Vasculopathy in the Diabetic Foot

This paper attempts to distil some of the results of vasculopathy studies performed on Jamaican diabetic clinic attendees. Doppler measurements of ankle/brachial pressure index (A/BI) revealed that 23 percent of the diabetics have peripheral occlusive arterial disease (POAD) which was mostly asymptomatic. Plethysmorgraphic blood flow studies revealed a profound reduction in the vasodilatory response to increased flow demand. Prevalence of POAD determined by Doppler testing of A/BI reported by other researchers ranged from 13 percent in a large community study, one-third of whom were diabetic, to 47 percent in patiens who had been diabetic for 20 years. Isolated posterior tibial disease has been reported to carry a three-fold risk of all cause mortality and a four-fold risk of coronary heart disease mortality. This underscores the need for regular Doppler A/BI testing in order to improve the recognition, and treatment of POAD, and prevent further cardiovascular morbidity and mortality.(Au)

Some clinical factors contributing to the development of the diabetic foot

Clinical neurological studies, blood pressure measurements and some haematological investigations were performed on a random sample of forty-four patients, at the Diabetes Out-Patient Clinic of the University Hospital of the West Indies (UHWI), to examine some of the factors that predispose to the development of the diabetic foot. Our results revealed that 86 percent of the patients had elevated glycosylated haemoglobin (HbA > 9.0 percent), 82 percent had clinical signs of peripheral sensory neuropathy. 29 percent had signs of autonomic neuropathy in addition to peripheral sensory neuropathy. Sixty-one percent (61 percent) of the patients had ankle/arm systolic blood pressure ration less than 1.0 and were diagnosed as having peripheral vascular disease (PVD). The group with neuropathy was found to have a significantly lower diastolic blood pressure (p < 0.0005) than the group without neuropathy. We believe that hyperglycaemia-induced vasodilation (indicated by a lower diastolic blood pressure) in a significant number of diabetics resulted in compensatory shunting of blood from the deeper tissues, including nerves, to periphery. The resulting endoneural hypoxia could be responsible for the unusually high incidence of peripheral sensory neuropathy detected in this sample of diabetic patients. Metabolic factors may also play a role.(AU)

Peripheral occlusive arterial disease in diabetic clinic attendees

Peripheral occlusive arterial disease occurs with a greater frequency in the diabetic population than in the general population. It can have debilitating effects and so early detection and intervention are important. The aim of this study was to investigate the prevalence of peripheral occlusive arterial disease (POAD) among a sample of diabetic patients attending the out-patient clinic at the University Hospital of the West Indies (UHWI), Mona. A sphygmomanometer was used to measure arm and ankle blood pressures in 80 diabetic patients, and the ankle-brachial systolic pressure index (ABI) was determined. The presence or absence of peripheral pulses was detected with the Multi-dopplex (model 1). POAD was defined by the absence of one or more peripheral pulses and/or an ABI < 0.09. Of the 80 diabetic patients examined, 18 (22.5 percent) were found to have POAD. Seventy-eight percent of diabetics with POAD had the disease in both legs. Intermittent claudication was diagnosed in 27.7 percent of patients with POAD. A significantly larger proportion of diabetics with POAD were hypertensive and/or neuropathic (p < 0.05). The results suggest that serious attention should be given to the quantitative screening for POAD in the diabetic patients attending the clinic at the UHWI (AU)

The effect of glycaemic control on peripheral blood flow in diabetics -Poster presentation

Many studies have shown that persistent uncontrolled blood glucose predisposes to several diabetic complications. The aim of this study was to determine the influence of blood glycated haemoglobin levels on plasma fibrinogen concentration - (PFC), relative plasma viscosity (RPV) and ankle blood flow (Qak) in a group of diabetic patients with vascular complications compared with non-diabetic control (C). Qak was measured by the technique of venous occlusion plethysmography. PFC was determined by a clot-weight method. RPV was determined by capillary viscometry. Glycaemic control was determined by measuring glycated haemoglobin levels (GHb). Patients were divided into three categories of glycaemic control, namely good (GHb 4 - 8 percent), moderate (GHb > 8 - 12 percent) and poor (GHb > 12 percent). Qak, PFC and RPV were compared among diabetics with and without peripheral occlusive arterial disease (POAD) and/or neuropathy of various categories of glycaemic control. Qak in diabetics without peripheral occlusive arterial disease (POAD) with good glycaemic control was significantly higher (p <0.05) than that of non-diabetic (C). Qak differed significantly (p < 0.05) between non-neuropathic diabetics (without POAD) (D) with good and poor or good and moderate glycaemic control. PFC was significantly higher (p < 0.05) in all diabetics with POAD, in D with moderate glycaemic control and in neuropathic diabetes (without POAD) (ND) with poor control than in C. RPV was significantly higher (p < 0.05) in D with moderate control and poorly controlled neuropathic diabetics with POAD than in C. RPV differed significantly (p < 0.05) between D with moderate and poor control. The results suggest that in the absence of POAD, an initial vasodilatation occurs in diabetics. The decrease in arterial flow as metabolic control worsens, may be a consequence of the simultaneous increase in plasma viscosity.(AU)

