Volume 1, Issue 2


Gastroenterological Emergencies Part I: Acute Upper Gastrointestinal Bleeding

June 22, 2010


Gastrointestinal (GI) bleeding is a common and costly medical condition. Approximately 1,000,000 hospitalizations occur annually for GI bleeding.1 Upper gastrointestinal (UGI) bleeding accounts for about half of these cases, and at a cost of $2.5 billion annually.1,2 The mortality rate of about 10% is unchanged despite widespread use of fiberoptic endoscopy, advances in medical and surgical care.1 Advanced age of patient population, multiple co-morbidities, increase in number of patients with variceal bleeding accounts for this unchanged mortality rate.1,2 This brief review addresses etiology, clinical features, endoscopic findings, therapeutic options and ideal management of  UGI bleeding.


UGI bleeding is defined as bleeding from a source (peptic ulcer, Dieulafoy lesion, varices etc.) from the oral cavity to the ligament of Treitz, a suspensory muscle that attaches the duodenojejunal junction to the diaphragm. Hematemesis is defined as emesis containing blood, whereas hematochezia is passage of  red blood per rectum. Hematemesis indicates bleeding from the esophagus, stomach or duodenum.1 Hematochezia usually occur with bleeding from the colon, rectum or anal canal. However, a rapid and severe UGI bleeding can present as hematochezia. Degeneration of blood by intestinal bacteria into hematin or other hemochromes is referred to as melena and this causes passage of black tarry stool with a characteristic odor.1 The amount of blood loss in the GI tract required to cause melena is only 50 ml. “Coffee grounds” emesis refers to a vomitus containing blood denatured by gastric acid. When the source of bleeding is not identified after a thorough upper endoscopy, colonoscopy and small bowel radiography, it is referred as occult GI bleeding.1


Hemorrhage from peptic ulcer accounts for majority of UGI bleeding. A variety of lesions with frequency of bleeding are listed in table 1.2,3


Frequency (%)

Peptic ulcer


Gastroduodenal erosions





Mallory-Weiss tear,

Dieulafoy lesion,

Gastric antral vascular ectasia (GAVE),


Aortoenteric fistula,

Cameron lesions.


Occult bleeding


Table 1. Frequency of bleeding in various causes of UGI bleeding.2,3

Risk assessment & management

It is imperative that the patient is first assessed for hemodynamic stability in any case of GI bleeding. Patients with advanced age; co-morbid conditions are predisposed to higher morbidity and mortality.2 Bleeding from varices has a very high one-year mortality rate (up to 70%).2 History and physical examination findings suggestive of variceal bleeding are previous history of variceal bleeding, history of chronic liver disease, thrombocytopenia and signs of portal hypertension. Patients older than 60 years, severe co-morbid conditions, with persistent tachycardia and hypotension despite aggressive resuscitation, evidence of ongoing hemorrhage, inability to improve hemoglobin despite blood transfusion should be admitted to the intensive care unit. Two wide bore (18 G or larger) peripheral or a central venous access must be obtained to provide fluids and blood rapidly. Periodic monitoring of hemoglobin / hematocrit to assess adequacy of resuscitation should be performed. A nasogastric lavage should be performed to assess severity of bleeding. A bilious gastric aspirate may rule out active bleeding. A timely consultation with gastroenterology service is of paramount importance. In patients with UGI bleeding, an upper endoscopic examination within the first 24 hours of hospitalization has a positive impact on duration of hospitalization, morbidity, and mortality.1,2

All patients should be kept NPO. Intravenous infusion of a proton pump inhibitor (PPI) to raise and maintain gastric pH above 6.0 is associated with positive outcomes in clinical trials.1,2 A higher gastric pH level helps in stabilizing the blood clot at the bleeding site. However, PPI use should be avoided in patients in whom clopidogrel is a critical medicine and H2 blockers should be used. In patients with suspected variceal bleeding, intravenous octreotide at 50 micrograms bolus dose followed by 50 micrograms per hour should be initiated and continued for 72 hours. In the presence of varices, hypervolemia should be avoided to prevent increase in portal hypertension and possibility of rupture of the varix. Gastric emptying should be achieved either with a thorough gastric lavage or with the use of promotility agents such as intravenous erythromycin or metochlopramide prior to endoscopy in order to improve the visibility. Reversal of coagulopathy and the correction of thrombocytopenia are essential before undertaking endoscopic hemostasis. However, recent studies showed that endoscopy could be safely performed in patients with acute GI bleeding with INR of 2-3.2,4,5

