Management of Gastrointestinal Bleeding

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23 Management of Gastrointestinal Bleeding

Nitin Dhamija, Robert Pousman, Omer Bajwa, Paul E. Marik

The interdisciplinary management of gastrointestinal (GI) bleeding involves volume resuscitation, correction of coagulation disorders, and protection of the airway while initiating diagnostic procedures to determine the site of bleeding.

The incidence of upper GI bleeding is estimated to be 37 to 172 per 10,000 population per year. Upper GI bleeding is nearly twice as common in males as in females, and its incidence increases with age, a pattern that has been attributed to increased incidence of predisposing comorbid conditions.^1,² The mortality rate for patients with upper GI bleeding has remained relatively stable over the past 40 years, ranging from 3% to 14%.¹ The risk of death depends on the patient’s age, presence of shock, comorbid medical conditions, presence of recent hemorrhage, location of the onset of bleeding (inpatient versus outpatient), and underlying cause of the hemorrhage (Table 23-1). Scoring systems to predict mortality and risk of rebleeding are based on host factors, the patient’s clinical course, and endoscopic findings.^1,² Variceal hemorrhage is associated with a mortality rate of 15% to 20%, and the risk of recurrent bleeding is about 30%.^3,⁴

TABLE 23-1 Risk Factors for Death After Hospital Admission for Acute Upper Gastrointestinal Hemorrhage

Advanced age

Shock on admission (pulse rate > 100 beats/min; systolic blood pressure < 100 mm Hg)

Comorbidity (particularly hepatic or renal failure and disseminated cancer)

Diagnosis (worst prognosis for advanced upper gastrointestinal malignancy)

Endoscopic findings (active, spurting hemorrhage from peptic ulcer; nonbleeding visible blood vessel; large varices with red spots)

Rebleeding (increases mortality 10-fold)

Causes of Upper Gastrointestinal Bleeding

The source of upper GI bleeding can be anywhere proximal to the ligament of Treitz. Note that bleeding from the nose, oropharynx, mouth, or lungs can present with symptoms suggestive of upper GI bleeding (e.g., emesis of bloody gastric contents). Upper GI bleeding can be classified into several broad categories based on anatomic and pathophysiologic factors:

1 Erosive or ulcerative lesions in the mucosa

2 Portal hypertension

3 Arteriovenous malformation(s)

4 Traumatic or postsurgical causes

5 Tumors

Causes of Lower Gastrointestinal Bleeding

Lower GI bleeding that occurs from a site distal to the ligament of Treitz can be grouped into multiple etiologies:

The most common cause of bleeding in patients younger than 50 years of age is hemorrhoids.⁵

Major Causes of Gastrointestinal Bleeding

Peptic Ulcer Disease

Peptic ulcer disease accounts for as many as half of the cases of upper GI bleeding. It is also the most common cause of bleeding in patients with portal hypertension and varices.¹ Bleeding from mucosal ulceration adjacent to a vessel can result from a Helicobacter pylori infection, use of nonsteroidal antiinflammatory drugs (NSAIDs), and/or critical illness. Concurrent aspirin and oral anticoagulation use further increases the risk of bleeding.⁶^–⁹ Acid suppression therapy (H₂-antagonists, proton pump inhibitors), however, has not affected the predominance of peptic ulcer bleeding as the cause of acute hemorrhage.¹⁰

Stress Ulcers

Owing to aggressive resuscitation and early enteral nutrition, bleeding from stress-related gastric ulcers among hospitalized patients is now relatively uncommon.

