Stanley AJ, Laine L. Management of acute upper gastrointestinal bleeding. BMJ. 2019 Mar 25;364:l536. doi: 10.1136/bmj.l536. PubMed PMID: 30910853.
Strate LL, Gralnek IM. ACG Clinical Guideline: Management of Patients With Acute Lower Gastrointestinal Bleeding. Am J Gastroenterol. 2016 Apr;111(4):459-74. doi: 10.1038/ajg.2016.41. Epub 2016 Mar 1. Erratum in: Am J Gastroenterol. 2016 May;111(5):755. PubMed PMID: 26925883; PubMed Central PMCID: PMC5099081.
RÃos Castellanos E, Seron P, Gisbert JP, Bonfill Cosp X. Endoscopic injection of cyanoacrylate glue versus other endoscopic procedures for acute bleeding gastric varices in people with portal hypertension. Cochrane Database Syst Rev. 2015 May 12;(5):CD010180. doi: 10.1002/14651858.CD010180.pub2. Review. PubMed PMID: 25966446.
Sreedharan A, Martin J, Leontiadis GI, et al. Proton pump inhibitor treatment initiated prior to endoscopic diagnosis in upper gastrointestinal bleeding. Cochrane Database Syst Rev. 2010 Jul 7;(7):CD005415. doi: 10.1002/14651858.CD005415.pub3. Review. PubMed PMID: 20614440.
Garcia-Tsao G, Sanyal AJ, Grace ND, Carey W; Practice Guidelines Committee of the American Association for the Study of Liver Diseases; Practice Parameters Committee of the American College of Gastroenterology. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007 Sep;46(3):922-38. Erratum in: Hepatology. 2007 Dec;46(6):2052. PubMed PMID: 17879356.
Barkun A, Fallone CA, Chiba N, et al; Nonvariceal Upper GI Bleeding Consensus Conference Group. A Canadian clinical practice algorithm for the management of patients with nonvariceal upper gastrointestinal bleeding. Can J Gastroenterol. 2004 Oct;18(10):605-9. PubMed PMID: 15497000.
Barkun A, Bardou M, Marshall JK; Nonvariceal Upper GI Bleeding Consensus Conference Group. Consensus recommendations for managing patients with nonvariceal upper gastrointestinal bleeding. Ann Intern Med. 2003 Nov 18;139(10):843-57. PubMed PMID: 14623622.
Ioannou G, Doust J, Rockey DC. Terlipressin for acute esophageal variceal hemorrhage. Cochrane Database Syst Rev. 2003;(1):CD002147. Review. PubMed PMID: 12535432.
Definition, Etiology, PathogenesisTop
Gastrointestinal (GI) bleeding may be divided into:
1) Upper gastrointestinal (GI) bleeding (from a source located above the ligament of Treitz), which occurs in ~80% of patients hospitalized due to GI bleeding. The most common causes include gastric or duodenal ulcers, acute hemorrhagic (erosive) gastropathy, esophageal varices, Mallory-Weiss syndrome, and esophagitis; less common causes include Dieulafoy lesions, duodenitis, neoplasms, esophageal ulcers, and vascular malformations. Acute upper GI bleeding may be precipitated by shock, systemic inflammatory response syndrome, sepsis, multiple trauma, acute respiratory failure, multiorgan failure, severe burns, and other acute and severe diseases.
2) Lower GI bleeding (from a source located below the ligament of Treitz), which occurs in ~20% of patients hospitalized due to GI bleeding. The most common causes of severe lower GI bleeding in adults are colonic diverticula and vascular malformations, while the less common causes include inflammatory bowel disease (IBD), hemorrhoidal disease, and neoplasms. In children and adolescents the causes may include intussusception (secondary to polyps), IBD, Meckel diverticular bleed, and small intestinal or colonic polyps.
Bleeding may be exacerbated by coagulopathy.
GI bleeding can be also divided into:
1) Overt GI bleeding: Bleeding that is visible, such as hematemesis (bloody or coffee-ground emesis), hematochezia (presence of blood and blood clots in feces), or melena (black tarry stools).
2) Obscure GI bleeding: Bleeding that may be obscure-overt or obscure-occult depending on the presence or absence of clinically evident bleeding.
1. Acute bleeding:
1) Upper GI bleeding: The most common presentation is melena (tarry, black, foul-smelling stools). If the bleeding is brisk, hematochezia or maroon stools may be observed. Sometimes the presenting symptom is hematemesis or coffee-ground emesis. Epigastric or diffuse abdominal pain may be present (chest pain mimicking coronary disease occurs in some patients) as well as symptoms of hypovolemia (shock).
