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Biomedical subjects

D J Ewing

Publications and source records attributed to D J Ewing.

At least 19 recordsLinked to original sources
PubMed1979

Diabetic autonomic neuropathy.

This review attempts to outline the present understanding of diabetic autonomic neuropathy. The clinical features have been increasinly recognised but knowledge of the localization and morphology of the lesions and their pathogenesis remains fragmentary. A metabolic causation as postulated in somatic nerves accords best with clinical observations. Most bodily systems, particularly the cardiovascular, gastrointestinal and urogenital, are involved with added disturbances of thermoregulatory function and pupillary reflexes. Possible effects on neuroendocrine and peptidergic secretion and respiratory control await definition. Current interest centres around the development of a new generation of tests of autonomic nerve function that are simple, non-invasive, reproducible and allow precision in diagnosis and accurate quantitation. Most are based on cardiovascular reflexes and abnormality in them is assumed to reflect autonomic damage elsewhere. Probably no single test suffices and a battery of tests reflecting both parasympathetic and sympathetic function is preferable. Little is known of the natural history. The prevalence may be greater than previously suspected and although symptoms are mild in the majority, a few develop florid features. The relation of control and duration of diabetes to the onset and progression of autonomic neuropathy is not clearly established. Once tests of autonomic function become abnormal they usually remain abnormal. Symptomatic autonomic neuropathy carries a greatly increased mortality rate possibly due to indirect mechanisms such as renal failure and direct mechanisms such as cardio-resiratory arrest. Improved treatment of some of the more disabling symptoms has been possible in recent years.

Autonomic Nervous System↗
PubMed1979

Non-invasive assessment of left ventricular response to Valsalva manoeuvre in normal and diabetic subjects using praecordial accelerocardiography.

The left ventricular response to the Valsalva manoeuvre was studied in 5 normal subjects (group 1), 6 diabetics without autonomic neuropathy (group 2), and 5 diabetics with autonomic neuropathy (group 3), using the maximum amplitude of the praecordial accelerocardiogram (DE) as a noninvasive index of left ventricular performance. During the Valsalva manoeuvre DE decreased in all 3 groups. In groups 1 and 2, DE increased significantly above the control value after release of the manoveuvre (DE overshoot) but this did not occur in group 3. It is suggested that the overshoot of DE in groups 1 and 2 reflects an increase in left ventricular contractility after release of the Valsalva manoeuvre and the absence of an overshoot in DE in the patients with autonomic neuropathy is the result of loss of cardiac adrenergic innervation. The ability to detect an abnormal cardiovascular response to the Valsalva manoeuvre using the non-invasive technique of praecordial accelerocardiography may be of practical value in the assessment of left ventricular function.

Adult↗
PubMed1979

Mononeuropathy in diabetes mellitus.

Fifty-one diabetic patients with mononeuropathies wereoneuropathy were studied to examine possible etiological factors, to determine the relationship with other diabetic complications, and to correlate with the presence and severity of background peripheral and autonomic neuropathy. The median, ulnar, and lateral popliteal nerves were most commonly affected and cranial neuropathy was relatively uncommon. When bilateral involvement of the same nerve was excluded, multiple mononeuropathies were found in only five patients. Median and ulnar mononeuropathy were gradual in onset and affected the dominant limb whereas other types of mononeuropathies were acute in onset with no predilection for either side. No consistent relationship was shown between the onset of mononeuropathy and age, sex, diabetic treatment, duration of diabetes, diabetic control, or other diabetic complications. In particular, there was no significant background peripheral and autonomic neuropathy, as assessed clinically and by objective tests, in almost one-half of the patients studied. It is concluded that diabetic mononeuropathy may occur independently of peripheral and autonomic neuropathy. It is possible, however, that a minimal degree of background damage, known to be present in all diabetic patients, may render them more susceptible than the general population to the various factors causing mononeuropathy.

Abducens Nerve↗
PubMed1978

Immediate heart-rate response to standing: simple test for autonomic neuropathy in diabetes.

The immediate heart-rate response to standing was measured in 22 normal controls and 25 patients with diabetes, 15 of whom had autonomic neuropathy. The response in the controls and patients without autonomic neuropathy was characteristic and consistent, with tachycardia maximal at around the 15th beat and relative bradycardia maximal at around the 30th beat. The diabetics with autonomic neuropathy, however, showed a flat response. In three controls the response was abolished with intravenous atropine but not with propranolol, showing that it is mediated through the vagus. A simplified test using routine ECGs and measuring the R-R interval at beats 15 and 30 with a ruler is easily performed as an outpatient procedure and may be used as a measure of autonomic function in diabetes.

Adult↗
PubMed1977

Gastric emptying in diabetic autonomic neuropathy.

Gastric emptying was studied in 12 diabetic patients, six with and six without objective evidence of autonomic neuropathy and in 20 non-diabetic controls, using a double isotope scinti-scanning technique which differentiated between solid and liquid emptying. Three patients with autonomic neuropathy exhibited gastric stasis, although this was detected by conventional radiology in only one. Neither the patients with stasis nor those without exhibited abnormally rapid early gastric emptying. In patients without stasis, the normal differentiation between solid and liquid emptying was impaired, suggesting an abnormality of antral peristalsis not attributable to vagal denervation. Both intravenous and oral metoclopramide produced symptomatic improvement in two patients with gastric stasis and restored their gastric emptying to normal.

Adult↗
PubMed1977

Peripheral and autonomic nerve function in newly diagnosed diabetes mellitus.

