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Gastrointestinal Bleeding

General Principles

Acute gastrointestinal (GI) bleeding is a common clinical problem that results in substantial morbidity and health care costs, especially when it develops in hospitalized patients (Gut 2011;60:1327  [PMID:21490373]).

  • Overt GI bleeding is the passage of fresh or altered blood in emesis or stool.
  • Occult GI bleeding refers to a positive fecal occult blood test (stool guaiac or fecal immunochemical test) or iron deficiency anemia without visible blood in the stool.
  • Obscure GI bleeding consists of GI blood loss of unknown origin that persists or recurs after negative initial endoscopic evaluation (Gastroenterology 2007;133:1697  [PMID:17983812]).

Diagnosis

Clinical Presentation

History

  • Hematemesis, coffee-ground emesis, and/or aspiration of blood or coffee-ground material from a nasogastric (NG) tube indicate an upper GI source of blood loss.
  • Melena, black sticky stool with a characteristic odor, usually suggests an upper GI source, although small bowel and right-sided colonic bleeds can also result in melena.
  • Various shades of bloody stool (hematochezia) are seen with distal small bowel or colonic bleeding, depending on the rate of blood loss and colonic transit. Rapid upper GI bleeding can present with hematochezia, typically associated with hemodynamic compromise or circulatory shock.
  • Anorectal bleeding usually results in bright red blood coating the exterior of formed stool associated with distal colonic symptoms (e.g., rectal urgency, straining, or pain with defecation).
  • Anemia from blood loss can cause fatigue, weakness, abdominal pain, pallor, or dyspnea.
  • Estimation of the amount of blood loss is often inaccurate. If the baseline hematocrit is known, the drop in hematocrit provides a rough estimate of blood loss. In general, lower GI bleeding causes less hemodynamic compromise than upper GI bleeding.
  • Coagulation abnormalities can propagate bleeding from a preexisting lesion in the GI tract. Disorders of coagulation (e.g., liver disease, von Willebrand disease, vitamin K deficiency, and disseminated intravascular coagulation) can influence the course of GI bleeding (see Chapter 20, Disorders of Hemostasis and Thrombosis).
  • Medications known to affect the coagulation process or platelet function include warfarin, heparin, low–molecular-weight heparin, aspirin, NSAIDs, thienopyridines (clopidogrel [Plavix], prasugrel [Effient], ticlopidine [Ticlid]), thrombolytic agents, glycoprotein IIb/IIIa receptor antagonists (abciximab [ReoPro], eptifibatide [Integrilin], tirofiban [Aggrastat]), direct thrombin inhibitors (argatroban, bivalirudin, dabigatran etexilate), and direct factor Xa inhibitors (rivaroxaban [Xarelto], apixaban).
  • NSAIDs and aspirin can result in mucosal damage anywhere in the GI tract. Therefore, dual antiplatelet therapy (e.g., clopidogrel plus aspirin) or concomitant aspirin and anticoagulation with warfarin can escalate the risk for GI bleeding by both initiating and propagating bleeding.

Physical Examination

  • Color of stool. Direct examination of spontaneously passed stool or on digital rectal examination (DRE) can help localize the level of bleeding. Moreover, DRE may identify anorectal abnormalities including anal fissures, which induce extreme discomfort during the DRE.
  • Fresh blood on an NG aspirate may indicate ongoing upper GI bleeding requiring urgent endoscopic attention (Gastrointest Endosc 2004;59:172  [PMID:14745388]). The aspirate should be considered positive only if blood or dark particulate matter (“coffee grounds”) is seen; hemoccult testing of NG aspirate has no clinical utility. A bleeding source in the duodenum can result in a negative NG aspirate. Gastric lavage with water or saline may be useful in assessing the activity and severity of upper GI bleeding and in clearing the stomach of blood and clots before endoscopy. After a diagnosis of upper GI bleeding is made, the NG tube can be removed in a stable patient.
  • Constant monitoring or frequent assessment of vital signs is necessary early in the evaluation, as a sudden increase in pulse rate or decrease in blood pressure (BP) may suggest recurrent or ongoing blood loss.
  • If the baseline BP and pulse are within normal limits, sitting the patient up and/or having the patient stand may result in orthostatic hemodynamic changes (drop in systolic BP of >20 mm Hg, rise in pulse rate of >10 bpm). Orthostatic changes are seen with loss of 10–20% of the circulatory volume; supine hypotension suggests a >20% loss. Hypotension with a systolic BP of <100 mm Hg or baseline tachycardia >100 bpm suggests significant hemodynamic compromise that requires urgent volume resuscitation (N Engl J Med 2008;359:928  [PMID:18753649]).

