Gastrointestinal Hemorrhage

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98 Gastrointestinal Hemorrhage

Horacio Hojman, Christina J. Wai, Stanley A. Nasraway

Definitions

Gastrointestinal (GI) bleeding can occur from anywhere throughout the GI tract. Classically, GI hemorrhage was classified into upper (source proximal to the ligament of Treitz) and lower (source distal to the ligament of Treitz) subgroups. However, new insights into the pathology of bleeding and therapeutic strategies have led to proposals for new categories. Bleeding that originates from the small bowel is now viewed as a separate entity,^1,² and the term lower GI hemorrhage is reserved for bleeding that arises in the colon and/or rectum. This chapter follows this classification scheme.

Epidemiology

Upper GI bleeding occurs more frequently than lower GI bleeding.³ In the United States, the annual incidence of hospitalization for upper GI bleeding is approximately 100 cases per 100,000 adults compared to about 20 cases per 100,000 patients for lower GI bleeding.^2,⁴ GI hemorrhage is most common among the elderly; in this population, the reported incidence is as high as 500 cases per 100,000 people per year. As demographic trends lead to increased numbers of elderly people in the general population, the incidence of GI hemorrhage is expected to steadily rise in the coming years.^5,⁶ Compared to patients with upper GI bleeding, patients with lower GI hemorrhage are less likely to experience shock and usually require fewer blood transfusions.² Despite improvements in the management of GI bleeding, mortality has remained relatively constant over the last 60 years.^7,⁸ Proposed reasons for the persistence of high mortality include an elderly patient population with many associated comorbidities.⁹^–¹¹ This leads to a high death rate independent of the GI bleeding, with 80% of the mortality attributable to other causes.¹²

Initial Assessment and Management

Patients with GI bleeding need to be approached like any patient with potentially life-threatening hemorrhage. Although most bleeding episodes are of low magnitude and self-limited, the potential for significant bleeding warrants a thorough evaluation of the patient. Evaluation begins with assessing vital signs and looking for signs of hemodynamic instability. As with any actively bleeding patient, obtaining adequate vascular access is essential. Preferably a large-bore intravenous (IV) catheter (at least 16 gauge) should be inserted in the antecubital fossa of each arm. If quick and easy access is needed due to instability of the patient, a central venous catheter can be inserted. However, the most commonly used central venous catheters are those designed for multiple infusions; since these catheters have multiple lumens with relatively small diameter and the catheters are relatively long, resistance to flow is higher than for short, wide-bore peripheral IV catheters, and achievable fluid administration rates are correspondingly slower.¹³

Initial resuscitation begins with a crystalloid solution. With ongoing bleeding, packed red blood cell transfusions may become necessary.

The initial laboratory panel should include a complete blood count, serum electrolytes, and a coagulation profile. If coagulopathy is detected, every effort should be made to correct the problem. Extra attention should be paid to certain patient populations. Cirrhotic patients and those taking warfarin will have decreased levels of coagulation factors reflected by an elevated international normalized ratio (INR). Consequently, fresh frozen plasma (FFP) should be administered to correct the coagulopathy. Platelets will be dysfunctional in patients taking aspirin or clopidogrel, and platelet transfusions may be indicated. Patients with renal failure and uremia or those with von Willebrand disease may respond to the administration of IV desmopressin (1-deamino-8-D-arginin vasopressin [DDAVP]; 0.3 µg/kg), a vasopressin analog that promotes von Willebrand factor release from endothelial cells.^14,¹⁵

Routine endotracheal intubation is not recommended.¹⁶^–¹⁸ However, the threshold for intubation should be low for patients who may be at high risk for aspiration secondary to severe vomiting or mental status changes secondary to conditions like shock or hepatic encephalopathy.

