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CHAPTER 75: Upper Gastrointestinal Bleeding 495 TABLE 74-3 Key Aspects to Address Before Discharging a Constipated Patient •  Possible  obstructing lesion •  Systemic  illness •  Medication  interaction/effect •  Electrolyte  imbalance •  Potential  for intestinal perforation with self-administered enemas  FECAL IMPACTION Physician resistance to manual disimpaction does the patient a dis service, as enemas provide little or no relief. Diarrhea does not rule out fecal impaction, especially in the elderly or debilitated patient. Failure to perform a rectal examination will result in misdiagnosis. Manual disimpaction is a painful procedure that often requires sedation. A novel instrument invented by an emergency physician termed The Dis - Impactor® is a U.S. Food and Drug Administration–registered dispos able medical device that is being retailed that claims that with its use, uncomfortable digital disimpaction can be avoided. After disimpaction, prescribe a regimen of medications and medical adjuncts to properly reestablish fecal flow.  INTESTINAL PSEUDO-OBSTRUCTION (OGILVIE’S SYNDROME) Ogilvie’s syndrome, or acute colonic pseudo-obstruction, is a clinical disorder with the signs, symptoms, and radiographic appearance of an acute large bowel obstruction with no evidence of distal colonic obstruction. The colon may become massively dilated (>10 cm). If the bowel is not decompressed the patient risks perforation, peritonitis, and death. 19,20 The exact mechanism is not known, but is thought to be secondary to a dysregulation of colonic motor activity by the autonomic nervous system. Predisposing factors include recent surgery, underlying neurologic disorders, and critical illness. 23 Treatment is varied and determined with surgical consultation. The symptoms may resolve with conservative management but may require operative or colonoscopic decompression of the dilated intestine.  ORGANIC CONSTIPATION Symptoms suggestive of organic constipation are acute onset, weight loss, rectal bleeding/melena, nausea/vomiting, fever, rectal pain, and change in stool caliber. 24 Intestinal obstruction or carcinoma is the primary consideration. If fecal impaction is the cause, manual disimpaction is the treatment. DISPOSITION AND FOLLOW-UP Many constipated patients can be safely discharged from the ED with the caveat that certain key aspects have been adequately addressed (Table 74-3). Fecal impaction requires disimpaction before discharge. Patients with organic constipation of a nonobstructive cause also can be managed safely as outpatients. The primary care provider should be contacted to ensure follow-up and to communicate concern for an organic process. Referral to a gastroenterologist is warranted for patients with nonorganic constipation of recent onset; chronic constipation associated with weight loss, anemia, or change in stool caliber; refractory constipation; and constipation requiring chronic laxative use. 10,26 Patients with organic constipation of obstructive origin require hospitalization, gastric decompression, and surgical consultation. Acknowledgments: The authors thank Vito Rocco and Arash Armin, who were coauthors of the chapter in the previous edition. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Upper Gastrointestinal Bleeding Christopher M. Ziebell Andrew D.

gastric decompression, and surgical consultation. Acknowledgments: The authors thank Vito Rocco and Arash Armin, who were coauthors of the chapter in the previous edition. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Upper Gastrointestinal Bleeding Christopher M. Ziebell Andrew D. Kitlowski Janna Welch Phillip Friesen INTRODUCTION AND EPIDEMIOLOGY Upper GI bleeding is any GI bleeding originating proximal to the liga ment of Treitz. The overall annual incidence of upper GI bleeding ranges from 39 to 172 per 100,000 in Western countries.1-3 Difference in prevalence between countries is attributed to variations in Helicobacter pylori rates, socioeconomic conditions, and prescription patterns of ulcerhealing and ulcer-promoting medications. 2 Increasing age, coexistent organ system disease, and recurrent hemorrhage are factors associated with increased morbidity and mortality. PATHOPHYSIOLOGY  PEPTIC ULCER DISEASE Despite a downward trend in prevalence over the past 20 years, peptic ulcer disease, which includes gastric, duodenal, esophageal, and stomal ulcers, is still considered the most common cause of upper GI bleeding. 2,4 However, the Analysis of Clinical Outcomes Research Initiative found gastric and duodenal ulcers in only 20.6% of 7822 endoscopies per formed for suspected upper GI bleeding. 4 This number is much lower than previous estimates of up to 50%.5,6 Awareness that aspirin, NSAIDs, and smoking cause bleeding and increased recognition and treatment of H. pylori infection may be responsible for decreased incidence. 7-10  EROSIVE GASTRITIS AND ESOPHAGITIS Erosive gastritis, esophagitis, and duodenitis are also common causes of GI hemorrhage. 11 Common predisposing factors include alcohol, salicylates, and NSAIDs. Infection, toxic ingestion, radiation, and stress from severe illness may also cause erosive gastritis. Stress-related mucosal disease occurs in patients with overwhelming sepsis, trauma, or respiratory failure requiring mechanical ventilation. Candida, herpes simplex virus, cytomegalovirus, and human immunodeficiency virus are potential sources of esophageal bleeding from infection.  