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66 Cymorek and Aziz
acute episode. Bleeding often precipitates encephalopathy and increases the risk of spontaneous bacterial peritonitis (SBP), which further complicates the management of these patients.
A common system used for endoscopic grading of esophageal varices classifies them by their size (5):
Grade I: Small varices without luminal prolapse.
Grade II: Moderate-sized varices with minimal luminal prolapse at gastroesophageal
junction.
Grade III: Large varices with significant luminal prolapse substantially obscuring the
gastroesophageal junction.
Grade IV: Very large varices completely obscuring the gastroesophageal junction.
Mainly, their anatomic location and relationship to esophageal varices classify gastric varices (6):
Type I: Gastric varices that appear as an inferior extension of esophageal varices.
Type II: Varices in the gastric fundus in continuity with esophageal varices.
Type III: Isolated gastric varices in the fundus, body or antrum of the stomach.
ENDOSCOPIC TREATMENT OF ESOPHAGEAL VARICEAL HEMORRHAGE
Endoscopy is the most commonly utilized therapeutic intervention in the initial attempt to control active hemorrhage. Initial management depends on patient hemodynamic sta­bility at the time of presentation. Hemodynamically unstable patients are resuscitated with supportive medical therapy, which includes intravascular volume resuscitation with iv fluids and blood products, and chemotherapeutic attempt to lower portal pressure with iv vasopressin or somatostatin. The patient’s condition is monitored in the Intensive Care Unit. Endoscopy is performed as soon as the patient is hemodynamically stable, for both diagnostic and therapeutic purpose. Hemodynamically stable patients undergo endoscopy as an initial diagnostic test, and therapeutic intervention to control bleeding. Portal pressure lowering agents are used in conjunction to endoscopic intervention to prevent early rebleeding. Patients who fail endoscopic and medical treatment are referred for transjugular intrahepatic portosystemic shunt (TIPS) placement or surgical treatment. Liver transplan­tation may be considered in selected cases for patients with end-stage liver disease.
INDICATIONS FOR ENDOSCOPIC INTERVENTION
Endoscopy is indicated for initial diagnosis as well as control of acute variceal hem­orrhage. Both endoscopic sclerotherapy and endoscopic variceal ligation are highly effective in controlling initial episodes of esophageal variceal bleeding (7). Endoscopic intervention is used for the initial control of bleeding, and as treatment for the prevention of recurrent esophageal variceal hemorrhage. Pharmacological therapy with nonselec­tive beta-blockers is added to endoscopic treatment for prevention of recurrent hemor­rhage (8). At the present time, endoscopic therapy is not recommended for the primary prophylaxis of a variceal hemorrhage (9).
CONTRAINDICATIONS
Endoscopic intervention should not be performed if the patient is hemodynamically unstable, when perforated viscus is suspected, and if the patient is combative, or is
Chapter 7 / Endoscopic Therapy 67
unwilling to cooperate. Endotracheal intubation should be considered for the prevention of aspiration, and for the treatment of patients with severe agitation or encephalopathy.
ENDOSCOPIC SCLEROTHERAPY (EST)
Indications and Technique
Endoscopic sclerotherapy is being performed on an emergent basis to stop acute bleeding, and selectively to prevent rebleeding after control of initial episode is achieved. The goal of sclerotherapy is initial thrombosis and further obliteration of varices by injection of sclerosing agent.
EST is performed with a short 25-gage needle that is directed into the veins (intravariceal injection) or into the esophageal wall next to the variceal vein (paravariceal injection). Both techniques are effective but the intravariceal injection is utilized most commonly. Several sclerosants are available for EST, including 1% sodium tetradecyl sulfate, 5% ethanolamine oleate, 5% sodium morrhuate, and 0.5%–1% polidocanol (not available in United States). 1 to 2 mL of sclerosant is injected under direct vision into each varix, starting just above the gastroesophageal junction (GEJ) (Fig. 1). The proce­dure is repeated at higher levels up to 5 cm from the GEJ. The injections should not be made at higher levels to avoid spinal cord injury. A maximal dose of 20 mL per session is recommended to avoid complications. Occasionally, two or more injections are needed to control bleeding from a very large varix. Preferentially, the injection is made just below the point of bleeding, though a precise location of source is not always possible, especially in cases with a very brisk bleeding.
After initial control of hemorrhage is achieved, EST is repeated initially 1 wk after an acute episode of bleeding, and then in 2-wk intervals thereafter, until varices are eradicated.
EST is also being used to control active bleeding from gastric (fundic) varices. En­doscopic management of bleeding gastric varices is more difficult, and usually higher volumes of sclerosing agent or multiple injections need to be used to control hemorrhage.
