Chapter 19. Gastrointestinal Bleeding

Gastrointestinal bleeding is an important cause of mortality for emergency department (ED) and critical care patients. This chapter discusses the two major types of bleeding, upper and lower, followed by detailed information on the management of these difficult patients.

Upper gastrointestinal bleeding (UGIB) is an important cause of mortality in the ED with rates from 3% to 16%.1–7 In the United States, UGIB represents 400,000 hospital admissions8 and 30,000 deaths annually.9 Hospital in-patients presenting with UGIB have a 2- to 6-fold increase of mortality compared with their ED counterparts.1–7 Increased risk of mortality is associated with increased age, severe comorbidity, hypotension, shock, rebleeding, and the timing of the bleeding event during an in-patient hospital stay.2,10

Clinical Presentation

Patients with UGIB often present with hematemesis, coffee ground vomiting, melena, or maroon stool, while hematochezia is typically associated with massive hemorrhage. The presentation of bleeding depends on the amount and location of hemorrhage. Patients may present with complications of anemia, including fatigue, chest pain, syncope, and shortness of breath. Untreated manifestations of progressive hemorrhagic shock are inevitable, including acute end-organ dysfunction and refractory hypotension.

The physical exam should include an assessment of airway, vital signs, and mentation. An abdominal exam, if tenderness is elicited, aids in localizing the source to a gastric or duodenal location. Blood on digital rectal exam may suggest both chronicity and degree of bleeding. The absence of rectal blood, however, does not exclude the existence of a gastrointestinal source. Stigmata of chronic liver disease including jaundice, telangiectasia, hemorrhoids, or caput medusae may indicate the presence of esophageal or gastric varices.

Etiology

UGIB can originate from a number of sources and are discussed below in order of frequency. A list of causes of upper GI bleeding is listed in Table 19-1.

Peptic Ulcer Disease

Despite the advent of H2 receptor antagonists and proton pump inhibitors (PPIs), peptic ulcer disease (PUD) remains the most common etiology of UGIB accounting for 140,000 hospitalizations each year in the United States.11 Approximately 28–59% of UGIB is represented by PUD, with the majority of duodenal, as opposed to gastric, origin.1,12 GI bleeding from a duodenal location is fairly common owing to its abundant blood supply and the posterior location of the gastroduodenal artery to the bulb. This is the case with most massive UGIBs. The presence of large ulcers in the posterior duodenal bulb or on the lesser curvature of the stomach is associated with increased mortality.

The pathophysiology of PUD results from the overproduction of gastric acid and pepsin. These overwhelm the mucosal barriers and reduce mucous and bicarbonate secretion.13 Nonsteroidal anti-inflammatory drugs (NSAIDs) cause ulcerative disease by submucosal erosion and reduction of prostaglandin production. The elevated rate of PUD witnessed in the United States parallels the high rate of NSAID use, which has been observed at 50%.1 NSAID use is currently considered the most significant risk factor associated with UGIB. Concurrent steroid use increases the risk of ulcer formation.

Helicobacter pylori, a gram-negative bacteria residing in the mucosal layer of the stomach, is the most common causative etiology of PUD via the stimulation of gastrin production. The majority of nonbleeding duodenal (90%) and gastric (75%) ulcers are associated with H. pylori infections. Consequently, one large Canadian study found 45% of nonvariceal UGIB cases were H. pylori positive.14 Recurrence of bleeding from H. pylori disease is rare when this organism is eradicated as part of ulcer treatment.15 When present with a history of NSAID use, H. pylori has an additive effect and a consequent increase in UGIB risk with an odds ratio (OR) of 6.13.16

Less common causes of PUD are high-gastrin-secreting states such as Zollinger–Ellison tumors. Smoking, history of alcohol abuse, and acute hepatic failure may exacerbate a preexisting ulcer, decrease healing, and increase recurrence and perforation rates.