ESOPHAGEAL AND GASTRIC VARICES Esophageal and gastric varices result from portal hypertension and, in the United States, are most often a result of alcoholic liver disease. Although varices account for a small percentage of all cases of upper GI hemorrhage, they can rebleed and carry a high mortality rate. However, many patients with end-stage cirrhosis never develop varices; many patients with documented varices never bleed; and many patients with a documented history of varices presenting with upper GI bleeding will actually bleed from nonvariceal sites. Variceal bleeding is the cause of upper GI bleeding in cirrhotics 59% of the time, followed by peptic ulcer disease in 16% of cases. 13 In-hospital mortality rates for any type of GI bleed in cirrhotics are essentially double those of noncirrhotic patients.  MALLORY-WEISS SYNDROME Mallory-Weiss syndrome is bleeding secondary to a longitudinal mucosal tear at the gastroesophageal junction. The classic history is repeated vomiting followed by bright red hematemesis. The syndrome can be associated with alcoholic binge drinking, DKA, or chemotherapy administration. The Valsalva maneuver, such as from coughing or sei zures, is also a reported cause. CHAPTER Tintinalli_Sec09_p0473-0562.indd 495 8/2/19 6:49 PM

The classic history is repeated vomiting followed by bright red hematemesis. The syndrome can be associated with alcoholic binge drinking, DKA, or chemotherapy administration. The Valsalva maneuver, such as from coughing or sei zures, is also a reported cause. CHAPTER Tintinalli_Sec09_p0473-0562.indd 495 8/2/19 6:49 PM 496 SECTION 9: Gastrointestinal Disorders  DIEULAFOY LESIONS Dieulafoy lesions are arteries of the GI tract that protrude through the submucosa. They are most commonly found in the lesser curvature of the stomach but may be found anywhere in the GI tract; 80% to 95% are found within 6 cm of the gastroesophageal junction. 15 These lesions are characterized by intermittent massive GI bleeding, without the standard predisposing factors of liver disease or NSAID use. Dieu lafoy lesions are difficult to diagnose endoscopically, and sometimes patients report multiple previous diagnostic maneuvers with negative results.  OTHER CAUSES Arteriovenous malformation and malignancy are other causes of upper GI hemorrhage. Significant bleeding from ear, nose, and throat sources can also masquerade as GI hemorrhage. An aortoenteric fistula secondary to a preexisting aortic graft is an unusual but important cause of bleeding to keep in mind. Classically, this presents as a self-limited “herald” bleed with hematemesis or hematochezia, which precedes massive hemorrhage and exsanguination. DIAGNOSIS  HISTORY Ask about hematemesis, coffee-ground emesis, or melena. Classically, hematemesis and coffee-ground emesis suggest an upper GI source. The presence of melena and age <50 years old more likely indicate an upper GI bleed versus a lower GI bleed, even in patients without hematemesis. Vomiting and retching, followed by hematemesis, suggest a Mallory- Weiss tear. Be sure to ask about prior episodes of GI bleeding and any interventions performed. A history of an aortic graft should suggest bleeding from an aortoenteric fistula. Review the patient’s medication list carefully. Salicylates, glucocorticoids, NSAIDs, and anticoagulants all place the patient at high risk for GI bleed. Alcohol abuse is strongly associated with a number of causes of bleeding, including peptic ulcer disease, erosive gastritis, and esophageal varices. Ingestion of iron or bismuth can simulate melena. Liquid medications with red dye, as well as certain foods, such as beets, can simulate hematochezia. In such cases, stool guaiac testing will be negative. Inquire about past history of GI bleeding, even though recurrent bleeding episodes may originate from different sources. Although the medical history may suggest the source of bleeding, history can also be misleading. For instance, what initially appears to be lower GI bleeding may actually be an upper GI bleed in disguise. Bright red or maroon rectal bleeding unexpectedly originates from upper GI sources about 14% of the time. 16 Although patients volunteer complaints of hematemesis or melena, if there is no vomiting or the patient has not noted tarry stools, signs may be subtle. Patients with hypoten sion, tachycardia, angina, syncope, weakness, confusion, or cardiac arrest may have underlying GI hemorrhage.  PHYSICAL EXAMINATION Visual inspection of the vomitus for a bloody, maroon, or coffeeground appearance is the most reliable way to diagnose upper GI bleeding in the ED. Consider keeping a sample of the vomitus or nasogastric aspirate at bedside for the gastroenterologist to view. Vital signs may reveal obvious hypotension and tachycardia or more subtle findings such as decreased pulse pressure or tachypnea. Y ounger patients and those without comorbidities can tolerate substantial volume loss with minimal or no changes in vital signs. Paradoxical bradycardia may occur even in the face of profound hypovolemia.