Once stabilized, the source of bleeding should be identified to direct treatment. Active vomiting of blood is indicative of a source of bleeding located in the upper GI tract. For patients who are passing blood per rectum, the bleeding can originate from either the upper GI tract (due to brisk bleeding) or the lower GI tract. A nasogastric tube should be inserted first.² If the nasogastric aspirate contains bile without blood, it is safe to assume the source of bleeding is distal to the ligament of Treitz.¹⁹ A rectal examination should always be performed to rule out anorectal pathology and evaluate the color of stool.²

Although frequently described as essential in aiding diagnosis, a complete history is generally not too useful and may be difficult to obtain from patients who are endotracheally intubated or in shock. The history also can obscure the diagnosis. For example, a history of cirrhosis secondary to alcohol abuse or hepatitis C may lead the clinician to suspect a variceal bleed when the actual bleeding source is a duodenal ulcer or gastric tumor. All potential etiologies for bleeding must be considered.

Whatever the type of GI bleeding, prompt endoscopy is of paramount importance, as this modality not only can help identify the source of bleeding but also offer therapeutic options.^20,²¹ For patients with lower GI bleeding, quick preparation of the colon is usually necessary to allow adequate visualization.^6,²² If the patient is hemodynamically unstable and cannot undergo timely colonic preparation, angiography is an alternative to identify and potentially treat the source of bleeding. Angiography can detect a bleeding vessel if the rate of hemorrhage is ≥0.5 mL/min.³ Once an arterial source is identified, treatment with embolization is performed, with a success rate of greater than 90%. Ischemic complications are rare in the upper GI tract, owing to the abundance of collaterals as compared to the lower GI tract.

Although done infrequently out of concerns for uncontrolled bleeding, provocative mesenteric angiography can reveal the source of bleeding in up to 60% of patients when an initial angiogram failed to do so.²³ This procedure entails systemic heparinization followed by sequential angiographic injections of a vasodilator and tissue plasminogen activator.

Another useful diagnostic modality is computed tomography (CT) angiography. Its role in the management of GI bleeding is less clear. Although CT angiography appears to be as accurate as conventional angiography for identifying the source of massive GI bleeding,^24,^25,²⁶ this modality is not useful therapeutically. If a bleeding site is identified using CT angiography, an additional procedure (i.e., surgery or conventional angiography) will be required for treatment.²⁷ Therefore, CT angiography should be employed only when conventional angiography is unavailable. Another proposed use is for identifying bleeding sources originating from the pancreatic ducts or biliary system, as these are not accessible by endoscopy.²⁸

Obtaining a gamma camera scan after injecting autologous technetium-99 (^99mTc)-labeled (“tagged”) red blood cells is another way to localize bleeding. This modality is more sensitive than angiography, since tagged red blood cell scans can detect bleeding at rates as low as 0.1 mL/min.³ Studies have shown that scans which become positive within 2 hours are more accurate at identifying the source of bleeding (95%–100%) than scans that show extravasation after 2 hours.^2,²⁹ Once the source of bleeding is identified, treatment is determined by the stability of the patient. If the patient is hemodynamically unstable, emergency surgery should be performed, whereas a second attempt at angiographic embolization is reasonable for more stable patients.

Unstable patients always should be admitted to an intensive care unit (ICU). For stable patients, the decision is based on clinical judgment. Criteria for ICU admission are hemodynamic instability, two or more comorbidities, age older than 60 years, and/or the need for hemodynamic monitoring or mechanical ventilation.

Upper GI Hemorrhage

Patients with upper GI bleeding tend to present with hematemesis. Upon evaluation, the nasogastric tube aspirate is often bloody. These patients commonly also have melena. If the bleeding is significant, it can be accompanied by hematochezia.² There are a multitude of potential etiologies for upper GI bleeding, including peptic ulcer disease, variceal hemorrhage, Dieulafoy’s lesion, stress ulceration, Mallory-Weiss tear, esophagitis, and aortoenteric fistulas. Careful evaluation of the patient will help make the appropriate diagnosis.