Diagnostic Testing

Laboratories

  • Complete blood cell (CBC) count
  • Coagulation parameters (international normalized ratio [INR], partial thromboplastin time [PTT])
  • Blood group, cross-matching of two to four units of blood
  • Comprehensive metabolic profile (creatinine, blood urea nitrogen, liver function tests)

Diagnostic Procedures

  • Endoscopy
    • Esophagogastroduodenoscopy (EGD), with high diagnostic accuracy and therapeutic capability, is the preferred investigative test in upper GI bleeding. Volume resuscitation or blood transfusion should precede endoscopy in hemodynamically unstable patients. Patients with ongoing bleeding or at risk for an adverse outcome (Table 18-1) benefit most from urgent EGD, while stable patients can be endoscoped electively during the hospitalization. IV erythromycin (infusion of 125–250 mg completed 30 minutes before EGD) empties the stomach of blood and clots and improves visibility for EGD (Gastrointest Endosc 2011;73:245  [PMID:21145052]). Second-look EGD after hemostasis has no proven benefit in reducing surgical intervention or overall mortality (J Gastroenterol Hepatol 2010;25:8  [PMID:20136971]).
      Table 18-1: Rockall Score for Risk Stratification of Acute Upper Gastrointestinal (GI) Bleeding


      VariablePoints
      Age
        <60 yr0
        60–79 yr1
        ≥80 yr2
      Shock
        Heart rate >100 bpm1
        Systolic blood pressure <100 mm Hg2
      Coexisting illness
        Coronary artery disease, congestive heart failure, other major illness2
        Renal failure, hepatic failure, metastatic cancer3

      Endoscopic diagnosis
        No finding, Mallory-Weiss tear0
        Peptic ulcer, erosive disease, esophagitis1
        Cancer of the upper GI tract2
      Endoscopic stigmata of recent bleeding
        Clean based ulcer, flat pigmented spot0
      Blood in upper GI tract, active bleeding, visible vessel, clot2

      A clinical score of 0 or a complete score of 2 or less indicate low risk for rebleeding or death.

      Adapted from Gralnek et al. N Engl J Med 2008;359:928  [PMID:18753649], with permission.

