Esophageal Bleeding

The general approach to upper gastrointestinal bleeding (UGIB) from an esophageal source does not differ from the approach for bleeding from other sources and is addressed in more depth in Chap. i70, "Gastrointestinal Bleeding." Resuscitation proceeds concurrently with the diagnostic effort of history, physical examination, and laboratory evaluation. Gastric lavage through a nasogastric tube or larger-bore gastric tube is generally accepted, and early airway management should be considered. Prompt mobilization of resources—including blood products, gastroenterology consult for endoscopy, and an appropriate inpatient level of care—is important.

About 60 percent of variceal bleeding will resolve with supportive care alone. 27 The rate of spontaneous cessation is higher for nonvariceal sources of UGIB. Patients who continue to bleed need specific intervention. Early endoscopy is generally accepted in patients with UGIB for its diagnostic and therapeutic applications. Pharmacologic treatment with an intravenous vasopressin/nitroglycerin combination, somatostatin, or octreotide can be used as well. Balloon tamponade is generally considered a last-resort therapy when pharmacologic management has failed and endoscopy is either not feasible secondary to massive bleeding or is ineffective. Surgical treatment also remains an option.

Varices develop in patients with chronic liver disease in response to portal hypertension. Around 60 percent of patients with chronic liver disease will develop varices. Of patients who develop varices, 25 to 30 percent experience hemorrhage.28 Patients who develop varices from alcohol abuse have a higher risk of bleeding, especially if there is ongoing alcohol consumption. About two-thirds of patients who have an index bleed experience recurrent hemorrhage, 50 percent occurring within 6 weeks of the initial episode.

With variceal bleeding, endoscopic therapy is often successful in controlling the hemorrhage. Sclerotherapy and ligation are the main alternatives, though in Europe the use of injected Histoacryl (a tissue adhesive) to obstruct the variceal lumen has gained popularity. Shunting procedures performed transvenously or by surgical approach should also be considered.29 Mortality is significant in esophageal variceal bleeding, quoted at 40 percent. 28 Concurrent hepatic failure is a risk factor for poor outcome.

Mallory-Weiss syndrome is arterial bleeding from longitudinal mucosal lacerations of the distal esophagus/proximal stomach. The majority of these lacerations are located at the GE junction, with only 10 percent found in the lower esophagus proper. Mallory-Weiss tears are responsible for between 5 to 15 percent of upper GI hemorrhage. They can occur at any age but are most common in the fourth through sixth decades. The pathophysiology of Mallory-Weiss syndrome is thought to be a transient, large pressure gradient between thorax and stomach, experienced maximally at GE junction.

Acute onset of upper GI bleeding is the usual presentation, though some patients can present with melana or hematochezia. Rarely the presentation will be one of isolated abdominal pain or syncope. Less than half of patients with Mallory-Weiss tears will report a history of vomiting prior to hematemesis. The spectrum of severity of bleeding is broad, but overall a low relative incidence of surgical intervention or adverse outcome is seen. Initial treatment is supportive as the vast majority of Mallory-Weiss tears stop bleeding spontaneously. Ongoing hemorrhage can require treatment with electrocoagulation, sclerotherapy, and laser photocoagulation. Angiographic embolization or surgical intervention remain options as well.

Esophageal cancer often results in heme-positive stools but is an uncommon cause of significant upper or lower GI bleeding. CHAPTER REFERENCES

1. Lang IM, Shaker R: Anatomy and physiology of the upper esophageal sphincter. Am J Med 103:50S, 1997.

2. Mittal RK, Balaban DH: The esophagogastric junction. N Engl J Med 336:924, 1997.

3. Berne RM, Levy MN: Physiology. St. Louis, Mosby, 1983.

4. Moore KL: Clinically Oriented Anatomy. Baltimore, Williams & Wilkins, 1985.

5. Pope CEN: The esophagus for the nonesophagologist. Am J Med 103:19S-, 1997.

6. Trate DM, Parkman HP, Fisher RS: Dysphagia: Evaluation, diagnosis, and treatment. Primary Care 1996; 23:417, 1996.

7. Falk GW, Richter JE: Approach to the patient with acute dysphagia, odynophagia and noncardiac chest pain, in Taylor MB (ed): Gastrointestinal Emergencies. Baltimore, Williams & Wilkins, 1997.

