Gastrointestinal Bleeding
Keywords
• Gastrointestinal bleeding • Emergency department • Gastrointestinal hemorrhage • Peptic ulcer disease
Gastrointestinal bleeding (GIB) is a common problem encountered in the emergency department (ED) and a significant cause of morbidity and mortality. The overall mortality rate is approximately 10% and has not changed significantly in the past several decades.1,2 The significant morbidity and mortality associated with GIB requires clinicians to be equipped with the skills to promptly diagnose, aggressively resuscitate, risk stratify, and request timely consultations. For hemodynamically or clinically unstable patients, early resuscitative measures focus on infusion of intravenous fluids or transfusion of blood products to reverse the direct consequences of bleeding; prevent end-organ damage, such as hypoxia or prerenal azotemia; and promote hemostasis.3 Although controversy exists regarding the management of gastrointestinal hemorrhage, the use of a treatment algorithm enables emergency medicine physicians to effectively care for these patients. This article reviews the initial assessment, management, differential diagnosis, and treatment modalities available for patients presenting to an ED with GIB.
Epidemiology
Gastrointestinal hemorrhage may be divided into upper GIB (UGIB) and lower GIB (LGIB) as defined by bleeding originating proximal or distal to the ligament of Treitz. Both UGIB and LGIB are more common in men and older adults.2,4,5 In general, UGIB is more common, accounting for a greater proportion of admissions in adults. The annual incidence for UGIB is estimated at 50 to 150 per 100,000 population,2,6 whereas that for LGIB is lower, at approximately 20 to 27 per 100,000 population.5,6 The mortality associated with UGIB is estimated to be anywhere from 6% to 13%, and even with the advent of endoscopic intervention, this mortality rate has not substantially decreased within the past 30 years.7 This is believed secondary to the increased number of older adults presenting with GIB, who are often on antiplatelet and anticoagulation agents and often have other comorbidities associated with their disease.3
Other independent markers of increased morbidity and mortality associated with GIB include the requirement of more than 5 units of packed red blood cells, hemodynamic instability, recurrent bleeding, endoscopic stigmata of recent hemorrhage, melena or hematochezia, esophageal varices, and bloody nasogastric aspirate.1,8,9 In general, most cases of GIB are self-limited, with the majority of patients having only one episode of bleeding.6 Compared with UGIB, LGIB has a decreased mortality rate of approximately 4%.5 Bleeds originating from the colon require fewer blood transfusions than those originating from the small intestine (36% vs 64%).10 In general, patients with LGIB are more likely to have higher hemoglobin levels (84% vs 61%) and less likely to go into shock (19% vs 35%).10,11
Etiology of UGIB
There are several causes of UGIB, with age playing a role in determining potential etiologies. The elderly are more likely to present with bleeds secondary to peptic ulcer disease, esophagitis, and gastritis. Together these account for 70% to 90% of hospital admissions for UGIB in this age group.12 Younger patients account for a larger percentage of cases secondary to causes such as Mallory-Weiss tears, gastrointestinal varices, and gastropathy, which are all less likely in older adults. Common causes of UGIB with prevalence are summarized in Table 1.
Causes | Prevalence |
---|---|
Peptic ulcer disease | 55% |
Gastric ulcer | 21.3%–23.1% |
Duodenal ulcer | 13.9%–24.3% |
Esophageal varices | 10.3%–23.1% |
Esophagitis | 3.7%–6.3% |
Duodenitis | 3.7%–5.8% |
Gastritis | 4.7%–23.4% |
Mallory-Weiss tears | 5%–10.2% |
Angiodysplasia | 6% |
Neoplasm | 2%–4.9% |
Stomal ulcer | 1.8% |
Esophageal ulcer | 1.7% |
Dieulafoy lesion | 1% |
Data from Cappell M, Friedel D. Initial management of acute upper gastrointestinal bleeding: from initial evaluation up to gastrointestinal endoscopy. Med Clin North Am 2008;92:491–509.
