Gastrointestinal Bleeding

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33 Gastrointestinal Bleeding

Scope

Demographic risk factors for patients with gastrointestinal (GI) bleeding include older age, male gender, and the use of alcohol, tobacco, aspirin, or nonsteroidal antiinflammatory drugs (NSAIDs).3 Risk for bleeding is significantly higher in elderly patients who have recently started a regimen of NSAIDs or regular-dose aspirin than in long-term users of these agents.4 Additional independent risk factors are unmarried status, cardiovascular disease, difficulty performing activities of daily living, use of multiple medications, and use of oral anticoagulants.5

Intensive resuscitation in the emergency department (ED) significantly decreases mortality in patients with hematemesis (vomiting blood), hematochezia (red bloody stools), or melena (black tarry stools).2 Application of the predictive mnemonic BLEED (ongoing bleeding, low systolic blood pressure, elevated prothrombin time, erratic mental status, unstable comorbid disease) at the initial ED evaluation can predict hospital outcomes in patients with acute upper or lower GI hemorrhage.6 Although the incidence of peptic ulcer bleeding has decreased, the decline in incidence has occurred only in patients younger than 70 years,7 and mortality from multiorgan failure, cardiopulmonary conditions, or terminal malignancy has remained constant.1

Lower GI bleeding (LGIB) afflicts 20 to 27 of every 100,000 persons annually in the United States.8 The rate of LGIB increases more than 200-fold from the third to the ninth decade of life, with 25% to 35% of all cases occurring in elderly patients. It is one of the common medical emergencies that can become life-threatening in elderly patients.9,10 Risk stratification for LGIB by Strate et al. has identified seven predictors of severe bleeding: heart rate higher than 100 beats/min, systolic blood pressure lower than 115 mm Hg, syncope, nontender abdominal examination, gross rectal bleeding, aspirin use, and more than two comorbid conditions. Patients with more than three risk factors have an 84% risk for severe bleeding, defined as transfusion of more than 2 units of red blood cells.1113

Pediatric GI bleeding is fairly common worldwide; however, the incidence of severe GI bleeding in U.S. children is very low.14 LGIB is a more common complaint in the practice of general pediatrics, and it accounts for 10% to 15% of referrals to a pediatric gastroenterologist.1517 In most children, bleeding is not life-threatening and ceases spontaneously, with only supportive care being required.16,17 The age of the child guides the clinician toward specific diagnoses.16,18

Pathophysiology

Upper Gastrointestinal Bleeding

Upper GI bleeding (UGIB) is defined as bleeding from a source proximal to the ligament of Treitz, which is located at the junction of the duodenum and jejunum. UGIB accounts for three quarters of cases of GI tract hemorrhage, with duodenal and gastric ulcers being the specific sources in more than half of patients with an upper tract cause.

Tips and Tricks

Patients with upper gastrointestinal bleeding should be instructed to avoid nonsteroidal antiinflammatory drugs (NSAIDs).19,20 Studies have shown that the risk for recurrent bleeding is significantly higher in long-term users of NSAIDs or regular-dose aspirin, especially if patients are elderly. For short-term users of NSAIDs or aspirin, cotreatment with proton pump inhibitors (but not with histamine H2 blockers) may reduce the risk for bleeding to less than the risk in nonusers.4

Hematochezia is generally a symptom of LGIB but may be associated with brisk upper tract hemorrhage. UGIB sources are identified in 11% of patients in whom LGIB was initially suspected.3 Melena most commonly results from bleeding proximal to the jejunum and should be considered a marker of UGIB.

Variceal hemorrhage is the most serious complication of portal hypertension and occurs in one third of patients with esophageal varices.3 It is more common in patients with Child B and C cirrhosis.21 The extent of severe bleeding depends on portal pressure, variceal size, and variceal wall thickness.22 Esophageal varices should be suspected in any alcoholic with unexplained anemia or obvious GI bleeding.

One study noted a decline in the frequency of peptic ulcer disease in patients with UGIB and reported that the proportion of bleeding ulcers with a nonvisible vessel is now 20%, which is less than previously reported.23 Such decline may be related to improved treatment of Helicobacter pylori infection.

