Abstract
The angiosome is a three-dimensional block of tissue supplied by a source vessel with its boundary outlined either by an anastomotic perimeter of reduced-caliber choke vessels or by true anastomoses with no reduction of vessel caliber. This article focuses on the role of these anastomotic vessels in defining flap survival or the necrotic pattern seen in fulminating meningococcal septicemia. Experiments in pigs, dogs, guinea pigs, and rabbits over the past 46 years were reviewed, focusing on the necrosis line of flaps, the effects of various toxins in vivo, and correlating these results in the clinical setting. Experimentally, choke anastomoses are functional and control flow between perforator angiosomes. They (1) permit capture of an adjacent angiosome when the flap is raised on a cutaneous perforator in 100 percent of cases, with the necrosis line occurring usually in the next interperforator connection; (2) confine flow to the territory of the involved artery when a toxin is introduced by spasm around its perimeter; and (3) lose this property of spasm when choke vessels are converted to true anastomoses following surgical delay, or where true anastomoses occur naturally, thereby allowing unimpeded blood flow and capture of additional angiosome territories. Clinical experience supports these observations. The functional angiosome is the volume of tissue that clinically can be isolated on a source vessel. The area extends beyond its anatomical territory to capture an adjacent territory if connections are by choke anastomoses, or more if they are by true anastomoses.
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