Peptic ulcer disease (PUD) is the most common cause of UGIB, accounting for approximately half of all cases.3 PUD occurs secondary to erosion of the gastric or duodenal tissue with symptoms of a gnawing epigastric discomfort and pain that worsens after eating and with lying down. Nausea and vomiting, along with anorexia and concomitant weight loss, are symptoms that are consistent with a diagnosis of PUD. Symptoms are often treated with the use of a proton pump inhibitor or H2 receptor antagonist. Infection with helicobacter pylori is the most common cause of PUD, with nonsteroidal anti-inflammatory drug (NSAID) use coming in second. Aspirin use, history of PUD, smoking, and alcohol use are all risk factors for PUD.13 Zollinger-Ellison syndrome, a disorder resulting in excess production of the hormone gastrin, is an uncommon cause of PUD. Although the overall prevalence of PUD as a cause of UGIB has decreased, an increase in PUD incidence secondary to NSAID use is noted in the elderly.14
Varices are responsible for approximately 10% to 25% of UGIB overall and 60% of UGIB in patients with cirrhosis.15 Cirrhotic patients develop portal hypertension secondary to blockage of the portal venous system, which lends itself to portosystemic collaterals, such as varices, and variceal bleeding. In patients with liver disease, the incidence of new esophageal varices is linear over time with a rate of approximately 9% per year.16 In addition, 30% of patients with portal hypertension and cirrhosis have bleeding secondary to these varices. Patients with portal hypertension–related bleeding, which includes esophageal and gastric varices and portal hypertensive gastropathy, have mortality rates of greater than 50% as compared with a 4% rate with bleeding from PUD.2 Other common causes of UGI bleeds are inflammatory pathologies, such as gastritis and duodenitis, and Mallory-Weiss tears. Less common causes include angiodysplasia and Dieulafoy lesions, which are large tortuous arterioles in the gastric wall that can erode and bleed.3
Etiology of LGIB
LGIB has decreased morbidity in comparison to UGIB and is often self-limited. Similar to UGIB, there are several factors that may be responsible for the bleed. The most common cause of LGIB is colonic diverticulosis, which presents with painless hematochezia. It is estimated that more than two-thirds of the population over the age of 80 are affected by diverticular disease. Approximately 60% of diverticular bleeds are found in the left aspect of the colon on colonoscopy.17 The recurrence rate of diverticular bleeds is 25% after 4 years.5
After colonic diverticulosis, angiodysplasia, colitis, and postpolypectomy bleeding follow in frequency of LGIB causes. Angiodysplasia is responsible for both acute and chronic LGIB but those are often asymptomatic because they do not frequently bleed. Patients taking NSAIDs, aspirin, and anticoagulants as well as coagulopathic patients or patients with platelet dysfunction are more likely to present with LGIB from angiodysplasia.17
Although there are poor data on the incidence of ischemic colitis, it is proposed that the disease is becoming more prevalent secondary to an increase in elderly patients with cardiovascular disease.17 Ischemic colitis is caused by a decrease in mesenteric blood flow as a result of hypotension or vasospasm, and patients often present with sudden onset of abdominal pain followed by diarrhea mixed with blood or hematochezia. LGIB is also a common manifestation of colitis secondary to inflammatory bowel disease but uncommonly leads to acute major gastrointestinal hemorrhage, with ulcerative colitis and Crohn’s disease responsible for 0.1% and 1.2% of massive bleeds, respectively.18 Table 2 lists common causes of LGIB with prevalence.
Causes | Prevalence |
---|---|
Diverticular disease | 17%–40% |
Angiodysplasia | 9%–21% |
Colitis | 2%–30% |
Inflammatory bowel disease | — |
Ischemia | — |
Infectious | — |
Radiation | — |
Postpolypectomy bleeding | 11%–14% |
Anorectal disease | 4%–10% |
Hemorrhoids | — |
Rectal varices | — |
Fissures | — |
Small bowel bleeding | 2%–9% |
Upper gastrointestinal bleeding | 0–11% |
Data from Barnert J, Messmann H. Diagnosis and management of lower gastrointestinal bleeding. Nat Rev Gastroenterol Hepatol 2009;6:637–46.
