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Biomedical subjects

J D Ward

Publications and source records attributed to J D Ward.

At least 145 records · Page 8Linked to original sources
PubMed1986

CSF brain creatine kinase levels and lactic acidosis in severe head injury.

The posttraumatic creatine kinase-BB isoenzyme (CKBB) activity and lactate concentration in ventricular cerebrospinal fluid (CSF) have been studied in 29 patients with severe head injuries. The CKBB activity reaches its maximum a few hours after trauma, and has a monoexponential drop with a half-time of approximately 10 hours. Ventricular CSF lactate concentration continues to rise in patients with a poor outcome, and decreases only slowly and inconsistently in most of the other patients. Thus, increase of lactate in the ventricular CSF is not, like CKBB, a direct one-stage consequence of the trauma but is due to continuous production from a derangement of metabolism caused by the trauma. Since even higher ventricular CSF lactate levels can be survived when not caused by head injury, and since no significant pH changes were related to the ventricular CSF lactic acidosis in these artificially ventilated patients, it is concluded that ventricular CSF lactic acidosis is indicative of a severe, although not necessarily intractable, disturbance of brain function associated with intracellular lactate production and acidosis.

Acidosis, Lactic↗
PubMed1986

Long term glycaemic control by alternative regimens in a feasibility study of continuous subcutaneous insulin infusion.

Of 382 insulin-treated diabetic patients participating in a feasibility study of continuous subcutaneous insulin infusion (CSII) and alternative regimens in a large British clinic, 63 used CSII for a 2-yr period. Additionally 74 patients persisted with an intensified injection regimen and 85 continued on non-intensified therapy. There was no significant difference in mean glycosylated haemoglobin between the 3 groups at the study onset. At month 24 only the CSII group had significantly reduced mean glycosylated haemoglobin (11.0 +/- 1.8 (SD) at month 0; 9.8 +/- 1.9 month 24, p less than 0.001) although the intensified injection group experienced a significant reduction in mean glycosylated haemoglobin until month 18 (11.0 +/- 1.8 month 0; 10.1 +/- 1.4, p less than 0.001). Serious hypoglycaemia was not increased in the CSII-treated group compared with the intensified injection group. Thus it proved feasible to achieve sustained, improved glycaemic control in a large group of patients by the use of insulin pump therapy and the level of control was superior to that achieved by an intensified injection regimen.

Blood Glucose↗
PubMed1985

Severe hyperkalaemia and ketoacidosis during routine treatment with an insulin pump.

During a feasibility study of the use of insulin pumps to treat diabetes ketoacidosis occurred at a rate of 0.14 episodes/patient/year in the first year but was lower in subsequent years. A case of cardiac arrest secondary to hyperkalaemia during ketoacidosis occurred in a patient treated with a pump. The mean (SD) serum potassium concentration on presentation to hospital with ketoacidosis was significantly higher in patients treated with a pump (5.7 (1.1) mmol(mEq)/l) than those treated with conventional injections of insulin (4.9(0.9) mmol/l; p less than 0.01). The high rate of ketoacidosis and raised serum potassium concentrations during treatment with the pump creates doubt about the use of this treatment as an alternative regimen for large numbers of patients in a busy diabetic clinic.

Acidosis↗
PubMed1985

Home blood glucose monitoring in non-insulin-dependent diabetics: the effect of gliclazide on blood glucose and weight control, a multicentre trial.

The efficacy of the sulphonylurea gliclazide was assessed in 229 non-insulin-dependent diabetics attending U.K. outpatient diabetic clinics. Patients inadequately controlled by diet alone or oral hypoglycaemic agents used reflectance meters to monitor their blood glucose. After a 4-week run-in, in those whose control remained unsatisfactory, gliclazide was either added to diet, or given in place of existing drugs. Patients continued home-monitoring and were followed for 3 months. Gliclazide reduced mean random blood glucose in all groups, particularly those previously treated by diet alone or a first-generation sulphonylurea. The patients improved in their ability to measure glucose at home and within 2 months a good correlation with laboratory measurements was found. Mean body weight was reduced, particularly in obese and elderly subjects and those treated previously with sulphonylurea drugs. Side effects were mild and only two patients were withdrawn for this reason.

Blood Glucose↗
PubMed1985

Small vessel disease in progressive diabetic neuropathy associated with good metabolic control.

