Gastrointestinal (GI) bleeding produces alarm and anxiety in parents and physicians. Most causes of GI bleeding do not result in significant blood loss, and many cases of GI bleeding cease spontaneously. Larger volume bleeding can lead to hemodynamic compromise that requires aggressive resuscitation and intervention. A systematic approach to diagnosis is required.
DEFINITIONS
Hematemesis: Vomiting of either fresh or altered blood (such as coffee grounds emesis). Implies recent or continuing bleeding proximal to the ligament of Treitz.
Hematochezia: Bright red blood per rectum or maroon-colored stools. Usually originates in the colon. Upper GI hemorrhage can also present with hematochezia secondary to decreased transit time in infants or with brisk bleeding. Blood-streaked stools suggest a bleeding source in the rectum or anal canal.
Melena: Dark or black, tarry stools with a characteristic odor. Indicative of blood that has been in the GI tract for a long time, allowing the denaturation of hemoglobin by bowel flora. Melenic stools are typically from a hemorrhage originating proximal to the ileocecal valve.
Occult blood: Presence of blood in the stool that is not visible but is confirmed by chemical testing (i.e. guaiac.)
The history can be helpful in identifying the cause and location of bleeding in the GI tract (Table 25-1). Quantifying the volume and acuity of blood loss is important in understanding the risk of hemodynamic compromise. The character of the blood may indicate a more likely location of bleeding, though brisk bleeding from an upper GI source can cause hematochezia. Fever, recent travel, or known sick contacts may implicate an infectious source, while longer-standing symptoms and associated weight loss may indicate a more serious underlying cause such as inflammatory bowel disease (IBD). A complete medication history is essential, including recent use of nonsteroidal anti-inflammatory drugs (NSAIDs) or antibiotics. Certain foods (e.g. beets) or medications can also cause a red discoloration of GI fluids and be mistaken for hematemesis or melena.
Characteristics of Bleeding |
Quantity: volume of blood (few drops vs. a cup) |
Duration: intermittent bleeding, isolated episode, ongoing bleeding |
Character: bright red blood, coffee grounds emesis, melena, hematochezia |
Abdominal Complaints |
Bowel patterns: diarrhea (infectious) or constipation (fissures), change in stool color |
Abdominal pain: indicates inflammation or ischemia of bowel wall |
Painless bleeding: indicates Meckel diverticulum, duplication, vascular malformation, or polyps |
Abdominal distention: possible bowel obstruction |
Tenesmus or urgency to defecate: consider IBD or infectious colitis |
Dietary History |
Cow milk or soy formula: consider allergic colitis |
Breastfeeding: consider ingested maternal blood |
Ingestion of products mistaken for hematemesis: artificial food coloring, gelatin, artificial fruit drinks, certain antibiotics, and cough syrups |
Ingestion of products mistaken for melena: beets, iron supplements, dark chocolate, bismuth, spinach, blueberries, grapes, licorice, others |
Review of Systems |
General: fever, weight loss or gain, anorexia |
Skin: rash, vascular malformations, edema, jaundice, lymphadenopathy, easy bruising |
Extremities: arthralgia, arthritis, clubbing |
Genitourinary: hematuria |
Abdomen: distention, pain, bowel patterns, vomiting |
Ears, nose, and throat: pharyngitis, epistaxis |
Past Medical History |
Previous GI bleeding |
Liver disease: indicates possible variceal bleeding or coagulopathy |
Previous or recent hospitalization: stress gastritis |
Medications or ingestions: NSAIDs, aspirin, steroids, anticoagulants, alcohol, toxins (rat poison) |
Umbilical artery catheterization: risk for portal vein thrombosis |
Coagulopathy |
Recent antibiotic exposure: pseudomembranous colitis |
Presence of gastrostomy or nasogastric tube |
Family History |
IBD, peptic ulcer disease, polyposis, bleeding diatheses |
Social History |
Immediate contacts with similar symptoms: may indicate infectious cause |
Travel, camping, or daycare: consider infectious causes |
The physical examination can be helpful in determining the etiology of GI bleeding (Table 25-2). The first priority is a quick assessment to identify patients with hemodynamic compromise or shock who need immediate resuscitation. Vital signs should be monitored closely. Patients may lose up to 15% of blood volume without evidence of hemodynamic compromise, and the blood pressure may be maintained until the patient has lost as much as 30% of the blood volume.1 Once the patient is determined to be stable, a comprehensive history and physical examination should be pursued.