Peripheral and autonomic nerve function was assessed in 10 newly diagnosed male diabetics (six insulin-treated and four sulfonylurea-treated) with repeated observations over the subsequent six months. There was significant impairment of motor-conduction velocity in the common peroneal nerve at diagnosis in both treatment groups, with improvement following treatment in only the insulin-treated patients. In contrast, although the blood glucose level fell in both groups, the mean level was significantly lower in the sulfonylurea-treated patients at two months and at each subsequent visit. In the autonomic function tests significant abnormality was found in the electrocardiographic R-R-interval (beat-to-beat) variation in resting heart rate in two of the insulin-treated patients and all of the sulfonylurea-treated group, with improvement in only one of the latter. One patient in the sulfonylurea-treated group also showed an abnormal response to the Valsalva maneuver (expressed as the Valsalva ratio), and this remained abnormal throughout the period of study. All other patients had normal responses to the Valsalva maneuver and sustained handgrip test. None of the patients had postural hypotension. Abnormalities in autonomic nerve function in diabetics at diagnosis have not been previously reported.

Adolescent↗
PubMed1976

Plasma renin activity in diabetic autonomic neuropathy.

Postural changes in plasma renin activity were studied in three groups of age and duration-matched male diabetics (potent, impotent and with postural hypotension) and in non-diabetic control subjects. Those diabetic subjects with postural hypotension due to automatic neuropathy had no increase in plasma renin activity to the erect posture whereas both the potent and impotent groups had similar plasma renin activity responses to the control subjects. There was a significant inverse correlation between the rise in plasma renin activity on standing and the postural drop in blood pressure (r = 0.476, P less than 0.01) but no correlation with other tests of autonomic reflex function such as the Valsalva manoeuvre and blood pressure response to sustained handgrip. The results suggested that the lesion responsible for the postural hypotension is in the efferent sympathetic pathway. However, neuropathy per se did not wholly explain the decreased postural plasma renin activity response. Diabetic nephropathy, with involvement of cells of juxtaglomerular apparatus, may also be implicated.

Adult↗
PubMed1976

Peripheral and autonomic nerve function in diabetic ketoacidosis.

Peripheral and autonomic nerve function was assessed at intervals over a 3-month period in seven diabetics after ketoacidosis. There was marked improvement in motor conduction velocity and terminal latency of both ulnar and common peroneal nerves in all patients. Five had one or more abnormal autonomic function tests but there were no consistent changes during the same period. It is postulated that peripheral nerves may be more susceptible to acute metabolic damage than autonomic fibres.

Adolescent↗
PubMed1976

Therapeutic experience with fludrocortisone in diabetic postural hypotension.

Fourteen patients with diabetic postural hypotension were treated with fludrocortisone for a mean 12 months (range 6-30 months). The mean daily dose of fludrocortisone was 0.2 mg (range 0.1 mg-0.4 mg). Standing systolic and diastolic blood pressures increased significantly (P less than 0.001) after treatment with fludrocortisone and the postural hypotension decreased significantly (P less than 0.001). Thirteen patients noted considerable symptomatic improvement. Fludrocortisone should be used cautiously in patients with congestive cardiac failure or the nephrotic syndrome.

Adult↗
PubMed1976

Mortality in diabetic autonomic neuropathy.

Thirty-seven diabetics with symptoms and clinical features suggestive of autonomic neuropathy were followed up for 33 months. Of the twenty with abnormal Valsalva or handgrip tests initially, ten (50%) died. There were no other features at presentation that differentiated those who subsequently died from those who survived. The causes of death were renal failure (six patients), cerebrovascular accident (two patients), hypoglycaemic coma (one patient), and "sudden death" (one patient). Of the survivors whose autonomic-function tests were repeated 18 months to 2 years later, five had new or worsening symptoms of autonomic neuropathy with corresponding deterioration of their autonomic-function tests; while two, with initially normal tests, had improved symptomatically. It is concluded that in diabetics with the clinical features of autonomic neuropathy simple autonomic-function tests give a good guide to prognosis, and that abnormal tests are associated with a high mortality.

Adult↗
PubMed1976

Peripheral motor nerve function in diabetic autonomic neuropathy.

Motor conduction velocity was measured in the median, ulnar and common peroneal nerves of 32 diabetics with clinical features of autonomic neuropathy. The responses to the Valsalva manoeuvre and sustained handgrip, and the postural fall in blood pressure were used to assess the integrity of the autonomic nervous system. Abnormalities in the three autonomic function tests were significantly correlated with the forearm conduction velocity of the ulnar nerve, the conduction velocity and motor latency of the common peroneal nerve, and the H reflex. These results show that, in diabetics with autonomic neuropathy, abnormalities in the autonomic nervous system parallel changes in the peripheral nerves. Any diabetic with peripheral neuropathy should be examined for evidence of autonomic nervous system involvement.

Adult↗
PubMed1975

A double-blind trial of patient-controlled nitrous-oxide/oxygen analgesia in myocardial infarction.

The analgesic effect of self-administered nitrous oxide 50%/oxygen 50% ('Entonox" analgesic apparatus) was compared with air given by the same method in a double-blind trial in 81 patients with myocardial infarction. Self-administered nitrous oxide/oxygen, which was associated with a low frequency of side-effects, proved significantly more effective than air in the early relief of severe cardiac pain, but not in the relief of moderate or slight pain or when administration was continued after ten minutes.

Adult↗