Clinical, electrophysiological, and electron microscopical data are presented on 10 diabetic patients with severe progressive neuropathy, predominantly motor in type, in the presence of good blood glucose control, and for one patient with painful neuropathy and third cranial nerve palsy. Endothelial cell hyperplasia was seen in small vessels in all cases, and seven patients showed plugging of the vascular lumen by degenerate cellular material and electron dense protein. It is suggested that these cells desquamate and occlude smaller peripheral vessels at a point of narrowing. In one case the lumen of a vessel was occluded by thrombus. Electron microscopical examination showed a vessel occluded by degranulated platelets. Electrophysiological studies showed a pattern of denervation that was asymmetrical and distally predominant in some patients, suggesting that the neuropathy, at least in part, relates to multiple small infarcts.

Adult↗
PubMed1985

Severe hypophosphatemia after head injury.

Hypophosphatemia occurs in a variety of clinical conditions. It develops in parallel with phosphate depletion from body losses or more commonly as a sequel to the redistribution of phosphate from the extracellular to the intracellular compartment. Hypophosphatemia is a multisystem disturbance capable of involving the neurological, immunological, and muscular systems, among others. In this report, we describe five patients with severe head injury who developed marked hypophosphatemia (less than 1 mg/dl) within 24 hours of hospitalization. This fall in serum phosphate coincided with the induction of respiratory alkalosis consequent to mechanical ventilation. In four of the five patients, as acid-base parameters returned to normal, serum phosphate values rose, in all instances reaching values greater than 2.5 mg/dl. Urinary phosphorus excretion, ordinarily negligible after hypophosphatemia induced by hypocapnia, was still present in Cases 1 and 4 (greater than 600 mg/24 hours). This is unexplained by any of the known hormonal or fluid alterations that accompany head injury. These five patients developed severe, yet transient, hypophosphatemia that resolved upon correction of hyperventilation-induced acid-base abnormalities. We discuss the pathophysiology of this entity and the implications for the head trauma patient.

Adolescent↗
PubMed1985

Plantar pressure measurements and the prevention of ulceration in the diabetic foot.

Static and dynamic measurements of foot pressure have been carried out on three groups of subjects: diabetic patients with neuropathy (with and without a history of ulceration), diabetic patients with no neuropathy, and normal subjects as controls. In many cases both techniques of measurement detected areas of abnormally high pressure under the foot, but in some cases a particularly high-pressure spot was detected on only one of the tests and sometimes both methods were needed to reveal all the areas of the foot which might be considered to be at risk. The dynamic measurements tended to show multiple areas of high pressure better than the static measurements. Our results indicate the importance of making both types of measurement when seeking to devise suitable means of protecting the foot from ulceration.

Diabetes Mellitus↗
PubMed1985

Failure of prophylactic barbiturate coma in the treatment of severe head injury.

In certain subgroups of severely head-injured patients, the mortality rate remains unacceptably high. The authors describe a randomized, controlled trial of prophylactic pentobarbital therapy in a group of these patients. Pentobarbital was started as soon as possible after the head injury, regardless of the intracranial pressure (ICP), and was continued for a prescribed period of time. The study included 53 consecutive head-injured patients over the age of 12 years, who had either an acute intradural hematoma (subdural and/or intracerebral, large enough to warrant surgical decompression), or no mass lesion but whose best motor response was abnormal flexion or extension. All patients in the study were randomly assigned to a control group (26 cases) or a pentobarbital-treated group (27 cases) once the diagnosis had been made and informed consent obtained. All patients were treated with the same protocol of aggressive resuscitation, prompt diagnosis and treatment of mass lesions, and intensive care, with close follow-up monitoring. The randomization was effective in producing a close match between the control and treated groups with respect to age, sex distribution, cause of injury, neurological status, intracranial lesions, prevalence of early systemic insults, midline shift, and initial ICP. Outcome was essentially the same in each group. There was no difference between groups in the incidence of elevated ICP, the duration of ICP elevation, or the response of ICP elevations to treatment. Arterial hypotension occurred in 14 patients (54%) in the treated group and only two patients (7%) in the untreated group. Based on these data the authors cannot recommend the prophylactic use of pentobarbital coma in the treatment of patients with severe head injury. They also believe that its use is accompanied by significant side effects which can potentially worsen the condition of a patient with severe head injury.

Adolescent↗
PubMed1984

Ventriculostomy-related infections. A prospective epidemiologic study.