2) Lower GI bleeding: Hematochezia is the most common presentation but ~10% of lower GI bleeding presents with melena. Symptoms of hypovolemia may occur (shock).
2. Chronic bleeding: Iron deficiency anemia, fecal occult blood. These patients often have obscure GI bleeding.
History may indicate the source of bleeding, but usually diagnosis can only be established on the basis of endoscopy or, in the case of a massive hemorrhage, during radiologic intervention or surgery.
1. Laboratory tests:
1) Complete blood count (CBC): A decrease in hematocrit, hemoglobin levels, and red blood cell (RBC) counts may not be evident until blood becomes diluted by the transition of the intercellular fluid into the intravascular space, which may take hours, or by infused fluids that contain no blood cells (eg, 0.9% NaCl).
2) International normalized ratio (INR) and other coagulation tests: These are particularly important in patients treated with anticoagulants, such as warfarin, especially because information concerning such treatment sometimes cannot be obtained from individuals with altered mental status. Coagulopathy may be also indicative of liver dysfunction or depletion of coagulation factors.
2. Endoscopy of the upper GI tract is the key diagnostic and often therapeutic modality for suspected upper GI bleeding. The most common lesion identified on upper endoscopy is peptic ulcer.
Ulcers are generally characterized by the Forrest classification, which reliably predicts the likelihood of rebleeding:
– Class I: Active spurting bleeding (Ia) or active oozing bleeding (Ib).
– Class IIa: Visible nonbleeding vessel.
– Class IIb: Adherent clot at the ulcer base.
– Class IIc: Flat pigmented spot at the ulcer base.
– Class III: Clean (white) ulcer base.
Classes Ia, Ib, and IIa are associated with high risk for rebleeding and are usually treated endoscopically in combination with injection therapy, coagulation, or clips. Class IIb lesions warrant targeted irrigation to attempt to dislodge the clot and then treat the underlying lesion. Classes IIc and III usually do not require endoscopic therapy, as they are associated with low risk for rebleeding.
If urgent endoscopy is not feasible, introduce a nasogastric tube (after securing the airway if needed). The presence of bile without blood in the gastric aspirate suggests a lower GI source of bleeding.
3. Colonoscopy is the initial diagnostic procedure for patients with lower GI bleeding. It should be performed after adequate bowel preparation ideally within 24 hours of presentation. Of note, urgent upper GI endoscopy may be indicated in patients who are unstable with hematochezia, as it is prudent to exclude a briskly bleeding upper GI source.
4. Computed tomography angiography (CTA) may be helpful in locating and potentially treating the source of active bleeding, using subsequently an interventional radiologic procedure.
5. Some patients with obscure GI bleeding (usually after repeat endoscopy or colonoscopy) may require small bowel evaluations with push enteroscopy, double balloon enteroscopy, and wireless capsule endoscopy; each may be combined with CT enterography.
Management algorithm for bleeding ulcers: Figure 6.1-9.
Management algorithm for bleeding varices: Figure 6.1-10.
1. Patients should be treated in an acute setting and then transferred to a general ward or monitored setting depending on the severity of their condition. In patients with significant blood loss and impaired mental status, maintain the airway and intubate if necessary.
2. Measure blood pressure. If it is normal, perform the measurement in a standing position. A decrease in systolic blood pressure >10 mm Hg, decrease in diastolic blood pressure >20 mm Hg, or increase in heart rate >30 beats/min indicates significant volume depletion. Check for signs of hypoperfusion, such as delayed capillary refill and other symptoms of shock. If the above signs are present, start treatment of shock (see Shock).
3. Correct blood volume for the blood lost due to the bleeding: Insert 2 large-bore peripheral vein catheters or a central venous catheter. Crystalloid is usually administered first as it is readily available. Packed RBCs should be administered as soon as possible in patients with signs of hemodynamic instability or shock.
4. Perform urgent endoscopy and make attempts to stop the bleeding using local injections of vasoconstrictors (such as epinephrine) or saline, electrocoagulation, argon coagulation, hemostatic clips, and ligation of esophageal varices.
