A systematic review6 documented the incidence of presentingsymptoms in patients with upper GI bleeding, as noted in Table 54-1. Melena, hematemesis, presyncope, and epigastric pain aremost common.

Physical ExaminationInitial physical examination should focus on hemodynamic stability and organ perfusion, signs of underlying comorbid conditions, and a careful abdominal and rectal examination.Measurement of vital signs with orthostatic measurements isessential in estimating the amount of intravascular volume loss,although this may not be as reliable in patients with chronic orrecurrent bleeding. Resting tachycardia and a systolic blood pres-sure <100 mm Hg correlate to an estimated acute volume loss of25% and >30%, respectively.

Laboratory and Other StudiesSpecific blood tests should be obtained in patients with suspectedacute upper GI bleeding. Hemoglobin with type and screen should be obtained initially in all patients, and serial hemoglobinvalues can help in identifying ongoing hemorrhage. It is impor-tant to consider that a drop in hemoglobin may not be seen until 24–72 hours after the start of bleeding; likewise, hemoglo-bin may continue to drop even once bleeding has stopped, espe-cially with hydration. Coagulation studies should be obtained inall patients, as well as liver aminotransferase levels, blood ureanitrogen (BUN), creatinine, electrolytes, and albumin. An ele-vated BUN/creatinine ratio is often present with upper GI bleed-ing due to diminished renal perfusion. Coagulation abnormalitiesand low albumin can be markers of decreased synthetic functionof the liver. Testing for Helicobacter pylori infection should be performed in those patients who are found to have peptic ulcerdisease on upper endoscopy.

Differential Diagnosis

The broad differential diagnoses of upper GI bleeding include the most common causes of peptic ulcer disease, esophagitis, gastritis, varices, and nonspecific mucosal abnormalities. Clini-cians should also consider Mallory-Weiss tears, arteriovenous malformations, and neoplasms. Less common sources includeCameron’s lesions (ulcers in the sac of a hiatal hernia), Dieulafoylesions (dilated aberrant submucosal vessels), traumatic or post-

BACKGROUND

Acute upper gastrointestinal (GI) bleeding requires rapid assess-ment and treatment by a clinician. Early recognition is crucial toreduce morbidity and mortality. Defined as bleeding derived froma source proximal to the ligament of Trietz, upper GI bleeding typ-ically presents with a history of hematemesis or melena, whereashematochezia suggests a lower source. However, this maxim isnot absolute, as patients with acute profuse upper GI bleeding canpresent with hematochezia, and melena can occur from bleedingsources in the small intestine or proximal colon.

Causes of upper GI bleeding are multiple, with nonspecificmucosal abnormalities, peptic ulcer disease, esophagitis, gastritis,and varices being the most common. Other common causesinclude Mallory-Weiss tears, arteriovenous malformations, andneoplasms.1–3

ASSESSMENT

Prevalence

The incidence of upper GI bleeding is approximately 100 casesper 100,000 people per year.4 This translates to approximately250,000–350,000 hospitalizations each year in the UnitedStates for acute upper GI bleeding. Bleeding from the upper GItract is approximately four times as common as bleeding from thelower GI tract. Upper GI bleeding is twice as common in men thanwomen and more common in the elderly.5

Clinical Presentation

HistoryA focused history should reveal risk factors for upper GI bleeding,comorbid conditions, medication use (both prescription and non-prescription), alcohol and illicit drug use, and symptomatology.As stated before, a history of hematemesis or melena suggests anupper GI source of bleeding; however, severe upper GI bleedingcan result in hematochezia. A prior history of use of aspirin ornonsteroidal anti-inflammatory drugs should raise the suspicionof gastritis or ulcers. A history of alcohol abuse or cirrhosis sug-gests the possibility of variceal bleeding, portal hypertensive gas-tropathy, or gastritis. A history of vomiting, especially in analcoholic, can suggest a Mallory-Weiss tear.

SECTION SEVEN GASTROENTEROLOGY

CHAPTER FIFTY-FOUR

Upper Gastrointestinal BleedingErica Brownfield, MD, FACP, and Marc D. Rosenberg, MS, MD

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surgical causes such as aortoenteric fistulas, foreign body inges-tion, and postsurgical anastomosis.

