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Biomedical subjects

J D Ward

Publications and source records attributed to J D Ward.

At least 127 records · Page 7Linked to original sources
PubMed1988

Enhanced specificity of prognosis in severe head injury.

Data from 523 patients admitted to the Medical College of Virginia with severe head injury and known 6-month outcomes were analyzed in order to determine the optimal combination of early-available prognostic factors. Twenty-one prognostic indicators noted in the emergency room at admission were used to predict outcomes into four categories: good, moderately disabled, severely disabled, or vegetative/dead. A combination of the patient's age (in years), the best motor response (graded in the usual six-point scale), and pupillary response (in both eyes) was found to be the most accurate indicator. The model correctly predicted outcome into one of the four outcome categories in 78% of cases ("specifically accurate predictions"). If predictions into an outcome category adjacent to the actual outcome were accepted, this model was accurate in 90% of cases ("grossly accurate predictions"). A set of three simple graphs based on this model can be used for rapid early estimation of probable outcome in a severely head-injured patient at admission.

Adult↗
PubMed1987

Changes in the factor VIII complex in diabetic ketoacidosis: evidence of endothelial cell damage?

Factor VIII-related antigen and von Willebrand factor are synthesised by and released from vascular endothelium. Acute increases in the plasma concentration of these proteins may reflect endothelial cell damage. We have thus measured the plasma concentration of factor VIII-related antigen and von Willebrand factor, together with procoagulant factor VIII, during the course of acute diabetic ketoacidosis in seven patients. In addition, evidence for qualitative changes in the factor VIII complex was sought. Plasma factor VIII-related antigen and von Willebrand factor were markedly increased (plasma factor VIII-related antigen at presentation, median 2.75 U/ml; von Willebrand factor 2.95 U/ml) and returned toward normal with clinical and biochemical resolution (plasma factor VIII-related antigen at clinical recovery, median 1.80 U/ml; von Willebrand factor 2.05 U/ml). Plasma procoagulant factor VIII followed a similar pattern, but levels were less elevated (plasma procoagulant factor VIII, at presentation, median 1.6 U/ml; at clinical recovery, 1.2 U/ml). Crossed immunoelectrophoresis and sodium dodecyl sulphate-acrylamide electrophoresis with autoradiographic identification of multimeric structure revealed no evidence of structurally abnormal factor VIII-related antigen in diabetic ketoacidosis. However, an extra peak on crossed immunoelectrophoresis ("pre-peak") was a feature in the acute phase ketoacidotic plasma in six subjects, and may represent aggregated factor VIII. Changes in plasma factor VIII are a feature of diabetic ketoacidosis and, whilst not specific to this condition, may be the result of endothelial cell damage.

Adult↗
PubMed1987

Brain tissue pH in severely head-injured patients: a report of three cases.

It is well established that low cerebrospinal fluid (CSF) pH and high CSF lactate concentration indicate the development of brain acidosis after severe human head injury. However, there is no direct evidence that tissue acidosis actually occurs. We measured brain extracellular pH (pHe) in three patients undergoing operation for the evacuation of acute subdural hematomas. A pH-sensitive polymer membrane electrode was inserted 500 micron into the cerebral cortex close to the damaged area. The pHe values obtained were correlated with ventricular CSF acid-based parameters and extension of the brain lesion. The CSF pH was higher than the pHe in all cases; the pHe was particularly low in areas of contusion or compression by mass lesion. The effect of focal brain tissue acidosis on clinical course after severe head injury is discussed.

Acid-Base Equilibrium↗
PubMed1987

Contribution of CSF and vascular factors to elevation of ICP in severely head-injured patients.

The authors studied the relative contribution of cerebrospinal fluid (CSF) and vascular parameters to the level of intracranial pressure (ICP) in 34 severely head-injured patients with a Glasgow Coma Scale score of less than 8. This was accomplished by first characterizing the temporal course of CSF formation and outflow resistance during the 5-day period postinjury. The CSF formation and outflow resistance were obtained from pressure responses to bolus addition and removal of fluid from an indwelling ventricular catheter. The vascular contribution to the level of ICP was assessed by withdrawing fluid at its rate of formation and observing the resultant change in equilibrium ICP level. It was found that, with the exception of patients with subarachnoid hemorrhage, CSF parameters accounted for approximately one-third of the ICP rise after severe head injury, and that a vascular mechanism may be the predominant factor in elevation of ICP.