8. Pera M, Cameron AJ, Trastek VF, et al: Increasing incidence of adenocarcinoma of the esophagus and esophagogastric junction. Gastroenterology 104:510, 1993.

9. Swann LA, Munter DW: Esophageal emergencies. Emerg Med Clin North Am 14:557, 1996.

10. Marshall JB, Kretschmar JM, Diaz-Arias AA: Gastroesophageal reflux as a pathogenic factor in the development of symptomatic lower esophageal rings. Arch Intern Med 150:1669, 1990.

11. Turkot S, Golzman B, Kogan J, et al: Acute upper-airway obstruction in a patient with achalasia. Ann Emerg Med 29:687, 1997.

12. Ouyang A, Cohen S: Motility Disorders of the esophagus, in Haubrich WS, Schaffner F, Berk JE (eds): Bockus Gastroenterology. Philadelphia, Saunders, 1995, pp 418-436.

13. Ho K: Noncardiac chest pain and abdominal pain. Ann Emerg Med 27:457, 1996.

14. Richter JE: Typical and atypical presentations of gastroesophageal reflux disease: The role of esophageal testing in diagnosis and management. Gastroenterol Clin North Am 25:75, 1996.

15. Dent J: Patterns of lower esophageal sphincter function associated with gastroesophageal reflux. Am J Med 103 (5A):29S, 1997.

16. Barbezat GO: Recent advances: Gastroenterology. BMJ 316:125, 1998.

17. Kahrilas PJ: Gastroesophageal reflux disease. JAMA 276:983, 1996.

18. Sontag SJ: Gastroesophageal reflux and asthma. Am J Med 103:84S, 1997.

19. Hogan WJ: Spectrum of supraesophageal complications of gastroesophageal reflux disease. Am J Med 103:77S, 1997.

20. de Caestecker J: Medical therapy for supraesophageal complications of gastroesophageal reflux. Am J Med 103 (5A):138S, 1997.

21. Kikendall JW, Friedman AC, Oyewole MA, et al: Pill-induced esophageal injury: Case reports and review of the medical literature. Dig Dis Sci 28:174, 1983.

22. Varghese GK, Crane LR: Evaluation and treatment of HIV-related illnesses in the emergency department. Ann Emerg Med 24:503, 1994.

23. Williamson WA, Ellis FHJ: Esophageal perforation, in Taylor MB (ed): Gastrointestinal Emergencies. Baltimore, Williams & Wilkins, 1997.

24. Levy F, Mysko WK, Kelen GD: Spontaneous esophageal perforation presenting with right-sided pleural effusion. J Emerg Med 13:321, 1995.

25. Janjua KJ: Boerhaave's syndrome. Postgrad Med J 73:265, 1997.

26. Ahmed A, Aggarwal M, Watson E: Esophageal perforation: A complication of nasogastric tube placement. Am J Emerg Med 16:64, 1998.

27. Terblanche J, Burroughs AK, Hobbs KEF: Controversies in the management of esophageal varices. N Engl J Med 320:1393, 1989.

28. Polio J, Groszmann RJ, Taylor MB: Acute management of portal hypertensive hemorrhage from the upper gastrointestinal tract, in Taylor MB (ed): Gastrointestinal Emergencies. Baltimore, Williams & Wilkins, 1997.

29. Rossle M, Siegerstetter V, Huber M, Ochs A: The first decade of the transjugular intrahepatic portosystemic shunt (TIPS): State of the art. Liver 18:73, 1998.

Was this article helpful?

0 0
Blood Pressure Health

Blood Pressure Health

Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...

Get My Free Ebook


Post a comment