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Emergency And Acute Medicine - Gastrointestinal Bleeding
Basic Overview
Gastrointestinal bleeding refers to blood loss originating anywhere along the GI tract. Upper gastrointestinal bleeding arises proximal to the ligament of Treitz, whereas lower gastrointestinal bleeding occurs distal to the ligament of Treitz to the anus. Overall mortality is approximately 10%, ranging from less than 5% in children to as high as 25% in adults older than 70 years. Upper GI bleeding accounts for most cases, with nonvariceal mortality of 6–8% and variceal bleeding mortality of 30–50%. Lower GI bleeding carries a mortality of 2–4%.
Common Causes And Mechanisms
Upper GI bleeding is most frequently due to ulcerative disease, particularly peptic ulcer disease associated with Helicobacter pylori infection or medication use such as NSAIDs, aspirin, glucocorticoids, potassium, and iron supplements. Other causes include gastric or esophageal erosions, reflux esophagitis, infectious esophagitis, pill-induced injury, foreign bodies, gastritis, and stress-related mucosal disease from trauma, burns, sepsis, or CNS injury. Portal hypertension leads to esophageal or gastric varices and portal hypertensive gastropathy. Vascular causes include arteriovenous malformations, Dieulafoy lesions, gastric antral vascular ectasia, and aortoenteric fistulas. Mallory–Weiss tears, tumors, pancreatic hemorrhage, hemobilia, and parasitic infections are less common causes.
Lower GI bleeding most often results from diverticulosis, colorectal cancer or polyps, colitis (ischemic, inflammatory, infectious, or radiation-induced), angiodysplasia, postpolypectomy bleeding, inflammatory bowel disease, anorectal sources such as hemorrhoids or fissures, rectal ulcers, and foreign bodies. In children, Meckel diverticulum and intussusception are the leading causes.
Clinical Presentation
Both upper and lower GI bleeding may present with hypovolemia. Upper GI bleeding typically causes hematemesis or coffee-ground emesis and melena, whereas lower GI bleeding usually presents with hematochezia. Rapid upper GI bleeding can also cause hematochezia. Patients may report abdominal pain, weakness, dizziness, dyspnea, confusion, or agitation.
History And Physical Examination
Key historical features include vomiting blood, black or tarry stools, bright red blood per rectum, abdominal pain, and symptoms of anemia or shock. Examination may reveal tachycardia, hypotension, pallor, dry mucous membranes, melena or hematochezia on rectal exam, and signs of shock.
Initial Evaluation Priorities
Essential evaluation includes CBC, coagulation studies, electrolytes, and assessment for hypovolemia. ENT examination helps differentiate hematemesis from hemoptysis. Nasogastric lavage may assist in identifying active upper GI bleeding, though its impact on outcomes is controversial. Rectal examination is necessary to assess stool color and identify anorectal sources while recognizing causes of false-positive or false-negative fecal occult blood tests.
Diagnostic Testing
Laboratory studies may reveal anemia, thrombocytopenia, coagulopathy, electrolyte abnormalities, elevated BUN-to-creatinine ratio suggestive of upper GI bleeding, and elevated lactate in shock. Imaging may include upright chest radiography if perforation or aspiration is suspected. Angiography and radionuclide scans can localize active bleeding. Endoscopic evaluation with esophagogastroduodenoscopy is diagnostic and therapeutic for upper GI bleeding, while colonoscopy is primarily diagnostic for lower GI bleeding after bowel preparation.
Differential Diagnosis
Alternative sources of apparent GI bleeding include epistaxis, oropharyngeal bleeding, hemoptysis, hematuria, vaginal bleeding, and traumatic injuries.
Prehospital Management
Airway protection is critical in massive bleeding or altered mental status. Large-bore IV access should be established, and crystalloid infusion initiated to maintain systolic blood pressure above 90 mm Hg.
