Management of Acute GI Bleeding in Primary Care: An Update

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Resident & Staff Physician®, September 2005, Volume 0, Issue 0

Upper gastrointestinal bleeding is a common medical emergency that continues to be a significant cause of morbidity and mortality. It requires rapid and appropriate intervention to control the associated hemodynamic instability and prevent continued or recurrent bleeding. Etiology is the key to prognosis. Lower gastrointestinal bleeding usually ceases spontaneously but may also result in hemodynamic instability or symptomatic anemia. Recognizing the signs and symptoms of upper versus lower gastrointestinal bleeding is crucial for prompt and appropriate treatment.

Upper gastrointestinal bleeding is a common medical emergency that continues to be a significant cause of morbidity and mortality. It requires rapid and appropriate intervention to control the associated hemodynamic instability and prevent continued or recurrent bleeding. Etiology is the key to prognosis. Lower gastrointestinal bleeding usually ceases spontaneously but may also result in hemodynamic instability or symptomatic anemia. Recognizing the signs and symptoms of upper versus lower gastrointestinal bleeding is crucial for prompt and appropriate treatment.

Ali Ahmed Siddiqui, MD

Robert M. Coben, MD

Jorge A. Prieto, MD

Anthony J. DiMarino, MD

Division of Gastroenterology

Philadelphia, Pa

PRACTICE POINTS

  • The cause of upper GI bleeding is the best indicator of prognosis. Variceal bleeding carries the highest risk of recurrence and death.
  • Colonoscopy is the initial diagnostic study of choice in patients with acute lower GI bleeding who are hemodynamically stable.

Gastrointestinal (GI) bleeding is a common clinical disorder responsible for more than 300,000 hospital admissions each year in the United States.1 Bleeding from the GI tract may present clinically as acute upper tract bleeding (proximal to the ligament of Treitz), acute lower tract bleeding (distal to the ligament of Treitz), or occult blood loss evidenced by either a positive stool test for blood or iron deficiency anemia. The annual rate of hospital admissions for upper GI bleeding is estimated to be 36 to 102 patients per 100,000 population2; for lower GI bleeding, it is 20 per 100,000 population.1

Assessing Acute Upper GI Bleeding

Upper GI bleeding leads to 10,000 to 20,000 deaths and costs $2.5 billion annually in the United States.3 More than 40% of patients are 60 years or older.2 Most episodes are self-limited, and patients require only supportive care. However, continued or recurrent bleeding is associated with a mortality rate as high as 25%.2

Etiology

Helicobacter pylori

Figure 1 provides an overview of the causes of upper GI hemorrhage. Peptic ulcer disease accounts for about 35% of upper GI bleeding.4 Aspirin or nonsteroidal anti-inflammatory drug (NSAID) use is common in these patients. Infection with is less prevalent in patients with bleeding ulcers than in those with uncomplicated ulcers.

Bleeding from gastric erosions, esophagitis, or arteriovenous malformations usually stops by itself and is not life threatening. Bleeding from Mallory- Weiss tears, usually a consequence of retching, also usually stops spontaneously, although endoscopic hemostatic treatment is sometimes required. Bleeding of an aberrant submucosal artery (Dieulafoy's lesion) that erodes into the lumen of the stomach is a rare cause of recurrent, vigorous upper GI bleeding. Bleeding from upper GI malignancy is usually not severe, whereas bleeding from varices is often severe and can lead to hepatic encephalopathy, renal failure, or sepsis. Consider an aortoduodenal fistula in patients with a history of abdominal aortic aneurysm surgery who develop profuse bleeding.

Because of its specific management, chronic liver disease should be considered in any patient with upper GI hemorrhage. Esophageal and gastric varices typically occur in the setting of cirrhosis. Although they account for only 9% of all cases of upper GI bleeding,5 they have a disproportionate impact on medical resources. Prognosis depends on the severity of underlying liver disease rather than the severity of bleeding.

Clinical presentation

Hematemesis and melena are the most common features of acute upper GI bleeding. Approximately 26% of patients present with melena, 30% with hematemesis, and 41% with both; only about 3% present with hematochezia.6 Whether the patient presents with hematochezia or melena is determined by the amount and rapidity of bleeding. Melena can occur when as little as 50 to 100 mL of blood is introduced into the upper GI tract.