Complications
EST is associated with local and systemic complications. The local complications like chest pain, transient dysphagia, odynophagia, and small pleural effusion are common, but usually minor and self-limiting. Mucosal ulcerations resulting from tissue necrosis are common and are seen in up to 70% of patients 1 wk after therapy (10). The deep esophageal ulcerations are an independent risk for bleeding. The tissue necrosis is also responsible for postprocedure esophageal perforation, which carries significant mortal­ity. Esophageal stricture formation is relatively common, though clinically significant dysphagia occurs in about 15% of cases. Proton pump inhibitors are being used to prevent local complications and to improve tissue healing (11). Mediastinitis and peri­carditis are less common and in part depend on the technique and amount of sclerosing agent being used.
Uncommon, but serious, systemic complications include aspiration pneumonia, sys­temic bacteriemia with risk for bacterial endocarditis and organ abscess, spinal cord paralysis, spontaneous bacterial peritonitis, and portal vein thrombosis. Aspiration dur­ing procedure and hypoxia can be prevented by use of elective intubation among patients at high risk. Infectious complications are prevented by prophylactic use of antibiotics when indicated.
68 Cymorek and Aziz
Fig. 1. Endoscopic sclerotherapy. (A) Endoscope with retracted sclerotherapy needle. (B) Endo- scope with extended sclerotherapy needle. (C) Injection of sclerosing agent into varix.
ENDOSCOPIC VARICEAL BAND LIGATION (EVL)
Indications and Technique
Endoscopic variceal ligation (EVL), also referred to as variceal banding, is an endo­scopic therapy for acute esophageal variceal bleeding, and for elective eradication of varices after the initial episode of hemorrhage. EVL technique for the esophageal varices is similar to endoscopic treatment of rectal hemorrhoids. The ligation is accomplished by placement of an elastic band on the varix, which strangulates a blood vessel, resulting in vessel thrombosis. The thrombosed varix undergoes necrosis and sloughs off, to be replaced by fibrous tissue in the process of mucosal healing.
A small cylinder, which is preloaded with bands, is loaded onto the tip of the endoscope and the connecting wire is passed down the biopsy channel of the endo­scope to be attached to a band-releasing device mounted into other end of that channel. Since the introduction of devices preloaded with multiple bands, there is no need for endoscope removal after each ligation, therefore, there is no need for overtube use. The endoscope with the device is placed over the varix, which is then suctioned into the device’s plastic cylinder at the end of an endoscope. With the use of the trigger device, a ligating band is deployed. After the ligation process is completed, suction is stopped, and a puff of air is used to release the ligated varix from the device (Fig. 2). It is important to start ligation at the level of gastroesophageal junction and proceed proxi­mally, because banded varices may obstruct esophageal lumen, making access to varices below them impossible. When ligating an actively bleeding varix, the band is placed directly over the bleeding point or just below it, but never above it, for the same reason. Typically, five to ten bands are placed in one session.
Chapter 7 / Endoscopic Therapy 69
Fig. 2. Esophageal variceal ligation. (A) Banding device including cylinder with rubber bands. (B). Banding device is placed over the varix. (C) Suction is applied to aspirate varix into the
cylinder. (D) Upon the release of the trip-wire, the rubber band strips off the cylinder and closes around the aspirated varix. (E) Ligated varix with endoscope removed.
After initial control of hemorrhage is achieved, the patient undergoes elective ligation 1 wk later and in 2-wk intervals thereafter for complete eradication of varices.
Complications
EVL has less potential for complications then EST (12). The ligation of varices causes mucosal ulceration in as many as 90% of patients at 1 wk, but because tissue injury is superficial and no sclerosing agent is being used, there is less potential for local compli­cations like perforation and mediastinitis. The reduced incidence of esophageal stricture has also been reported (13). A less-tissue necrosis with the use of EVL provides theo­retical ground for reduction of systemic infectious complications, which are related to the degree of bacteriemia during and postprocedure. EVL carries a similar risk for respiratory complications as EST does; therefore, the same precautions are needed. Proton-pump inhibitors are also being used to promote mucosal healing.
ENDOSCOPIC SCLEROTHERAPY WITH TISSUE ADHESIVE
BUCRYLATE (HYSTOACRYL) (FIG. 3)
Standard endoscopic methods used in the treatment of esophageal varices have not been found effective for gastric varices. In the United States, at present, most patients with type II and III gastric variceal hemorrhage are treated with transjugular intrahepatic portosystemic shunt (TIPS). A new sclerotherapy technique for bleeding gastric varices, utilizing cyanoacrylate glue (Histoacryl) injection, was introduced in Europe. In the United States, Histoacryl is not approved by the FDA for clinical use.
70 Cymorek and Aziz
Fig. 3. View of the retroflexed endoscope for injection of tissue adhesive into the gastric cardia verix.
