Blood flow in the diabetic neuropathic foot

Edmonds, M E; Roberts, V. C.; Watkins, P J

doi:10.1007/bf00253862

Cited by 259 publications

(126 citation statements)

References 16 publications

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“…Abnormalities of blood flow [6] and venous oxygenation [7] have been reported in the foot with diabetic neuropathy and arteriovenous shunting [8] could partly explain these findings. While our patients had no clinical evidence of significant peripheral vascular disease or neuropathy, early changes in blood flow or nerve conduction could still be present.…”

Section: Discussionmentioning

confidence: 95%

Reduced transcutaneous oxygen tension and impaired vascular response in type 1 (insulin-dependent) diabetes

Railton¹,

Newman²,

Hislop

et al. 1983

Diabetologia

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Summary. Measurements of transcutaneous oxygen tension were made on the foot and arm in 16 Type 1 (insulin-dependent) diabetic patients with no evidence of vascular or neurological disease on simple clinical examination and in 30 nondiabetic subjects. The mean transcutaneous oxygen tension measured at 45 ~ on the foot was significantly lower in the diabetic patients than in the non-diabetic subjects. The hyperaemic response in the arm after cuff occlusion (measured by transcutaneous oxygen tension at 37 ~ was also significantly lower in the diabetic patients. These results may reflect abnormal capillary blood flow in diabetic patients. As the methods are simple and non-invasive, they may prove useful in the early assessment and subsequent monitoring of peripheral vascular problems in diabetes.Key words: Transcutaneous oxygen tension, vascular response, Type 1 diabetes, capillary blood flow.The technique of transcutaneous oxygen tension (TcPO2) measurement can provide a non-invasive method of estimating both arterial PO2 and tissue perfusion [1]. If the vascular bed is maximally dilated by heating to 45 ~ and adequately perfused, there is a good correlation between TcPO2 values and arterial PO2 in healthy adults [2]. With the electrode operating at a lower temperature (usually 37 ~ the TcPO2 reading is then related to skin perfusion and the technique can be used to assess reactive hyperaemia in the skin [3].We have reported previously a reduction in TcPO2 values at 45 ~ in patients with peripheral vascular disease [4], but whether such abnormalities in TcPO2 can be detected in diabetic patients with no clinical evidence of vascular disease is unknown. Reduction in vascular reactivity in diabetic children has been reported [5] and we have, therefore, investigated a group of adult Type 1 (insulin-dependent) diabetic patients to determine whether there are any differences in TcPO2 or in vascular reactivity compared with normal subjects. Patients and MethodsSixteen Type 1 diabetic patients, eight females and eight males, mean +SD age 28_6years (range 18-39years) were studied (Tablet). None had any symptoms of leg pain or claudication and all had palpable lower limp pulses including dorsalis pedis and posterior tibial pulses. Lower limb reflexes, pin prick and touch sensation and ankle vibration sense using a tuning fork (128 Hz) were also normal in all patients. Thirty normal subjects (11 females and 19 males) aged from 20 to 63 years were also studied. Twenty-two of this group (11 females and It males) were aged < 40 years (mean + SD: 28.4 + 6.1 years) and were used as control subjects. All gave informed consent. Six of the diabetic patients and 11 of the control subjects were regular smokers of 20-40 cigarettes daily. All subjects refrained from smoking for a minimum of 1 h before the procedure and were studied supine. The left arm and left foot were exposed and clothing loosened around the arm and leg to prevent any obstruction to blood flow. The examination room was maintained close to 26 ~ to prevent vasoconstri...

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Section: Discussionmentioning

confidence: 95%

Reduced transcutaneous oxygen tension and impaired vascular response in type 1 (insulin-dependent) diabetes

Railton¹,

Newman²,

Hislop

et al. 1983

Diabetologia

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“…This increase is now thought to be due to the dilation of denervated arteriovenous shunts [2][3][4][5][6][7][8][9] normally controlled by sympathetic nerves.…”