Diagnosis

Patients who present with suspected upper GI bleeding (except forpatients assumed to have esophageal varices) should have anasogastric tube lavage to help confirm the diagnosis and toassess the severity of bleeding. Lavage can also be helpful inremoving residual blood and other gastric contents to aid in diag-nosis. Silverstein et al.7 found that 15.9% of patients with a clearaspirate, 29.9% with coffee-ground aspirate, and 48.2% with redblood aspirate had an active upper GI source of bleeding at thetime of endoscopy. However, lavage without blood does notexclude an upper GI bleed, as it may miss up to 16% of activelybleeding lesions.8 On the other hand, a lavage with a bilious aspi-rate suggests but does not guarantee that the bleeding is distal tothe ligament of Treitz.9 Identification of bleeding is a visual test,and guaiac testing of lavage fluid is not useful. Additionally, onceperformed the nasogastric (NG) tube should be removed forpatient comfort and to prevent subsequent morbidity from thetube.

Upper endoscopy is the diagnostic modality of choice for acuteupper GI bleeding and should be performed as quickly as possibleto speed appropriate intervention. It is highly sensitive and spe-cific for identifying bleeding lesions in the upper GI tract. Allpatients with acute upper GI bleeding should undergo upperendoscopy, unless the risks outweigh the benefits. Patients con-sidered to be at high risk for complications (i.e., those within 30days after myocardial infarction or very ill patients with anApache II score >16) have higher complication rates; therefore,individual decisions need to be made regarding whether or not toproceed with endoscopy,10 In all patients, endoscopy should onlybe done once hemodynamic stability, endotracheal intubation (ifneeded), and adequate monitoring in an intensive care unitsetting have been achieved.

Angiography and radionuclide red blood cell scans detect activebleeding and can be useful if upper endoscopy does not reveal asource of bleeding or cannot reach the source for therapy.

Prognosis

Mortality rates from upper GI bleeding are 6–10% overall.4

Despite advances in endoscopy and other minimally invasive pro-cedures, the mortality figures are largely unchanged over the past30 years, largely due to an aging patient population with anincreasing prevalence of associated medical comorbidities.6 Poorprognostic indicators such as being elderly, markers of severebleeding, comorbidities, and certain causes are associated withhigher mortality and are listed in Box 54-1. In the majority offatal cases, death is caused by deterioration of underlying ill-nesses rather than by GI bleeding.7

Persistent or recurrent bleeding occurs in 5–30% of patients.Risk of rebleeding can be predicted by endoscopic characte-ristics of a lesion. Patients with oozing or pumping lesions andvisible vessels on endoscopy have a higher risk of rebleed-ing and mortality rate than patients without active bleeding8,11

(Fig. 54-1).Prognostic factors should be used when determining hospital

management and therapeutic options for patients.

MANAGEMENT

Treatment

Hemodynamic resuscitation and stabilization should be the firstpriorities in management. Two large-bore peripheral intravenouscatheters or a central venous line should be placed for intra-

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Table 54-1 Presenting Symptoms in Upper GI Bleeding6

Symptom Incidence (%)

Hematemesis 40–50Melena 70–80Hematochezia 15–20Either hematochezia or melena 90–98Presyncope 43.2Epigastric pain 41Heartburn 21Dyspepsia 18Syncope 14.4Weight loss 12Diffuse abdominal pain 10Jaundice 5.2Dysphagia 5

Box 54-1 Factors Associated with Poor Prognosis in Upper GI Bleeding

Age over 60

Markers of severe bleeding

• Red blood in nasogastric aspirate

• Red blood in stool

• Requirement for blood transfusion

• Use of anticoagulants

• Hemodynamic instability.

Comorbid conditions

• Active coronary artery disease

• Renal failure

• Congestive heart failure

• Active lung disease

• Sepsis

• Metastatic cancer

• Advanced liver disease

Bleeding etiology

• Varices

• Neoplasms

• Rendu-Osler-Weber syndrome

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venous access. In patients with massive hematemesis, end-otracheal intubation should be considered to protect against aspi-ration. Intravenous fluids should be administered to maintainhemodynamic stability. Any patient who is hemodynamicallyunstable or who has varices should be admitted to an intensivecare unit (ICU). ICU placement should also be considered for those patients with a high risk of rebleeding (i.e., visible vessel in a peptic ulcer).

Blood products should be given when necessary. As a generalrule, in the setting of an acute GI bleed, young otherwise healthyadults should maintain a hematocrit of at least 20%; elderlypatients and those with severe comorbidities (such as coronaryartery disease) should maintain a hematocrit of at least 30% inorder to maintain adequate oxygen delivery. Patients with a coag-ulopathy or thrombocytopenia should be given fresh frozenplasma and platelets, respectively.