Indications and Technique
Cyanoacrylate compound in a liquid form has a consistency similar to water; there­fore, it is suitable for intravariceal injection with the use of a sclerotherapy needle. Upon injection into a varix, cyanoacrylate undergoes a polymerization process, which is triggered by its contact with a physiological fluid such as blood. In this process, cyanoacrylate glue is transformed from liquid into a solid form compound, which obliterates variceal lumen, and provides a rapid homeostasis of active bleeding. At present, there is no standardization of injection technique in treatment of varices. A sclerotherapy needle is being used as an injector (Huang). Histoacryl is being used in its undiluted form, as well as in dilution with Lipiodol, which delays the polymeriza­tion process and allows the operator more time to complete the injection and remove the needle. Undiluted Histoacryl undergoes instantaneous transformation into the solid compound; such a rapid process may not allow complete varix obliteration and, in addition, may cause clogging of the endoscope channel. The accessory channel needs to be lubricated with silicone oil prior to the procedure in order to prevent adherence of cyanoacrylate. Personnel participating in the procedure need to wear protective goggles to avoid eye injury.
Endoscopic sclerotherapy with use of cyanoacrylate was shown to be highly effective in the treatment of active hemorrhage from gastric varices, as well as in elective variceal obliteration (14). Term obliteration is used, rather then eradication of varices because varices are filled with a solid substance and are visible up to several weeks after comple­tion of treatment.
Chapter 7 / Endoscopic Therapy 71
Complications
Endoscopic sclerotherapy using cyanoacrylate glue, a tissue adhesive, was reported to be a safe procedure, but not free from serious complications. A main concern with the use of cyanoacrylate is the risk of embolization. Reports of cerebral stroke (15), pulmo­nary embolism (16), portal vein embolism, and splenic infarction (17) raised questions about the safety of this procedure. Additional complications in the form of visceral fistulas were also reported (18). Though embolic complications are rare in most series, they carry the risk for a significant morbidity and mortality.
COST EFFECTIVENESS OF AVAILABLE THERAPIES
Data on the cost of treating an episode of variceal bleeding and cost comparison of particular therapeutic modalities is limited. The difficulty in comparing the cost of commonly used therapies is a result of institutional and national differences in cost calculations between different healthcare models.
Medical therapy was shown to be the most cost-effective form of primary prophylaxis for esophageal variceal hemorrhage (19). Estimated cost of treatment for the prevention of recurrent variceal hemorrhage is the lowest for medical treatment and increases gradu­ally for the endoscopic intervention and TIPS, with surgical treatment being the most expensive therapy (20). A recent multicenter prospective trial comparing the cost of EVL and EST at 1-yr follow-up showed similar costs between EVL and EST. The total median direct cost was $9700 for EVL and $13,200 for EST with a p value of 0.46 (21).
SUMMARY
1. Endoscopic treatment of esophageal variceal hemorrhage has become the standard of treatment in recent years. Both EST and EVL are highly effective in controlling active variceal bleeding and variceal eradication.
2. EVL is reported to have a lower rate of rebleeding, mortality, and complications, however the initial choice of treatment for active bleeding depends greatly on the experience of the endoscopist.
3. The rate of variceal bleeding and limited visibility during the procedure may dictate EST as an initial choice because it is easier to perform under such circumstances.
4. Treatment of gastric varices with a newer sclerotherapy agent, Histoacryl, is promis­ing, but there are concerns over its safety and the product is not approved for use in the United States.
5. Endoscopic therapy is not recommended for primary prevention of variceal hemor­rhage at present.
REFERENCES
1. Navarro VJ, Garcia-Tsao G. Variceal hemorrhage. Crit Care Clin 1995;11:391–414.
2. Wiliams SG, Westaby D. Fortnightly review: management of variceal hemorrhage. Br Med J 1994;308:
1213–1217.
3. Graham DY, Smith JL. The course of patients after variceal hemorrhage. Gastroenterology 1981;80:
800–809.
4. Garcia-Tsao G, Grace ND, Groszmann R, et al. Portal pressures, presence of gastroesophageal varices
and variceal bleeding. Hepatology 1985;5:419–424.
5. Paquet KJ. Prophylactic endoscopic sclerosing treatment of the esophageal varices-a prospective
controlled randomized trial. Endoscopy 1982;14:4-5.
72 Cymorek and Aziz
6. Hashizume M, Sugimachi K. Classification of gastric lesions associated with portal hypertension.
J Gastroenterol Hepatol 1995;10:339–343.
7. Kitano S, Baatar D. Endoscopic treatment for esophageal varices: will there be a place for sclero-
therapy during the forthcoming era of ligation? Gastrointest Endosc 2000;52:226–232.
8. Lo GH, Lai KH, Cheng JS, et al. Endoscopic variceal ligation plus nadolol and sucralfate compared
with ligation alone for the prevention of variceal rebleeding: a prospective, randomized trial. Hepatology 2000;32:461–465.