Prognostic indicators

Prognostic indicators include etiology, severity of initial bleeding, age, comorbid diseases, ulcer size, and hospitalization.

Etiology.

The cause of bleeding is the most important determinant of prognosis. Patients with bleeding from esophageal or gastric varices (Figure 2) have much higher rates of rebleeding (24%) and mortality (22%) than those with bleeding from other etiologies.7

Severity of initial bleed.

Indicators of severe bleeding or a high risk of continued bleeding include hemodynamic instability at time of presentation, repeated red hematemesis or hematochezia, and failure of the gastric aspirate to clear with lavage. Patients with a bloody nasogastric aspirate are about 3 to 4.5 times more likely to have a high-risk lesion than those with a clear aspirate.8

Age.

Patients older than 60 years are at increased risk of death. In a study of more than 3000 patients with upper GI bleeding, 73% of deaths occurred in patients older than 60 years.2

Comorbid diseases.

Upper GI bleeding concomitant to chronic diseases, such as coronary artery disease, chronic renal insufficiency, chronic obstructive pulmonary disease, or chronic liver disease, is associated with increased mortality risk.

Ulcer size.

The mortality rate in patients with ulcers larger than 2 cm is as high as 40%.9

Events in the hospital.

Bleeding during hospitalization is associated with an approximate 10% rate of mortality.10

Endoscopy

can predict the risk of rebleeding in a patient with nonvariceal upper GI bleeding (Figure 3). Endoscopic prognostic factors are listed in the Table. Evidence suggests that patients with low-risk lesions on endoscopy can be treated safely?and obviously less expensively?as outpatients.11 The key to triaging patients with upper GI bleeding is to obtain an early endoscopy to determine an accurate prognosis and hence the need for hospital admission.

Initial Management of Upper GI Hemorrhage

An algorithm for the management of upper GI bleeding is presented in Figure 4. The first focus for any patient with significant blood loss should be an evaluation of the severity of bleeding. Carefully measure blood pressure and pulse, with special attention to any orthostatic changes suggestive of shock. Large-bore central intravenous (IV) line access and vigorous volume replacement should be initiated immediately in all patients with significant bleeding to decrease morbidity. An infusion of isotonic electrolyte solutions can restore volume until vital signs stabilize. The rate of infusion depends on the severity of shock. Ameta-analysis has shown that crystalloids (eg, normal saline) should be used rather than colloids.12 However, normal saline should be used carefully in patients with suspected liver disease to avoid precipitating ascites. If blood transfusion is required, the goal is to maintain a hemoglobin concentration of at least 100 g/L. Packed erythrocytes are the preferred form for blood transfusions.

Blood samples for analysis of hemoglobin, platelets, coagulation factors, and typing should be sent to the laboratory immediately. Note that hemoglobin concentration is an unreliable marker of acute blood loss, but it is helpful to obtain as a baseline value.

Therapy for nonvariceal upper GI hemorrhage

The role of proton pump inhibitors (PPIs) in patients with acute nonvariceal upper GI hemorrhage has been studied extensively. A review of studies using IV omeprazole (which is now in clinical studies in the United States but is not yet approved by the Food and Drug Administration) for bleeding caused by peptic ulcer disease concluded that PPIs should be used whenever upper GI bleeding is severe enough to warrant endoscopic therapy. That review recommends considering PPIs when peptic ulcer is suspected in a patient who is hemodynamically unstable, when endoscopic evaluation is delayed or unavailable, and when blood transfusions are required.13 Further studies comparing IV omeprazole and IV omeprazole plus endoscopic therapy in patients with a nonbleeding visible vessel or adherent clot showed that those in the combination therapy group had fewer episodes of recurrent bleeding and a reduced need for blood transfusion.14

One randomized, placebo-controlled trial showed that oral omeprazole (Prilosec), at a dose of 40 mg every 12 hours for 5 days, reduced the rate of bleeding and the need for surgery in patients with bleeding peptic ulcers.15

Endoscopy, which can be used to diagnose and treat most patients with upper GI bleeding, reduces blood transfusion requirements and intensive care unit (ICU) and total hospital stays,16 particularly when performed within 24 hours of hospital admission. Almost half of hemodynamically stable patients with upper GI bleeding who are evaluated with upper endoscopy are found to have low-risk stigmata for recurrent bleeding and can be safely discharged and followed as outpatients.17 Most nonpeptic ulcer and nonvariceal causes of upper GI bleeding are treated with the same endoscopic modalities used for peptic ulcer bleeding; the major methods include thermal coagulation, injection therapy, and/or mechanical compression.

