Michael Huang, David H. Kerman Gastrointestinal (GI) bleeding is a common finding in the ambulatory care setting. Patients may report the symptoms as black tarry stools (melena), bright red stools (hematochezia), and even bright red vomitus (hematemesis).1 GI hemorrhage can occur anywhere in the GI tract from the mouth to the anus and can be overt or occult2 (Box 136-1). Overt GI bleeding is considered major when it is accompanied by hemodynamic instability and minor when it is not. Occult bleeding is nonvisible bleeding that can be detected by stool testing or indirectly suggested by iron deficiency anemia.3 GI bleeding may be related to ulceration, inflammation, erosion of a blood vessel, or neoplasm. Management of GI bleeding has remained constant for several decades. Hemodynamic stabilization of the patient, cessation of active bleeding, and prevention of recurrent bleeding have long remained the goals of medical management for this disorder, which occurs in approximately 100 individuals per 100,000 per year.4 Many of these patients require emergency treatment, hospitalization, and intensive care monitoring. Upper and lower GI tract bleeding are differentiated according to anatomic source. Patients with upper gastrointestinal tract bleeding (UGIB) from a source proximal to the ligament of Treitz may be asymptomatic, have subtle signs of anemia and hypovolemia, or have a dramatic presentation with hematemesis, melena, or hematochezia.5 Causes of UGIB are classified as variceal and nonvariceal bleeding. The most common cause of nonvariceal bleeding is peptic ulcer disease, with gastric ulcers occurring more frequently than duodenal ulcers.5 Nonspecific mucosal abnormalities, such as erosions, are the second most common cause of nonvariceal bleeding.6 Low-dose aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently implicated in UGIB and are associated with morbidity and mortality.5,7,8 Other causes of UGIB include anticoagulants, antiplatelets, esophagitis, and gastroesophageal varices. Lower gastrointestinal tract bleeding (LGIB) from a source distal to the ligament of Treitz can cause occult blood loss or massive hematochezia and shock. The most common cause of LGIB is diverticulosis (40%). Other sources include cancer, polyps, colitis, ulcers, angiodysplasia, and miscellaneous causes such as postpolypectomy bleeding, aortocolonic fistula, stercoral ulcer, anastomotic bleeding, anorectal hemorrhoids, fissures, and rectal ulcers. GI bleeding can be associated with esophagitis, peptic ulcer disease, gastritis, Helicobacter pylori, esophageal or gastric varices, diverticulosis, gastric and colonic cancers, gastric and colonic polyps, and angiodysplasia.2,4 Peptic ulcers are defects in the mucosa of the duodenum or stomach caused by a breakdown in normal mucosal defenses and ulcer erosion into a blood vessel. Contributing factors include smoking, NSAIDs, excess stomach acid production, and H. pylori. Bleeding caused by gastritis is related to diffuse superficial lesions in the gastric mucosa that are usually associated with local irritants or H. pylori. Gastritis can also be caused by major physiologic stressors, including burns, sepsis, trauma, and long-distance running, secondary to decreased splanchnic blood flow and the resultant decrease in mucus production, bicarbonate secretion, and prostaglandin synthesis, all leading to a breakdown in the normal mucosal defenses. NSAIDs inhibit cyclooxygenase, decreasing the synthesis of protective prostaglandins, and may have direct effects on the gastric mucosa, causing both irritation and superficial lesions. Alcohol ingestion causes gastric mucosa production of leukotrienes, which may be responsible for vascular stasis, engorgement, and increased vascular permeability, resulting in hemorrhage.9,10 H. pylori was first described in 1984. This gram-negative spiral bacterium has adaptive mechanisms to survive in the human stomach, including the conversion of urea, water, and acid to ammonia and bicarbonate. It is the secretions of toxins, disruption of the mucous layer, and direct adherence to the gastroduodenal surface epithelium that render the underlying mucosa vulnerable to peptic acid damage. Excluding NSAIDs, approximately 100% of cases of chronic superficial gastritis, 90% to 95% of duodenal ulcers, and 80% of gastric ulcers are believed to be caused by H. pylori. However, improved hygiene and eradication have caused the prevalence of H. pylori in peptic ulcer disease to markedly decrease.11 Treatment of this organism has been shown to cure ulcer disease and to decrease the incidence of ulcer recurrence and rebleeding.12,13,14 Esophageal varices are dilated submucosal veins arising as a consequence of portal hypertension.15 The most common cause of portal hypertension in the United States is cirrhosis from alcoholic and chronic active hepatitis; however, worldwide the most common cause is parasitic disease (particularly schistosomiasis).12–16 Approximately one third of all patients with cirrhosis will bleed from varices; overall mortality is 30%.,17 Diverticulosis is a common cause of acute LGIB.4 Diverticula can occur at the penetration site of colonic arteries, which can rupture into the diverticular sac, resulting in LGIB.10 Angiodysplasias, small vascular tufts formed by capillaries, veins, and venules, representing an acquired arteriovenous malformation14,15 are the most common vascular lesions found in the GI tract. A small percentage of these lesions are present at birth, but most angiodysplasias are detected in people older than 60 years.14,18 Although massive bleeding is occasionally associated with these lesions, bleeding is more often slow, chronic, and occult. Overt blood loss from the GI tract can manifest in numerous ways. Hematemesis is bloody vomitus that is either fresh and bright red or older and like coffee grounds in appearance. Melena is stool that is black, shiny, and foul smelling as a result of blood degradation. These clinical signs generally originate from an upper GI source. The presence or history of black or red hematemesis confirms an upper GI source after bleeding from the nose and oropharynx has been excluded. Melena represents