9. The Veterans Affairs Cooperative Variceal Sclerotherapy Group. Prophylactic sclerotherapy for esoph-
ageal varices in men with alcoholic liver disease: a randomized, single-blind, multicenter clinical trial. N Engl J Med 1991;324:1779–1784.
10. Sarin SK. Endoscopic sclerotherapy for esophago-gastric varices: a critical reappraisal. Aust N Z J Med 1989;19:162–171.
11. Gimson A, Polson R, Westaby D, et al. Omeprazole in the management of intractable esophageal ulceration following injection sclerotherapy. Gastroenterology 1990;99:1829–1831.
12. Laine L, El-Newihi HM, Migikovsky B, et al. Endoscopic ligation compared with sclerotherapy for the treatment of bleeding varices. Ann Intern Med 1993;119:1–7.
13. Laine L, Cook D. Endoscopic ligation compared with sclerotherapy for treatment of esophageal variceal bleeding. A meta-analysis. Ann Intern Med 1995;123:280–287.
14. Kind R, Guglielmi A, Rodella L, et al. Bucrylate treatment of bleeding gastric varices: 12 years’ expe­rience. Endoscopy 2000;32:512–519.
15. See A, Florent C, Lamy P, et al. Cerebrovascular accidents after endoscopic obturation of esophageal varices with isobutyl-2-cyanoacrylate in 2 patients. Gastroenterol Clin Biol 1986;10:604–607.
16. Roesch W, Rexeoth G. Pulmonary, cerebral and coronary emboli during bucrylate injection of bleed­ing fundic varices. Endoscopy 1998;30:S89–S90.
17. Cheng PN, Sheu BS, Chen CY, et al. Splenic infarction after histoacryl injection for bleeding gastric varices. Gastrointest Endosc 1998;48:426–427.
18. Battaglia G, Morbin T, Patarnelo E, et al. Visceral fistulae as a complication of sclerotherapy for esoph­ageal and gastric varices using isobutyl-2-cyanoacrylate. Gastrointest Endosc 2000;52:267–270.
19. Teran JC, Imperiale TF, Mullen KD, et al. Primary prophylaxis of variceal bleeding in cirrhosis: a cost­effectiveness analysis. Gastroenterology 1997;112:473–482.
20. Sharara AI, Rockey DC. Gastroesophageal variceal hemorrhage. N Engl J Med 2001;345(9):669–681.
21. Gralnek I A, Jensen DM, Kovacs TO, et al. The economic impact of esophageal variceal hemorrhage: Cost effectiveness implications of endoscopic therapy. Hepatology 1999;29:44–50.
Chapter 8 / Peptic Ulcer Disease 73
II
GASTRIC SURGERY
74 Miedema and Rangnekar
Chapter 8 / Peptic Ulcer Disease 75
8
Surgical Treatment of Peptic Ulcer Disease
Brent W. Miedema,
CONTENTS
INTRODUCTION OPERATIVE TECHNIQUES CURRENT SURGICAL TREATMENT OF ULCER COMPLICATIONS COMPLICATIONS AND MANAGEMENT OF PEPTIC ULCER SURGERY SPECIAL CONSIDERATIONS IN ULCER SURGERY COST-EFFECTIVE SURGERY IN PUD
UMMARY
S REFERENCES
INTRODUCTION
The surgical treatment of peptic ulcer disease (PUD) has undergone a radical shift in the past 10 years. This is primarily because of the recognition that most gastric and duodenal ulcers are caused by Helicobacter pylori ( H. pylori). The recognition that PUD is an infectious problem, rather than a problem with excess acid production, and can be definitely cured, has rendered most peptic ulcer operations obsolete. Eradication of the H. pylori eliminates recurrence of the ulcer disease, whereas healing an ulcer with antacid therapy alone results in a 70–80% recurrence rate. Thus, most surgical literature prior to the recognition of H. pylori was based on controlling acid production is no longer relevant to modern day ulcer surgery.
This chapter will focus on the indications and operative techniques for gastroduodenal ulcer disease. The traditional understanding and surgical treatment of ulcer disease will be reviewed. The current approach to complications of ulcer disease will be detailed. The few areas where elective surgical treatment is applicable for PUD will be discussed. Finally, the complications and cost effectiveness of ulcer surgery will be reviewed.
MD
and Nitin Rangnekar,
MD
OPERATIVE TECHNIQUES
The evolution of operations for ulcer disease has progressed as surgical techniques and understanding of gastric physiology advanced. Gastrojejunostomy and subtotal
From: Clinical Gastroenterology: An Internist's Illustrated Guide to Gastrointestinal Surgery
Edited by: George Y. Wu, Khalid Aziz, and Giles F. Whalen © Humana Press Inc., Totowa, NJ
75