In children, the pathophysiology of the bleeding is determined by the specific causes of hemorrhage for each age group.24

Lower Gastrointestinal Bleeding

LGIB refers to bleeding that originates from an intestinal source distal to the ligament of Treitz. The majority of patients with hematochezia bleed from a colonic source. Diverticular disease, angiodysplasia, and neoplasm are the leading causes of LGIB in adults. Anal fissure and hemorrhoids are the most benign causes of LGIB. Approximately 10% of all patients will never have a source identified, and up to 40% of patients with LGIB have more than one potential bleeding source.11

Comorbid illnesses and decreased physiologic reserve make elderly patients more vulnerable to the adverse consequences of acute blood loss and prolonged hospitalization.10,25 Specifically, hematochezia is more commonly associated with syncope, dyspnea, altered mental status, stroke, falls, fatigue, and acute anemia in older patients. Poor prognostic indicators also include continued bright red rectal bleeding, excessive transfusions, orthostasis, shock, and altered mental status on admission.9

image Red Flags

Data from Swaim M, Wilson J. GI emergencies: rapid therapeutic responses for older patients. Geriatrics 1999;54:20.

Ulcerative colitis accounts for the majority of cases of massive LGIB in young adults in the second or third decade of life. Diverticulosis and arteriovenous malformation are found in older adults.15

The independent risk factors listed earlier are useful prognostic indicators, and outcomes are poorer in patients with either upper or lower tract bleeding.5 Specifically, use of over-the-counter NSAIDs may represent an important cause of peptic ulcer disease and ulcer-related hemorrhage in those with UGIB.4,26

Although most causes of LGIB in children are self-limited and benign, it is imperative to consider Meckel diverticulum, midgut volvulus, and intussusception in appropriate age groups.15

Clinical Presentation

Patients with GI bleeding can be rapidly assessed by their reported volume of blood loss and initial hemodynamic status. Massive hemorrhage is associated with signs or symptoms of hemodynamic instability, including tachycardia (heart rate greater than 100 to 120 beats/min), systolic blood pressure less than 90 to 100 mm Hg, symptomatic orthostasis, syncope, ongoing bright red or maroon hematemesis, transfusion requirements in the first 24 hours, and inability to stabilize the patient.27

Vital signs and postural changes should be assessed in patients who appear sufficiently stable. An increase of 20 beats/min or more in pulse or a decrease of 20 mm Hg in systolic blood pressure between the supine and upright positions indicates loss of more than 20% of blood volume in normal adult patients.9 Tachycardia, low blood pressure, reduced urine output, and conjunctival pallor in patients with GI bleeding are signs that mandate immediate volume replacement. Hypovolemic shock implies at least a 40% loss of blood volume. Note that abnormalities in vital signs, especially postural vital sign, are unreliable in pediatric and elderly patients.

The history should focus on the quantity, frequency, and duration of bleeding (differentiating between melena and hematochezia) to characterize the nature of the GI bleeding. Comorbid status, including other GI disorders, anticoagulant use, syncope, weight loss, alcohol intake, and cardiovascular disease, should be assessed.

In addition to continuous monitoring of vital signs, physical examination should include assessment of mental status, skin (for jaundice or pallor), and pulmonary and cardiovascular compromise (especially in the elderly because of ischemia from blood loss), as well as a thorough abdominal examination for distension, tenderness, or masses. Digital rectal examination and testing of stool for gross or occult blood should be performed in patients with suspected GI bleeding.

Complaints associated with LGIB include hematochezia or melena, although patients may have additional findings, such as anemia, light-headedness, hypovolemia, weakness, malaise, chest pain, and dyspnea. It is important to note that patients with LGIB may be asymptomatic and have complaints seemingly unrelated to intestinal bleeding (e.g., fatigue, weight loss); dramatic findings consisting of massive rectal bleeding in acutely ill and unstable patients are less common.28

Delayed black tarry stools may occur from a source of bleeding in the small bowel or ascending colon and may not be noted by the patient until several days after the bleeding has stopped.29

A thorough history and complete physical examination are important for evaluation of a child with GI bleeding. Bright red blood that coats but is not mixed with stool suggests an anorectal source. Hematochezia indicates bleeding from the distal part of the small bowel or proximal part of the colon. Bloody diarrhea usually suggests colonic bleeding. Currant-jelly stools are indicative of the vascular congestion and hyperemia seen with intussusception.