Emergency Department Stabilization
Airway, breathing, and circulation are prioritized. Two large-bore IV lines are placed, cardiac monitoring initiated, and volume resuscitation started with crystalloid boluses. Blood transfusion is indicated for significant anemia or hemodynamic instability, with attention to balanced transfusion strategies in massive hemorrhage. Coagulopathy is corrected with fresh frozen plasma, vitamin K, and platelets as indicated.
Definitive Emergency Treatment
Early gastroenterology consultation is essential. Proton pump inhibitor infusion is initiated for suspected upper GI bleeding, and octreotide is added when variceal bleeding is suspected. Vasopressin may be considered for refractory variceal bleeding with caution. Emergent endoscopy provides definitive diagnosis and therapy, including cauterization, injection, or banding. Balloon tamponade is reserved as a last resort. In cirrhotic patients, prophylactic antibiotics reduce mortality. For lower GI bleeding, angiography or surgical intervention may be required for ongoing massive hemorrhage.
Medication Therapy
Management includes IV proton pump inhibitors, octreotide or somatostatin analogs, vasopressors when indicated, nitroglycerin with vasopressin to limit ischemia, and vitamin K for coagulopathy.
Disposition And Admission Criteria
Admission is required for active bleeding, advanced age, comorbid illness, coagulopathy, anemia, or any episode of hemodynamic instability. Discharge may be considered for resolved bleeding with negative evaluation, stable hematocrit, and reliable follow-up in otherwise healthy patients.
Follow-Up And Referral
Patients discharged from the emergency department require close follow-up within 24–36 hours and clear return precautions. Upper GI bleeding patients should continue proton pump inhibitor therapy and avoid alcohol, NSAIDs, aspirin, caffeine, and tobacco.
Key Clinical Pearls And Pitfalls
A significant proportion of upper GI bleeding presents with hematochezia. Failure to aggressively resuscitate with fluids and blood products is a common and dangerous error. In elderly patients, peptic ulcer disease remains the most common cause and is associated with higher mortality.
Basic Overview
Gastrointestinal bleeding refers to blood loss originating anywhere along the GI tract. Upper gastrointestinal bleeding arises proximal to the ligament of Treitz, whereas lower gastrointestinal bleeding occurs distal to the ligament of Treitz to the anus. Overall mortality is approximately 10%, ranging from less than 5% in children to as high as 25% in adults older than 70 years. Upper GI bleeding accounts for most cases, with nonvariceal mortality of 6–8% and variceal bleeding mortality of 30–50%. Lower GI bleeding carries a mortality of 2–4%.
Common Causes And Mechanisms
Upper GI bleeding is most frequently due to ulcerative disease, particularly peptic ulcer disease associated with Helicobacter pylori infection or medication use such as NSAIDs, aspirin, glucocorticoids, potassium, and iron supplements. Other causes include gastric or esophageal erosions, reflux esophagitis, infectious esophagitis, pill-induced injury, foreign bodies, gastritis, and stress-related mucosal disease from trauma, burns, sepsis, or CNS injury. Portal hypertension leads to esophageal or gastric varices and portal hypertensive gastropathy. Vascular causes include arteriovenous malformations, Dieulafoy lesions, gastric antral vascular ectasia, and aortoenteric fistulas. Mallory–Weiss tears, tumors, pancreatic hemorrhage, hemobilia, and parasitic infections are less common causes.
Lower GI bleeding most often results from diverticulosis, colorectal cancer or polyps, colitis (ischemic, inflammatory, infectious, or radiation-induced), angiodysplasia, postpolypectomy bleeding, inflammatory bowel disease, anorectal sources such as hemorrhoids or fissures, rectal ulcers, and foreign bodies. In children, Meckel diverticulum and intussusception are the leading causes.