reveal obvious hypotension and tachycardia or more subtle findings such as decreased pulse pressure or tachypnea. Y ounger patients and those without comorbidities can tolerate substantial volume loss with minimal or no changes in vital signs. Paradoxical bradycardia may occur even in the face of profound hypovolemia. Remember that comorbid conditions and medications may mask the body’s physiologic response to volume loss. β-Blockers, for example, will prevent tachy cardia. Patients with baseline hypertension may have relatively normal blood pressure in the setting of hypovolemia. Cool, clammy skin is an obvious sign of shock. Spider angiomas, palmar erythema, jaundice, and gynecomastia suggest liver disease. Petechiae and purpura suggest an underlying coagulopathy. Facial lesions, cutaneous macules, or telangiectasias may be suggestive of the Peutz-Jeghers, Rendu-Osler-Weber, or Gardner’s syndromes. A careful ear, nose, and throat examination can reveal an occult bleeding source that has resulted in swallowed blood and subsequent coffee-ground emesis. Abdominal examination may disclose tenderness, masses, ascites, or organomegaly. Perform rectal examination to detect the presence of blood and its appearance, whether bright red, maroon, or melanotic.  LABORATORY TESTING In patients with significant bleeding, the single most important labora tory test is to obtain blood for type and cross-match in case transfusion is needed. A CBC is also important, although the initial hematocrit level may not reflect the actual amount of acute blood loss. In addition, consider BUN, creatinine, electrolyte, glucose, coagulation, and liver function studies. Upper GI hemorrhage will elevate BUN levels through digestion and absorption of hemoglobin. A BUN:creatinine ratio ≥30 suggests an upper GI source of bleeding. 17 Coagulation studies, including INR, partial thromboplastin time, and platelet count, are useful in patients taking anticoagulants and those with underlying hepatic disease. Obtain an ECG in patients with underlying coronary artery disease. Silent cardiac or mesenteric ischemia can develop if bleeding decreases cardiac or mesenteric perfusion. A single elevated lactate level is a sentinel sign of severe illness. The success or failure of resuscitation efforts can be assessed by following dynamic lactate levels, because a rising lactate level in the hospital setting is a clear predictor of in-hospital mortality. Routine abdominal and chest radiographs are of limited value and are not needed in the absence of specific clinical indications. Barium contrast studies are contraindicated because barium may hinder subsequent endoscopy or angiography. In cases where traditional endoscopy is unavailable or endoscopic visualization is unable to find the source, consider tagged red-cell scintigraphy or visceral angiography. Both of these tests will demonstrate the source only in cases of active bleeding. Scintigraphy and angiography help localize the source of bleeding to determine whether medical or surgical management is optimal.  NASOGASTRIC LAVAGE A negative nasogastric aspirate does not conclusively exclude an upper GI source. Intermittent bleeding, pyloric spasm, or edema preventing reflux of duodenal blood can cause false-negative results. Ultimately, nasogastric aspiration yields a positive result in only 23% of patients without hematemesis who have occult upper GI bleeding. Nasogastric intubation and aspiration are diagnostically useful. 20 In patients without a history of hematemesis, a positive aspirate provides strong evidence for an upper GI source of bleeding. High-risk lesions are more likely in patients with bloody aspirates. Visual inspection of the aspirate to identify bloody, maroon, or coffee-ground material verifies upper GI bleeding.