Esophageal Varices

Gastroesophageal variceal hemorrhage is a major complication of portal hypertension from cirrhosis and accounts for 5% to 15% of all cases of bleeding from the upper GI tract.¹¹^–¹⁴ The most common site of varices is the distal 2 to 5 cm of the esophagus. Superficial veins in this anatomic region lack support from surrounding tissues (Figure 23-1).¹⁵ The dilation of distal esophageal varices depends on a threshold pressure gradient, most commonly measured by the hepatic venous pressure gradient, defined as the difference between the wedged, or occluded, hepatic venous pressure and the free hepatic venous pressure (normal gradient < 5 mm Hg). If the hepatic venous pressure gradient is below 12 mm Hg, varices do not form.^16,¹⁷ Varices do not invariably develop in patients with gradients ≥12 mm Hg, so this pressure gradient is necessary but may not be sufficient in and of itself for varix formation.^16,¹⁷ Gastroesophageal varices are present in 40% to 60% of patients with cirrhosis; their presence and size are related to the underlying cause, duration, and severity of cirrhosis.¹⁸

Figure 23-1 Transjugular intrahepatic portosystemic shunt (TIPS).

Esophagitis

Significant bleeding from esophagitis and erosive disease is the second most common cause of upper GI hemorrhage, often causing occult blood loss rather than acute bleeding.⁶^–⁹ Clinically obvious bleeding is most likely in patients with extensive ulcerative disease or with an underlying coagulopathy.

Mallory-Weiss Tear

Mallory-Weiss tears usually occur in gastric mucosa, although 10% to 20% occur in esophageal mucosa. They account for approximately 5% to 7% of cases of upper GI hemorrhage.⁶^–⁹ A history of retching is obtained in less than one third of patients.¹⁹ Bleeding from Mallory-Weiss tears remits spontaneously in most patients; 5% experience rebleeding. Patients who experience rebleeding from a Mallory-Weiss tear usually have an underlying bleeding diathesis.^20,²¹

Angiodysplasia

Angiodysplasia of the GI tract is a common source of bleeding that can occur anywhere from stomach to colon. The cause of these lesions is not clear. These lesions also occur in patients with Osler-Weber-Rendu syndrome.

Diverticulosis

The prevalence of diverticular disease is age dependent, increasing from less than 5% at age 40 to 30% by age 60, to 65% by age 85. The high prevalence of the disease explains why diverticulosis is the most common cause of lower GI bleeding even though fewer than 15% of patients with diverticulosis develop significant diverticular bleeding. Diverticular bleeding typically occurs in the absence of diverticulitis, and the risk of bleeding is not further increased if diverticulitis is present.²² Risk factors for diverticular bleeding include²³:

1 Relative lack of dietary fiber

2 Aspirin and NSAID use

3 Advanced age

4 Constipation

Colitis

Infectious, ischemic, and idiopathic colitis (inflammatory bowel disease) can all manifest initially with hematochezia. Mucosal inflammation (colitis) is the common response to acute or chronic injury, resulting in activation of the immune system and inflammatory cascades. Establishing a specific diagnosis is paramount in the treatment of acute colitis, since therapy is dependent on the underlying disease process. The diagnosis requires an interpretation of the histologic and gross findings within the clinical context.

Neoplasms

Colon cancer is a relatively less common but serious cause of hematochezia. Neoplasms are responsible for approximately 10% of cases of rectal bleeding in patients older than 50 years, but neoplasms are rarely implicated as the etiology for GI bleeding in younger individuals.²⁴ Bleeding occurs as the result of erosion or ulceration of the overlying mucosa. The bleeding tends to be low grade and recurrent. Bright red blood suggests left-sided lesions; right-sided lesions can manifest with maroon blood or melena.

Hemorrhoids

Hemorrhoidal bleeding typically is painless, often presenting as bright red blood on stools, in the toilet, or on toilet paper. Hemorrhoids are dilated submucosal veins in the anus, located above (internal) or below (external) the dentate line.²⁵ They usually are asymptomatic but can manifest with hematochezia, thrombosis, strangulation, or pruritus. Hematochezia results from rupture of internal hemorrhoids that are supplied by the superior and middle hemorrhoidal arteries.