Clinical Presentation
Both upper and lower GI bleeding may present with hypovolemia. Upper GI bleeding typically causes hematemesis or coffee-ground emesis and melena, whereas lower GI bleeding usually presents with hematochezia. Rapid upper GI bleeding can also cause hematochezia. Patients may report abdominal pain, weakness, dizziness, dyspnea, confusion, or agitation.
History And Physical Examination
Key historical features include vomiting blood, black or tarry stools, bright red blood per rectum, abdominal pain, and symptoms of anemia or shock. Examination may reveal tachycardia, hypotension, pallor, dry mucous membranes, melena or hematochezia on rectal exam, and signs of shock.
Initial Evaluation Priorities
Essential evaluation includes CBC, coagulation studies, electrolytes, and assessment for hypovolemia. ENT examination helps differentiate hematemesis from hemoptysis. Nasogastric lavage may assist in identifying active upper GI bleeding, though its impact on outcomes is controversial. Rectal examination is necessary to assess stool color and identify anorectal sources while recognizing causes of false-positive or false-negative fecal occult blood tests.
Diagnostic Testing
Laboratory studies may reveal anemia, thrombocytopenia, coagulopathy, electrolyte abnormalities, elevated BUN-to-creatinine ratio suggestive of upper GI bleeding, and elevated lactate in shock. Imaging may include upright chest radiography if perforation or aspiration is suspected. Angiography and radionuclide scans can localize active bleeding. Endoscopic evaluation with esophagogastroduodenoscopy is diagnostic and therapeutic for upper GI bleeding, while colonoscopy is primarily diagnostic for lower GI bleeding after bowel preparation.
Differential Diagnosis
Alternative sources of apparent GI bleeding include epistaxis, oropharyngeal bleeding, hemoptysis, hematuria, vaginal bleeding, and traumatic injuries.
Prehospital Management
Airway protection is critical in massive bleeding or altered mental status. Large-bore IV access should be established, and crystalloid infusion initiated to maintain systolic blood pressure above 90 mm Hg.
Emergency Department Stabilization
Airway, breathing, and circulation are prioritized. Two large-bore IV lines are placed, cardiac monitoring initiated, and volume resuscitation started with crystalloid boluses. Blood transfusion is indicated for significant anemia or hemodynamic instability, with attention to balanced transfusion strategies in massive hemorrhage. Coagulopathy is corrected with fresh frozen plasma, vitamin K, and platelets as indicated.
Definitive Emergency Treatment
Early gastroenterology consultation is essential. Proton pump inhibitor infusion is initiated for suspected upper GI bleeding, and octreotide is added when variceal bleeding is suspected. Vasopressin may be considered for refractory variceal bleeding with caution. Emergent endoscopy provides definitive diagnosis and therapy, including cauterization, injection, or banding. Balloon tamponade is reserved as a last resort. In cirrhotic patients, prophylactic antibiotics reduce mortality. For lower GI bleeding, angiography or surgical intervention may be required for ongoing massive hemorrhage.
Medication Therapy
Management includes IV proton pump inhibitors, octreotide or somatostatin analogs, vasopressors when indicated, nitroglycerin with vasopressin to limit ischemia, and vitamin K for coagulopathy.
Disposition And Admission Criteria
Admission is required for active bleeding, advanced age, comorbid illness, coagulopathy, anemia, or any episode of hemodynamic instability. Discharge may be considered for resolved bleeding with negative evaluation, stable hematocrit, and reliable follow-up in otherwise healthy patients.
Follow-Up And Referral
Patients discharged from the emergency department require close follow-up within 24–36 hours and clear return precautions. Upper GI bleeding patients should continue proton pump inhibitor therapy and avoid alcohol, NSAIDs, aspirin, caffeine, and tobacco.
Key Clinical Pearls And Pitfalls
A significant proportion of upper GI bleeding presents with hematochezia. Failure to aggressively resuscitate with fluids and blood products is a common and dangerous error. In elderly patients, peptic ulcer disease remains the most common cause and is associated with higher mortality.
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