Food allergy may lead to GI bleeding from food-induced colitis and could result in dehydration in infants younger than 3 months.17 Anal fissures are common in infants and produce red streaks or spots of blood in the diaper.15 Other causes of dark stool are iron, charcoal, flavored gelatin, red fruits, bismuth, and food dyes. Maternal blood swallowed by neonates during delivery may be diagnosed with the Apt test.17

Differential Diagnosis

The most common causes of UGIB in adults are listed in Box 33.1, and causes of LGIB in adolescents and adults are listed in Box 33.2.

The exact cause of the GI bleeding is less important to the emergency physician (EP) than differentiation between upper and lower tract sources.

An aortoenteric fistula may have developed in a patient with massive LGIB and recent surgery.9

Differential Diagnosis for Pediatric Gastrointestinal Bleeding

Table 33.1 lists the differential diagnosis for UGIB and LGIB according to patient age. Ingestion of maternal blood is the most common cause of suspected GI bleeding in neonates; blood is swallowed during either delivery or breastfeeding (from a fissure in the mother’s breast). Other causes of GI bleeding in neonates include bacterial enteritis, milk protein allergies, intussusception, anal fissures, lymphonodular hyperplasia, and erosions of the esophageal, gastric, and duodenal mucosa.

Table 33.1 Causes of Gastrointestinal (GI) Bleeding in Children by Age

AGE GROUP CAUSES OF UPPER GI BLEEDING CAUSES OF LOWER GI BLEEDING
Neonates

Infants (1 mo-1 yr)

Infants (1-2 yr) Children (2-12 yr)

From Arensman R, Abramson L. Gastrointestinal bleeding: surgical perspective. EMedicine 2004. Available at www.emedicine.com/ped/topic3027.htm.

Mucosal injuries presumably result from a dramatic rise in gastric acid secretion and laxity of the gastric sphincters in infants. Maternal stress in the third trimester has also been proposed to increase maternal gastrin secretion and enhance infantile peptic ulcer formation.

Some drugs have been implicated in neonatal GI bleeding, including NSAIDs, heparin, and tolazoline, which are used for persistent fetal circulation. Indomethacin, administered to maintain a patent ductus arteriosus in neonates, may cause GI bleeding through intestinal vasoconstriction and platelet dysfunction. Maternal medications can also cross the placenta and incite GI problems in the developing fetus and neonate on delivery. Aspirin, cephalothin, and phenobarbital are well-known causes of coagulation abnormalities in neonates. Stress ulcers in newborns are associated with dexamethasone, which is used for fetal lung maturation.

Rarer causes of GI bleeding in a neonate are volvulus, coagulopathies, arteriovenous malformations, necrotizing enterocolitis (especially in preterm infants), Hirschsprung enterocolitis, and Meckel diverticulitis.14

In infants, GI mucosal lesions and irritations are the most common causes of bleeding and include esophagitis, gastritis, duodenitis, ulcers, colonic polyps, and anorectal disorders. Intussusception is a common and important cause of GI bleeding in this age group. The incidence of intussusception is greatest in infants aged 3 months to 1 year, but it can occur in children up to 5 years of age. Approximately 80% of all cases of intussusception occur in infants younger than 2 years.

Other causes of infantile GI bleeding are infectious diarrhea, midgut volvulus, Meckel diverticulum, arteriovenous malformation, and GI duplication. Rare causes include foreign body ingestion, variceal disease, irritable bowel disease, and acquired thrombocytopenia.