eful. 20 In patients without a history of hematemesis, a positive aspirate provides strong evidence for an upper GI source of bleeding. High-risk lesions are more likely in patients with bloody aspirates. Visual inspection of the aspirate to identify bloody, maroon, or coffee-ground material verifies upper GI bleeding. Early nasogastric lavage is associated with decreased time to endoscopy. 21 Nasogastric tube placement and lavage can confirm the diagnosis of upper GI bleeding and correlate with risk of high-risk lesions on endoscopy. Guaiac testing of nasogastric aspirate can yield both false-negative and false-positive results. Conventional stool guaiac cards may be falsely negative. However, guaiac cards specifically designed for upper GI sources are available. Conversely, even minimally traumatic nasogastric intubation can result in positive guaiac testing even in the face of a clear aspirate. Visual inspection of the aspirate for a bloody, maroon, or coffee-ground appearance is the most reliable way to diagnose upper GI bleeding in the ED. If bright red blood or clots are found in the nasogastric aspirate, perform gentle gastric lavage. Room temperature water is the preferred irrigant. Maintain the nasogastric tube on mild, intermittent suction. Suction that is too vigorous may produce gastric erosions that can con fuse findings on subsequent endoscopy. As of this writing, there is no evidence to support concerns that nasogastric tube passage may provoke bleeding in patients with varices. Tintinalli_Sec09_p0473-0562.indd 496 8/2/19 6:49 PM

ntermittent suction. Suction that is too vigorous may produce gastric erosions that can con fuse findings on subsequent endoscopy. As of this writing, there is no evidence to support concerns that nasogastric tube passage may provoke bleeding in patients with varices. Tintinalli_Sec09_p0473-0562.indd 496 8/2/19 6:49 PM CHAPTER 75: Upper Gastrointestinal Bleeding 497  RISK STRATIFICATION Risk stratification depends on clinical judgment. There are no uni versally accepted pre-endoscopy risk stratification practice guidelines. However, the literature does seem to agree on those individuals that qualify as very low risk ( Table 75-1). Pre-endoscopic predictors of higher risk include advanced age, comorbidities, red hematemesis, hematochezia, red blood on nasogastric aspirate, hemodynamic instability, and abnormal laboratory studies. 24-28 Other high-risk factors include prior variceal banding, clamping or cauterization of an ulcer bed, or the transjugular intrahepatic portosystemic shunt procedure. TREATMENT Initial management is stabilization. Patients in hemorrhagic shock require emergent resuscitation, including two large-bore IVs, typed and cross-matched blood with the consideration of massive transfusion protocols, and in selected cases, early airway management. Intubating a patient with an upper GI bleed who is hemodynamically unstable can be a perilous procedure. Aggressively resuscitate prior to intubation, and consider using smaller doses of the induction agent to minimize peri-intubation hypotension or arrest. 29 ED treatment is summarized in Table 75-2.  BLOOD TRANSFUSIONS When upper GI bleeding is severe, blood transfusions can be lifesaving. If a large amount of blood product is anticipated, use massive transfusion protocols. 30 See Chapter 13, “ Approach to Traumatic Shock, ” for discussion of massive transfusion. In less severe cases, the decision to transfuse can be difficult because hemoglobin concentrations do not fall until after hemodilution has occurred. Individualize thresholds for transfusion based on underlying comorbidities and hemodynamic status. 31 Liberally transfusing all bleeding patients using a high threshold (hemoglobin <9 grams/dL) can cause harm. 5 A restrictive transfusion threshold using hemoglobin concentrations of <7 grams/dL in most patients and <9 grams/dL in older patients with comorbidities who are not tolerating the acute anemia is recommended. 5,31  COAGULOPATHY In patients with life-threatening bleeding receiving anticoagulants, reverse the coagulopathy without concern for the INR unless there are contraindications to reversal, such as cardiac or vascular stents or prosthetic valves. In less severe bleeding, carefully consider the risks of reversal therapy. An INR ≥1.5 is a significant predictor of mortality in patients with an upper GI bleed who are receiving anticoagulants. International consensus guidelines recommend reversal of coagulopathy for upper GI bleed patients who have an elevated INR or platelet counts <50,000/μL. 31,33 Coagulopathies from other causes such as the newer oral antithrombin and Xa inhibitors should be managed according to institutional protocols. See Figure 239-1 and Table 239-4 in Chapter 239, “Thrombotics and Antithrombotics, ” for recommendations for anticoagulant reversal. Reversal should not delay time to endoscopy. Tranexamic acid, in a small systematic review study, has been shown to reduce the risk of death in patients with upper GI bleeding, 34 but a much larger randomized controlled trial is due to be published soon.  PROTON PUMP INHIBITORS Consensus guidelines continue to recommend proton pump inhibitors for patients with nonvariceal bleeding from peptic ulcer disease. 35 When proton pump inhibitors are given at high dose, the gastric pH remains neutral.