Absorption↗
PubMed1987

Outcome after severe head injury. Relationship to mass lesions, diffuse injury, and ICP course in pediatric and adult patients.

A consecutive series of 330 severely head-injured patients was studied prospectively. All of the patients were treated with the same protocols by the same physicians and staff in the same intensive care unit. All of the patients had intracranial pressure (ICP) monitoring. Of the 330 patients, 100 were in the pediatric age group (0 to 19 years of age) and 230 were in the adult group (20 to 80 years of age). Statistical analyses were performed with regard to outcome, Glasgow Coma Scale (GCS) score, ICP course, and incidence of surgical lesions. The average emergency room GCS score as well as the 24-hour GCS score for each group was the same. The percentage of patients having ICP that was normal, increased but reducible, and increased but not reducible in each group was the same. The pediatric patients had a significantly higher percentage of good outcomes (43%) than the adult patients (28%) (p less than 0.01). They also had a significantly lower mortality rate (24%) than the adult patients (45%) (p less than 0.01). At 1 year following injury, 55% of pediatric patients had a good outcome compared to 21% of adults (p less than 0.001); this trend was evident at 3 months, with the same p value. Pediatric patients with normal ICP had a higher percentage of good outcomes (70%) than the adult patients with normal ICP (48%) (p less than 0.05). There was no significant difference in outcome in pediatric and adult patients with mass lesions or with increased ICP, regardless of whether or not the pressure was reducible. There was a much higher incidence of surgical mass lesions in adult patients (46%) than in pediatric patients (24%) (p less than 0.001).

Adolescent↗
PubMed1987

Pressure-volume index in head injury.

The authors studied intracranial pressure (ICP) and intracranial compliance as defined by the pressure-volume index (PVI) in 34 severely head-injured patients with a Glasgow Coma Scale score of 8 or less. The objective of the research was to determine if there was a correlation between the pressure-volume status and subsequent increase in ICP. The PVI and ICP measurements were obtained serially, and the temporal course of the pressure-volume status and ICP was determined during the 5-day period following injury. Aggressiveness of ICP was quantified by a therapy intensity level scale. A clear relationship between the PVI measured soon after injury and subsequent development of ICP emerged. Following mechanical trauma the PVI is reduced, and the degree of reduction and extent of biomechanical recovery are closely related to outcome and development of raised ICP.

Adolescent↗
PubMed1987

Glycaemic control in diabetic patients transferred from therapy with animal insulins to human crystalline zinc insulin of recombinant DNA origin: a multicentre study.

87 stable insulin-dependent diabetic patients from 6 diabetic clinics within the UK were transferred from their existing once or twice daily regimen of subcutaneous animal insulin to a similar regimen of human insulin of recombinant DNA origin in neutral soluble and crystalline zinc suspension formulations. Seven point blood glucose profiles, glycosylated haemoglobin concentrations and insulin dose were examined, in each patient, before and after 6 weeks therapy with human insulins. The 67 patients on twice daily insulin showed no significant change in mean blood glucose values or glycosylated haemoglobin but required a significantly higher dose of human crystalline zinc suspension than their previous long-acting animal insulin. In contrast the 17 patients on a once daily regimen experienced a significant deterioration in glycaemic control without a significant change in insulin dose or glycosylated haemoglobin. Three patients on twice daily insulin withdrew shortly after transfer to human insulin. The combination of human soluble and crystalline zinc suspension appears to be a more satisfactory substitute for animal insulin when used in a multi-dose regime rather than on a once daily basis.

Animals↗
PubMed1987

The natural history of foot pressure abnormalities in neuropathic diabetic subjects.