5. Start pharmacologic treatment:
1) In patients with high-risk bleeding gastric or duodenal ulcers or acute hemorrhagic gastropathy, administer an IV proton pump inhibitor (PPI) (eg, esomeprazole, omeprazole, or pantoprazole). Our pattern of practice is to administer a bolus injection followed by a continuous infusion for 3 days (this also includes patients in whom bleeding was successfully stopped using endoscopy). If no further bleeding has occurred after 3 days of monitoring, the patient can be switched to an oral PPI. Low-risk lesions can be managed with initial oral PPI therapy. Of note, there is insufficient evidence to reach a firm conclusion about the superiority or noninferiority of PPI regimens for acute ulcer bleeding based on route (oral vs IV) and dose (high vs medium or low) of PPIs.Evidence 1Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to risk of bias and imprecision. Neumann I, Letelier LM, Rada G, et al. Comparison of different regimens of proton pump inhibitors for acute peptic ulcer bleeding. Cochrane Database Syst Rev. 2013 Jun 12;(6):CD007999. doi: 10.1002/14651858.CD007999.pub2. Review. PubMed PMID: 23760821. All patients with peptic ulcers should be tested and, if positive, treated for Helicobacter pylori infection. Nonsteroidal anti-inflammatory drugs should be avoided if possible with the exception of acetylsalicylic acid (ASA), which should be continued if there is a good indication for cardiovascular protection.
2) In patients with bleeding esophageal varices, administer one of the following IV agents lowering portal pressure:
a) Terlipressin, a synthetic analogue of vasopressin with fewer adverse effects: 5 to 20 microg/min in a 20- to 40-minute infusion; if necessary, repeat the infusion every 8 hours for a maximum of 5 days. Alternatively injections of 1 to 2 mg every 4 to 6 hours may be used.
b) Somatostatin: 250 microg injection followed by a continuous infusion of 250 microg/h for 5 days.
c) Octreotide: 50 microg injection followed by a continuous infusion of 50 microg/h for 5 days.
3) Patients with cirrhosis and GI bleeding should receive antibiotics (eg, ceftriaxone for 1 week; switch to oral ciprofloxacin is possible if the patient is discharged earlier), as this is associated with a mortality benefit.Evidence 2Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to the risk of bias. Chavez-Tapia NC, Barrientos-Gutierrez T, Tellez-Avila F, et al. Meta-analysis: antibiotic prophylaxis for cirrhotic patients with upper gastrointestinal bleeding - an updated Cochrane review. Aliment Pharmacol Ther. 2011 Sep;34(5):509-18. doi: 10.1111/j.1365-2036.2011.04746.x. Epub 2011 Jun 27. PubMed PMID: 21707680.
4) In patients treated with anticoagulants, neutralize the anticoagulant effects (vitamin K antagonists: see Table 3.1-5; heparin: see Heparins; fibrinolytic agents: see ST-Segment Elevation Myocardial Infarction). However, this should not delay endoscopy once needed. Hematology consultation may be required in case of use of direct oral anticoagulants. Also see Perioperative Direct Oral Anticoagulant Management.
6. In patients with bleeding esophageal varices in whom endoscopic attempts to stop the bleeding have failed, you can introduce a Sengstaken-Blakemore tube into the esophagus and stomach or another type of tube (eg, Linton-Nachlas) allowing for balloon compression of the varices; the tubes should be removed within 24 hours.
7. If endoscopic and pharmacologic treatment is ineffective, proceed with visceral angiography and selective embolization of the bleeding vessel or administration of terlipressin into the visceral vessels.
8. Since patients may require emergency surgery, involve a surgeon in the management at early stages of treatment. Indications for consideration of surgery include uncontrolled massive bleeding (ie, causing uncontrolled hemodynamic instability), also after an endoscopic or angiographic attempt to stop the bleeding; recurrent bleeding (following 2 endoscopic procedures); prolonged bleeding combined with an estimated blood loss >50% of circulating volume; and repeated hospitalizations due to a bleeding ulcer. The following surgical procedures are used:
1) Bleeding duodenal ulcer: Usually pyloroplasty or antrectomy are performed, both with oversewing of the bleeding ulcer. Vagotomy was historically performed as well, but it is now generally avoided as effective pharmacologic suppression of gastric acid is available.
2) Bleeding gastric ulcer or gastric erosions: Various types of resection, depending on the clinical situation and patient’s condition.
3) Bleeding esophageal varices unresponsive to pharmacotherapy and insertion of tubes compressing varices: Transvenous intrahepatic portosystemic shunt (TIPS) is a minimally invasive method. If this is ineffective, perform portosystemic anastomosis or revascularization and transection (dissection and suturing) of the esophagus as well as splenectomy.
4) Lower GI bleeding: Colonoscopy performed during surgery and guided by the operating surgeon sometimes enables localization of the source of bleeding. If this is successful, segmental intestinal resection with anastomosis is performed; if the source of bleeding in the colon cannot be located, partial colectomy with ileorectal anastomosis is performed.
Figure 6.1-9. Management algorithm for bleeding ulcers.
Figure 6.1-10. Management algorithm for bleeding esophageal varices.