9.2 GI Hemorrhage, Abdominal Trauma & Peritonitis

Acute Gastrointestinal Hemorrhage in Children

Pediatric GI bleeding ranges from self-limited mucosal oozing to exsanguinating hemorrhage from varices, peptic ulceration, Meckel diverticulum, or vascular malformations. The anatomic divider used on exams remains the ligament of Treitz: bleeding proximal to it is upper GI bleeding (UGIB); bleeding distal to it is lower GI bleeding (LGIB).

Hematemesis (bright red or coffee-ground) and melena point to an upper source. Hematochezia usually indicates a lower source, but a brisk upper bleed in a small child can transit rapidly and appear as bright red blood per rectum with shock—never exclude UGIB solely because blood is red. Age narrows the differential: neonates may have swallowed maternal blood, vitamin K deficiency bleeding, or coagulopathy; infants and toddlers may have anal fissure (painless streaks with hard stool), milk-protein colitis, intussusception, or Meckel diverticulum; older children and adolescents add peptic ulcer disease, varices from portal hypertension (biliary atresia sequelae, extrahepatic portal vein obstruction), inflammatory bowel disease, and Dieulafoy or polyp bleeding.

Resuscitation and Source Control

Protect the airway early if hematemesis is massive or consciousness is impaired—aspiration of blood is lethal. Establish reliable IV or intraosseous access, obtain type and crossmatch, CBC, coagulation studies, blood gas, and lactate, and begin volume resuscitation. Use blood products for hemorrhagic shock; massive transfusion protocols in children target balanced ratios of red cells, plasma, and platelets while monitoring ionized calcium and avoiding hypothermia. A restrictive transfusion threshold near 7 g/dL is appropriate for hemodynamically stable children without active coronary ischemia, but unstable ongoing hemorrhage overrides a fixed number—resuscitate to perfusion.

Pharmacologic adjuncts depend on etiology. High-dose proton-pump inhibition supports clot stability in peptic ulcer bleeding. In portal hypertensive variceal bleeding, octreotide (or similar somatostatin analogue) reduces splanchnic blood flow and portal pressure pending endoscopy. Correct thrombocytopenia and clotting factor deficiencies; vitamin K is given when deficiency is plausible. Definitive control is usually endoscopy (banding for esophageal varices; injection, clipping, or thermal therapy for ulcers). Refractory arterial bleeding may need angiographic embolization; surgical exploration remains the rescue for uncontrolled hemorrhage or perforation.

Abdominal Trauma

Children’s compliant rib cages and relatively large solid organs make blunt abdominal trauma common after motor vehicle collisions, falls, bicycle handlebar injuries, and nonaccidental trauma. The spleen and liver are the most frequently injured solid organs; kidney, pancreas, and hollow viscus injuries occur less often but carry high morbidity when missed.

Initial ATLS-style priorities remain airway, breathing, and circulation with hemorrhage control. A FAST exam can detect free intraperitoneal fluid in unstable patients, while CT with IV contrast defines injury grade in stable children. Contemporary pediatric trauma practice favors nonoperative management of hemodynamically stable solid-organ injuries: bed rest appropriate to grade, serial abdominal exams, hemoglobin trending, and activity restriction. Operative or angioembolization pathways are reserved for persistent hemodynamic instability, peritonitis suggesting hollow-viscus injury, or expanding hemorrhage.

PICU nursing surveillance focuses on delayed hemorrhage (especially spleen), rising abdominal girth, referred shoulder pain (Kehr sign with splenic blood irritating the diaphragm), tachycardia out of proportion to fever, and falling hematocrit. Handlebar or seat-belt signs raise concern for duodenal hematoma, pancreatic injury, or bowel perforation—persistently bilious output, amylase/lipase rise, or free air change the plan from observation to intervention. Always consider nonaccidental trauma when the history and injury pattern conflict.

Abdominal Compartment Syndrome

Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) threaten children after trauma, massive fluid resuscitation, burns, ascites, omphalocele/gastroschisis closure, and postoperative bowel edema. Rising pressure impairs venous return, cardiac output, renal perfusion, and diaphragmatic excursion, producing oliguria, escalating peak airway pressures or PaCO2, and progressive shock.

Intra-abdominal pressure is commonly estimated with bladder-pressure transduction via a Foley catheter using a standardized fill volume appropriate for pediatric size. Sustained elevation with new organ dysfunction—classically pressure in the range associated with ACS (often cited around >20 mmHg in adults, interpreted in children with size-adjusted concern and clinical context)—defines ACS. Medical decompression includes nasogastric and rectal decompression, maximizing abdominal wall compliance with adequate sedation and neuromuscular blockade when appropriate, draining ascites or fluid collections, and carefully managing fluids. Refractory ACS requires decompressive laparotomy and often temporary abdominal closure; closing the abdomen too tightly after congenital defect repair or trauma laparotomy can recreate the syndrome.

Peritonitis

Peritonitis is peritoneal inflammation from chemical irritation or bacterial contamination. In children, common PICU causes include perforated appendicitis, NEC-related perforation, trauma to hollow viscus, anastomotic leak after GI surgery, and spontaneous bacterial peritonitis in portal hypertension with ascites. Clinical findings include fever, tachycardia, abdominal rigidity, rebound tenderness, guarding, absent bowel sounds, and progression to septic shock with capillary leak.

Management pairs source control with resuscitation: IV fluid boluses titrated to perfusion, early broad-spectrum antibiotics covering enteric organisms and anaerobes (expand coverage for healthcare-associated flora when indicated), gastric decompression, and prompt surgical or interventional drainage. Imaging may show free air, abscess, or free fluid, but a board-like abdomen with sepsis should not wait indefinitely for perfect imaging. Postoperative peritonitis after intestinal anastomosis demands a high index of suspicion—new tachycardia, rising lactate, bilious wound drainage, or wound dehiscence are red flags.

Putting Hemorrhage, Trauma, and Peritonitis Together

A child with handlebar trauma who develops peritonitis and free air has hollow-viscus perforation until proven otherwise—antibiotics and surgery, not prolonged observation. A cirrhotic adolescent with massive hematemesis needs airway protection, octreotide, balanced transfusion without overfilling portal pressure unnecessarily, and banding. A trauma patient with climbing ventilator pressures, anuria, and high bladder pressure needs decompression, not more indiscriminate crystalloid. These pattern-recognition pathways are the high-yield CCRN Pediatric approach to abdominal emergencies.