The pressures under the feet of 39 subjects with diabetic neuropathy were initially assessed during walking using an optical pedobarograph. The upper limit of normality for pressure readings in non-diabetic subjects had previously been established as 10 kg/sq.cm. These subjects were then followed for a mean period of 3 years after which foot pressure studies were repeated. 39 feet had abnormal results when initially studied, compared with 33 at the follow-up study (p = NS). However, changes in the distribution of pressure under the metatarsal heads were seen in 13 feet, while 20 feet showed changes in abnormal pressures under the same site. Recurrent metatarsal ulcers occurred in 6 feet during the study, with 5 occurring at documented sites of high pressure. It is concluded that important changes in the distribution and level of pressures under diabetic neuropathic feet occur during a relatively short time. As it has previously been demonstrated that increased foot pressures are associated with foot ulceration, it is important for the orthotist to re-assess the feet regularly to establish whether significant changes in pressure distribution that might warrant new insoles or footwear have occurred.

Adult↗
PubMed1986

Sural nerve oxygen tension in diabetes.

Peripheral nerve oxygen tensions were assessed in vivo by using microelectrodes to measure endoneurial oxygen tension in exposed sural nerve. In 11 diabetic patients with chronic sensorimotor neuropathy the mean endoneurial oxygen tension was 39.7 (SD 10.2) mm Hg. In all but one patient compared with none of four non-neuropathic subjects the mean nerve oxygen tensions were below dorsal foot vein values. This unphysiological state may have a role in the aetiology of diabetic neuropathy.

Adult↗
PubMed1986

Diabetic neuropathies and pain.

Many of the diabetic neuropathic syndromes are characterized by painful symptoms with a sensation of burning and associated with troublesome hyperaesthesia. It is important to distinguish between the acute and chronic forms of peripheral sensory neuropathy; while the former carries an excellent prognosis for symptomatic improvement within one year, the latter may cause persistent symptoms for many years. In contrast to the acute form, in which symptoms are particularly severe but abnormal neurological signs are minimal, patchy stocking and glove sensory loss together with peripheral small muscle wasting are often present in chronic sensorimotor neuropathy. Peripheral polyneuropathies are more common in patients with poor metabolic control, although recent evidence implicates blood glucose flux as a possible contributory factor to neuropathic pain. It is possible that blood glucose flux or altered peripheral blood flow leads to increased spontaneous activity in nociceptive afferent fibres which are present in the axonal sprouts that characterize small fibre neuropathy. In the diagnosis of the neuropathies, exclusion of other aetiological factors is of paramount importance as there is no specific diagnostic test for diabetic nerve damage. If there is no symptomatic improvement after a period of stable and optimal metabolic control together with simple analgesics, then the tricyclic drugs should be regarded as first line therapy. The rapid effect of these drugs suggests a peripheral rather than central mode of action.

Diabetic Neuropathies↗
PubMed1986

Arteriovenous shunting in quadriplegia.

Arterio-venous shunting has been demonstrated in the limbs of ten subjects with traumatic quadriplegia, as shown by increased venous oxygen concentration and a Doppler sonogram pattern indicative of continuous forward flow. This phenomenon is similar to that seen in the diabetic neuropathic foot, suggesting that autonomic dysfunction is a major factor in the development of foot ulceration in the quadriplegic and in the diabetic.

Foot↗
PubMed1986

Laser Doppler flowmetry: in the assessment of peripheral vascular disorders? A preliminary evaluation.

Skin is a representative microvascular bed providing easy access for the study of capillary haemodynamics. In this preliminary evaluation we have used laser Doppler flowmetry to measure the response of skin capillary blood flow to local thermal stimulation. The purpose of our study was to see if such measurements can be used to derive useful clinical information. Thirty subjects, 15 male and 15 female, were selected to establish "normal' patterns of behaviour. All normal subjects studied showed similar patterns of response. There was a slight downward trend in red-blood-cell flux with age. Periods of vasomotor activity were present at rates ranging from 4-17 cycles/min. The mean temperature rise in the heated skin area was 4 degrees C. Blood flow over this range increased by a factor of 10 or more. Clinical cases studied were strictly limited to three categories of disease with known or suspected microvascular changes: algodystrophy, lower-limb ischaemia and diabetic neuropathy. All the clinical cases studied showed deviations from the normal pattern. Patients with algodystrophy had impaired peripheral vascular function in the affected area. Patients with lower-limb ischaemic problems all had poor peripheral perfusion. In the limited number of diabetic neuropathic feet studied two patterns emerged: patients with no evidence of ulceration displayed striking vasomotor activity; those with more severe problems had reduced red-blood-cell flux and little evidence of vasomotor control.

