Treatment of bleeding esophageal varicesA new technique

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Treatment of Bleeding Esophageal Varices A New Technique

Roberto Blanco-Benavides, MD, FACS, Mexico City, Mexico

Bleeding from esophageal varices secondary to portal hypertension caused by cirrhosis of the liver is a frequent clinical problem that is difficult to treat. There is a high mortality rate and recurrent bleeding in a number of patients [I]. A new surgical technique for treatment of bleeding esophageal varices is presented. It is based on an increase in the periesophageal pressure and the creation of a gastroesophageal antireflux mechanism. Operative Technique A wide, and not tight Nissen fundoplication [2] 6 to 8 cm long is performed through the abdomen, with a Sengstaken-Blakemore tube (balloons deflated) in situ. Five to 7 cm incisions into the stomach are made parallel to the suture line. A gastrogastro anastomosis is performed with continuous 3-O catgut suture and a second row of 2-O silk sutures is added (Figure 1). The Sengstaken-Blakemore tube is removed and the abdomen is closed in the usual manner. A liquid diet is begun after 48 hours.

We have used this technique in 17 adult patients with active bleeding from esophageal varices who were diagnosed endoscopically and who did not respond to medical treatment for 24 hours. These patients had presented with bleeding one or more times previously and all had histologic diagnoses of hepatic cirrhosis. Utilizing Child’s classification of surgical risk [5], 10 patients were considered to be in class C and 7 patients were considered to be in class B. In all of the patients the bleeding was stopped. At present, the seven class B patients have lived for a postoperative period of 1 to 3 years and five of the class C patients are alive 1 to 2 years postoperatively. Five

Comments The most widely accepted factor in the pathogenesis of bleeding from esophageal varices is increased hydrostatic pressure in the portal venous system and the esophagus due to gastroesophageal reflux [3,4]. However, the pressure can be modified with the application of this new technique of placing the inferior end of the esophagus into the abdominal cavity and surrounding it with the stomach. In this way, the intraabdominal and intragastric pressures are transmitted directly to the esophagus, acting like a permanent external tourniquet (Figures 2 and 3); it also creates a gastroesophageal antireflux mechanism.

From the Department of Sugery, Hospital Gabriel Mancera, Mexico Institute of Social Security, Mexico City, Mexico. Requests for reprints should be addressed to Roberto Blanco-Benavides, MD, Apartado Postal 85-004, Mexico 20, D.F.

Volume 145, June 1993

Ffgure 1. Gastrogastro anastomosis affer a N&en t/on.




Figure 2. Transverse section of the esophagus and stomach showing the transmisskm of intraabdominai and intragastric pressures to the esophagus.

of the class C patients died from hepatic insufficiency, one in the immediate postoperative period (5 days), two 6 months after the operation, one 12 months after operation, and one 16 months after operation. Five patients presented with transitory dysphagia of solids which disappeared spontaneously within 4 to 5 weeks after institution of a liquid diet. No patient has had renewed bleeding of the esophageal varices since operation. Summary A technique for the treatment of bleeding esophageal varices has been described. It is based on an increase in the periesophageal pressure and the creation of an antireflux mechanism that modifies the pathogenic factors of the bleeding. It has been utilized in 17 high-risk patients with satisfactory results.


Figure 3. Postoperative esophagogram of a class 6 patient.

References 1. Johnson WC, Nabseth CC, Widrich WC, Bush HL Jr, O’tlara ET, Robbins AH. Bleeding esophageal varices. Ann Surg 1982; 195:393-400. 2. Shackelford FIT. Surgery of the alimentary tract. Second ed. Philadelphia: WB Saunders, 1978:423. 3. Liebowitz HR. Pathogenesis of esophageal varix rupture. JAMA 1981;175:874-9. 4. Crloff MJ, Thomas l-U.Pathogenesisof esophageal varix rupture. Arch Surg 1963;87:301-7. 5. Child CG III. The liver and portal hypertension. Philadelphia: WB Saunders, 1964:82.

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