uncommon in contemporary pediatric surgical practice.

Preoperative endoscopy can identify bleeding sites in the stomach in most patients. The presence or absence of associated duodenal bleeding from either duodenitis or peptic ulcer disease should be established prospectively. In the absence of duodenal bleeding, the initial operative maneuver should be a gastrotomy and the walls of the stomach inspected. The least ablative surgery should be performed. If possible, superficial erosions should be oversewn. Focal ulcers, Dieulafoy lesions, or isolated areas of bleeding can be resected locally or with a standard partial gastrectomy, but this is rarely necessary. Problems arise in patients with life-threatening hemorrhage from multiple sites on the gastric wall. Gastric devascularization has been used successfully to treat this condition (8). If this fails to stop the bleeding, total gastrectomy is an option. It is difficult to identify the appropriate application of vagotomy in these situations, but it may be recommended in children with associated duodenal ulcer disease.

Having discussed the operative management of the child with stress gastritis, it is important to emphasize the importance of prophylaxis. Stressed children should have aggressive attempts to raise their gastric pH to above 4.5 with either H₂-antagonists, proton pump inhibitors, or antacids. This is usually sufficient therapy.

Peptic ulcer disease can afflict children in all age groups. The capacity of the stomach to produce acid is present in the premature and full-term newborn infant (9). About one-half of children with acute ulcers present with GI hemorrhage. Gastric and duodenal ulcer disease is responsible for 18% and 11% of upper GI hemorrhage, respectively. Fortunately, this bleeding is usually not life threatening. Endoscopy should accurately localize the ulcer. Endoscopic techniques, such as heater probe coagulation or bipolar cautery, may be used to arrest the bleeding focus. If this fails, operation is necessary. Standard therapy includes exposure of the ulcer and three-point suture ligation of the ulcer bed. Ligation of the gastroduodenal artery may be beneficial. Vagotomy and a drainage procedure do not appear necessary for acute bleeding ulcers in children. After successful medical or surgical management, children are placed on an H₂-antagonist for 3 to 6 months. The Zollinger-Ellison syndrome should be considered in any child with multiple ulcers or recurrent ulcers. Serum gastrin levels are obtained to rule out this syndrome.

Lower GI hemorrhage is a common complication of a Meckel’s diverticulum. Most children affected are younger than 5 years of age (10). In 95% of cases, bleeding results from ulceration of adjacent ileal mucosa by heterotopic acid secreting gastric or pancreatic mucosa contained in the diverticulum. Bleeding is usually painless. The diagnostic test of choice is a technetium-99m pertechnetate scan (Fig. 71-1). Uptake of the isotope by the heterotopic mucosa allows identification of the bleeding source. The technetium scan is 85% sensitive and 95% specific for a Meckel’s diverticulum presenting with hemorrhage. Diagnostic yield of the scan can be increased by
pharmacologic intervention with H₂-blockers to inhibit isotope excretion from ectopic gastric mucosa. In addition, pentagastrin stimulates isotope uptake by the ectopic mucosa and glucagon decreases peristalsis, thereby increasing isotope retention time within the diverticula (11). Nonbleeding Meckel’s diverticuli can also be diagnosed by visceral angiography (12).

After the child is stabilized, the diverticulum is excised surgically. Care is taken to assess the adjacent ileum for the presence of an ulcer that may need to be resected with the diverticulum. Many Meckel’s diverticuli are amenable to laparoscopic excision.