The patient with PUD classically presents with intermittent burning epigastric pain that occurs 1–3 hours after meals and is relieved by food and antacid. Constant epigastric pain suggests that there is transmucosal penetration of the ulcer. Referred back pain can be a sign of pancreatic inflammation. Diffuse peritoneal irritation and severe abdominal pain can be signs of perforation. Approximately 5% of penetrating duodenal ulcers will erode into the peritoneal cavity and cause a chemical peritonitis. Typically the patient can recall the exact time of onset of the abdominal pain, which is frequently accompanied by tachycardia and, later, dehydration, fever, and ileus. Free air underneath the diaphragm on upright chest radiograph is pathognomonic of perforated viscous. This complication constitutes an emergency, which warrants the initiation of appropriate fluid resuscitation, pain management, and surgical consultation. In general, the elderly are at increased risk for gastric perforation. GI bleeding is the most common cause of death in PUD patients with comorbidities or over the age 65 years.17

The prevalence of mucosal erosive disease in UGIB ranges from 1% to 31% and is often reported as the second leading cause of UGIB. These diseases may present as esophagitis, gastritis, duodenitis, or esophageal ulcer. The pathophysiology and risk factors mimic those of PUD. The lack of standardization in reporting esophagitis and other erosive diseases across study cohorts may explain the wide spectrum of prevalence observed.12

Stress ulcers, a relevant subset of mucosal erosive disease, deserve particular mention in critical care patients. Uncommonly present in ED patients, stress ulcers are mucosal defects, which are induced during periods of increased physiologic demand and critical illness. Illnesses such as massive burns, trauma, elevated intracranial pressure, sepsis, and severe shock are all causes of stress ulcers. The pathophysiology of stress ulcer is unclear, but is generally thought to be caused by splanchnic hypoperfusion and poor reperfusion. The concomitant reduction in bowel motility and mucosal secretion of protective substrates are contributory. The increased acidic milieu promotes the progression of these superficial diffuse changes to ulcerative lesions. Unlike PUD, H. pylori plays a limited role in stress ulcers. Patients presenting with stress ulcers may be distinguished from the typical ED presentations of PUD by the following risk factors: profound persistent hypotension or shock, high-dose vasopressor use, chronic mechanical ventilation, severe burns, uremic renal failure, greater than 6 days of nasogastric tube placement, acute CNS illness, and high-dose steroid utilization.18 Stress ulcers typically heal when the underlying clinical condition is addressed. Variants of stress ulcers include Cushing's and Curling's ulcers.

Esophageal Varices

Gastric and esophageal varices remain an important cause of UGIB accounting for 6–14% of presentations. Populations with high ethanol consumption observe higher rates secondary to liver cirrhosis. It is not uncommon for patients with no prior diagnosis of cirrhosis to present to the ED with a herald bleeding event. Varices account for 50–60% of UGIB events in the cirrhotic patient.12 Often a consequence of cirrhosis-induced portal hypertension, varices are dilated submucosal veins in the lower esophagus or gastroesophageal junction. Varices place the patient at risk for developing a life-threatening bleeding. The sequence of events that lead to variceal rupture begins with increased hepatic resistance and increased portal blood flow. These two factors cause an increase in the portal pressure, causing dilation of preexisting vessels and the formation of varices. Repeated increases in portal pressure due to meals, ethanol, exercise, and increased abdominal pressure all cause further dilation of varices. Rupture and bleeding occur when the elastic limit of the vessel wall is exceeded.19 Bleeding is characteristically severe and is associated with an in-patient mortality of 11–34%: the highest rates are observed in cirrhotics.20

Mallory–Weiss

Mallory–Weiss (MW) syndrome accounts for 2–7% of UGI bleeds.1,5,21 The pathogenesis of MW syndrome is not completely understood, although any disease that causes retching or vomiting can induce MW. Alcoholism is the most frequently associated condition, although eating and coughing disorders, pregnancy, heavy lifting, diabetic ketoacidosis, and blunt abdominal trauma have all been described.22,23 Linear tears, thought to occur as a result of a transient high transmural pressure gradient across the region of the gastroesophageal junction, characterize MW syndrome. Overdilation of the noncompliant lower esophagus can also produce an injury as described in postcardiopulmonary resuscitation patients.24 There is a 0.07–0.49% incidence of MW as an iatrogenic consequence of gastroesophageal endoscopy.25,26

The presence of a hiatal hernia may be a predisposing factor for MW. It has been proposed that, in hiatal hernia patients, a higher pressure gradient develops in the hernia compared with the rest of the stomach during retching, thereby increasing the potential for mucosal laceration.27 MW tears typically result in mild to moderate GI bleeding, but are rarely severe in nature. These superficial mucosal tears tend to heal rapidly and are often self-limited. Bleeding spontaneously stops in about 90% of cases, although coagulopathy or preexisting comorbidities such as thrombocytopenia and liver failure can result in refractory bleeding.28 Low admission hematocrit (HCT), shock, or active bleeding during endoscopy is predictive of a complicated course.29,30

Vascular Anomalies

Vascular anomalies or angiodysplasia account for about 2–5% of acute UGIB. Upper gastrointestinal angiodysplasia occurs most commonly in the stomach, rarely in the duodenum or esophagus. Bleeding from angiodysplasia is associated with advanced age, aortic stenosis, chronic renal failure, and calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia (CREST) syndrome.