Initial Management of Gastrointestinal Bleeding

Bleeding stops spontaneously in most patients, but aggressive management is required when bleeding does not quickly resolve or when patients are at high risk for rebleeding. Priorities include achieving hemodynamic stability and preventing complications such as pulmonary aspiration.^26,²⁷ The rate of bleeding dictates the urgency of management:

1 Patients with trace hemoccult test–positive stools and without severe anemia can be managed as outpatients.

2 Visible blood requires hospitalization and inpatient evaluation.

3 Persistent bleeding or rebleeding with hemodynamic instability necessitates admission to the intensive care unit (ICU).

4 Massive bleeding, defined as loss of 30% or more of estimated blood volume or bleeding requiring blood transfusion of 6 or more units in 24 hours, requires aggressive diagnostic and resuscitative methods in the ICU and the involvement of the intensivist, the gastroenterologist, and, frequently, the GI surgeon.

In patients with upper GI bleeding, the amount of blood loss can be estimated by measuring the return from a nasogastric tube. An approximate estimate of blood loss can be made by the hemodynamic response to a 2-L crystalloid fluid challenge:

1 If blood pressure returns to normal and stabilizes, blood loss of 15% to 30% has occurred.

2 If blood pressure rises but falls again, blood volume loss of 30% to 40% has occurred.

3 If blood pressure continues to fall, blood volume loss of greater than 40% has probably occurred.

The degree of blood loss also can be estimated clinically by an evaluation of the heart rate, blood pressure, respiratory rate, urine output, and mental status (Table 23-2). The clinical estimation of blood loss is somewhat more difficult in patients with cirrhosis who have hyperdynamic circulation at baseline and a lower-than-normal systolic blood pressure and widened pulse pressure.

TABLE 23-2 Clinical Indicators as to Degree of Blood Loss

History and Examination

Assessment of comorbidities, careful cardiopulmonary evaluation including measurement of blood pressure and postural changes, heart rate, chest auscultation, ability of the patient to protect his or her airway, and a digital rectal exam to evaluate stool quality and assess for mass, hemorrhoids, fissures, or fistula are essential.

The clinical features of the GI bleeding provide clues to the probable source of bleeding within the GI tract (Table 23-3). When small amounts of bright red blood are passed per rectum, the lower GI tract can be assumed to be the source. In patients with large-volume maroon stools, aspiration via a nasogastric tube should be performed to assess the possibility of upper GI bleeding. Examination of nasogastric aspirate has diagnostic value, although in approximately 15% of patients with upper GI bleeding, the nasogastric aspirate fails to reveals blood or “coffee ground” material.^26,²⁷

TABLE 23-3 Clinical Indicators of Gastrointestinal Bleeding and the Probable Source Location Within the Gastrointestinal Tract

Clinical Indicator	Probability of Upper Gastrointestinal Source	Probability of Lower Gastrointestinal Source
Hematemesis	Almost certain	Rare
Melena	Probable	Rare
Hematochezia	Possible	Probable
Blood-streaked stool	Rare	Almost certain
Occult blood in stool	Possible	Possible

All patients with upper GI bleeding should have a nasogastric tube placed. Iced-saline lavage does not prevent or decrease upper GI bleeding.²⁸ Gastric lavage with lukewarm tap water offers an equally safe and cost-effective alternative.²⁹ Coffee-ground material or a frankly bloody gastric aspirate confirms an upper GI source of bleeding, whereas a nonbloody yellow-green nasogastric aspirate that contains duodenal secretions suggests the absence of bleeding proximal to the ligament of Treitz.³⁰ However, in up to 50% of patients with a bleeding duodenal ulcer, a nonbloody gastric aspirate is obtained,²⁹ possibly because of insufficient reflux of blood from the duodenum through the pylorus. Similarly, an intermittently bleeding upper GI lesion may result in a nonbloody gastric aspirate. The color of the gastric aspirate is of prognostic significance. Patients with coffee-ground or black gastric aspirates and whose stool is melanotic have a reported mortality rate of 9%.³⁰ However, patients who have bright red blood per gastric aspirate and red blood per rectum have a 30% mortality rate.³⁰ Red blood per rectum from an upper GI source usually signifies rapid bleeding.³¹