Any modifiable factors that may have contributed to bleed-ing should be eliminated (i.e., aspirin, nonsteroidal antiinflam-matory medications, anticoagulants, alcohol). Patients should be kept non per os (nothing by mouth) (NPO) until endoscopy.

Acid suppression with high-dose antisecretory therapy, withadministration of proton pump inhibitors (PPI), significantlyreduces the rate of rebleeding in patients with bleeding ulcers.This has not been shown with H2 receptor antagonists.12–14 Sincepeptic ulcer disease accounts for a large percentage of upper GIbleeds, it is reasonable to give a PPI while awaiting endoscopy. Ofnote, when given orally, PPIs are more effective with faster onsetof action and raising of pH compared to intravenous administra-tion and are far less expensive. However, if the patient needs to beNPO and endoscopy is imminent, intravenous administration isacceptable.

Octreotide, a somatostatin analog, may also be considered intreatment, as it has been shown to reduce the risk of rebleedingfrom variceal and nonvariceal causes.15

Consultation by a gastroenterologist is imperative in order toobtain both diagnostic and therapeutic upper endoscopy. Endoscopic therapy varies, depending on the findings, source of bleeding, availability of equipment, and the expertise of

the endoscopist. If a bleeding lesion is identified, therapeuticendoscopy can achieve acute hemostasis and prevent recurrentbleeding in most patients.

Upper GI bleeding caused by peptic ulcer disease should betreated with antimicrobial agents targeted toward H. pylori whenserologies are present. Antibiotic regimens are listed in Box 54-2.It is important to follow up on biopsy results of ulcers (Fig. 54-2).

Any patient who presents with significant upper GI bleeding(multiple blood transfusions required) or who remains refractoryto endoscopic therapy should be managed in consultation with asurgeon. Patients who are not surgical candidates can be consid-ered for angiography with embolization.

Secondary prophylactic measures are needed to decrease therisk of recurrent bleeding in patients with peptic ulcer disease andvarices. Patients with these diagnoses should be discharged onantisecretory therapy and beta-blockers, respectively.

DISCHARGE/FOLLOW-UP PLANS

Repeat endoscopy with follow-up by a gastroenterologist shouldbe arranged prior to discharge in any patient found to have agastric ulcer. This is necessary in order to document healing

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Visible vessel

Figure 54-1 • Endoscopic picture of ulcer with visible blood vessel.

Box 54-2 Antibiotic Regimens for Helicobacter pylori

1. PPI (twice daily) + amoxicillin (1 g twice daily) +clarithromycin (500 mg twice daily) × 7–14 days

a. For patients allergic to penicillin, metronidazole (500mg twice daily) can be used instead of amoxicillin

b. For patients allergic to macrolides, metronidazole(500 mg twice daily) can be used instead ofclarithromycin × 14 days

2. PPI (twice daily) + Bismuth (525 mg four times daily) + 2antibiotics (e.g., metronidazole and tetracycline both 500mg four times daily) × 7–14 days

Figure 54-2 • Endoscopic picture of hemostasis being achieved withuse of hemostatic clip on a bleeding ulcer.

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of these lesions, as biopsy may be required of a nonhealing ulcer in order to exclude underlying malignancy. Patients foundto be positive for H. pylori, should have follow-up studies such asstool antigen or breath test to document eradication. Patientswith variceal bleeding will need close follow-up by a hepatologist.

SUGGESTED READINGBoonpongmanee S, Fleischer DE, Pezzullo JC, et al. The frequency of

peptic ulcer as a cause of upper-GI bleeding is exaggerated.Gastrointest Endosc 2004; 59:788–794.

Fallah MA, Prakash C, Edmundowicz S. Acute gastrointestinal bleeding.Med Clin North Am 2000; 84(5):1183–1208.

Peter DJ, Dougherty JM. Evaluation of the patient with gastrointestinalbleeding: an evidence based approach. Emerg Med Clin North Am1999; 17(1):239–261.

Cappell MS, Iacovone FM. Safety and efficacy ofesophagogastroduodenoscopy after myocardial infarction. Am J Med1999; 106:29–35.

Gisbert JP, Gonzalez L, Calvet X, et al. Proton pump inhibitors versusH2-antagonists: a meta-analysis of their efficacy in treating bleedingpeptic ulcer. Aliment Pharmacol Ther 2001; 15:917–926.