Section: Resultsmentioning

confidence: 99%

Blood flow patterns in painful diabetic neuropathy

1984

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Summary.Peripheral blood flow is known to be qualitatively increased in diabetic patients with neuropathy. We have measured the actual blood flow in the feet of diabetic patients with neuropathy using non-invasive mercury strain gauge plethysmography and Doppler sonogram techniques and shown that it is increased on average five times above normal at an ambient temperature of 20 ~ -22 ~ Moreover, reduction of this high flow by sympathetic arousal stimuli proved possible in those with severe painful neuropathy contrasting strongly with failure to reverse it in those with severe non-painful sensory neuropathy. Reduction of blood flow was associated with reduction in neuropathic pain. We studied 22 diabetic patients with severe sensory neuropathy and eight with painful neuropathy. High resting foot blood flows were demonstrated in both groups with neuropathy. The big toe flow in those with severe sensory neuropathy was 29.3 + 9.2 ml. rain-1. 100m1-1 (mean+-SD) and in the painful neuropathy group, 25.9+_7.5, compared with 5.2+2.4ml.min -1. 100m1-1 in the non-diabetic control subjects (p<0.001). High foot skin temperatures were also recorded in the groups with neuropathy, reflecting the high blood flow. The subjects with painful neuropathy retained the ability to constrict peripheral blood vessels in response to arousal stimuli, and reduce peripheral flow on average by 32% compared with the patients with sensory neuropathy who responded on average by only 10%. The demonstration of a peripheral sympathetic defect, responsible for the high blood flow and the potential reversal of such flow in painful neuropathy may be important in our further understanding of the aetiology of such pain and its treatment.Key words: Diabetes mellitus, peripheral blood flow, sensory neuropathy, painful neuropathy, peripheral sympathetic neuropathy.During the nineteenth century, the feet of diabetic patients with peripheral neuropathy were observed to be hot and erythematous [1] and the blood flow in such feet was considered to be increased. This increase is now thought to be due to the dilation of denervated arteriovenous shunts [2-9] normally controlled by sympathetic nerves.Measurement of actual blood flow in diabetic neuropathic feet has only been undertaken in one previous study [10]. Blood flow was not found to be increased in neuropathic subjects probably because the studies were conducted by waterbath plethysmography at 32~ causing vasodilatation and increased flow in the control subjects.The aim of this study was to measure the magnitude of resting foot blood flow in a group of diabetic patients with severe sensory neuropathy and to discover whether the hot, burning foot, so characteristic of distal painful neuropathy, also has a high resting flow resulting from a peripheral sympathetic defect. In addition, the sympathetic responses of both types of neuropathy were tested to discover whether either retained the ability to reduce peripheral flow by vasoconstriction, and whether any benefits might result from this. Subjects and metho...

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“…It is well established that there is arterio-venous shunting in the diabetic neuropathic leg which leads to distended, "arterialised" veins [39][40][41][42] that have elevated oxygen ten-sion [42]. The presence of epineurial arterio-venous shunts in the neuropathic subjects and the reduced intensity of fluorescence has led us to speculate that similar mechanisms may be taking place at the surface of the nerve leading to a "steal" effect rendering the endoneurium ischaemic.…”

Section: Discussionmentioning

confidence: 99%

Impaired blood flow and arterio-venous shunting in human diabetic neuropathy: a novel technique of nerve photography and fluorescein angiography

et al. 1993

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Summary. New techniques of sural nerve photography and fluorescein angiography which are able to provide an index of nerve blood flow have been developed. Under local anaesthetic, 3 cm of sural nerve was exposed at the ankle using an operating microscope. Without disturbing the epineurium, vessels were identified and photographed at a standard magnification ( x 30). These were independently graded by an ophthalmologist not otherwise involved with the study. Fluorescein angiography was then carried out on the exposed nerve. The fluorescein appearance time and intensity of fluorescence were quantified, using computer analysis of digitised images. Thirteen subjects with chronic sensory motor neuropathy, five non-neuropathic diabetic and nine normal control subjects were studied. The mean epineurial vessel pathology score of the neuropathic group was significantly higher than the combined normal control and non-neuropathic diabetic groups (p < 0.01). Direct epineurial arteriovenous shunting was observed in six neuropathic and one non-neuropathic diabetic patients and not in any of the normal control subjects. The nerve fluorescein appearance time was significantly delayed in subjects with chronic sensory motor neuropathy (51.5 + 12 s) compared to both normal (34.7 _+ 9 s, p < 0.01) and non-neuropathic diabetic subjects (33.4 + 11 s,p < 0.025). The mean intensity of fluorescence at 96, 252 and 576 s, was significantly lower in subjects with chronic sensory motor neuropathy compared with both of the other groups (p < 0.05). The epineurial vessel pathology score was significantly related to reduced sural (p < 0.01) and peroneal (p < 0.001) nerve conduction velocities, elevated vibration (p < 0.01) and thermal (p < 0.001) perception and the severity of retinopathy (p < 0.002). The fluorescein appearance time was significantly related to reduced sural sensory (p <0.02) conduction velocity, elevated vibration (p < 0.01) perception and epineurial vessel (p < 0.002) pathology score, but it failed to relate to peroneal motor (p = 0.06) conduction velocity, thermal (p = 0.1) perception and the severity ofretinopathy (p = 0.3). Intensity of fluorescence was significantly related to fluorescein appearance time (at 96 s,p < 0.001; at 576 s,p < 0.05) but did not relate to measures of neuropathic severity. These techniques have enabled us to observe that epineurial vessel anatomy is abnormal and that nerve blood flow is impaired in subjects with chronic sensory motor neuropathy. In addition epineurial arterio-venous shunting may be a feature of diabetic neuropathy. These techniques may further be applied to study nerve blood flow in early diabetic neuropathy.

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Blood flow in the diabetic neuropathic foot

Cited by 259 publications

References 16 publications

Reduced transcutaneous oxygen tension and impaired vascular response in type 1 (insulin-dependent) diabetes

Reduced transcutaneous oxygen tension and impaired vascular response in type 1 (insulin-dependent) diabetes

Blood flow patterns in painful diabetic neuropathy

Impaired blood flow and arterio-venous shunting in human diabetic neuropathy: a novel technique of nerve photography and fluorescein angiography

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