Vital Signs |
Fever: infectious causes or inflammatory diseases (IBD or HSP) |
Weight loss: chronic diseases (IBD, cystic fibrosis, liver disease) |
Tachypnea: hemodynamic compromise or acidosis |
Tachycardia: earliest sign of hemodynamic compromise |
Hypotension: present with significant blood volume loss |
General |
Distressed or toxic-appearing patient: hemodynamic compromise from significant hemorrhage or underlying process causing systemic illness (toxic colitis, intussusception, ischemic bowel, necrotizing enterocolitis) |
Well-appearing patient: less urgent causes of bleeding |
Failure to thrive: malnutrition from chronic diseases (IBD, cystic fibrosis, liver disease) |
Head, Eyes, Ears, Nose, and Throat |
Nose: evidence of epistaxis |
Eyes: scleral icterus (liver disease), iritis (IBD) |
Oropharyngeal: mucosal trauma or bleeding from posterior pharynx |
Cardiovascular |
Evidence of hemodynamic compromise: tachycardia, gallop rhythm, delayed capillary refill, poor perfusion |
Abdominal |
Abdominal tenderness: nonspecific but indicates inflammation or ischemic injury of the bowel |
Abdominal mass: intussusception, intestinal duplication may result in right lower quadrant masses |
Evidence of portal hypertension: hepatosplenomegaly, ascites |
Rectal examination: stool specimen for hemoccult testing, palpable polyp |
Perineal and anal inspection: skin tags (IBD), fissures, superficial skin breakdown or inflammation (streptococcal cellulitis) |
Extremities |
Clubbing: chronic diseases (cystic fibrosis, IBD, liver disease) |
Arthritis: IBD |
Skin |
Vascular malformations: syndromes with associated Gl vascular malformations (e.g. Klippel-Trénaunay syndrome, Rendu-Osler-Weber syndrome) |
Cutaneous or oral pigmentation: Peutz-Jeghers syndrome |
Purpura or petechiae: vasculitis (HSP) or bleeding diathesis |
Erythema nodosum: IBD |
The differential diagnosis of GI hemorrhage can be divided into upper and lower GI bleeding. Although certain causes are more likely in certain ages, there is considerable overlap between age groups. Patients with complex medical issues have special diagnostic considerations in the evaluation of GI bleeding. The causes of upper and lower GI bleeding are summarized in Tables 25-3 and 25-4, respectively.
Neonates and Young Infants | Older Infants, Children and Adolescents |
---|---|
Ingested maternal blood At delivery During breastfeeding Milk protein allergy Trauma (nasogastric tube) Gastritis Overwhelming illness Medications Idiopathic Ischemia Acidosis Esophagitis Reflux Infectious Necrotizing enterocolitis Coagulopathy Congenital malformations Duplication cyst Vascular malformation | Gastritis/ gastroduodenal ulceration Sepsis Stress Medications Ingestion Burns Increased ICP Ischemia Acidosis Helicobacter pylori* Esophagitis Reflux Infectious Ingestion Eosinophilic Esophageal foreign body Gastroesophageal varices Cirrhosis Extrahepatic portal vein thrombosis† Budd-Chiari syndrome± Nasopharyngeal bleeding source Epistaxis Tonsils Tooth extraction Coagulopathy Hemobilia Hepatic injury Trauma to intestinal mucosa Nasogastric tube Gastrostomy tube Mallory-Weiss tear Prolapse gastropathy Vascular anomalies† Hemangioma Dieulafoy lesion Telangiectasia Other Henoch-Schönlein purpura Crohn disease Pulmonary hemorrhage Congenital malformations† Duplication cyst |