Common Causes of Upper Gi Bleeding

Peptic Ulcer Disease

Peptic ulcer disease (PUD) is the most common cause of upper GI bleeding. Common underlying etiologies for PUD include the use of nonsteroidal antiinflammatory drugs (NSAIDs) and Helicobacter pylori infection. Many patients with PUD do not have H. pylori infection of the stomach.³⁰ Even when H. pylori infection is present, eradication of H. pylori is unnecessary in the acute setting but is important for long-term prevention of recurrence.³¹

Significant PUD bleeding is frequently due to a posterior penetrating ulcer in the first portion of the duodenum that erodes into the gastroduodenal artery. The bleeding stops spontaneously in approximately 80% of cases. However, the remaining 20% of patients have recurrent bleeding or do not stop bleeding spontaneously at all.^32,³³ Historically, surgery was indicated to control the bleeding in a significant number of patients. It is rarely required these days because other less invasive therapies are available.

Early initiation of therapy with a proton pump inhibitor (PPI) is effective in reducing intragastric pH and the need for endoscopic treatment.³⁴ PPIs are more effective than histamine receptor 2 (H₂) blockers³⁵^–³⁷ or somatostatin.^38,³⁹ Administration of large doses of omeprazole after endoscopy (80 mg bolus injection followed by 8 mg/h continuous infusion for 72 hours, and then 40 mg/d orally for 1 week) compared to standard doses has been found to decrease the incidence of recurrent bleeding,^32,^38,^40,⁴¹ decrease the need for surgery, and prevent development of shock that leads to death. Unless there is a contraindication, a PPI always should be administered.

Prompt endoscopy is essential, as it allows identification and treatment of the bleeding vessel.²⁰ Some groups report performing endoscopy within 3 hours of admission.⁹ Endoscopy within 24 hours^10,⁴² has been associated with significant decreases in the incidence of recurrent bleeding, need for surgery, and length of stay. Administration of the prokinetic agent, erythromycin (3 mg/kg IV), before endoscopy can improve visibility during the procedure.^43,⁴⁴

Local injection of epinephrine, thermocoagulation, and application of endoscopic clips are approaches that can be used to stop bleeding. When used alone or in combination,⁴⁵ these methods are successful in over 90% of cases.⁴⁶ A detailed description of these endoscopic procedures is beyond the scope of this chapter and will therefore only be discussed briefly to inform the intensivist about possible complications. Injection of diluted epinephrine (1 : 10,000 solution) is effective in stopping bleeding, especially when used in higher volumes.^47,⁴⁸ Several proposed mechanisms include direct vasoconstriction, a tamponade effect related to the volume of injection, and induction of platelet aggregation. Although less frequent with high-volume injections,⁴⁹ rebleeding can occur in up to 20% of patients treated with epinephrine alone.³² Thermal coagulation is more effective than epinephrine in preventing rebleeding and the need for surgery,³² but it is associated with a 1% risk of perforation.³³ Hemoclips can also be applied endoscopically to control a bleeding vessel.^50,⁵¹ Although very safe, they are difficult to deploy and require expertise that is unavailable in many centers.

Even after initial endoscopic control, rebleeding occurs in as many as 20%³³ of patients, resulting in a significant increase in morbidity and mortality.⁵² In a review of the literature, Elmunzer et al.⁴⁶ reported several predictive factors for rebleeding, including hemodynamic instability, multiple comorbidities, active bleeding, large ulcer size (>2 cm),³³ a posterior duodenal ulcer, and a lesser curvature ulcer.