After the gastric contents have been aspirated, the nasogastric tube should be left in place to monitor ongoing bleeding and prevent pulmonary aspiration until there is no longer any evidence of bleeding. Maintaining this tube for a prolonged period, especially when the tube is attached to suction, may injure gastric mucosa and exacerbate GI hemorrhage.³²

Initial Resuscitation

Volume resuscitation with crystalloids is the first priority in the management of any patient with GI bleeding. Two large-bore peripheral intravenous (IV) catheters should be inserted and/or a large-bore central line venous catheter should be established. Resuscitation should be initiated with crystalloid solutions, either normal saline (2 L) or lactated Ringer’s solution. Large-volume resuscitation with normal saline alone may cause a hyperchloremic metabolic acidosis and is possibly associated with coagulation abnormalities. Colloidal solutions have no role in the management of patients with acute GI bleeding. A complete blood count including platelet count should be obtained. Other key laboratory studies should include blood typing and cross-matching, prothrombin time (or international normalized ratio), activated partial thromboplastin time, blood chemistry panel, liver function panel. Transfusion of packed red blood cells should be initiated for patients with an estimated blood loss greater than 15%. Transfusion of fresh frozen plasma should be initiated for patients with preexisting coagulopathy (from liver disease or anticoagulation; see Table 23-2). Platelet transfusion is indicated if the platelet count is less than 50,000/µL.

The endpoints of resuscitation include normalization of heart rate, blood pressure, and indices of end-organ perfusion. Vasopressor agents initially should be avoided because pressor-mediated vasoconstriction in a hypovolemic patient can cause severe end-organ ischemia.³³ Patients with a history of congestive heart failure, renal failure, or cirrhosis may require monitoring to assess cardiac parameters such as central venous pressure, cardiac output, stroke volume, and/or preload responsiveness. Although bedside pulmonary artery catheterization was widely used in the past for cardiac monitoring in the ICU, the recent trend in critical care medicine has been to use less invasive approaches such as bedside echocardiography or monitoring of pulse pressure variation.

Once venous access has been established, a nasogastric or orogastric tube should be placed to facilitate removal of particulate matter, fresh blood, and clots to facilitate endoscopy and decrease the risk of massive aspiration. Endotracheal intubation is recommended for patients with a high risk of aspiration, such as those with massive bleeding or altered mental status. In addition, endotracheal intubation facilitates endoscopy. While awaiting endoscopy or surgical intervention, octreotide infusion should be commenced in patients with severe upper GI bleeding.

Triage: Who to Admit to the Intensive Care Unit

Patients should be categorized as either low risk or high risk based upon prognostic scales that incorporate clinical, laboratory, and endoscopic data. Risk factors for rebleeding or mortality include age older than 65 years; shock; poor health status; comorbidities; low initial hemoglobin level; melena; need for transfusion; and fresh red blood on rectal examination, in emesis, or in nasogastric aspirate. Sepsis and elevated blood urea concentration, creatinine concentration, or serum aminotransferase level are additional risk factors. Endoscopic predictors include active bleeding, nonbleeding visible blood vessel, adherent clot, ulcer size greater than 2 cm, adverse ulcer location (posterior lesser gastric curvature or posterior duodenal wall), and adverse lesion type (ulcer, varices, or neoplasm).

The rate of rebleeding is approximately 3% in the low-risk group and 25% in the high-risk group. Patients in the low-risk group can be managed safely on a general medical floor. The decision regarding ICU admission should be individualized based on the patient’s risk stratification, age, comorbid diseases, clinical presentation, and endoscopic findings. Patients with active bleeding and two or more comorbidities have a mortality rate above 10% and should be observed in an ICU.³⁴ Patients with coronary artery disease are best managed in an ICU because of the risk of myocardial ischemia secondary to hypovolemia and hypoperfusion.⁴⁵ Admission to an ICU should be considered when endoscopic stigmata of recent hemorrhage, particularly visible vessels, are noted.