an upper GI source 85% to 95% of the time, and hematochezia from a briskly bleeding upper GI source accounts for 15% of cases. Patients with UGIB with hematochezia have a worse prognosis in terms of morbidity and mortality than those with melena.6 Hematochezia is the passage of bright red to mahogany-colored blood from the rectum as pure blood, blood mixed with stool, blood clots, or bloody diarrhea. These manifestations are more overt or obvious, but occult blood loss is often more subtle. In general, patients with a lower GI source of bleeding have hematochezia, a clear nasogastric (NG) aspirate, and a normal blood urea nitrogen (BUN)/creatinine ratio.19 In addition, patients can have symptoms associated with blood loss, such as presyncope, dyspnea, angina, postural hypotension, and shock, with no overt bleeding source. Occult blood loss can manifest as iron deficiency anemia or as a positive result of a routine fecal occult blood test (FOBT) with use of a chemical reagent.18 Patient history should include the amount, duration, and source of any signs of bleeding along with any associated symptoms, including dizziness, abdominal pain, chest pain, shortness of breath, diaphoresis, and weakness. The patient should be questioned about prior episodes of bleeding and about other illnesses that can result in bleeding, such as cirrhosis, cancer, coagulopathies, and connective tissue disease. All significant past medical and surgical conditions as well as any allergies and medication use, including alendronate, potassium chloride, anticoagulants, and over-the-counter preparations (especially aspirin and NSAIDs), should be elicited and documented. A careful history of alcohol, tobacco, and illicit drug use is also necessary. The physical examination is brief and focused. The initial general appearance and mental status of the patient should be noted. Vital signs are the most important factor in considering initial triage and should be obtained early and frequently. The earliest sign of hypovolemia is tachycardia; hypotension does not occur until volume loss approaches 40%.18 The skin should be examined for color, temperature, turgor, moisture, and capillary refill. Cutaneous lesions on upper extremities, lips, and oral mucosa may reveal hereditary hemorrhagic telangiectasia or blue rubber bleb nevus syndrome. These can be related to a family history of GI bleeding. Other cutaneous manifestations that should be noted on the physical examination include signs of cirrhosis such as spider nevi, palmar erythema, and scleral icterus. The cardiovascular examination should focus on the heart rate and the character of the peripheral pulses. Postural change in blood pressure should be immediately noted. Orthostasis suggests a blood volume loss of 15% to 20%.18 If the systolic blood pressure falls more than 20 mm Hg, the diastolic blood pressure decreases more than 10 mm Hg, or the heart rate increases by more than 20 beats per minute when an adult patient stands from a supine position, intravascular fluid loss is likely and hospital admission should be considered (level of evidence: moderate).20 The abdomen should be auscultated and palpated to identify a mass, tenderness, guarding, or rigidity. Abdominal pain, particularly cramping in the periumbilical area and abdominal distention, may indicate rapid intestinal transit of blood and a major bleed. A careful rectal examination can detect hemorrhoids, fissures, or rectal carcinoma. The stool should be examined for gross blood or melena, indicating acute bleeding that may require urgent intervention. Occult blood testing is usually reserved for colorectal cancer screening purposes, although it can be useful in the appropriate context.21 One must be aware of the highly variable specificity and sensitivity rates of stool occult blood testing. After the patient is stabilized, a thorough physical examination should be performed in search of non-GI sources of bleeding, such as increased or irregular menstrual bleeding in the presence of iron deficiency anemia.22 Laboratory evaluation of all patients with GI bleeding should include hemoglobin, hematocrit, and platelet count to assess baseline blood loss and platelet adequacy.19 The patient’s blood should be typed and crossmatched for 4 to 6 units of packed red blood cells. Laboratory studies include BUN, creatinine, and glucose concentration; liver function tests (LFTs); and prothrombin time (PT) and activated partial thromboplastin time (aPTT). An increased BUN level with normal creatinine concentration is suggestive of an upper GI source.12 Arterial blood gases (ABGs) may be helpful in assessing oxygenation and clarifying the patient’s acid-base status. Electrocardiography (ECG) should be performed for all patients older than 40 years with chest or abdominal pain or a history of cardiac or pulmonary disease. Radiographic studies may include an acute abdominal series if there is suggestion of a perforated viscus or intestinal obstruction accompanying bleeding. NG tube lavage that reveals blood or coffee ground–like material confirms the diagnosis of UGIB and may suggest that the bleeding is caused by a high-risk lesion.23 It is worth noting that 16% of patients with actively bleeding lesions at endoscopy may not demonstrate blood in the NG tube aspirate and therefore have a low sensitivity for UGIB.21,22,24 The gastric lavage may not be positive for blood if the bleeding has ceased or if the bleeding is occurring beyond a closed pylorus in cases such as duodenal ulcers. Bilious fluid return on NG lavage indicates an open pylorus, thus increasing the sensitivity for detection of postpyloric bleeding. NG tube lavage has also been used to clear the stomach for improved visualization before endoscopic evaluation. Further diagnostic studies, such as endoscopy, barium studies, bleeding scans, and angiography, should be performed at the discretion of the consulting gastroenterologist or surgeon.19,21,22,25 Early consultation should be prompted if an acute bleed is suspected.
Gastrointestinal Hemorrhage
Definition and Epidemiology
Pathophysiology
Clinical Presentation
Physical Examination
Diagnostics
Gastrointestinal Hemorrhage
Chapter 136