Rare Causes of UGIB

Leiomyomas and gastrointestinal stromal tumors constitute about 1% of primary gastrointestinal tumors, mostly occur in the stomach, and often present with overt UGIB. Adenocarcinoma is the most common primary malignancy. It presents as a gastric mass, nonhealing ulcer, or stricture. Gastric lymphomas constitute about 5% of gastric tumors. Specifically, gastric mucosa-associated lymphoid tissues (MALTomas) are early B-cell lymphomas highly associated with chronic H. pylori infection. They rarely cause acute bleeding. Gastric metastases most commonly arise from lung cancer, breast cancer, and cutaneous melanoma. These malignancies frequently rebleed and have a poor long-term prognosis. Radiation and chemotherapy treatment for gastric malignancies can result in UGIB that are difficult to manage and usually require a multidisciplinary approach.31

Aortoenteric fistula often presents with a mild “herald bleed” followed by massive hemorrhage. This diagnosis constitutes a high mortality with delayed diagnosis. For this reason, emergency esophagogastroduodenoscopy (EGD) is indicated if this diagnosis is suspected. Aortoenteric fistula is a rare consequence of prior aortic surgery, aortic aneurysms, and severe atherosclerosis. These fistulas are typically located at the distal duodenum underscoring the role of endoscopic investigation up to this location. During EGD, if a prosthetic graft mesh is found, the scope should be withdrawn without attempting therapeutic intervention and the lesion should be treated intraoperatively due to the risk of massive bleeding.32,33

Lower gastrointestinal bleeding (LGIB) accounts for about one quarter to one third of all admissions for gastrointestinal bleeding.34 The incidence of acute LGIB is estimated at 20–27 per 100,000 adult population at risk, significantly lower compared with UGIB with 100–200 cases per 100,000 population.35 The incidence of LGIB increases with age and is higher in men, presumably because of the increased frequency of vascular disease and diverticulosis in older men. Mortality rates of acute LGIB are consistently in the range of less than 5%.

LGIB is defined as hemorrhage that arises distal to the ligament of Treitz and encompasses a broad clinical spectrum that ranges from insignificant hematochezia to severe hemorrhage with shock.36 Acute LGIB is defined as bleeding of less than 3 days' duration. Severe hemorrhage is defined as a decrease in HCT by 20% or a transfusion requirement of ≥2 U of blood. Other clinical data associated with severe bleeding include heart rate ≥100/min, syncope, systolic blood pressure ≤115 mm Hg, nontender abdominal examination, aspirin use, bleeding per rectum during the first 4 hours of evaluation, and more than two active comorbid conditions.37

Clinical Presentation

Acute LGIB often presents as hematochezia, melena, or dark red blood with clots. A digital rectal exam is required. Hematochezia is the most common presentation of LGIB. However, 10–15% of hematochezia presentations are from a UGIB source.38 Melena suggests a source of bleeding proximal to the cecum, while dark red blood with clots suggests the ascending colon.

Etiology

The most common etiologies of LGIB will be discussed in order of frequency. A list of causes of lower GI bleeding is included in Table 19-2.