Further Management of Upper Gastrointestinal Bleeding

Endoscopy is the modality of choice for determining diagnosis, prognosis, and therapy for upper GI bleeding. Endoscopy should be performed after the patient has been adequately resuscitated and has achieved a degree of hemodynamic stability, but within 24 hours of presentation. In patients who have had relatively minor bleeding, endoscopy can be performed on a semielective basis.

Nonvariceal Bleeds

A meta-analysis of a large number of studies of nonvariceal bleeds demonstrated that endoscopic intervention decreased the mortality rate.³⁵ Multiple endoscopic therapies, including injection of epinephrine, injection of alcohol, injection of thrombin, injection of fibrin glue, thermal contact, or application of hemostatic clips, have been evaluated. Monotherapy with epinephrine provides suboptimal hemostasis. However, epinephrine plus a second method significantly reduces the risk of rebleeding, surgery, or mortality.

Variceal Bleeding

Variceal bleeding stops spontaneously in more than half of patients; however, in those who continue to bleed, the mortality rate approaches 80%. Without treatment to obliterate the varices, there is a 60% to 70% risk of rebleeding. The risk for acute recurrent bleeding is highest within the first 72 hours of the initial bleed and decreases with time, similar to the case for peptic ulcer hemorrhage.^36,³⁷ Another option is variceal band ligation^37,³⁸; advantages over injection sclerotherapy include fewer local and systemic complications, lower rebleeding rates, fewer endoscopic treatment sessions to obliterate varices, and lower mortality rate.³⁸^–⁴²

The diagnostic and therapeutic value of endoscopy in patients with upper GI bleeding is often limited by the presence of residual blood or clots.⁴³ To avoid this problem, gastric lavage is usually performed with a large-diameter nasogastric tube just before endoscopy.⁴⁴ Erythromycin induces rapid gastric emptying in healthy subjects and in patients with diabetic gastroparesis.⁴⁴^–⁴⁶ Infusion of erythromycin (250 mg) just prior to endoscopy improves esophagogastroduodenal cleansing and enhances the quality of endoscopic findings.⁴⁵

Further Management of Bleeding Peptic Ulcers

Pharmacologic Therapy

Although gastric acid–suppressing agents such as histamine receptor 2 blockers (H₂ blockers) have long been available as treatment options for patients with peptic ulcer disease, in acutely bleeding patients, their use has not reduced the number of transfusions, episodes of further bleeding or rebleeding, or the need for surgery.⁴⁶

Proton pump inhibitors (PPIs) are now widely used to suppress gastric acid secretion in patients with a variety of acid-related disorders.⁴⁷ Data from a number of studies⁴⁸^–⁵⁴ suggest that IV administration of a PPI reduces the risk of recurrent upper GI bleeding, but this therapy may not affect other outcome variables. Somatostatin is effective for controlling hemorrhage from esophageal varices,⁵⁵^–⁵⁷ but its efficacy in the setting of nonvariceal upper GI hemorrhage has not been demonstrated.⁵⁸

Role of Surgery

Although surgical intervention for peptic ulcer bleeding is less common than in the past, the indications for operation remain unchanged, including severe hemorrhage unresponsive to initial resuscitative measures; unavailability or failure of endoscopic or other nonsurgical therapies to control persistent or recurrent bleeding; and a coexisting second indication for operation, such as perforation, obstruction, or suspicion of malignancy.^59,⁶⁰

In a clinical trial that enrolled patients with recurrent upper GI hemorrhage, patients who were randomized to receive endoscopic retreatment had significantly fewer complications and tended to have decreased transfusion requirements, 30-day mortality rate, and use of the ICU than patients who were randomized to surgery.⁶¹ Nevertheless, 10% to 12% of patients with acute ulcer hemorrhage still require operative intervention for adequate hemostasis.⁶²

