Although the exact incidence of gastrointestinal (GI) bleeding in children is unknown, hematemesis, hematochezia, and melena are common and often anxiety-provoking medical conditions for parents, children, and emergency department (ED) providers. In healthy children, most GI bleeding is minor and self-limited, but occasionally can be life-threatening.

Although most children will be clinically stable, a child with massive GI bleeding may present critically ill and hemodynamically unstable, requiring rapid stabilization. The Pediatric Assessment Triangle facilitates a quick bedside assessment.¹

Once stability of a child’s airway, breathing, and circulation has been confirmed, obtain further history and a more complete physical examination to direct secondary management. Information regarding the color (red, coffee-ground, black, or tarry), timing, and volume (drops, “spoonful,” “cupful”) of bleeding is essential, although often difficult to accurately assess.² Associated symptoms such as abdominal pain, vomiting, fever, diarrhea, and stooling patterns may be helpful. A history of certain pre-existing medical conditions known to be associated with GI bleeding, such as coagulopathy, liver or bowel disease, or recent surgical procedures, may further direct care. A thorough medication history including prescription and non-prescription medicines, such as NSAIDs, corticosteroids, and anticoagulants, that are known to increase the risk for bleeding may help identify the cause.³ Also consider inadvertent or accidental ingestion of medications prescribed to close contacts.

The origin of GI bleeding is often difficult to visualize on physical examination. However, beyond the initial assessment, a focused methodical examination can reveal key diagnostic findings. Examine the nose and pharynx for extra-gastrointestinal bleeding sources such as epistaxis, oropharyngeal trauma, or post-tonsillectomy hemorrhage. Look for signs of liver disease, including jaundice, hepatosplenomegaly, and ascites. Bruising or petechiae may indicate an underlying coagulopathy or platelet disorder. In patients with suspected rectal bleeding, carefully examine the perineum, rectum, and anus for anal fissures, hemorrhoids, excoriated skin from diaper rashes, or signs of physical or sexual abuse.

Direct the diagnostic evaluation and treatment according to the child’s level of hemodynamic stability, history, and physical examination. Patients with small and self-limited GI bleeding who are clinically well-appearing require minimal diagnostic testing. If there is any question about the presence of blood, perform a guaiac or gastroccult test.⁴ Seemingly apparent bloody stool or vomitus may be caused by ingestions of red food dyes, medications (e.g., cefdinir and rifampin), and foods (e.g., beets) rather than true bleeding. Bismuth salicylate, iron supplementation, spinach, licorice, cranberries, and other foods can turn stools very dark and be mistaken for melena. False positive guaiac tests are rare but may be seen with ingestions of red meat or peroxidase-containing fruits and vegetables such as cauliflower, broccoli, turnips, or radishes.⁵

It is important to differentiate extra-gastrointestinal sources of bleeding, such as epistaxis, hemoptysis, hematuria, or menstrual blood, from GI bleeding. Newborns may present with either hematemesis or melena secondary to ingested maternal blood. Close examination of the mother’s breasts for fissures or bleeding or testing of breastmilk obtained via a breast pump may help identify the source of blood. When it is clinically necessary to differentiate maternal from infant blood, utilize the Apt–Downey test, in which adult hemoglobin turns brown in an alkaline environment, whereas infant hemoglobin remains pink. In confirmed GI bleeding, obtain a hematocrit to assess for anemia. However, since acute blood loss prior to crystalloid administration will not immediately result in a drop in hematocrit, serial hematocrit measurements are also needed. Order a platelet count and coagulation studies in patients with evidence of life-threatening GI bleeding. If there is concern for large or continued blood loss, order a type and screen (or type and cross if hemodynamic instability is imminent).

Gastric lavage may help identify an upper GI bleed as well as help assess the volume of ongoing hemorrhage. However, gastric lavage is rarely beneficial in practical management and is associated with significant discomfort and risk of aspiration.⁶ Patients with recurrent, continued, or massive GI bleeding may require specialty consultation for emergent endoscopy.