Endoscopy in Diagnosis and Intervention

Upper endoscopy is the standard of care for diagnosis and treatment of acute UGI bleeding with up to 95% sensitivity.2,22 Some scoring systems such as Rockall scoring system utilizes findings at endoscopy along with several clinical parameters.2,6 Several important prognostic factors can be estimated using these scoring systems in patients with nonvariceal UGI bleeding, such as longer hospitalization, need for a surgical intervention, recurrent bleeding, and the risk of death.2

Patients with active spurting (18% cases) have 55% recurrent bleeding with 11% mortality rate, while patients with clean-base ulcer have 5% recurrent bleeding with 2% mortality rate.2 All patients with evidence of active bleeding at endoscopy should be treated with endoscopic therapy. Several anatomic and pathological factors prohibit or limit effectiveness of endoscopic therapy such as ulcers on the lesser curvature of the stomach, ulcers on the posterior or superior duodenal bulb, large visible vessels, and the ulcers larger than 2 cm in diameter. Injection of dilute epinephrine, thermal cautery, argon plasma coagulation, and placement of clips or bands are frequently utilized methods to achieve hemostasis. A combination of injection and thermal therapy achieved superior results compared to epinephrine injection alone to prevent recurrent bleeding, need for surgical intervention, and death.7

Endoscopic therapy should be applied to bleeding or nonbleeding visible vessels. An adherent clot should be removed and underlying lesion should be treated. Nonbleeding ulcers with a clean base and flat, pigmented spots do not require endoscopic therapy. Endoscopic therapy achieves hemostasis in up to 90% of cases. Recurrent bleeding occurs in up to 25% cases.8 Angiography with embolization or surgery should be reserved for the patients with refractory bleeding. Endoscopy prior to embolization or surgery helps to determine the diagnosis and to locate the bleeding site. A “second look” endoscopy is reserved for the patients with recurrent bleeding and in whom adequate examination was not possible at the time of initial endoscopy. A routine repeat endoscopy reduces the rate of recurrent bleeding without reducing the rate of the need for surgery and the risk of death.9

In patients with variceal bleeding, endoscopic therapy with variceal ligation or injection of sclerosant to obliterate the varices should be used.  A combination of endoscopic therapy and sandostatin use improves the chances to achieve hemostasis and reduces rebleeding rates compared with endoscopic therapy alone.10 The placement of transjugular intrahepatic portosystemic shunt (TIPS) should be reserved in patients with refractory or recurrent variceal bleeding.

GI bleeding and myocardial infarction

Concomitant presentation of myocardial infarction (MI) and UGI bleeding is ominous and common.2 UGI bleeding can precipitate an acute MI due to hypovolemia, hypoperfusion and increased myocardial contractile demand. Conversely, GI bleeding can be precipitated by use of antiplatelet and thrombolytic agents in the treatment of MI.2 The majority of UGI bleeding cases precipitated by the treatment of MI is self-limiting and resolve with correction of coagulopathy. However, an acute MI precipitated by a GI bleeding tends to be massive.2 Endoscopy in patients with an acute MI has higher mortality of 1% compared to usual rate of 0.0004% (2-59).2,11 The use of warfarin causes a five-fold increase in risk of GI bleeding.2

Antiplatelet agents and GI bleeding

Prostaglandins protect the gastric and duodenal lining from gastric acid. Aspirin decreases the production of prostaglandins from the GI mucosa and predisposes to the development of mucosal ulceration.2 Mucosal prostaglandin production is decreased with doses as low as 10 mg a day.2,12 The risk of UGI bleeding doubles at the dose of 75 mg a day and quadruples with dose of 300 mg a day and enteric coating does not reduce this risk.2,13-16 Clopidogrel should be recommended when there is an GI adverse event or if aspirin cannot be tolerated. Clopidogrel is associated with lower GI bleeding rate (0.52%) compared with aspirin (0.72%; p<0.5).2,17 A low dose aspirin with a PPI lowers incidence of GI bleeding.2 Recently, several PPIs were shown to inhibit CYP2C19 enzyme, thereby reducing the antiplatelet effects of clopidogrel. Thus, concomitant use of PPI in patients taking clopidogrel should be avoided.

