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J Thorac Cardiovasc Surg 1996;111:176-180
© 1996 Mosby, Inc.


SURGERY FOR CONGENITAL HEART DISEASE

AUGMENTATION OF PULMONARY BLOOD FLOW WITH AN AXILLARY ARTERIOVENOUS FISTULA AFTER A CAVOPULMONARY SHUNT

Alan Magee, MD, Eugene Sim, MD, Lee N. Benson, MD, FRCP(C), William G. Williams, MD, FRCS(C), George A. Trusler, MD, FRCS(C), Robert M. Freedom, MD, FRCP(C)


Toronto, Ontario, Canada

From the Departments of Pediatrics and Surgery, University of Toronto School of Medicine, and the Divisions of Cardiology and Cardiovascular Surgery, The Hospital for Sick Children, Toronto, Ontario, Canada.

Received for publication June 23, 1994. Accepted for publication April 12, 1995. Address for reprints: Robert M. Freedom MD, FRCP(C), The Hospital for Sick Children, 555 University Ave., Toronto, Ontario, Canada, M5G 1X8.

Abstract

Of 320 children with cyanotic congenital heart malformations who had previously undergone cavopulmonary shunt operations, 11 had increasing cyanosis and exercise intolerance and were considered unsuitable for definitive repair, a Fontan procedure, or other palliation. Eight had a previous Glenn shunt and three had a previous bidirectional cavopulmonary connection. To augment pulmonary blood flow, 10 patients underwent creation of an ipsilateral axillary arteriovenous fistula. Mean oxygen saturations were 80% ± 2% before operation, 85% ± 2% immediately after operation, and 84% ± 3% at a mean follow-up interval of 7.4 years (range 0.1 to 15.5 years). Mean hemoglobin values were 202 ± 10 gm/L before operation, 177 ± 10 gm/L after operation, and 191 ± 14 gm/L at latest review. The only complication was mild swelling of the arm distal to the fistula in one patient. All patients reported improvement in exercise tolerance. Eight patients have continued evidence of fistula patency. Development of ipsilateral pulmonary arteriovenous fistulas has not been observed in any patient. Creation of an axillary arteriovenous fistula to augment pulmonary blood flow after a cavopulmonary shunt provides useful palliation for complex cyanotic heart disease when other options are limited. Such additional sources of pulmonary blood flow may influence the development of pulmonary arteriovenous fistulas. (J THORACCARDIOVASCSURG1996;111:176-80)




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