Upper GI bleeding is classically defined as occurring proximal to the ligament of Treitz, and may originate in the esophagus, stomach, or duodenum, with common pediatric causes varying by age (Table 72-1). Although hematemesis is the typical presentation of an upper bleed, 75% of children with bright red rectal bleeding will also have an upper source originating from a brisk upper bleed and rapid intestinal transit time. The distinction is important, as upper GI bleeding carries a higher mortality rate than lower GI bleeding.⁷ The primary focus should be resuscitation and stabilization followed by a diagnostic evaluation. Acute therapeutic interventions may depend on the source of bleeding, including vitamin K, parenteral proton pump inhibitors (PPIs), and octreotide infusion for significant variceal hemorrhage. ⁸

ESOPHAGUS

Inflammatory disorders of the esophagus can result in irritation of the mucosa and subsequent bleeding. Gastroesophageal reflux is the most common cause of esophageal inflammation and may present with regurgitation, abdominal or chest pain, cough, and food refusal.⁹ (See Chapter 73 for a detailed review of gastroesophageal reflux.) Esophageal infections from Candida, cytomegalovirus, and herpes occur most commonly in immunocompromised children presenting with severe chest or abdominal pain, fever, dysphagia, and odynophagia; if bleeding occurs, it is typically small in volume. Many patients with reflux esophagitis can be treated empirically with lifestyle modifications and acid suppression with either an H² antagonist or a PPI (Table 72-2). Children with infections of the esophagus often require further evaluation and possibly inpatient treatment depending on the severity of their symptoms.

Lacerations of esophageal mucosae (Mallory–Weiss tears) occur in patients with repeated retching, vomiting, or paroxysmal cough, typically occurring at the gastroesophageal junction or in the cardia of the stomach.^8,10,11 Abdominal pain is usually minimal, and bleeding is self-limited and relatively small in volume.^11,12 Most patients are successfully treated with antiemetics and acid suppression.¹²

Children with known liver disease and portal hypertension are at risk for esophageal varices, coagulopathy, and significant GI bleeding (Fig. 72-1). There is insufficient evidence to guide the management of children with esophageal varices. Much of the current evidence is extrapolated from adult studies and there is variation in care to some children.^12,13 Although self-limited in up to 50% of patients, variceal bleeding is associated with a mortality rate of up to 8%.^10,12 These patients may require packed red blood cells, platelet transfusions, and/or correction of coagulation defects with fresh frozen plasma (10–15 mL/kg) and vitamin K (5–10 mg, subcutaneously for non–life-threatening bleeding, intravenous for life-threatening bleeding). Endoscopy offers diagnosis as well as therapeutic sclerotherapy or banding in severe cases. Medical therapy with intravenous octreotide (loading dose: 1–2 μg/kg IV, max 50 μg; maintenance infusion: 1–2 μg/kg/h IV, max 50 μg/h) or vasopressin (starting dose: 0.002 units/kg/min IV; titrate to max of 0.01 units/kg/min) may control variceal bleeding in children with portal hypertension, either alone or in conjunction with endoscopic management.^10–12,14 Placement of a Senstaken–Blakemore tube can be a life-saving temporizing measure if pharmacologic and endoscopic methods fail to control massive variceal bleeding.^8,12

STOMACH/DUODENUM

Gastritis and peptic ulcer disease are common etiologies of upper GI bleeding (Fig. 72-2). Medications such as NSAIDs, corticosteroids, and iron increase the risk for gastric and duodenal mucosal inflammation.³ Infection with Helicobacter pylori is a common cause of gastric and duodenal ulcers in healthy children.¹⁵ Critically ill children are particularly at risk for development of “stress gastritis,” and prophylactic acid–suppression therapy is essential. Patients with gastritis or ulcers often present with epigastric or left upper quadrant abdominal pain relieved by eating. Hematemesis and melena are usually self-limited, although can be massive and even life threatening, particularly in the setting of ulceration and perforation.^8,12 Although the gold standard for the diagnosis of H. pylori infection is endoscopy with biopsy, noninvasive testing for H. pylori immunoglobulin G (IgG) serology and fecal antigen testing are reliable and highly sensitive.^15,16 In contrast to current guidelines for adults, the “test-and-treat” practice (the detection of H. pylori infection by a noninvasive test followed by treatment if positive test) is not recommended in children; antimicrobial therapy should be initiated only when H. pylori infection has been documented by histology, and whenever possible, an H. pylori strain antibiogram utilized in order to optimize the treatment.¹⁵ Gastritis and peptic ulcers can be treated with PPIs (Table 72-3) and close follow-up provided the bleeding is minimal and self-limited.¹⁵