Older children may have any of the preceding conditions, but duodenal ulcer, Mallory-Weiss tear, and nasopharyngeal bleeding are important causes of bleeding in this age group. Less common causes are gastritis or ulcers induced by salicylates or NSAIDs, Henoch-Schönlein purpura, ingestion of caustic substances, hemolytic-uremic syndrome, inflammatory bowel disease, and vasculitis. In adolescents older than 12 years, the most common causes of UGIB are duodenal ulcers, esophagitis, gastritis, and Mallory-Weiss tears.14

Diagnostic Testing

Upper Endoscopy

Esophagogastroduodenoscopy (EGD) is now the diagnostic test of choice for establishing the source of UGIB. The overwhelming majority of existing data suggest that early endoscopy is a safe and effective procedure in all risk groups.34,35 Patients without active hematemesis may benefit from immediate upper endoscopy by a gastroenterologist to confirm the site of bleeding rather than undergoing the potential additional discomfort and morbidity associated with placement of a nasogastric tube. Endoscopy is both diagnostic and therapeutic in many cases.36 One study noted that live-view video capsule endoscopy (VCE) accurately indentifies high- and low-risk patients in the ED with UGIB. The use of VCE to risk-stratify these patients significantly reduced time to performance of emergency EGD and therapeutic intervention.37

Arteriography

Angiography is appropriate for initial testing of patients with massive bleeding.39 When the bleeding cannot be identified and controlled by endoscopy, intraoperative enteroscopy or arteriography may help localize the bleeding source and facilitate segmental resection of the bowel.40 Mesenteric angiography can detect bleeding at a rate of 0.5 mL/min or greater.41 Either angiography or angiographic computed tomography may be used to identify aortoenteric fistulas.

Intraarterial injection of vasopressin or other vasoconstrictors at the site of bleeding can control hemorrhage; embolization is an option when intraarterial injection is unsuccessful.42,43

Treatment

Figure 33.1 presents an algorithm for the treatment of GI bleeding. Insert two 18-gauge or larger intravenous lines and administer 0.9% normal saline or lactated Ringer solution on arrival of the patient.41 Quickly evaluate the patient’s hemodynamic status and determine the extent of blood or fluid resuscitation necessary. Standard resuscitative measures for the management of shock should precede or occur in parallel with definitive diagnostic testing. Management should otherwise be directed toward the underlying source of bleeding. Note that in 80% of cases, LGIB spontaneously stops.25

image

Fig. 33.1 Management of lower gastrointestinal hemorrhage.

EGD, Esophagogastroduodenoscopy; IV intravenous; RBC, red blood cell; (+), positive test result; (−), negative test result.

(Adapted from Hoedema RE, Luchtefeld MA. The management of lower gastrointestinal hemorrhage. Dis Colon Rectum 2005;48:2010-24.)

If the patient is hemorrhaging, consult a gastroenterologist and surgeon. Upper endoscopy is the diagnostic and therapeutic procedure of choice for acute UGIB. Surgery is indicated for patients with active bleeding when medical therapy proves ineffective and continued hemorrhage requires more than 5 units of blood within the first 4 to 6 hours.28,29,41,48 Bowel resection may be required for pronounced LGIB.

In the absence of consultants, massive esophageal hemorrhage as a result of variceal bleeding may be temporarily treated with the placement of a gastroesophageal balloon tamponade device (Blakemore-Sengstaken tube). Although this is an uncommon procedure, EPs in remote practice locations should be familiar with the indications for and proper use of such potentially lifesaving devices.

Octreotide acetate is a synthetic analogue of somatostatin that should be administered intravenously to all patients with suspected UGIB from esophageal varices to induce splanchnic vasoconstriction and a reduction in portal hypertension. The loading dose is 50 mcg intravenously, followed by infusion of 25 to 50 mcg/hr for 5 days.

Comorbid condition, such as coagulopathies, hyperkalemia, and cardiac ischemia, should be identified and treated. The EP should consider the administration of fresh frozen plasma, platelets, recombinant factor VIIa (NovoSeven), or desmopressin (DDAVP) as appropriate.

References

1 Lanas A. Upper GI bleeding—associated mortality: challenges to improving a resistant outcome. Am J Gastroenterol. 2010;105:90–92.

2 Baradarian R, Ramdhaney S, Chapalamadugu R, et al. Early intensive resuscitation of patients with upper gastrointestinal bleeding decreases mortality. Am J Gastroenterol. 2004;99:619–622.

3 Peura DA, Lanza FL, Gostout CJ, et al. The American College of Gastroenterology Bleeding Registry: preliminary findings. Am J Gastroenterol. 1997;92:924–928.