Determining the source of LGIB can be a challenging task for clinicians. Although most lesions responsible for LGIB are due to colonic or anorectal disease, diagnosis may be difficult because LGIB may be intermittent and may originate from the small intestine or an upper tract source of brisk bleeding. Lower tract sources of GIB have a rebleeding rate of approximately 10% to 20%, require operative intervention in 10% to 15% of cases, and have a mortality rate of 4%.2,5,6 Chronic LGIB is responsible for 18% to 30% of patients with iron deficiency anemia presenting to the ED.17
Initial evaluation
The initial evaluation of patients presenting with GIB should focus on assessment of vital signs, the obtainment of a thorough yet focused medical history, a physical examination with particular attention paid to evidence of GIB and hemodynamic compromise, and laboratory diagnostic testing. Prompt and accurate assessment of these factors guides medical decision making, allowing for early diagnosis, aggressive resuscitation, and timely consultations. Vital signs, in particular heart rate and blood pressure, provide clinicians with diagnostic clues regarding the stability of patients. The loss of approximately less than 250 mL of blood does not usually affect heart rate or blood pressure. Greater than 800 mL of blood loss, however, may cause a drop in blood pressure of 10 mg Hg and a rise in heart rate of 10 beats per minute.17 Significant tachycardia, tachypnea, hypotension, decreased mental status, and shock may result from blood loss totaling more than 1500 mL.17 Although abnormal vital signs are concerning, normal vital signs do not preclude the presence of a significant bleed.
Nature of the bleed
The medical history can provide important diagnostic information with regards to the severity of disease and help focus triage and treatment of patients. Pertinent historical questions are detailed in Box 1. Historical questions include defining the nature of the bleed as hematemesis, hematochezia, or melena. Hematemesis usually signifies a UGIB and can be defined as bright red blood or darker coffee ground emesis. Approximately 50% of patients with UGIB present with hematemesis.6 The return of bright red blood or coffee grounds through the passage of a nasogastric tube and subsequent nasogastric lavage has high predictive value for a bleed proximal to the ligament of Treitz; however, a negative lavage does not exclude UGIB.3 Hematochezia is characterized by bright red or maroon-colored blood per rectum and suggests a source distal to the ligament of Treitz. Approximately 14% of bleeds presenting with hematochezia are caused by a brisk upper source with rapid transit.19 Hematochezia due to an upper tract source of bleeding has been shown associated with a higher transfusion requirement, need for surgery, and mortality rate.6,19 Dark tarry or melanotic stools, which may also signify either an upper or lower source for the bleed, are associated with a lower mortality rate compared with hematochezia.6 It is estimated that 90% of melanotic stools arise proximal to the ligament of Treitz and take on a dark tarry appearance secondary to prolonged transit and degradation of blood.3 Approximately 70% of patients with UGIB present with melena in contrast to only 20% to 30% of patients with LGIB.6,11 In addition to characterizing the nature of the bleed, it is important to define the duration, quantity, and frequency of bleeding episodes.
Clinical features
Medications and past medical, family, and social histories are also useful tools to help diagnose patients presenting with signs and symptoms suggestive of GIB. Medication history includes patient use of NSAIDs, aspirin, glucocorticoids, anticoagulants, and antiplatelet agents. Both aspirin and NSAID use have been shown to contribute to UGIB and LGIB, which are dependent on dose and duration of use.11,20,21 Additionally, the use of aspirin (<100 mg/d), anticoagulation agents in the therapeutic range, and antiplatelet agents, such as clopidogrel, all increase the risk of UGIB threefold.22,23 Important past medical history includes episodes of prior gastrointestinal hemorrhage, because up to 60% of UGI bleeds arise from prior gastrointestinal lesions that have bled.24 Other relevant medical history includes presence of hemorrhoids, hepatic disease, coagulopathies, vascular disease, HIV infection, prior radiation therapy for prostate or pelvic cancer, inflammatory bowel disease, and recent colonoscopy with polypectomy. Family history of colon cancer and social history, specifically pertaining to alcohol and tobacco intake, also help to risk stratify patients. Both alcohol and cigarette smoking are associated with gastrointestinal malignancies.25 Alcohol abuse is independently associated with an increased incidence of PUD and may also result in cirrhosis and varices.25