Lau JY, Sung JJ, Lee KK, et al. Effect of intravenous omeprazole onrecurrent bleeding after endoscopic treatment of bleeding pepticulcers. N Engl J Med 2000; 343:310–316.

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Key Points

•Though hematemesis or melena suggests upper GI bleedingand hematochezia a lower source, acute profuse upper GIbleeding can present with hematochezia, and melena can occurfrom bleeding sources in the small intestine or proximal colon.

•Bleeding from the upper GI tract is about four times more fre-quent than bleeding from the lower GI tract, twice as commonin men as women, and more common in the elderly.

•Resting tachycardia and a systolic blood pressure <100 mm Hgcorrelate with an estimated acute volume loss of 25% and>30%, respectively.

•Patients with suspected upper GI bleeding should undergogastric lavage, recognizing that identification of bleeding is avisual test, and guaiac testing of lavage fluid is not useful. Oncecompleted, the NG tube should be removed for patientcomfort and to prevent subsequent morbidity from the tube.

•Upper endoscopy is the diagnostic modality of choice for acuteupper GI bleeding and should be performed as quickly as pos-sible to speed appropriate intervention. Persistent or recur-

rent bleeding occurs in 5–30% of patients and can be pre-dicted by endoscopic characteristics of a lesion.

•Patients with upper GI bleeding require IV access (preferablytwo peripheral 18-gauge catheters or larger), volume resusci-tation, and correction of coagulation abnormalities.

•In the majority of fatal cases, death is caused by deteriorationof underlying illnesses rather than by GI bleeding.

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REFERENCES1. Boonpongmanee S, Fleischer DE, Pezzullo JC, et al. The frequency

of peptic ulcer as a cause of upper-GI bleeding is exaggerated.Gastrointest Endosc 2004; 59:788–794.

2. Jutabha R, Jensen DM. Management of severe uppergastrointestinal bleeding in the patient with liver disease. MedClin North Am 1996; 80:1035–1068.

3. Silverstein FE, et al. The national ASGE survey on uppergastrointestinal bleeding. I. Study design and baseline data.Gastrointest Endosc 1981; 27:73–79.

4. Fallah MA, Prakash C, Edmundowicz S. Acute gastrointestinalbleeding. Med Clin North Am 2000; 84(5):1183–1208.

5. Longstreth, GF. Epidemiology of hospitalization for acute uppergastrointestinal hemorrhage: a population-based study. Am JGastroenterol 1995; 90:206–210.

6. Peter DJ, Dougherty JM. Evaluation of the patient withgastrointestinal bleeding: an evidence based approach. EmergMed Clin North Am 1999; 17(1):239–261.

7. Silverstein FE, et al. The national ASGE survey on uppergastrointestinal bleeding. II. Clinical prognostic factors.Gastrointest Endosc 1981; 27:80–93.

8. Silverstein FE, et al. The national ASGE survey on uppergastrointestinal bleeding. III. Endoscopy in upper gastrointestinalbleeding. Gastrointest Endosc 1981; 27:94–103.

9. Jensen DM, Machicado GM. Diagnosis and treatment of severehematochezia: the role of urgent colonoscopy after purge.Gastroenterology 1988; 95:1569–1574.

10. Cappell MS, Iacovone FM. Safety and efficacy ofesophagogastroduodenoscopy after myocardial infarction. Am JMed 1999; 106:29–35.

11. Katschinski B, Logan R, Davies J, et al. Prognostic factors in uppergastrointestinal bleeding. Dig Dis Sci 1994; 39:706–712.

12. Gisbert JP, Gonzalez L, Calvet X, et al. Proton pump inhibitorsversus H2-antagonists: a meta-analysis of their efficacy intreating bleeding peptic ulcer. Aliment Pharmacol Ther 2001;15:917–926.

13. Kaviani MJ, et al. Effect of oral omeprazole in reducing re-bleedingin bleeding peptic ulcers: a prospective, double-blind, randomized,clinical trial. Aliment Pharmacol Ther 2003; 17:211–216.

14. Lau JY, Sung JJ, Lee KK, et al. Effect of intravenous omeprazole onrecurrent bleeding after endoscopic treatment of bleeding pepticulcers. N Engl J Med 2000; 343:310–316.

15. Imperiale TF, Birgisson S. Somatostatin or octreotide comparedwith H2 antagonists and placebo in the management of acutenonvariceal upper gastrointestinal hemorrhage: a meta-analysis.Ann Intern Med 1997; 127:1062–1071.

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