    • Colonoscopy can be performed after a rapid bowel purge in clinically stable patients; the purge solution can be infused through an NG tube when not tolerated orally. While diagnostic yield is highest with colonoscopy performed within 24 hours of presentation, (Am J Gastroenterol 2005;100:2395  [PMID:16279891]), patient outcome does not necessarily improve (Am J Gastroenterol 2010;105:2636  [PMID:20648004]). Therapeutic colonoscopy, however, may reduce transfusion requirements, need for surgery, and length of hospital stay. All patients with acute lower GI bleeding from an unknown source should eventually undergo colonoscopy during the initial hospitalization, regardless of the initial mode of investigation.
    • Anoscopy may be useful in the detection of internal hemorrhoids and anal fissures but does not replace the need for colonoscopy.
    • Push enteroscopy allows evaluation of the proximal small bowel beyond reach of a standard EGD, especially if no source is found on careful colonoscopy.
    • Capsule endoscopy is most useful after the upper gut and the colon have been thoroughly examined and the bleeding source is suspected in the small bowel (Gastroenterology 2007;133:1697  [PMID:17983812]). In overt obscure GI bleeding, capsule endoscopy has higher diagnostic yield with similar long-term outcomes when compared with angiography (Am J Gastroenterol 2012;107:1370  [PMID:22825363]). However, images cannot be viewed in real time, exact localization within the small bowel cannot be pinpointed, and therapy cannot be administered; consequently, improvements in diagnostic yield may not translate into better outcomes (Gastroenterology 2010;138:1673  [PMID:20138043]).
    • Single- and double-balloon enteroscopy allows visualization of most of the small bowel through either an oral or anal approach. Balloons at the endoscope tip and overtube can be consecutively inflated and deflated to facilitate deep insertion into the small bowel.
    • Intraoperative enteroscopy may assist endoscopic therapy or surgical resection of an actively bleeding source in the small bowel.
  • CT enteroclysis has value when both conventional endoscopy and capsule endoscopy are nondiagnostic in obscure-overt bleeding with prominent anemia (Gastrointest Endosc 2011;73:1002  [PMID:21396638]).
  • Tagged red blood cell (RBC) scanning involves labeling RBCs with technetium-99m that may extravasate into the bowel lumen with active bleeding, detected as pooling of the radioactive tracer on gamma camera scanning, to identify the potential bleeding site. CT angiography may have similar benefit in localizing bleeding prior to catheter angiography (J Vasc Interv Radiol 2010;21:848  [PMID:20400333]). These tests are particularly useful in unstable active bleeding precluding urgent colonoscopy.
  • Arteriography demonstrates extravasation of the dye into the intestine when bleeding rates exceed 0.5 mL/min, thereby localizing bleeding. Arteriography is often performed after bleeding is initially localized by other means. Selective cannulation and infusion of vasopressin vasoconstrict the bleeding vessel; moreover, the vessel can be embolized.

Treatment

  • Restoration of intravascular volume. Two large-bore (16- to 18-gauge) IV lines or a central venous line should be urgently placed to provide IV fluid resuscitation. Circulatory shock may require volume administration using pressure infusion devices, guided by the patient’s condition and degree of volume loss (N Engl J Med 2008;359:928  [PMID:18753649]). Packed RBC transfusion should be used for volume replacement whenever possible; O-negative blood or simultaneous multiple-unit transfusions may be indicated if bleeding is massive. Transfusion should be continued until hemodynamic stability is achieved and the hematocrit reaches ≥25–30%. Overcorrection of volume and blood counts does not necessarily improve outcome and may even be detrimental in variceal bleeding (Aliment Pharmacol Ther 2010;32:215  [PMID:20456308]).
  • Oxygen administration. Supplemental oxygen enhances the oxygen-carrying capacity of blood and should be universally administered in acute GI bleeding.
  • Correction of coagulopathy. Coagulopathy (INR ≥1.5) increases morbidity and mortality in acute GI bleeding (Aliment Pharmacol Ther 2011;33:1010  [PMID:21385193]) and should be corrected if possible. Platelet infusion may be indicated when the platelet count is <50,000/μL.
  • Endotracheal intubation protects the airway and prevents aspiration in obtunded patients with massive hematemesis and in active variceal bleeding.
  • Risk stratification. Validated risk stratification tools, such as the Rockall and Glasgow-Blatchford scores, are available to identify patients at highest risk for an adverse outcome (Aliment Pharmacol Ther 2011;34:470  [PMID:21707681]). The Rockall score (see Table 18-1) has a clinical component that is rapidly calculated at presentation and a complete final score that takes endoscopic findings into account (Gut 1996;38:316  [PMID:8675081]).