Diverticular Disease

Diverticular diseases are the most common cause of significant and life-threatening LGIB, accounting for 50% of cases.38,39 Diverticula develop where the vasa recta (intramural branches of the marginal artery supplying the colon) penetrate the colonic wall.40 They most frequently occur in the left colon, but can exist anywhere in the colon, except the rectum. Abnormal colonic motility, defective muscular structure, increased cross-linking of collagen, and aging are all causes of diverticula. In addition, a diet low in fiber can lead to firm, small stools, which cause reduced transit time. Over time, vigorous contractions in the colon push the inner intestinal lining outwards through vulnerable points in the muscle walls.41 High intraluminal pressure and a weak colonic wall at the sites of vessel penetration into the muscularis lead to herniation.42 The pouches that develop are called diverticula. Diverticular hemorrhage is thought to occur when the damaged vessel ruptures at the dome or the neck of the diverticulum. The most common presentation of diverticular bleeding is massive painless rectal hemorrhage. Severe blood loss is noted in 3–5% of patients with diverticulosis. In approximately 80% of patients, diverticular bleeding resolves spontaneously.43

Angiodysplasia

Angiodysplasias of the intestine or arteriovenous malformations (AVMs) account for up to 30% of LGIB.44 AVMs are found in patients older than 50 years of age and are distributed equally between the sexes. These lesions are notably associated with aortic stenosis and renal failure, especially in elderly patients. The exact mechanism of development of angiodysplasia is not fully known. Development is related to age and strain on the bowel wall.45 Chronic venous obstruction is proposed to play an important role. When applied to the bowel lumen, the Laplace law states tension is highest in bowel segments with the greatest diameter, such as the right colon. Repeated episodes of colonic distention are associated with transient increases in lumen pressure and size. Over time, this process causes gradual dilation of the submucosal veins, the venules, and the arteriolar capillary units feeding them. Ultimately, the capillary rings dilate, the precapillary sphincters lose their competency, and a small arteriovenous communication forms.46 A link between a deficiency of high-molecular-weight multimers of von Willebrand factor, aortic stenosis, and colonic angiodysplasia has also been proposed.45 The hemorrhage tends to arise from the right side of the colon, with the cecum being the most common location. However, AVMs can occur anywhere in the colon, rectum, and small bowel. Most patients experience chronic bleeding, but up to 15% of patients can present with massive hemorrhage.47

AIDS/HIV

Patients with HIV/AIDS may have unique etiologies of gastrointestinal bleeding compared with their non-HIV cohorts. Sources of UGIB, although frequently unrelated to HIV, may include cytomegalovirus and Kaposi's sarcoma. LGIB, however, are often HIV related with etiologies including CMV colitis, hemorrhoids, and anal fissures. Because of concomitant thrombocytopenia, HIV patients may present with significant bleeding from an otherwise self-limiting source (i.e., hemorrhoid).48

Other Causes of LGIB

Patients with a previous history of atherosclerotic disease, vasopressor use, or shock should be assessed for ischemic colitis. Other less frequent etiologies of LGIB include malignancy, inflammatory bowel disease, NSAID use, infectious colitis, anorectal disorders, small bowel sites (i.e., Crohn's, Meckel's diverticula), and postpolypectomy bleeding.34,36

Careful consideration of the management approach of gastrointestinal bleeding is needed due to the high morbidity and mortality associated with this condition. Despite advances in medical management and therapeutic interventions, the mortality from UGIB remains unchanged over the past 40 years.49,50 For critical patients, consultation with gastroenterology and surgery should occur early in the patient's course. Several management considerations are discussed in detail below.

Resuscitation

The management of patients with GIBs includes initial and ongoing resuscitation. Aggressive replacement of lost volume with crystalloids and colloids is obligatory in hemodynamically unstable patients. Initial resuscitation should begin with the placement of two large-bore intravenous catheters, and administration of one to two 20 mL/kg bolus of crystalloid with the short-term goal of resolution of tachycardia and hypotension to restore tissue perfusion. Refractory hypotension or evidence of end-organ hypoperfusion should prompt the administration of packed red blood cells (PRBCs). Blood administration should not be delayed pending the results of a repeat hemoglobin (Hb) or the visualization of hematemesis, melena, or hematochezia in the setting of hemodynamic compromise.

Airway Considerations

Massive hematemesis can result in a compromised, visibly obscured airway. Manifestations of hemorrhagic anemia may cause decline in mentation and increased aspiration risk. Moreover, endoscopic interventions in patients with frequent bouts of hematemesis, vomiting, or retching can prove challenging and may lead to further complications. Consequently, establishing a definitive airway in the anticipation of potential cardiovascular compromise and need for therapeutic endoscopic or surgical intervention may be warranted in the setting of large-volume hematemesis.