Venous function study in diabetics with neuropathy: a preliminary study

In a previous study, we found a significantly impaired vasodilatory reserve, a reflection of abnormal vasodilation in the feet of diabetics with neuropathy. No study has been done to establish whether our diabetics have abnormal venous function. The present study was designed to examine venodynamic variables in order to determine whether venous impairment was present in our diabetic patients. Venous circulation in the leg was examined in 27 diabetic patients with neuropathy (ND) and compared with 35 non-neuropathic diabetics (NND) and 19 non-diabetic controls (C). Patients and controls were free from signs and symptoms of peripheral occlusive arterial disease. Glycaemic control in the patients was assessed by the measurement of glycated haemoglobin.(AU)

Impaired vasodilatory reserve in diabetes with and without neuropathy - abstract

Several studies have shown that resting blood flow is increased in the diabetic neuropathic foot, It has been proposed that the mechanism involved is the loss of sympathetic tone which occurs when nervesto peripheral blood vessels are damaged resulting in blood vessels being constantly dilated. The extent to which further dilatation can be achieved when interrupted flow is resumed we termed vasodilatory reserve (VDR). This has not previously been investigated. We, therefore, attempted to assess the VDR in diabetes' blood vessels by measuring reactive hyperaemia at the ankle. The VDR was determined in 23 neuropathic (ND), and 16 non-neuropathic diabetic (D) patients and compared with 16 non-diabetic control subjects (C). Patients and controls were free from signs and symptoms of peripheral occlusive arterial disease. Glycaemic control are assessed by glycosylated haemoglobin levels. Ankle blood flow (Q) was measured by venous occlusion plethsmography. Reactive hyperaemia was induced by occlusion of the ankle at 200 mm Hg for 4 minutes. Blood flow was then measured at 1 minutes deflation of the occlusive cuff to 60 Hg. The VDR is expressed as the precentage change in blood flow from the resting value 1 minute after reactive hyperaemia. VDR was 14.49 percent, 20.8 percent and 114.75 percent in the ND, D and C groups respectively. Our present finding indicated and impaired vasodilatory reserve in the ankle of neuropathic and non-neuropathic diabetes pointing to their inability to adequately increase blood supply to the feet after interrupted flow(AU)

Haemorrheological changes in diabetic neuropathies - abstract

Chronic hyperglycaemia leads to disturbances in metabolic pathways in nerves. However, the underlying mechanisms are still not fully understood. One of the theories of diabetic neuropathy has implicated a vascular factor, which we believe may be associated with abnormal haemorrheological changes. Persistent hyperglycaemia creates a "stressful" conditions which triggers increased production of the acute-phase-reactant protein, fibrinogen, causing the development of a hyperfibrinogenaemic state. Apart from the red cell concentration, fibrinogen is the next most important determinant of whole blood viscosity. Therefore, an hyper-viscosity syndrome is commonly seen in diabetic patients. The increased viscosity could be an important factor in the development of endothelial damage in the vaso nervorum, hence contributing to the pathogenesis of diabetic neuropathy. The present study examined changes in haemorrheological parameters, with particular emphasis on plasma fibrinogen concentration in diabetics with and without peripheral neuropathy. Forty-seven (47) diabetics, 39 females and 8 males, were selected randomly during routine attendance at the Diabetic Clinic at the Unversity Hospital of the West Indies. Patients underwent a comprehensive medical check and were screened for peripheral neuropathy. Twenty-one patients were classified as insulin-treated and 26 as non-insulin-treated. For the diabetic patients, the mean (ñ SD): Age = 53.71 ñ 15.22 years, duration of diabetes mellitus = 12.96 ñ 7.97 years, B.M.I. = 30.00 ñ 10.00, blood pressue = 162.58 ñ 33.91/91.78 ñ 11.65 mm Hg; HbA1 = 13.99 ñ 4.83 percent. Only 2 (4.35) of the patients smoked or drank alcohol. A sex and age-matched non-diabetic control group consisting of 30 subjects were also studied. Venous blood was analysed for plasma fibrinogen concentration (PFC), packed-cell volume (PCV), haemoglobin concentration (HB) and glycosylated haemoglobin (HbA1) levels. The prevalence of peripheral neuropathy in the diabetic patients was 73.87 percent. PFC was significantly (p < 0.001) elevated in diabetic group, 5.06 ñ 1.26 g/l, compared with non diabetic groups, 3.19 ñ 0.65 g/l. However there was no significant difference in PFC betwen diabetics with (4.19 ñ 1.36 g/l) and without (5.14 ñ 1.14 g/l) neuropathy. Both PCV and Hb values were significantly less (p<0.05) in diabetics than in non-diabetics. Neither PCV nor Hb showed any significant variation between deabetics with and without neuropathy (AU)