Medications

  • Nonvariceal upper GI bleeding. Pre-endoscopic IV proton pump inhibitors (PPIs) (40 mg IV bolus bid or 80 mg IV bolus followed by 8 mg/h continuous infusion) impact the proportion of patients who have high-risk stigmata of hemorrhage and reduce need for endoscopic therapy in bleeding peptic ulcer disease (PUD) (Am J Gastroenterol 2012;10:345). However, meta-analysis does not show benefits in rebleeding, surgical intervention, or mortality between IV infusions and IV bolus therapy in unselected cases (Arch Intern Med 2010;170:751  [PMID:20458081]). PPI therapy, IV or oral (e.g., omeprazole 40 mg PO bid or equivalent), is more effective than IV histamine-2 receptor antagonist (H2RA) therapy (Am J Gastroenterol 2014;109:1005  [PMID:24777150]).
  • Variceal bleeding. Octreotide (an octapeptide that mimics endogenous somatostatin) infusion acutely reduces portal pressures and controls variceal bleeding, improving the diagnostic yield and therapeutic success of subsequent endoscopy. Octreotide should be initiated immediately (50- to 100-μg bolus, followed by infusion at 25–50 μg/h) and continued for 3–5 days after EGD if variceal hemorrhage is confirmed (Gastrointest Endosc 2014;80:221  [PMID:25034836]). Both terlipressin and octreotide achieve similar hemostatic effects with comparable safety to octreotide as adjuvants to endoscopic therapy in variceal bleeding (Hepatology 2014;60:954  [PMID:24415445]; Aliment Pharmacol Ther 2012;35:1267  [PMID:22486630]). A 7-day course of antibiotic prophylaxis with an IV third-generation cephalosporin (ceftriaxone) is recommended (see Chapter 19, Liver Diseases) in any patient with cirrhosis and variceal bleeding; a fluoroquinolone is an alternative (Hepatology 2009;49:2087  [PMID:19475696]).
  • Thalidomide may be an effective approach for refractory chronic bleeding from GI vascular malformations (Gastroenterology 2011;141:1629  [PMID:21784047]).

Other Nonpharmacologic Therapies

  • Endoscopic therapy
    • Therapeutic endoscopy offers the advantage of endoscopic hemostasis. Therefore, EGD should be performed early in acute upper GI bleeding (within 12–24 hours).
    • Variceal ligation or banding is the endoscopic therapy of choice for esophageal varices, with endotracheal intubation for airway protection if bleeding is massive or the patient is obtunded (Gastrointest Endosc 2014;80:221  [PMID:25034836]). Variceal banding has value in both primary and secondary prophylaxis of variceal bleeding, with benefits similar to that from β-blocker therapy alone (Gastroenterology 2010;139:1238  [PMID:20547163]). Complications include superficial ulceration, dysphagia, and transient chest discomfort.
    • Sclerotherapy is also effective but is used mostly when variceal banding is not technically feasible.
    • Endoscopic injection of cyanoacrylate (glue) is more effective than β-blocker therapy in primary and secondary prophylaxis of gastric variceal bleeding, but not esophageal variceal bleeding (Gut 2010;59:729  [PMID:20551457]).
  • Transjugular intrahepatic portosystemic shunt (TIPS) is a radiologic procedure wherein an expandable metal stent is deployed between the hepatic veins and the portal vein to reduce portal venous pressure in refractory esophageal and/or gastric variceal bleeding from portal hypertension (Hepatology 2007;46:922  [PMID:17879356]). Early TIPS may be of value in reducing treatment failure and mortality in acute variceal bleeding (N Engl J Med 2010;362:2370  [PMID:20573925]). Encephalopathy may occur in up to 25% of patients and is treated medically (see Chapter 19, Liver Diseases). Assessment with duplex Doppler ultrasound for TIPS stenosis is recommended if variceal bleeding recurs or if esophageal or gastric varices redevelop.
  • Balloon-occluded retrograde transvenous obliteration (BRTO) is a newer treatment option for gastric variceal bleeding, where gastric varices are obliterated through a gastrorenal shunt (J Gastroenterol Hepatol 2009;24:372  [PMID:19032446]). BRTO appears to be equivalent to TIPS for short-term management of bleeding gastric varices (J Vasc Interv Radiol 2014;25:355  [PMID:24468043]).

Surgical Management

  • Emergent total colectomy may rarely be required for massive, unlocalized, colonic bleeding; this should be preceded by EGD to rule out a rapidly bleeding upper source whenever possible. Certain lesions (e.g., neoplasia, Meckel diverticulum) require surgical resection for a cure.
  • Total or partial colectomy may be required for ongoing or recurrent diverticular bleeding.
  • Splenectomy is curative in bleeding gastric varices from splenic vein thrombosis.
  • Shunt surgery (portacaval or distal splenorenal shunt) is now rarely performed; this can be considered in patients with good hepatic reserve.