Mallory-Weiss bleeding usually stops spontaneously; continued bleeding is treated similarly to bleeding from peptic ulcers.

In thermal coagulation, electrical current (multipolar or bipolar electrode) or the direct application of a heated device (ie, heater probe) is used to seal the vessel. Hemostasis can be effectively achieved in 90% of patients with active bleeding, and rebleeding rates are reduced by more than 50%.18

Injection therapy, using saline or diluted epinephrine, yields initial results similar to those of thermal therapy, but it may not be as effective for long-term hemostasis.19 Thermal and injection therapy can be combined to control bleeding and treat the lesion definitively. Mechanical treatment methods include the use of hemostatic clips. In the few patients who have recurrent bleeding after initial endoscopic therapy, a second attempt is often successful and can reduce the need for surgery.20

Therapy for variceal upper GI hemorrhage

Because variceal hemorrhage is associated with an increased risk of mortality, aggressive resuscitation is vital. Antibiotics are also helpful in reducing mortality. Early endoscopy is essential for diagnosis and therapy. If early endoscopy is not possible, administer the vasoactive drug octreotide acetate (Sandostatin). Octreotide reduces portal venous blood flow and arterial flow to the stomach and the duodenum while maintaining renal arterial flow.11 Evidence suggests that variceal band ligation is the most effective therapy for esophageal varices.7,21 The best treatment for gastric varices found at the index endoscopy is currently undetermined, although transjugular intrahepatic portosystemic stents (TIPS) are reportedly beneficial.22 When initial treatments fail, initiate rescue therapy. Many experts believe that TIPS is the rescue therapy of choice.23,24

Acute Lower GI Bleeding

The annual incidence of lower GI bleeding is estimated to be 20.5 per 100,00 population, making it about one fifth as common as upper GI bleeding.1 The incidence increases more than 200-fold from the third to ninth decade of life.1 The mean patient age is 70 years,25 and mortality is approximately 4%.26

Etiology

The most common causes of lower GI bleeding are colonic diverticula, vascular ectasias, and tumors?all of which increase in prevalence with age (Figure 5).

Hematochezia, the most frequent presenting feature in lower GI bleeding, is variously described as bloody diarrhea, blood and clots per rectum, maroon-colored stool, and blood mixed with the stool. However, hematochezia is also sometimes a sign of upper GI bleeding, which is manifested as hemodynamic instability, hematemesis, and bloody nasogastric tube aspirate.

Diagnosis and treatment

An algorithm for the management of lower GI bleeding is presented in Figure 6. The initial approach to the patient is the same as with upper GI bleeding, namely, careful assessment of vital signs and vigorous volume replacement. A history of bleeding, inflammatory bowel disease, radiation therapy, and/or NSAID use may be helpful to obtain but will not identify the bleeding source. Patients with factors such as orthostatic hypotension, a decrease in the hematocrit value of 6% or less, transfusion of more than 2 units of packed red blood cells, or continuous active bleeding require admission to the ICU for observation.11

Diagnostic colonoscopy

is the study of choice in patients with acute lower GI hemorrhage, but it should only be used for patients who are hemodynamically stable. In a recent study, colonoscopy yielded a diagnosis in 85% of patents.27 The bleeding site can often be identified by the presence of a fresh clot or active bleeding (Figure 7). Endoscopic therapy of these lesions, using methods similar to those described for upper GI bleeding, can reduce the risk of rebleeding and the need for surgery. Vascular lesions can be treated with injection, contact thermal methods, or endoscopic laser therapy.