4 Pilotto A, Franceschi M, Leandro G, et al. The risk of upper gastrointestinal bleeding in elderly users of aspirin and other non-steroidal anti-inflammatory drugs: the role of gastroprotective drugs. Aging Clin Exp Res. 2003;15:494–499.

5 Kaplan RC, Heckbert SR, Koepsell TD, et al. Risk factors for hospitalized gastrointestinal bleeding among older persons. J Am Geriatr Soc. 2001;49:126–133.

6 Kollef MH, O’Brien JD, Zuckerman GR, et al. BLEED: a classification tool to predict outcomes in patients with acute upper and lower gastrointestinal hemorrhage. Crit Care Med. 1997;25:1125–1132.

7 Loperfido S, Baldo V, Piovesana E, et al. Changing trends in acute upper-GI bleeding: a population-based study. Gastrointest Endosc. 2009;70:212–224.

8 Brackman MR, Gushchin VV, Smith L, et al. Acute Lower Gastroenteric Bleeding Retrospective Analysis (the ALGEBRA study): an analysis of the triage, management and outcomes of patients with acute lower gastrointestinal bleeding. Am Surg. 2003;69:145–149.

9 Akhtar AJ. Lower gastrointestinal bleeding in elderly patients. J Am Med Dir Assoc. 2003;4:320–322.

10 Strate LL. Lower GI bleeding: epidemiology and diagnosis. Gastroenterol Clin North Am. 2005;34:643–664.

11 Lee J, Costantini TW, Coimbra R. Acute lower GI bleeding for the acute care surgeon: current diagnosis and management. Scand J Surg. 2009;98:135–142.

12 Strate LL, Orav EJ, Syngal S. Early predictors of severity in acute lower intestinal tract bleeding. Arch Intern Med. 2003;163:838–843.

13 Strate LL, Saltzman JR, Ookubo R, et al. Validation of a clinical prediction rule for severe acute lower intestinal bleeding. Am J Gastroenterol. 2005;100:1821–1827.

14 Hsai R, Wang N, Halpern J, et al. Pediatrics, gastrointestinal bleeding. EMedicine. 2005.

15 Arensman R, Abramson L. Gastrointestinal bleeding: surgical perspective. EMedicine. 2004.

16 Fox VL. Gastrointestinal bleeding in infancy and childhood. Gastroenterol Clin North Am. 2000;29:37–66. v

17 Leung AK, Wong AL. Lower gastrointestinal bleeding in children. Pediatr Emerg Care. 2002;18:319–323.

18 Arain Z, Rossi TM. Gastrointestinal bleeding in children: an overview of conditions requiring nonoperative management. Semin Pediatr Surg. 1999;8:172–180.

19 Blot WJ, McLaughlin JK. Over the counter non-steroidal anti-inflammatory drugs and risk of gastrointestinal bleeding. J Epidemiol Biostat. 2000;5:137–142.

20 Thomas J, Straus WL, Bloom BS. Over-the-counter nonsteroidal anti-inflammatory drugs and risk of gastrointestinal symptoms. Am J Gastroenterol. 2002;97:2215–2219.

21 Sorbi D, Gostout CJ, Peura D, et al. An assessment of the management of acute bleeding varices: a multicenter prospective member-based study. Am J Gastroenterol. 2003;98:2424–2434.

22 Roberts L, Kamath P. Pathophysiology of variceal bleeding. Gastrointest Endosc Clin N Am. 1999;2:167–174.

23 Boonpongmanee S, Fleischer DE, Pezzullo JC, et al. The frequency of peptic ulcer as a cause of upper-GI bleeding is exaggerated. Gastrointest Endosc. 2004;59:788.

24 Lazzaroni M, Petrillo M, Tornaghi R, et al. Upper GI bleeding in healthy full-term infants: a case-control study. Am J Gastroenterol. 2002;97:89–94.

25 Swaim M, Wilson J. GI emergencies: rapid therapeutic responses for older patients. Geriatrics. 1999;54:20.

26 Wilcox CM, Shalek KA, Cotsonis G. Striking prevalence of over-the-counter nonsteroidal anti-inflammatory drug use in patients with upper gastrointestinal hemorrhage. Arch Intern Med. 1994;154:42–46.