Special Considerations

Cardiac Patients and Gastrointestinal Bleeding

  • In acute coronary syndromes (ACS), GI bleeding increases 30-day all-cause mortality rates by a factor of almost 5 (J Am Coll Cardiol 2009;29:1293). Antiplatelet and anticoagulant therapy, especially dual antiplatelet therapy (e.g., aspirin plus clopidogrel), are significant risk factors. Among patients on low-dose aspirin with history of PUD bleeding, continuous aspirin therapy increases the risk for recurrent PUD bleeding (Ann Intern Med 2010;152:1  [PMID:19949136]).
  • PPI prophylaxis decreases the risk of GI bleeding, without significant effects on the incidence of hospital-acquired pneumonia or 30-day mortality (Aliment Pharmacol Ther 2011;34:519  [PMID:21726257]).
  • Despite concerns that PPIs competitively inhibit the cytochrome P450 enzyme that activates clopidogrel, randomized controlled trials have not substantiated higher vascular events with concurrent use of clopidogrel and PPI (N Engl J Med 2010;11:363; Heart 2013;99:520  [PMID:22851683]). Among PPIs, pantoprazole may have the least pharmacodynamic interaction with clopidogrel (Eur J Gastroenterol Hepatol 2011;23:396  [PMID:21464720]).
  • Left ventricular assist devices (LVADs), used in end-stage heart failure, are associated with GI bleeding rates significantly higher than those seen with dual antiplatelet therapy or anticoagulation (Clin Gastroenterol Hepatol 2014;12:1461  [PMID:24480675]). Bleeding is predominantly overt and from upper GI sources, especially angiodysplastic lesions, making EGD or push enteroscopy the initial investigation of choice (Gastrointest Endosc 2012;75:973  [PMID:22341716]).

Outline


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Citation

Williams, Dominique, et al., editors. "Gastrointestinal Bleeding." Washington Manual of Medical Therapeutics, 35th ed., Wolters Kluwer Health, 2016. Washington Manual, www.unboundmedicine.com/washingtonmanual/view/Washington-Manual-of-Medical-Therapeutics/602609/4/Gastrointestinal_Bleeding.
Gastrointestinal Bleeding. In: Williams D, Ramgopal R, Gdowski M, et al, eds. Washington Manual of Medical Therapeutics. 35th ed. Wolters Kluwer Health; 2016. https://www.unboundmedicine.com/washingtonmanual/view/Washington-Manual-of-Medical-Therapeutics/602609/4/Gastrointestinal_Bleeding. Accessed June 18, 2019.
Gastrointestinal Bleeding. (2016). In Williams, D., Ramgopal, R., Gdowski, M., Dretler, A., & Bhat, P. (Eds.), Washington Manual of Medical Therapeutics. Available from https://www.unboundmedicine.com/washingtonmanual/view/Washington-Manual-of-Medical-Therapeutics/602609/4/Gastrointestinal_Bleeding
Gastrointestinal Bleeding [Internet]. In: Williams D, Ramgopal R, Gdowski M, Dretler A, Bhat P, editors. Washington Manual of Medical Therapeutics. Wolters Kluwer Health; 2016. [cited 2019 June 18]. Available from: https://www.unboundmedicine.com/washingtonmanual/view/Washington-Manual-of-Medical-Therapeutics/602609/4/Gastrointestinal_Bleeding.
* Article titles in AMA citation format should be in sentence-case
TY - ELEC T1 - Gastrointestinal Bleeding ID - 602609 ED - Williams,Dominique, ED - Ramgopal,Rajeev, ED - Gdowski,Mark, ED - Dretler,Alexandra, ED - Bhat,Pavat, BT - Washington Manual of Medical Therapeutics UR - https://www.unboundmedicine.com/washingtonmanual/view/Washington-Manual-of-Medical-Therapeutics/602609/4/Gastrointestinal_Bleeding PB - Wolters Kluwer Health ET - 35 DB - Washington Manual DP - Unbound Medicine ER -