Identification and treatment of those ulcers with potential for rebleeding is necessary to avoid complications. The Forrest classification is very useful at predicting recurrent bleeding.⁵³ There are three categories based on endoscopic findings. Forrest I lesions are those that are actively bleeding. Forrest II lesions have stigmata of recent bleeding. They are further classified into Forrest IIa lesions where a non-bleeding vessel is visible and Forrest IIb lesions defined by the presence of an adherent clot. Forest III lesions are those that do not have signs of recent bleeding. Forrest I and II lesions have a high incidence of rebleeding. Nearly all Forrest I lesions rebleed.⁵⁴ In some series, Forrest IIa lesions have rebleeding rates as high as 81%,⁵⁵^–⁵⁷ although 40% is probably a more accurate number.⁵⁸ They also are associated with a high mortality rate of 11%. Endoscopic treatment is recommended for Forrest I and IIa lesions.⁵⁹ The role of endoscopic treatment for Forrest IIb lesions is less clear. Consensus is lacking on the definition of an adherent clot. Many clinicians are reluctant to mobilize a clot because of the potential to promote bleeding.⁶⁰ Nevertheless, administration of PPIs at high doses can help stabilize the clot and decrease the rebleeding rate.³² Due to poor interobserver reliability in identifying a visible vessel,^61,⁶² Doppler ultrasound has been proposed as another diagnostic modality. Riemann and Rosenbaum⁵⁵ reported in a prospective randomized controlled trial that Doppler ultrasound is more effective than direct visualization for locating vessels. Patients treated after identification with Doppler ultrasound had a lower incidence of rebleeding and a significant decrease in mortality (0% versus 10%).

Angiography may be needed for patients who continue to bleed despite endoscopic treatment ⁶³ or in whom endoscopy cannot be performed. Super-selective embolization controls the bleeding and decreases the complication rate.⁶⁴ Embolization of an actively bleeding vessel has a high success rate. If a bleeding site cannot be identified, blind embolization is not recommended. However, if the source of bleeding was previously identified endoscopically, blind embolization of the suspected vessels can be as effective as targeted embolization.⁶⁵^–⁶⁷ A metallic clip placed at the time of endoscopy may be helpful for identifying the area where bleeding occurred.⁶⁸ If rebleeding takes place, embolization can be attempted a second time for a combined success rate of 95%.⁶⁵ A potential complication of embolization is contrast-induced acute renal failure, particularly when infusion of a dye load occurs in combination with intravascular volume depletion secondary to hemorrhage.⁶³ Duodenal ischemia is rare and usually can be treated conservatively with PPIs. Mortality is in the range of 10% to 45%, and death is most often related to the presence of comorbid conditions.^69,⁷⁰

A minority of patients require surgical intervention to control the bleeding.^71,⁷² Because surgery is usually performed after failure of endoscopic and/or angiographic embolization, the patients are usually sicker and have a higher mortality rate. Although the reported mortality with surgery is similar to angiographic embolization, the mortality rate after failed embolization has been reported to be as high as 83%.⁶³ The procedure of choice is oversewing of the bleeding vessels with or without an acid-reducing procedure such as a vagotomy and pyloroplasty, a vagotomy and antrectomy, or a highly selective vagotomy. With the current availability of highly effective acid-suppressive medications and H. pylori treatment, extensive surgery is not indicated in these very sick patients.

Variceal Hemorrhage

The second most common cause of upper GI bleeding is variceal hemorrhage. Varices are present in approximately 50% of patients with cirrhosis and become more prominent with advanced liver disease.⁷³ They commonly develop in the lower esophagus and stomach secondary to portal hypertension. The hepatic vein pressure gradient is the main determinant of the propensity for variceal bleeding.^74,⁷⁵ These thin-walled varicose veins, located in the weak lamina propria of the lower esophagus, are especially predisposed to rupture and bleeding.⁷⁶