Laboratories

In the evaluation of the bleeding patient, blood should be immediately sent for CBC, electrolytes, calcium, renal function, glucose, prothrombin time, partial thromboplastin time, and INR, and typed for cross-matched blood. While a low Hb is the rule in cases of massive GI bleeding, slow, intermittent bleeds or early presentations can have Hb levels within normal range. In a study that identified 51% of UGIB patients who ultimately required transfusion, the mean presenting Hb was 11.3.51 Because of the potentially dynamic nature of gastrointestinal bleeding, serial Hb and HCT should be collected to identify significant changes over time. These changes may or may not be heralded by a disruption in hemodynamics, change in clinical appearance, or symptoms such as chest pain, shortness of breath, or altered mentation. An elevated blood urea nitrogen (BUN) to creatinine ratio is suggestive of an upper GI source.51 However, rapid transit may preclude the elevation of BUN and present with a normal ratio. The existence of thrombocytopenia or coagulopathic disturbances should prompt judicious correction with platelets, fresh frozen plasma, and/or cryoprecipitate.

Gastric Tubes and Lavage

The placement of a gastric tube should be considered in the appropriate setting to ascertain both the existence and degree of severity of a UGIB. While nasogastric tube placement can be performed in the alert mentating patient with a gag reflex, there are multiple potential issues. Serious risks include aspiration pneumonitis, laryngospasm, and perforation of the pharyngeal and gastrointestinal structures.52 Contraindications to placement include history of esophageal varices or strictures, recent alkaline ingestion, and a history of gastric bypass surgery. Patients with an altered level of consciousness should be intubated in order to provide airway protection prior to placement of a gastric tube. In the event of maxillofacial trauma, patients should have an orogastric tube placed to avert passing the tube through the cribriform plate. If immediate endoscopy is available, the gastric tube offers little incremental benefit and may be omitted.

Room-temperature tap water or saline lavage prior to endoscopy is considered safe and an important adjunct in management of suspected UGIB from PUD.53 Ice water lavage was once considered an acceptable therapeutic intervention for UGIB via gastric vessel vasoconstriction; however, this is not supported by the literature.54 The aspiration of fresh blood indicates active bleeding, whereas an aspirate with a coffee ground appearance is associated with a subacute or chronic etiology of the UGIB. The lack of bloody aspirate does not rule out the possibility of a UGIB.55,56

Blood Product Administration

Blood products provide obvious benefits in repleting lost volume, replacing blood components, and correction of acidosis. However, a number of studies have demonstrated that blood product administration has been associated with immune suppression, increased nosocomial infection rates, and death.57 Hence, it is important to properly select patients who would receive the greatest benefit from blood administration.

Patients exhibiting signs of end-organ hypoperfusion benefit from the additional oxygen-carrying capacity of PRBCs. Findings suggestive of global tissue hypoxia may include altered mental status, seizures, hypoxemia, ischemic electrocardiographic changes, or elevation of lactate, creatinine, hepatic transaminases, or troponin. In the absence of these findings, Hb should be kept at ≥757 in patients without history of coronary artery disease (CAD) and ≥10 in those with a history of CAD.58

Coagulopathy

GI bleeding may result from the use of anticoagulants such as warfarin, antiplatelet agents such as aspirin or clopidogrel, or NSAIDs. In addition, a history of factor deficiency or cirrhosis may indicate that a disruption in the homeostasis of the coagulation cascade exists. Therapy should be directed at correcting the underlying etiology in these cases.

Warfarin toxicity is treated with the administration of 4–6 U of FFP. Vitamin K administration will also reverse the effects of warfarin; however, its onset of action is much delayed and its effect will last 1–2 weeks. Such reversal with vitamin K should be carefully weighed against the future need to chronically anticoagulate the patient. Platelets may be administered to actively bleeding patients with a history of thrombocytopenia, salicylate, or NSAID use. Cryoprecipitate and individual clotting factors may be administered if appropriate. DDAVP or desmopressin should be considered in patients who present with chronic renal failure or uremia to increase the production of von Willebrand factor as these patients have poor platelet aggregation.