4 but a much larger randomized controlled trial is due to be published soon.  PROTON PUMP INHIBITORS Consensus guidelines continue to recommend proton pump inhibitors for patients with nonvariceal bleeding from peptic ulcer disease. 35 When proton pump inhibitors are given at high dose, the gastric pH remains neutral. Clot formation from platelet aggregation is dependent on a pH >6.0. 36 Administer a high-dose proton pump inhibitor such as omepra zole 80 milligrams IV bolus followed by infusion of 8 milligrams/h 37 because the cause of bleeding cannot be determined without endoscopy. In patients with peptic ulcer bleeding, proton pump inhibitors reduce the need for surgery, the length of stay in the hospital, and signs of bleeding.  SOMATOSTATIN ANALOGUES/OCTREOTIDE Octreotide is a long-acting analogue of somatostatin that elicits several actions in patients with upper GI bleeding. It inhibits the secretion of gastric acid, reduces blood flow to the gastroduodenal mucosa, and causes splanchnic vasoconstriction. 39 The dose is a 50-microgram bolus followed by a continuous infusion of 25 to 50 micrograms/h. Octreotide does not appear to provide a clear benefit on mortality, 40 but when combined with early endoscopy, it may reduce bleeding.41  ANTIBIOTICS Patients with cirrhosis have an impaired immune system and have an increased risk of gut bacterial translocation during an acute bleeding episode. Prophylactic antibiotics (e.g., ciprofloxacin 400 milligrams IV or ceftriaxone 1 gram IV) reduce infectious complications, rebleeding, days of hospitalization, mortality from bacterial infections, and all-cause mortality, 42 and should be started as soon as possible.  PROMOTILITY AGENTS Erythromycin and metoclopramide are examples of promotility agents used to enhance endoscopic visualization. 43 Consider administration if the patient is undergoing endoscopy in the ED and the patient is sus pected to have large amounts of blood in the upper GI tract. 31 ENDOSCOPY Upper GI endoscopy is the diagnostic study of choice. Endoscopy allows visualization of the source of bleeding (in most cases) and administra tion of hemostatic therapy. 44 The optimal timing relates to the severity of the bleeding. Early endoscopy (within 6–24 hours of presentation for unstable patients if adequately resuscitated and 12–36 hours for stable patients 45) is recommended for most patients because it is associated TABLE 75-1 Upper GI Bleeding Risk Very Low Risk High Risk <60 y old Advanced age No major comorbidities Comorbidities and prior endoscopic or transjugular intrahepatic portosystemic shunt procedures No history of red hematemesis Red hematemesis No hematochezia Hematochezia or melena Negative nasogastric aspirate Positive nasogastric aspirate Hemodynamically stable at ED presentation Hemodynamically unstable Normal laboratory studies Abnormal laboratory studies TABLE 75-2 Treatment of Upper GI Bleed Treatment Dose Comments Blood transfusion Transfuse if ≤7 grams/dL in most; ≤9 grams/dL in older patients or patients with comorbidities Correct coagulopathy Correct if INR is elevated or platelets <50,000; or if bleeding severe, correct coagulopathy unless contraindications to correction (e.g., stents, valves) Omeprazole 80-milligram IV bolus then infusion of 8 milligrams/h Labeled use for ulcer bleeding Octreotide 50-microgram bolus then infusion of 25–50 micrograms/h Unlabeled use for varices; for elderly, begin at lower dose range of 25-microgram bolus and infusion of 25 micrograms/h Antibiotics Ciprofloxacin 400 milligrams IV or ceftriaxone 1 gram IV Antibiotics for cirrhotics with upper GI bleeding Tintinalli_Sec09_p0473-0562.indd 497 8/2/19 6:49 PM