Despite recent improvements in medical management of these patients, mortality remains high at 20% in the first 6 weeks.^73,⁷⁷ The rebleeding rate ranges between 30% and 40% in the first 6 weeks and is associated with a 30% mortality rate.⁷⁸ Because of the high mortality rate, prompt management is crucial. If the diagnosis of variceal hemorrhage is suspected, pharmacologic therapy should be instituted in transit to the hospital.⁷⁹ If not initiated during transport, vasopressin, the vasopressin analog, terlipressin, somatostatin, or the somatostatin analog, octreotide,⁸⁰ should be administered upon arrival at the hospital. These agents are effective at controlling hemorrhage from varices in up to 80% of cases. These medications also can facilitate endoscopic visualization by reducing the rate of active bleeding.^77,⁸¹

Terlipressin is the only agent proven to reduce mortality.⁸²^–⁸⁴ Unfortunately, terlipressin is not available in the United States. It is administered at a dose of 2 mg every 4 to 6 hours for the first 48 hours, followed by half this dose for up to 5 days.⁸⁵^–⁸⁹ Somatostatin causes splanchnic arteriolar vasoconstriction and decreases the portal venous pressure by decreasing inflow into the portal circulation. It is administered as an initial bolus of 250 µg, which can be repeated up to three times, followed by an infusion of 250 µg/h for up to 5 days to prevent rebleeding.⁸⁵

The role of octreotide is unclear. Although it has a longer half-life compared to somatostatin, its hemodynamic effects are not as pronounced. It is administered by continuous infusion at 25 or 50 µg/h preceded by a 50- or 100-µg bolus. Although somatostatin and octreotide are similarly successful for controlling variceal hemorrhage, use of these agents alone has not been shown to decrease mortality.⁹⁰^–⁹² Accordingly, these agents should be used in combination with endoscopic therapy.

Historically, vasopressin has been used successfully to control acute variceal hemorrhage.⁹³ However, administration of vasopressin is associated with serious side effects (myocardial ischemia, mesenteric and limb ischemia, cerebrovascular accidents, and hyponatremia) in a significant number of patients, and it requires the concurrent administration of IV nitroglycerin (10 to 50 µg/minute). Vasopressin is administered as an infusion starting at 0.4 U/min, and the infusion rate can be increased incrementally to 1 U/minute as indicated by the clinical response. Although it controls bleeding in up to 80% of the cases, it does not decrease mortality, most likely because of its propensity to promote ischemia in other vital organs. Therefore, vasopressin should be reserved for those rare circumstances when other more effective drugs are unavailable.

Antibiotics should be started early in a prophylactic fashion, since as many as 20% of patients with cirrhosis and GI bleeding develop infections. Antibiotics have been shown to be effective in reducing the number of infections in these patients, and early administration of appropriate antibiotics has been shown to decrease the incidence of early rebleeding and improve survival.^94,⁹⁵ Ceftriaxone (1 gm IV daily) is the recommended antibiotic. Studies show it to be superior to fluoroquinolones.⁷⁷ For patients with a history of penicillin allergy, fluoroquinolones can be used as an alternative.^73,⁷⁷

Patients should be admitted to an ICU for close monitoring and management. Endotracheal intubation is usually indicated,⁷⁷ as these patients are at risk for aspiration and/or hepatic encephalopathy. Resuscitation with crystalloids and packed red blood cells should be initiated promptly to avoid hypovolemia and subsequent complications like renal failure. However, hypervolemia should be avoided. Intravascular volume overload has the potential to exacerbate variceal bleeding.

Upper endoscopy should be performed next to determine the exact source of bleeding. Despite esophageal and gastric varices being a common source of bleeding in patients with cirrhosis, in as many as 25% of cases, acute GI bleeding arises from a non-variceal source.