Factor VII, which is available in a recombinant formulation, complexes with tissue factor and activates factor Xa inducing the production of clot. It is approved for use in bleeding patients with hemophilia A. In cirrhosis, factor VII administration remains controversial as there are conflicting results from trials evaluating its use in the management of acute variceal bleeding.59 Novel agents such as prothrombin complex concentrate may serve a future role in massive hemorrhage in patients with a known deficiency of Vitamin K, although they are contraindicated in patients with disseminated intravascular coagulation or liver disease.60

Massive Blood Transfusion

Bleeding patients who require greater than 10 U of PRBC over a 24-hour period are also at risk for the depletion of coagulation factors and platelets because of the dilutional effect. Once the first 10 U of PRBC has been administered, consideration should be made for the administration of fresh frozen plasma and platelets. The precise ratios that would render most benefit are unclear.61,62 Patients should also be monitored for volume overload, hypothermia, hyperkalemia, hypocalcemia, and iron toxicity.60

Proton Pump Inhibitors

PPIs act via the Na–K-ATPase channels to interrupt the production of H+ ions. Increasing the gastric pH promotes platelet aggregation that is impaired in acidic environments.63 The PPI should be administered intravenously and the patient kept NPO. When compared with placebo or H2 receptor antagonist, PPI reduces the risk of rebleeding and the need for subsequent surgery in endoscopically diagnosed UGIB from peptic ulcer. PPI, however, has not been shown to reduce the overall mortality from peptic ulcer bleeding,64 but may reduce the mortality in patients with high-risk endoscopic findings such as active bleeding or a visible vessel. PPI remains an important adjunct to endoscopy as it reduces the need for therapeutic intervention during the procedure.65 The optimal dose and route of administration have not yet been clearly elucidated; however, suggested dosing is an initial intravenous bolus equivalent to 80 mg of omeprazole followed by an intravenous infusion of 8.0 mg/h for up to 72 hours, at which point high-dose oral PPI treatment may be initiated.11

Octreotide/Somatostatin

Somatostatin and its analogue, octreotide, inhibit the exocrine function of glandular tissue, which reduces both acid and pepsin secretion. Moreover, they reduce gastroduodenal mucosal blood flow that, in concert with the reduction in acid production, should theoretically prove to be of benefit in PUD. Evidence is lacking, though, in their role in the management of PUD.66 The role of octreotide in variceal bleeding has been clearly demonstrated to facilitate hemostasis when used in conjunction with endoscopy.67,68 The recommended regimen includes an initial bolus of 50 mcg followed by an infusion of 50 mcg/h.

Vasopressors

Generally, the use of vasopressors should be discouraged in hemorrhagic shock. Hypotension should primarily be addressed by volume resuscitation with crystalloid and colloid administration. The placement of a central line in the internal jugular or subclavian veins can facilitate administration of fluids directly into the cardiac circuit as well as provide guidance in fluid administration via monitoring of the central venous pressure (CVP). A CVP reading below 8 would indicate the need for additional volume infusion.

Vasopressin, used commonly in the pre-PPI era, is an endogenous pressor normally secreted by the posterior pituitary in response to hypotensive states. It preferentially vasoconstricts sphlancnic vessels to reduce portal venous inflow and pressure. In the presomatostatin era, vasopressin was frequently utilized in cirrhotic patients who, at an advanced stage of the disease, have an impaired ability to generate systemic vascular resistance. However, vasopressin's lack of selectivity at high doses makes it a less desirable agent. Vasopressin use has been reserved for massive refractory bleeding and is administered intravenously in a dose of 0.1–1.0 U/min. Concomitant intravenous administration of nitroglycerin at 40–400 ucg/min can be used to counteract cardiac and bowel ischemic sequela of vasopressin. A synthetic analogue of vasopressin, terlipressin, is used more commonly in Europe, and may have a role in the chronic management of hepatorenal syndrome given its limited side effect profile and longer half-life.69

Balloon Tamponade

The Sengstaken–Blakemore tube, introduced in the 1950s, is a double-balloon esophageal tamponade system used in life-threatening UGIB from esophageal or gastric varices. The gastric balloon occludes feeding vessels at the gastroesophageal junction, reducing the pressure in the esophageal varices, while the esophageal balloon provides direct compression.70 Complications associated with its placement include esophageal or gastric rupture, pressure necrosis, and aspiration pneumonitis. An updated version, the Minnesota tube, has an added esophageal suction port to minimize aspiration. Because of the prohibitively high complication and mortality rate associated with balloon tamponade, the exhaustion of medical and endoscopic therapies prior to placement is recommended.71 However, massive refractory hemorrhage, which precludes endoscopy or is associated with hemodynamic instability, may warrant the placement of a balloon tamponade system.