Further Management of Esophageal Varices

Pharmacologic Interventions

Vasopressin causes direct splanchnic and systemic vasoconstriction mediated via the V₁ receptor on vascular smooth muscle and thereby decreases portal venous flow and portal pressure.⁶³ Vasopressin can be administered either IV or directly into the superior mesenteric artery. As with other potent vasoconstrictors, vasopressin must be administered via a central venous line. Higher doses are associated with increased toxicity without further benefit. Vasopressin achieves hemostasis in about 55% of patients.⁶⁴ Systemic side effects, which occur in 20% to 30% of patients, can include myocardial ischemia, cerebral ischemia, acrocyanosis, congestive heart failure, cardiac arrhythmias, hyponatremia, hypertension, and phlebitis at the venous infusion site. Concomitant administration of nitroglycerin, either IV or sublingually, improves the safety and efficacy of vasopressin.⁶⁵ The combination of vasopressin and nitroglycerin more effectively controls bleeding and reduces toxicity but does not reduce mortality compared to vasopressin alone.⁶⁶ Terlipressin, a synthetic vasopressin analog, has been used instead of vasopressin to attempt to reduce the toxicity.⁶⁷ Terlipressin can be administered as intermittent boluses and has a better side-effect profile than vasopressin. A recent meta-analysis showed reduction in all-cause mortality with terlipressin compared to placebo. No statistical difference in outcome was noted among terlipressin and octreotide, vasopressin, or balloon tamponade. Terlipressin is not currently available for use in the United States.

Somatostatin causes splanchnic vasoconstriction, reduces azygos blood flow, reduces portal collateral circulation, and decreases portal pressure.⁶⁸ Somatostatin has been used successfully as an alternative to vasopressin to control variceal bleeding owing to its safer side-effect profile.⁶⁹ Octreotide, a synthetic somatostatin analog, is more commonly used than somatostatin and is the drug of choice in the United States. Somatostatin or octreotide therapy in addition to sclerotherapy is superior to either therapy alone in controlling bleeding and preventing rebleeding but has not been shown to improve long-term mortality. Likewise, the combination of somatostatin and endoscopic variceal ligation does not improve long-term mortality. Although both agents control acute bleeding and prevent rebleeding, neither somatostatin nor octreotide have a clearly demonstrated role in improving mortality.⁷⁰^–⁷⁴

Balloon Tamponade

Variceal hemorrhage that is unresponsive to combination therapy with octreotide and endoscopic therapy should be temporarily controlled by balloon tamponade, which initially can control hemorrhage in up to 90% of cases.^75,⁷⁶ Rebleeding occurs in approximately 50% of cases after balloon deflation if balloon tamponade is used alone.⁷⁷ Endotracheal intubation and adequate sedation is essential before placement of the balloon.^78,⁷⁹ Relative contraindications to balloon tamponade include esophageal stricture, recent caustic ingestion, recent esophageal surgery, large hiatal hernia, recent sclerotherapy, an unproven variceal source of bleeding, and an improperly trained support staff.^80,⁸¹ Esophageal rupture occurs in about 3% of cases. Other complications include pulmonary aspiration, alar necrosis, nasopharyngeal bleeding, and balloon impaction.^77,^80,⁸¹

Transjugular Intrahepatic Portosystemic Shunt

Transjugular intrahepatic portosystemic shunt (TIPS) is an intrahepatic low-resistance shunt between the hepatic and portal veins created by angiographic methods (see Figure 23-1). The shunt is kept patent by a fenestrated metal stent and decompresses the portal vein, similar to a surgical side-to-side portacaval shunt, but avoids the need for laparotomy.

