Edmonds M E, Roberts V C, Watkins P J
Diabetologia. 1982 Jan;22(1):9-15. doi: 10.1007/BF00253862.
The mechanisms which underlie the development of Charcot joints and foot ulceration are poorly understood. The present study using non-invasive Doppler techniques demonstrates that in the neuropathic leg, the arteries are rigid, peripheral blood flow is increased and associated with arteriovenous shunting. We studied 10 diabetics with severe neuropathy (including five with Charcot changes), 16 diabetics without neuropathy and 10 control subjects. Markedly abnormal blood velocity profiles (sonograms) were demonstrated only in those patients with severe neuropathy. They showed increased diastolic flow (indicated by a reduced Pulsatility Index of 2.88 +/- 0.8 (mean +/- SD) compared with 9.53 +/- 4.0 (p less than 0.001) in the diabetics without neuropathy and 10.8 +/- 3.7 (p less than 0.001) in the control subjects) suggesting arteriovenous shunting. Increased rigidity was indicated by decreased transit times -57 +/- 6.3 ms (mean +/- SD) in the diabetics with neuropathy compared with 66 +/- 7.6 ms (p less than 0.01) in the diabetics without neuropathy and 67 +/- 9.1 ms (p less than 0.05) in the control subjects. This was accompanied by raised ankle systolic pressures -199 +/- 22 mmHg (mean +/- SD) in the diabetics with neuropathy compared with 151 +/- 15 mmHg, (p less than 0.001) in the diabetics without neuropathy and 146 +/- 18 mmHg (p less than 0.001) in the control subjects. Medial wall calcification occurred almost exclusively in the neuropathic subjects. These alterations in blood flow which include arteriovenous shunting may be important in the pathogenesis of complications of the neuropathic leg.
夏科关节和足部溃疡形成的潜在机制目前还知之甚少。本研究采用非侵入性多普勒技术表明,在神经性腿部,动脉僵硬,外周血流增加并伴有动静脉分流。我们研究了10名患有严重神经病变的糖尿病患者(包括5名有夏科氏改变的患者)、16名无神经病变的糖尿病患者和10名对照者。仅在那些患有严重神经病变的患者中显示出明显异常的血流速度曲线(超声图)。他们表现出舒张期血流增加(搏动指数降低,为2.88±0.8(平均值±标准差),而无神经病变的糖尿病患者为9.53±4.0(p<0.001),对照者为10.8±3.7(p<0.001)),提示存在动静脉分流。神经病变的糖尿病患者的通过时间缩短,为57±6.3毫秒(平均值±标准差),表明僵硬增加,而无神经病变的糖尿病患者为66±7.6毫秒(p<0.01),对照者为67±9.1毫秒(p<0.05)。同时,神经病变的糖尿病患者的踝部收缩压升高,为199±22毫米汞柱(平均值±标准差),而无神经病变的糖尿病患者为151±15毫米汞柱(p<0.001),对照者为146±18毫米汞柱(p<0.001)。内侧壁钙化几乎仅发生在神经病变患者中。这些包括动静脉分流在内的血流改变可能在神经性腿部并发症的发病机制中起重要作用。