The risk of GI bleeding is higher with the use of antiplatelet agents in patients with a history of peptic ulcer bleeding.2 The rate of recurrent bleeding within one year in such patients approaches 15%.2,18 Treatment of H.pylori prior to starting an antiplatelet agent may reduce the risk of GI bleeding.2

NSAIDS and GI bleeding

Approximately one in twenty NSAID users develop GI complications and ulceration and accounts for up to 30% hospitalization for UGI bleeding.2 NSAIDs inhibit prostaglandin production and misoprostol, a synthetic prostaglandin is used to reduce NSAID associated GI complications. However, its use is limited due to the development of diarrhea and abdominal cramps.2 The use of PPI in NSAID users significantly reduces risk of UGI bleeding.2,19-21


Figure 1. Algorithm for the management of patients with acute UGI bleeding.2 Adapted with permission from Laine L, Peterson WL. Bleeding peptic ulcer, N Engl J Med 1994; 331:717-727. Copyright 1994 Massachusetts medical society. All rights reserved.


Duodenal Arteriovenous malformation (AVM).                  S/p endoscopic thermal ablation.


Visible vessel with clot in duodenal bulb.                     S/p endoscopic cauterization.


Clean-based ulcer in the duodenum.                          Esophageal varices s/p endoscopic ligation.

Active spurting from an artery in the duodenum.

Figure 2. Endoscopic stigmata of various sources of UGI bleeding.


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2) Albeldawi M, Qadeer MA, Vargo JJ. Managing acute upper GI bleeding, preventing recurrences. Cleve clin J med 2010; 77 (2):131-142.

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5) Choudari CP, Rajgoapl C. Palmer KR. Acute gastrointestinal hemorrhage in anticoagulated patients: diagnoses and response to endoscopic treatment. Gut 1994; 35:464-466.

6) Rockall TA, Logan RF, Devlin HB et al. Risk assessment after acute upper gastrointestinal hemorrhage. GUT 1996; 38:316-321.

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8) Lau JY, Sung JJ, Lam YH et al. Endoscopic retreatment compared with surgery in patients with recurrent bleeding after initial endoscopic control of bleeding ulcers. N Engl J Med 1999; 340:751-756.

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13) Weil J, Colin-Jones D, Langman M, et al. Prophylactic aspirin and risk of peptic ulcer bleeding. BMJ 1995; 310:827–830.

14) De Abajo FJ, Garcia Rodriguez LA. Risk of upper gastrointestinal bleeding and perforation associated with low-dose aspirin as plain and enteric-coated formulations. BMC Clin Pharmacol 2001; 1:1.

15) Kelly JP, Kaufman DW, Jurgelon JM, Sheehan J, Koff RS, Shapiro S. Risk of aspirin-associated major upper gastrointestinal bleeding with enteric coated or buffered product. Lancet 1996; 348:1413–1416.

16) Garcia Rodriguez LA, Hernandez-Diaz S, De Abajo FJ. Association between aspirin and upper gastrointestinal complications: systematic review of epidemiological studies. Br J Clin Pharmacol 2001;52:563–571.

17) CAPRIE Steering Committee. A randomized, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). Lancet 1996; 348:1329–1339.

18) Wilcox CM, Ladabaum U. A patient with high risk of gastrointestinal bleeding requiring nonsteroidal anti-inflammatory drugs. Clin Gastroenterol Hepatol 2006; 4:1090–1093.

19) Lanas A, Garcia-Rodriguez LA, Arroyo MT, et al; Investigators of the Association Española de Gastroenterología (AEG). Effect of antisecretory drugs and nitrates on the risk of ulcer bleeding associated with nonsteroidal anti-inflammatory drugs, antiplatelet agents, and anticoagulants. Am J Gastroenterol 2007; 102:507–515.

20) Chin MW, Yong G, Bulsara MK, Rankin J, Forbes GM. Predictive and protective factors associated with upper gastrointestinal bleeding after percutaneous coronary intervention: a case-control study. Am J Gastroenterol 2007; 102:2411–2416.

21) Chan FK. NSAID-Induced peptic ulcers and Helicobacter pylori infection: implications for patient management. Drug Saf 2005; 28:287–300.

22) Chak A, Cooper GS, Lloyd LE, Kolz CS, Barnhart BA, Wong RC. Effectiveness of endoscopy in patients admitted to the intensive care unit with upper GI hemorrhage. Gastrointest Endosc 2001; 53:6–13.


GI- Gastrointestinal

UGI- Upper gastrointestinal

GAVE- Gastric antral vascular ectasia

NPO- Nothing per oral

PPI- Proton pump inhibitor

INR- International normalized ratio

TIPS- Transjugular intrahepatic portosystemic shunt

MI- Myocardial infarction

NSAID- Non steroidal anti-inflammatory



Upper gastrointestinal bleeding; endoscopy; hemostasis; recurrent bleeding.