Approximately 10% to 20% of patients fail to stop bleeding with standard medical therapy. Others rebleed in the first few days after cessation of the index bleed. A second attempt at endoscopic hemostasis is sometimes effective and is generally recommended.⁸² TIPS has been shown to achieve hemostasis in patients with refractory hemorrhage from varices. Among high-risk patients, placement of TIPS should be considered sooner rather than later, as significant improvement in mortality has been demonstrated in recent studies. TIPS also has been shown to improve long-term outcomes in patients who are poor candidates for surgery, such as those with sepsis, multiorgan failure, or cardiopulmonary compromise.⁸³^–⁸⁶ Principal complications of TIPS are listed in Table 23-4.

TABLE 23-4 Complications of Transjugular Intrahepatic Portosystemic Shunt (TIPS)

Technique-Related Complications	Complications Related to Portosystemic Shunting	Stent-Related Complications
Neck hematoma Cardiac arrhythmias Perihepatic hematoma Extrahepatic puncture of portal vein	Hepatic encephalopathy Increased risk of bacteremia Liver failure	TIPS-associated hemolysis
Infection of stent
Stent stenosis or ruptured liver capsule malfunction

Nonselective Beta-Blockers

Nonselective beta-blockers such as propranolol and nadolol have been used to prevent recurrent bleeding. Treatment with these agents can reduce the risk of recurrent bleeding and death from bleeding by about 40%. Sympathetic adrenergic activity regulates splanchnic arteriolar resistance.⁸⁷ Blockade of β-adrenergic receptors allows unrestricted α-adrenergic activity, producing splanchnic arteriolar vasoconstriction and decreasing portal venous inflow.

After an oral or IV dose of propranolol, portal pressure decreases by 9% to 31%.⁸⁸^–⁹⁵ It has been suggested that a decrease in heart rate and cardiac output also contributes to the decrease in portal venous inflow.⁸⁷^–⁹⁰ Findings suggest that the portal decompressive effect of propranolol is a specific splanchnic effect rather than a consequence of its systemic effects.⁹⁶ Nitrates such as isosorbide mononitrate have been shown to act synergistically with beta-blockers in reducing hepatic venous pressure gradient. The cumulative risk of hemorrhage was decreased from 29% among those who received nadolol alone to 12% among those who received the combination of nadolol and isosorbide mononitrate.⁹⁷ Nitrates, however, may worsen systemic arteriolar vasodilation due to cirrhosis and impair tissue oxygenation, presumably by dilation of arteriovenous channels in the peripheral circulation.

Nadolol has a longer half-life of biological activity ^98,⁹⁹ and can be administered once a day. It is more hydrophilic than propranolol; hydrophilicity limits intestinal absorption after oral administration as well as passage across the blood-brain barrier.^100,¹⁰¹ Propranolol is administered orally twice a day. The dose should be increased slowly until the heart rate decreases by 25% from baseline but remains above 55 beats per minute. Once a stable dose is achieved, propranolol can be changed to a once-a-day, sustained-release form¹⁰² that is equally effective.¹⁰³^–¹⁰⁹

Patients with a history of variceal bleeding should receive either combination pharmacologic therapy, including beta-blockers and nitrates, or a combination of endoscopic variceal ligation in addition to blood component therapy. The latter strategy has a significantly lower rate of bleeding, but it does not appear to affect survival rate. Combined use of endoscopic variceal ligation and nonselective beta-blockers is recommended for prevention of recurrent variceal bleeding. Combined drug therapy (beta-blockers and nitrates) should be reserved for patients who are not candidates for endoscopic variceal ligation.