Esophageal varices can be treated with sclerotherapy or band ligation. The type of endoscopic treatment depends on the experience and expertise of the endoscopist as well as the magnitude of bleeding. Band ligation appears to be superior for reducing the risk of recurrent bleeding after the acute event and has been associated with fewer complications. However, band ligation can be difficult to perform in patients with massive bleeding. In these cases, sclerotherapy is preferred.⁷⁷ The success of endoscopic treatment is similar to vasoactive drugs, with a rate of 80% to 85%.^77,⁹⁶^–⁹⁹ However, despite similar success rates to vasoactive drugs for controlling bleeding, a recent Cochrane meta-analysis found that sclerotherapy could not be recommended as a first-line treatment, given its higher complication rate. Its use should be reserved for pharmacologic failures.¹⁰⁰ Conversely, the combination of pharmacologic and endoscopic treatment in selected patients appears to be superior to vasoactive drugs alone.^96,¹⁰¹

Gastric varices bleed less frequently but more intensely than esophageal varices, leading to higher transfusion requirements and mortality.¹⁰² The recommended treatment is sclerotherapy with histoacryl glue (N-butyl-2-cyanoacrylate).¹⁰³ Complications include ulceration of the mucosa and embolic events from the glue.^32,⁷⁷

With massive bleeding, a Sengstaken-Blakemore (S-B) tube or one of its variations can be inserted as a temporizing measure. The S-B tube has fallen out of favor as more effective therapies have become available. The risks of its use include aspiration, esophageal rupture, and an inability to control the bleeding.¹⁰⁴^–¹⁰⁷ However, for selected patients, it can be life saving. The S-B tube has a gastric and an esophageal balloon. The tube does not have to be cooled before insertion.¹⁰⁸ Tube placement should be preceded by endotracheal intubation. The tube should be introduced through the nose or, more frequently, through the mouth into the stomach. The position of the distal tube in the stomach should be confirmed by insufflation of air combined with auscultation. Radiographic confirmation has been advocated to avoid insufflation of the gastric balloon in the esophagus, resulting in esophageal rupture.¹⁰⁹ After confirming the position of the S-B tube, the gastric balloon is inflated with 500 mL of saline, and gentle traction is applied (approximately 1 kg or the weight of a 1-L IV bag). This maneuver stops bleeding from varices high in the fundus and occludes collaterals from the stomach to the submucosa of the esophagus. If the bleeding stops, the balloon is secured in place using a football helmet or a pulley system connected to an IV pole. If esophageal bleeding persists, the esophageal balloon is inflated next. The inflation port is connected to a manometer, and pressure is gradually increased until the bleeding stops or the pressure equals 45 mm Hg, whichever comes first. Once the bleeding is controlled, the S-B tube is kept in place, usually for 24 hours, before deflating the balloons. This allows preparation for other therapies such as endoscopy or a transjugular intrahepatic portosystemic shunt (TIPS). If bleeding recurs after deflation, the balloons can be reinflated. A method of inserting the S-B under direct vision by endoscopy has been described¹¹⁰; however, it is not clear that this approach reduces the incidence of complications.

If the previously described treatments are unsuccessful, TIPS should be attempted. TIPS placement reduces the hepatic vein pressure gradient and effectively controls bleeding in 90% to 100% of the cases.⁷⁸ However, emergency TIPS placement is associated with a high incidence of hepatic encephalopathy and a mortality rate as high as 50%.¹¹¹ In the event TIPS placement is unavailable, a surgical portosystemic shunt should be considered. One surgical approach entails interposition of an 8-mm ringed polytetrafluoroethylene shunt between the portal vein and the inferior vena cava.¹¹² Because of the relatively small diameter of the graft, its placement creates only a “partial” portocaval shunt with preservation of hepatopetal flow, leading to a lower incidence of encephalopathy. In experienced hands, the graft has a 95% patency rate at 7 years. However, even its advocates advise against using this approach if the patient is a candidate for liver transplantation.¹¹³ A splenorenal shunt (with or without splenectomy) is another surgical option. The operative mortality for distal splenorenal shunt placement has been reported to be less than for portocaval shunt placement; however, not all experts share this view.¹¹³ Although some studies report a similar complication rate and mortality compared to TIPS,¹¹⁴ only a few specialized centers have surgeons who are experienced in performing these difficult procedures for very sick patients.