Prior to insertion of a balloon tamponade system, patients should be mechanically ventilated. The balloons and aspiration ports should be checked for integrity and patency. In the event there is no esophageal aspiration port, a nasogastric tube can be sutured onto the Sengstaken–Blakemore tube proximal to the esophageal balloon. The tube should be advanced orally approximately 50 cm into the gastric cavity. The stomach should then be aspirated of its contents. The gastric balloon can then be inflated in increments of 100 mL to a maximum of 400–500 mL. The Sengstaken–Blakemore tube should then be placed on a traction device to achieve hemostasis. If bleeding persists, the esophageal balloon may be inflated to 30–40 mm Hg. Malpositioning is not uncommon and placement should be confirmed by chest radiograph.69,70,72,73 The Linton-Nachlas tube has a single distal balloon that may be used in patients with documented gastric varices only.74

Special Management Considerations in Hepatic Cirrhosis

Resuscitation and management of the hepatic cirrhosis patient deserves special attention.

Varices typically occur in the third to fourth stages of cirrhosis; these patients often preferentially pool their intravascular volume in the markedly vasodilated mesenteric circulation. Thus, persistent hypotension in these patients may be the rule. Markers of adequate resuscitation in these patients are less clear. In addition, aggressive fluid resuscitation can raise portal pressures, increasing shear stress against the already compromised varix. Moreover, dilution of coagulation factors in the cirrhotic may lead to increased or refractory bleeding.

The use of crystalloid, while appropriate initially, should be limited. The resuscitation strategy should be promptly transitioned to one that utilizes colloid in the form of PRBCs, fresh frozen plasma, platelets, or albumin as needed. Maintaining a systolic blood pressure of 80–90 mm Hg may be adequate, provided the patient is not exhibiting other signs of hypoperfusion.

Approximately 20% of UGIB cirrhotic patients are infected on admission, and 50% subsequently develop infection during hospitalization. Antibiotic administration has been shown to enhance survival in these patients.75,76 Quinolones or cephalosporins are recommended for these patients.77,78

Endoscopy

Esophagogastroduodenoscopy

Following adequate resuscitation, EGD is the diagnostic and therapeutic modality of choice for UGIB and may be indicated in certain cases of LGIB with unclear etiology. EGD serves the role of diagnosis, triage, and therapy.79

Early assessment of the etiology and severity of bleeding will dictate further therapy and need for critical care monitoring. Endoscopic management is successful in greater than 75% of patients. Despite endoscopic therapy, rebleeding occurs in about 7–29% of cases, and is most common with variceal bleeding. The benefits of EGD over other therapeutic modalities are decreased rates of further bleeding, fewer blood transfusions, lower mortality, shorter hospital stays, and lower hospital costs.80 Treatment of UGIB with EGD depends on the etiology of the bleed.

In PUD, hemostasis can be achieved by injection therapy with epinephrine or alternative agent, mechanical clipping, or thermal treatment. Visible vessels or the presence of spurting or oozing blood predict further rebleeding and increased mortality. Almost all fatal rebleeding occurs within the first 24 hours.63

In MW syndrome, the occurrence of shock or active bleeding during endoscopic evaluation is predictive of recurrent bleed and warrants intensive care monitoring.29 Sclerotherapy or injection with epinephrine may be of benefit with some MW lesions.

Endoscopic therapy of variceal bleeding may be achieved by sclerotherapy or ligation. The administration of somatostatin or octreotide early in suspected variceal bleeding facilitates achievement of hemostasis during emergent endoscopy.81,82 The addition of antibiotic prophylaxis in cirrhotic patients appears to also reduce postendoscopic treatment failures. Endoscopy has not been shown, however, to reduce overall mortality in acute variceal bleeding, with rebleeding occurring in 10–15% of cases.83

Colonoscopy

Colonoscopy is the modality of choice in evaluating LGIB. Patients with hematochezia or hypotension, however, should have upper endoscopy performed first to evaluate for a brisk UGIB.84 Although studies have demonstrated successful endoscopy can be achieved without bowel preparation, the American Society of Gastroenterology recommends thorough colon cleansing to enhance visualization of occult lesions.85 Hemostasis is achieved by thermocoagulation, injection therapy of various agents, and mechanical methods. The incidence of complication is 1 in 1,000 with perforation occurring rarely. The diagnostic yield of urgent colonoscopy is high if performed within 12–24 hours, although may not necessarily reduce mortality, transfusion requirement, or length of stay.86 Evidence of active bleeding, visible vessels, or adherent clot during colonoscopy is associated with a complicated course and rebleeding.87