Surgical Management

Surgery for bleeding esophagogastric varices continues to be the most reliable method to control acute hemorrhage and prevent its recurrence. Operative approaches generally consist of either (1) decompression of the high-pressure portal venous system into the low-pressure systemic venous system by creation of a shunt or (2) devascularization of the distal esophagus and proximal stomach with or without disconnection of the portal and azygous venous systems. In most instances, surgical procedures are used for prevention of recurrent hemorrhage rather than treatment of the initial bleeding episode. Because of the effectiveness of endoscopic therapies, emergency surgery for variceal hemorrhage in most centers is reserved for patients who have failed initial nonsurgical treatment and have reasonable hepatic function.¹¹⁰

Antibiotics in Variceal Bleeding

Bacterial infections are very common in patients with cirrhosis. Most common causes are urinary tract infections and spontaneous bacterial peritonitis (SBP). Mortality has been shown to be higher in patients with infections than in noninfected patients.^111,¹¹² Infections also predispose patients to recurrent variceal hemorrhage.¹¹³ A meta-analysis of five trials of short-term antibiotic prophylaxis in patients with variceal bleeding showed both a decrease in the number of infections in treated patients and improved survival.¹¹⁴ Any patient with cirrhosis and GI bleeding should receive a short course of antibiotic therapy (oral norfloxacin, 400 mg twice a day; or IV ciprofloxacin, 1 g once a day).¹¹⁵ The latter therapy may be appropriate in areas with high prevalence of fluoroquinolone-resistant organisms.

Further Management of Lower Gastrointestinal Bleeding

Eliciting a medical history and identifying pertinent risk factors help in determining the cause of lower GI bleeding. Use of aspirin or NSAID use is strongly associated with diverticular bleeding. Bleeding associated with antecedent hypovolemia should raise the possibility of ischemic colitis, whereas prior radiation therapy for prostate or pelvic cancer suggests radiation proctitis, which can appear months or years after radiation. A history of severe constipation should raise the possibility of a stercoral ulcer, and a recent colonoscopic polypectomy suggests postpolypectomy bleeding.

A careful digital rectal examination and sigmoidoscopy should be done to exclude anorectal pathology and confirm the patient’s description of the symptoms. Of rectal carcinomas diagnosed by proctoscopy, 40% are palpable on digital rectal examination.¹¹⁶

Colonoscopy

Colonoscopy is the mainstay of early and rapid diagnosis and treatment of lower GI bleeding. Colonoscopy has a very high diagnostic yield for patients presenting with lower GI bleeding.¹¹⁷ In addition, endoscopic therapy is applied to lower GI bleeding for many cases. Modes of endoscopic therapy for acute lower GI bleeding, in particular for angiodysplasia and diverticular disease, include thermal contact probes, laser, monopolar electrocautery (hot biopsy forceps), injection sclerotherapy, and band ligation.

Scintigraphy and Angiography

If the source of bleeding is not detected on colonoscopy, a bleeding scan followed by angiography should be considered if bleeding is severe. Although not as precise in identifying the site of bleeding as angiography, scintigraphy is safe and more sensitive, detecting active bleeding reliably at rates less than 0.1 mL/min.^118,¹¹⁹ Angiographic demonstration of a tumor, neovascularization, or vascular lesions may identify a presumed source of bleeding in the absence of extravasation. The specificity of this procedure is 100%, but sensitivity varies from 47% with acute bleeding to 30% with recurrent bleeding.

Angiography permits transcatheter administration of vasoconstrictors (vasopressin or terlipressin) for lower GI bleeding.¹²⁰ Although hemostasis is frequently achieved, rebleeding can occur in up to 50% of patients after cessation of therapy. Complications include abdominal pain, fluid retention, hyponatremia, transient hypertension, sinus bradycardia, premature ventricular contractions, and atrial fibrillation. Major complications have been reported and include pulmonary edema, serious arrhythmias, myocardial ischemia, and hypertension.¹²¹

Transcatheter embolization with various embolic agents (e.g., surgical gelatin sponges, microcoils, polyvinyl alcohol particles, detachable balloons) has been used with great success to control massive lower GI bleeding. Ischemic complications appear to be more common when embolization is performed for colonic rather than for upper GI hemorrhage because of the relatively sparse colonic collateral circulation. Embolic therapy may have utility in patients with coronary artery disease or in other situations where vasopressin therapy is relatively contraindicated or has failed. Embolization is an alternative to emergency surgery, primarily in non-neoplastic lesions and in high-risk patients.