[The clinico-pathological aspects of acute exacerbation of arteriosclerosis obliterance].
Arteriosclerosis obliterance (ASO) is defined as the ischemic status of lower extremity produced by a stenotic and/or occlusive lesion of lumens of major arterial stress based on the pathology of atherosclerotic change. The sign and symptom of ASO are usually thought to be progressed slowly by natural progression process of atherosclerosis, however, in certain occasion, the progression of clinicopathological status of leg ischemia is acute as well as grave, so as to manifest rest pain or necrosis of the lower extremity. The basic mechanism of acute exacerbation of lower leg ischemia is attributed to the acute extended thrombus formation in arterial lumen. The factors influencing to the thrombus formation are represented as Virchow's Trias such as the changes in arterial wall, the stasis of blood flow and the coagulability of blood. One of the characteristic feature associated with massive and extended ischemia of lower leg is myonephropathic metabolic syndrome proposed by Haimovich in 1960. This syndrome is particularly seen immediately following the restoration of blood flow to the severely damaged leg and characterized by renal as well as systemic organs disorder. The relationship between the extent of muscle damage and the duration of ischemia is analysed through our data.
Nakajima
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First Department of Surgery, Chiba University School of Medicine, Japan.
D058186:Acute Kidney Injury / Q000209:etiology; D000210:Acute-Phase Reaction; D001162:Arteriosclerosis Obliterans / Q000150:complications / Q000503:physiopathology*; D018450:Disease Progression; D006801:Humans; D007511:Ischemia / Q000209:etiology / Q000601:surgery; D007866:Leg / Q000098:blood supply; D009132:Muscles / Q000473:pathology; D009336:Necrosis; D011183:Postoperative Complications / Q000209:etiology; D015427:Reperfusion Injury / Q000209:etiology; D012206:Rhabdomyolysis / Q000209:etiology; D013577:Syndrome