Radionuclide imaging and angiography

may be used when urgent colonoscopy cannot identify a bleeding source or when the bleeding is too rapid to permit colonoscopy.

Radionuclide imaging can detect active bleeding of 0.1 to 0.5 mL/min. It is more sensitive than angiography but less specific than a positive endoscopic or angiographic study.28 Radionuclide imaging is well tolerated by patients but is limited by its variable ability to localize bleeding, with a precision rate of around 45%.27 An advantage of tagged red blood cell scintigraphy is the ability to detect intermittent bleeding by performing serial scans over the lifetime of the radionuclide.

Angiography has a specificity of 100% but a sensitivity of only 30% to 47%.29 This study requires a bleeding rate of at least 1 mL/min. When a bleeding site is identified, intra-arterial infusion of vasopressin (Pitressin) or arterial embolization may be performed via the catheter. Intra-arterial vasopressin controls lower GI bleeding in 59% to 90% of patients, but bleeding recurs in 36% to 43% of cases once the vasopressin infusion is stopped.30 Transcatheter embolization may be better at controlling bleeding; newer studies indicate that the high rates of intestinal infarction reported in early series have been reduced to almost 0%.30 Other complications of arteriography, which occur in approximately 2% to 4% of patients, include arterial thrombosis, embolization, and renal failure.31

Small bowel evaluation

should be performed in patients with hematochezia when upper GI endoscopy and colonoscopy cannot detect the bleeding source. Push enteroscopy that allows evaluation of the proximal 60 cm of the jejunum is preferred.

A video capsule endoscopy, which can image the entire small bowel, identifies the site of bleeding in 55% to 65% of patients.32 One study showed that the most common capsule endoscopy findings were angiodysplasia (45%), fresh blood (23%), jejunal ulcers (10%), ileal inflammatory mucosa (6%), and ileal tumor (6%).33 Consider a nuclear medicine scan in young patients with lower GI bleeding to evaluate for Meckel's diverticulum.31 A new method of enteroscopy using a double-balloon technique allows not only diagnostic but also therapeutic endoscopic interventions for small bowel lesions. It is easy to handle and seems to be safe. Visualization of the entire small bowel is possible using both oral and anal approaches. It may one day become the gold standard modality for the small bowel.

Surgery

Surgical consultation is appropriate in all cases of GI bleeding but is most critical in patients with severe lower GI bleeding. Every effort should be made to diagnose the bleeding lesion. Even if the site cannot be identified, the physician will be able to guide surgical therapy to the most plausible segment of the colon. Surgical repair of a lesion identified endoscopically or radiographically is often curative. Empiric colectomy is reserved for life-threatening bleeding that cannot be localized and has not responded to available therapeutic approaches.

Conclusion

The approach to GI bleeding depends on the hemodynamic status of the patient. Rapid stabilization is required if signs and symptoms of shock or severe blood loss are present. Once the patient is stable, determine the likely source of bleeding. Vomited blood, melena, and/or bright red blood streaked in the feces suggest upper GI tract lesions. Such patients require early endoscopy. Bloody diarrhea or stools is more typical of lower GI bleeding and is evaluated with colonoscopy. Modern endoscopic therapeutic techniques have eliminated the need for surgery in most patients with GI bleeding, but surgical consultation should always be considered.

SELF-ASSESSMENT TEST

1. Which of these signs and symptoms is the most common presentation of upper GI bleeding?

  • Bright red blood from the rectum without feces
  • Tarry stools without vomiting of blood

2. All these factors indicate a poor prognosis in patients with upper GI bleeding, except:

  • Ulcer size less than 2 cm
  • Age older than 60 years

3. All these are recommended therapy for upper GI hemorrhage, except:

  • Oral omeprazole in a patient with peptic ulcer disease
  • Antibiotic therapy in a patient with variceal bleeding

4. Which of these is the diagnostic study of choice in patients with lower GI bleeding?

  • Radionuclide imaging
  • Colonoscopy

5. Which of these are the most common causes of upper and lower GI bleeding, respectively?

  • Varices and diverticulosis
  • Gastric erosions and polyps

(Answers at end of reference list)

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Answers:

1. C; 2. B; 3. C; 4. D; 5. A