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Biomedical subjects

M E Edmonds

Publications and source records attributed to M E Edmonds.

54 records · Page 3Linked to original sources
PubMed1984

Diabetic autonomic neuropathy and iritis: an association suggesting an immunological cause.

Of 47 insulin requiring diabetics aged 21-40 years with autonomic neuropathy (heart rate variability less than 10), 14 had previously developed iritis. In all except two cases the iritis preceded the autonomic symptoms. The autonomic neuropathy was very severe, 10 patients having two or more characteristic symptoms. Ten of the patients with iritis were women. The association of iritis (itself an immune disorder) with severe symptomatic autonomic neuropathy raises the possibility of an underlying immunological basis for autonomic neuropathy.

Adult↗
PubMed1983

Ephedrine: a new treatment for diabetic neuropathic oedema.

Peripheral oedema secondary to diabetic neuropathy is poorly understood and difficult to treat. Ephedrine markedly reduced neuropathic oedema in four insulin-dependent diabetics. Mean weight-loss (p less than 0 . 05) after 7 days' treatment was 7 . 43 +/- 4 . 51(SD) kg. The oedema returned (mean weight increase 6 . 33 +/- 1 . 73 kg; p less than 0 . 01) when ephedrine was withdrawn but resolved (weight-loss 4 . 85 +/- 1 . 57 kg; p less than 0 . 01) when ephedrine treatment was repeated. In one patient mean 24 h sodium excretion increased from 177 +/- 5 . 20 mmol before ephedrine to 502 +/- 78 mmol on ephedrine therapy (p=0 . 028). Ephedrine also reduced excessive peripheral blood flow produced by the neuropathy; both arterial diastolic flow and arteriovenous shunting as demonstrated by Doppler blood velocity profiles were reduced and the pulsatility index increased from 2 . 50 +/- 0 . 61 to 4 . 75 +/- 1 . 76 (p less than 0 . 001). Ephedrine continues (12-15 months) to be an effective treatment for neuropathic oedema in these four patients.

Adult↗
PubMed1983

Sympathetic nerve failure in diabetes.

Sympathetic damage is a striking feature of diabetic neuropathy, probably much more common and important than previously suspected. Degeneration of arterial medial smooth muscle with subsequent medial calcification is a feature of diabetic neuropathy and represents a structural abnormality probably resulting from sympathetic denervation. Loss of vasomotor control is responsible not only for postural hypotension but also for the remarkable increase of peripheral blood flow and arteriovenous shunting in the neuropathic foot. Demineralisation of bones and neuroarthropathic bone and joint destruction may result. Intractable oedema is another consequence of these haemodynamic abnormalities, while in other cases there is a close association of sympathetic defects with painful neuropathies. The possibility of new treatments using sympathomimetic agents to reverse these abnormalities now exists, and ephedrine has already been shown to be highly effective in reducing neuropathic oedema.

Arrhythmias, Cardiac↗
PubMed1982

Medial arterial calcification and diabetic neuropathy.

X-ray examinations of the feet, knees, and hands were performed on 20 diabetics with severe neuropathy and 20 diabetics with no evidence of neuropathy but with a similar mean age and duration of diabetes. All were under 53 years old with no clinical evidence of peripheral vascular disease. Medial arterial calcification was much more common and extensive in the patients with neuropathy, occurring in the feet in 15 and in the hands in eight compared with in four (p less than 0.001) and none (p less than 0.001) of the controls respectively. Although there was some correlation between calcification and both proteinuria (p less than 0.05) and proliferative retinopathy (p less than 0.02), the association between calcification and neuropathy (p less than 0.001) was much stronger. Neuropathy, with sympathetic denervation of the smooth muscle of the tunica media, may be important in the aetiology of medial arterial calcification.

Adult↗
PubMed1982

Blood flow in the diabetic neuropathic foot.

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.

Adult↗
PubMed1979

Autonomic neuropathy in rheumatoid arthritis.

Patients with seropositive and seronegative rheumatoid arthritis (RA) and age-matched controls were investigated for the presence of autonomic neuropathy. Significantly more patients with RA had abnormal autonomic function, suggesting that autonomic neuropathy occurs more commonly in RA than hitherto suspected. The existence of an autonomic neuropathy may be an important complicating factor in rheumatoid disease and may lead to increased morbidity and mortality.

Adult↗
PubMedDate not supplied

Vascular calcification, autonomic neuropathy, and peripheral blood flow in patients with diabetic nephropathy.