27 Peter D, Dougherty J. Evidence based emergency medicine: evaluation of the patient with gastrointestinal bleeding: an evidence based approach. Emerg Med Clin North Am. 1999;17:239–261.

28 Hoedema RE, Luchtefeld MA. The management of lower gastrointestinal hemorrhage. Dis Colon Rectum. 2005;48:2010–2024.

29 Vernava AM, 3rd., Moore BA, Longo WE, et al. Lower gastrointestinal bleeding. Dis Colon Rectum. 1997;40:846–858.

30 Cuellar RE, Gavaler JS, Alexander JA, et al. Gastrointestinal tract hemorrhage. The value of a nasogastric aspirate. Arch Intern Med. 1990;150:1381–1384.

31 Witting MD, Magder L, Heins AE, et al. Usefulness and validity of diagnostic nasogastric aspiration in patients without hematemesis. Ann Emerg Med. 2004;43:525.

32 Pitera A, Sarko J. Just say no: gastric aspiration and lavage rarely provide benefit. Ann Emerg Med. 2010;55:365–366.

33 Anderson RS, Witting MD. Nasogastric aspiration: a useful tool in some patients with gastrointestinal bleeding. Ann Emerg Med. 2010;55:364–365.

34 Dam JV, Brugge WR. Endoscopy of the upper gastrointestinal tract. N Engl J Med. 1999;341:1738–1748.

35 Spiegel BM, Vakil NB, Ofman JJ. Endoscopy for acute nonvariceal upper gastrointestinal tract hemorrhage: is sooner better? A systematic review. Arch Intern Med. 2001;161:1393–1404.

36 Spiegel BM. Endoscopy for acute upper GI tract hemorrhage: sooner is better. Gastrointest Endosc. 2009;70:236–239.

37 Rubin M, Hussain SA, Shalomov A, et al. Live view video capsule endoscopy enables risk stratification of patients with acute upper GI bleeding in the emergency room: a pilot study. Dig Dis Sci. 2011;56:786–791.

38 Howarth DM, Tang K, Lees W. The clinical utility of nuclear medicine imaging for the detection of occult gastrointestinal haemorrhage. Nucl Med Commun. 2002;23:591–594.

39 Suzman MS, Talmor M, Jennis R, et al. Accurate localization and surgical management of active lower gastrointestinal hemorrhage with technetium-labeled erythrocyte scintigraphy. Ann Surg. 1996;224:29–36.

40 Manning-Dimmitt LL, Dimmitt SG, Wilson GR. Diagnosis of gastrointestinal bleeding in adults. Am Fam Physician. 2005;71:1339–1346.

41 Cagir B, Cirincione E. Lower gastrointestinal bleeding, surgical treatment. EMedicine. 2009.

42 Gady JS, Reynolds H, Blum A. Selective arterial embolization for control of lower gastrointestinal bleeding: recommendations for a clinical management pathway. Curr Surg. 2003;60:344.

43 Khanna A, Ognibene SJ, Koniaris LG. Embolization as first-line therapy for diverticulosis-related massive lower gastrointestinal bleeding: evidence from a meta-analysis. J Gastrointest Surg. 2005;9:343–352.

44 Zuckerman GR, Prakash C. Acute lower intestinal bleeding. Part II: etiology, therapy, and outcomes. Gastrointest Endosc. 1999;49:228–238.

45 Jensen DM, Machicado GA, Jutabha R, et al. Urgent colonoscopy for the diagnosis and treatment of severe diverticular hemorrhage. N Engl J Med. 2000;342:78–82.

46 Liang HH, Wang W, Wei PL. Unusual cause of lower GI bleeding. Gastroenterology. 2010;138:e7–e8.

47 McSweeney SE, O’Donoghue PM, Jhaveri K. Current and emerging techniques in gastrointestinal imaging. J Postgrad Med. 2010;56:109–116.

48 Messmann H. Lower gastrointestinal bleeding—the role of endoscopy. Dig Dis. 2003;21:19.

49 Zuccaro G, Jr. Management of the adult patient with acute lower gastrointestinal bleeding. American College of Gastroenterology. Practice Parameters Committee. Am J Gastroenterol. 1998;93:1202–1208.