Adolescent↗
PubMed1986

Experience of continuous subcutaneous insulin infusion in the outpatient management of diabetic teenagers.

Of forty-five adolescent diabetic patients offered continuous subcutaneous insulin infusion (CSII) as part of a large feasibility study, 13 (28.9%) initially chose the treatment, but only 4 out of 11 who actually started CSII continued for one year (64% discontinuation rate). In contrast 30.4% of adults approached chose CSII, and 32% had discontinued after one year. Improvement in glycaemic control was poor, and clinical problems were more common in pump-treated teenagers than in adults. CSII does not appear to be a therapeutic solution for adolescents having difficult management problems.

Adolescent↗
PubMed1986

Diabetic neuropathies. Current concepts in prevention and treatment.

Diabetic nerve damage leads to a wide variety of unpleasant problems: painful sensations, muscle weakness, numb feet predisposing to ulcers, impotence, and a series of distressing effects due to autonomic dysfunction. At present, there is no single effective treatment for the many clinical syndromes--each of which may well have a different cause. Improved blood glucose control must remain the first line of treatment, hopefully to improve nerve structure and function but also to raise the pain threshold. A variety of sedatives and analgesics may also help some patients. Inhibition of the enzyme aldose reductase with resultant interference with neural sorbitol and myo-inositol metabolism would seem to have a good theoretical basis in therapy, and detailed results of long term clinical trials of aldose reductase inhibitors such as sorbinil and tolrestat are awaited with interest. Their role in the future could be more important in prevention of nerve damage than in attempting to reverse gross end-stage nerve destruction. In diabetic subjects with loss of pain sensation in the foot due to neuropathy or in the more advanced state of foot ulceration, intensive educational and clinical efforts should be exerted to prevent this distressing and common problem. In the future, a more detailed understanding of the biochemical abnormalities occurring in nerves and their effect on nerve function, structure and vasculature may lead to more satisfactory and logical treatments for this the commonest single complication of diabetes.

Diabetic Neuropathies↗
PubMed1986

Prognostic significance of ventricular CSF lactic acidosis in severe head injury.

Brain-tissue acidosis inferred by cerebrospinal fluid (CSF) lactic acidosis is considered to play an important role in the clinical course of severe head injury. Ventricular CSF lactate concentration was studied in 19 patients during the first 5 days after severe head injury. All patients were intubated, paralyzed, and artificially ventilated so that PaCO2 was kept at 33.2 +/- 5.0 mm Hg and PaO2 at 122 +/- 18 mm Hg (mean +/- standard deviation). The mean Glasgow Coma Scale score on admission was 5.73 +/- 2.42. The first CSF sample was drawn within 18 hours after head injury. Over the first 4 days postinjury, patients with a poor outcome had significantly higher ventricular CSF lactate levels than did those with moderate disabilities or a good outcome. Patients showing favorable outcome had a significant decrease in ventricular CSF lactate levels 48 hours after injury. This decrease was not observed in patients with a poor outcome. Increased ventricular CSF lactate concentration was also reliably associated with increased intracranial pressure (ICP). Ventricular CSF lactate levels did not correlate with the magnitude of intraventricular bleeding. Arterial and jugular venous blood lactate levels, although high after head injury, were usually lower than the levels in the ventricular CSF and reached a normal range by the 3rd day following head trauma. At that time, the ventricular CSF lactate concentration was still above normal in patients with a poor outcome but had decreased to normal in patients with moderate disabilities or a good outcome. Ventricular CSF pH did not generally correlate with the ventricular CSF lactate concentration in patients under controlled ventilation; however, in a few patients close to death or with ventricular infection, a correlation was noted. Ventricular CSF lactate levels were not related to cerebral blood flow. In this study, profiles of ventricular CSF lactate concentration are defined in relation to the patients' clinical course and outcome. High ventricular CSF lactate concentration is present within 18 hours after severe head injury. Its decrease to normal in the following 48 hours is a reliable sign of clinical improvement; however, ventricular CSF lactate levels that are persistently high or that increase over time indicate the patient's deterioration. Serial assessment of ventricular CSF for acid-base status and metabolites in head-injured patients with a ventricular catheter already placed for ICP monitoring is useful in the evaluation of prognosis and clinical course.

Acidosis, Lactic↗