The possibility that digital gangrene in patients with diabetic nephropathy might be due to abnormalities of peripheral blood flow secondary to vascular calcification has been investigated. Twenty patients with renal failure due to diabetic nephropathy were studied. Peripheral blood flow was measured using venous occlusion plethysmography, together with an assessment of medial arterial calcification on plain radiographs of the hands and feet, and transcutaneous oxygen tension (TcPO2). Hallux blood flow was markedly raised (median 22.5, range 11.5-56.5, ml min-1 100-ml-1) compared with non-diabetic control subjects (4.7, 1.1-10.5, ml min-1 100-ml-1; p less than 0.01) and similar to that in diabetic patients with autonomic neuropathy (29.5, 16.7-49.6, ml min-1 100-ml-1). Although vascular calcification was common and extensive in the patients with diabetic nephropathy, TcPO2 measurements in the supine foot were normal and did not indicate tissue ischaemia. We conclude that despite extensive vascular calcification high peripheral blood flow occurs in the feet of these patients at rest together with normal transcutaneous oxygen tension.

Adult↗
PubMedDate not supplied

Raised ankle/brachial pressure index in insulin-treated diabetic patients.

The ankle/brachial blood pressure index (A/B PI) is important in the vascular laboratory assessment of peripheral vascular disease. However it is falsely elevated in diabetes, hence underestimating the true severity of disease. We have therefore examined the influence of diabetes on the A/B PI in 2092 patients, 538 with diabetes, all referred for evaluation of peripheral vascular disease. The prevalence of a raised A/B PI (greater than or equal to 1.5) in insulin-treated patients (18.3%) was much higher (p less than 0.001) than that in both non-insulin-treated diabetic patients (4.5%) and patients with no diabetes (2.8%). Insulin-treated patients with a duration of diabetes of greater than 30 years had a higher prevalence of raised A/B PI than those with a duration of less than or equal to 9 years. No significant age effects were seen.

Ankle↗
PubMedDate not supplied

Paradoxical blood flow responses in the diabetic neuropathic foot: an assessment of the contribution of vascular denervation and microangiopathy.

Blood flow is abnormal in the diabetic neuropathic foot, and this may be of importance in the pathogenesis of complications. Arteriovenous shunting is increased, and blood flow through these channels may paradoxically decrease in response to local heating. Peak skin blood flow is also reduced in these patients. It is not known whether these blood flow abnormalities may reflect diabetic microangiopathy, or whether they simply reflect vascular denervation. The skin blood flow response to a local thermal stimulus was studied in four non-diabetic patients with a unilateral traumatic neuropathy and foot ulceration. All showed a decrease in skin blood flow (to 68% of basal) at the great toe during local heating in the neuropathic limb, in contrast to the normal limb, in which blood flow increased to 180% of basal. Peak skin blood flow was also greatly reduced in the neuropathic limb, being only 29% of the normal limb. Neuropathy alone can be responsible for abnormal skin blood flow responses in the neuropathic foot.

Adolescent↗
PubMedDate not supplied

Is neuropathic ulceration the key to understanding increased mortality due to ischaemic heart disease in diabetic foot ulcer patients? A population approach using a proportionate model.

Ischaemic heart disease (IHD) is the commonest cause of death in diabetic foot ulcer patients and non-ulcerated diabetic patients, yet the mortality rate of diabetic foot ulcer patients is over twice that of non-ulcerated patients. As the cause of this increased mortality is not understood, we plotted the ratio of deaths due to ischaemic heart disease (IHDn) to other causes of death (i.e. IHDn:OCDn) against age for 242 diabetic foot ulcer patients and 121 controls (non-ulcerated diabetic patients). The IHDn:OCDn ratio rose above 1.0 from age 40 years onwards for diabetic foot ulcer patients, but from age 70 years onwards for controls, demonstrating differentially increased mortalities due to IHD. A population model involving summation of IHDn:OCDn ratios for neuropathic and neuroischaemic diabetic foot ulcer patients calculated an overall increased mortality rate of 1.8 compared with that of non-ulcerated diabetics. The model predicted that a 25% reduction in neuropathic diabetic foot ulcer patients dying from IHD would eliminate the increased mortality, demonstrating that neuropathic rather than ischaemic ulceration defines the cause of increased mortality among diabetic foot ulcer patients.

Adult↗