Diagnostic and Interventional Radiology

Angiography

Formal peripheral angiography has the capacity to identify a lesion that is actively bleeding at a rate of 0.5–1.0 mL/min. Advantages of angiography include the ability to identify the precise location of the bleed and the potential for a therapeutic intervention via embolization. Disadvantages include an inability to identify venous bleeding and a major complication rate of up to 9.1% associated with contrast administration, femoral artery thrombosis, and transient cerebral ischemic events.88 Multidetector computed tomography angiography is equivalent to peripheral angiography in its ability to detect the site of active bleeding and is increasingly used for this purpose.89

Embolization can be used for UGIB lesions particularly in the case of active massive bleeding that precludes the performance of endoscopy. Embolization in this setting rarely causes ischemia and has the advantage of averting surgery but is associated with rebleeding in up to 30% of cases.90,91

Angiography is indicated in patients with persistent recurrent LGIB without an identified source on endoscopy or with active massive bleeding that again precludes the performance of endoscopy. If identified during angiography, most LGIB are amenable to embolization with a high success rate. In the event that hemostasis is not achieved, the interventionalist may inject methylene blue at the bleeding site to facilitate a subsequent intraoperative surgical approach.91

Bleeding Scan

Nuclear scintigraphy with 99mTc-labeled red blood cells or 99mTc-sulfur colloid is indicated in patients who have an occult or intermittent source of LGIB that is undetected by endoscopy or angiography. It has the advantage of increased sensitivity compared with angiography and is able to detect bleeding at a rate of 0.1 mL/min. A significant drawback to nuclear scintigraphy is that its accuracy in localizing the bleeding source rapidly declines 2 hours after study initiation.92

TIPS

Endoscopic treatment failures in the management of esophageal varices require transjugular intrahepatic portosystemic shunt (TIPS). The right hepatic and portal veins are accessed percutaneously via the right internal jugular vein. A cannula is then inserted to create a portosystemic communication to reduce portal pressures. When embolization of varices is performed during TIPS, the success rate is high. Complications include worsening liver function, hepatic encephalopathy, and pulmonary hypertension.93 TIPS can be used as a bridge to liver transplantation or for palliation in advanced-stage cirrhosis. Contraindications include severe hepatic failure, hepatic encephalopathy, polycystic liver disease, right-sided congestive heart failure, malignancy, sepsis, and severe coagulopathy.94

Surgery

UGIB

The advent of PPIs and therapy for H. pylori infection have greatly reduced the need for surgical intervention in bleeding PUD.91 The classic indications for surgical intervention for patients with refractory bleeding despite medical or endoscopic therapy include loss of 30% of the estimated blood volume in the first 24 hours, a requirement of greater than 1,500 mL of transfused blood per 24 hours to maintain stable hemodynamics, hemorrhage to the point of hypotension or shock, and recurrent bleeding during medical therapy.50 Patients who require surgery carry a mortality of up to 25%. Repeat endoscopic therapy, however, has been shown to reduce the need for surgical intervention without increasing mortality.95 Moreover, when compared with surgery, angiographic embolization appears to be equally efficacious and is associated with lower morbidity.91

LGIB

LGIB lesions that are not amenable to endoscopic intervention or angiographic embolization should be considered for surgery. Since intraoperative identification is not feasible, preoperative localization of the bleeding lesion is necessary to prevent blind resection of bowel segments.

It can be difficult to predict the outcome of patients with gastrointestinal bleeding from their initial presentation; however, some literature is available on this subject. Using the Glasgow-Blatchford scoring system, UGIB patients may be safely discharged if they meet the following criteria: Hb >12.9 g/dL in men or 11.9 g/dL in women, a systolic blood pressure >109 mm Hg, pulse <100/min, BUN level <18.2 mg/dL, no melena, no history of syncope, or no past or present liver disease or heart failure. Predictors of adverse outcome and severity in LGIB include hemodynamic instability 1 hour after initial evaluation, active gross bleeding per rectum, and initial HCT ≤35%.96