We concluded a prospective epidemiologic study of ventriculostomy-related infections (ventriculitis or meningitis) in 172 consecutive neurosurgical patients over a two-year period to determine the incidence, risk factors, and clinical characteristics of the infections. Ventriculitis or meningitis developed in 19 of 172 patients (11 per cent) undergoing a total of 213 ventriculostomies. When data from all these cases plus five cases of nonventriculostomy-related infection were combined, cerebrospinal-fluid pleocytosis was more significantly associated with the diagnosis of ventriculitis or meningitis (P less than 0.0001) than were fever and leukocytosis (P = 0.07). Risk factors for ventriculostomy-related infections included intracerebral hemorrhage with intraventricular hemorrhage (P = 0.027), neurosurgical operations (P = 0.016), intracranial pressure of 20 mm Hg or more (P = 0.019), ventricular catheterization for more than five days (P = 0.017), and irrigation of the system (P = 0.021). Previous ventriculostomy did not increase the risk of infection with subsequent procedures. We conclude that ventriculostomy-related infections may be prevented by maintenance of a closed drainage system and by early removal of the ventricular catheter. If monitoring is required for more than five days, the catheter should be removed and inserted at a different site.

Bacteria↗
PubMed1984

The diabetic foot.

Neuropathic ulceration and gangrene in the diabetic foot is related to lack of sensation of the foot to painful stimuli, the easy access and development of infection. High pressure areas lead to rapid breakdown of tissue and the presence of abnormally fast blood flow leading to arteriovenous shunting leave peripheral tissues gravely at risk from ischaemia. The knowledge of these basic facts involved in the development of foot ulceration should allow a more logical approach to prevention-indeed with care through medical attention and an understanding of the social background of at risk patients, should lead to a major reduction in the incidence of foot ulceration in the diabetic patient and hence to a lowering of morbidity and on occasions, mortality. Leaving all the medical and scientific matters aside, it should be stated that diabetic foot ulceration in the warm diabetic foot is a failure on the part of the diabetic physician to identify problems, educate his patient and provide correct social services to totally prevent this unhappy complication of diabetes.

Anti-Bacterial Agents↗
PubMed1984

Genetic and metabolic studies in diabetic neuropathy.

Forty-one diabetic patients with symptomatic diabetic neuropathy were studied together with an equal number of matched diabetic subjects without neuropathy. The acetylator status was determined and HLA-A, B, C and DR antigens were investigated. Metabolic control was assessed by measurement of glycosylated haemoglobin and by the mean of multiple random clinic blood glucose values. No significant difference was observed between the two groups in the proportion of fast and slow acetylators. The distribution of HLA frequencies was similar in subjects with and without neuropathy for both Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic patients. When compared with diabetic subjects without neuropathy, the neuropathy group had higher levels of both glycosylated haemoglobin (mean +/- SEM: 50.1 +/- 1.4 versus 57.5 +/- 1.8 mmol hydroxymethylfurfural/mol haemoglobin (10.5 +/- 0.3 versus 12.0 +/- 0.4% haemoglobin A1, p less than 0.01) mean blood glucose (9.3 +/- 0.4 versus 11.3 +/- 0.5 mmol/l, p less than 0.005). This study provides no evidence that genetic factors increase the susceptibility of diabetic patients to develop neuropathy. In contrast, the elevated glycosylated haemoglobin and blood glucose levels strengthen the association between hyperglycaemia and diabetic neuropathy.

Adult↗
PubMed1984

Near-normal glycaemic control does not correct abnormal platelet reactivity in diabetes mellitus.

The effect of improved glycaemic control, effected by 16 weeks continuous subcutaneous insulin infusion (CSII), on platelet aggregation and platelet prostaglandin biosynthesis has been assessed in a group of 11 diabetic patients with painful peripheral neuropathy. Before CSII and compared with results obtained on samples from age- and sex-matched control subjects, there was enhanced reactivity of the platelets from diabetic patients to ADP, collagen and sodium arachidonate (NaAA). There was also increased thromboxane B2 (TXB2) production after platelet stimulation by NaAA. In contrast, collagen-induced thromboxane production by platelets from diabetic patients was significantly less than that of platelets from controls. Treatment by CSII resulted in a statistically significant improvement in glycaemic control and this was maintained for the 16 week period of the study. At 16 weeks and in the presence of near-normal glycaemic control, the enhanced platelet reactivity in response to collagen and NaAA persisted and that to ADP was further increased. Collagen-induced thromboxane production was, however, corrected by CSII.

Adenosine Diphosphate↗
PubMed1984

The effects of the pneumatic antishock garment on intracranial pressure in man: a prospective study of 12 patients with severe head injury.

Changes in intracranial pressure, mean arterial blood pressure, and cerebral perfusion pressure in response to sequential inflation of the pneumatic antishock garment were monitored in 12 patients with severe head injury and initial intracranial pressure less than 20 mm Hg. The small incremental increases in intracranial pressure that occurred with inflation of the pneumatic antishock garment were compensated for by improved hemodynamic stability and elevated mean arterial blood pressure which produced a simultaneous rise in cerebral perfusion pressure. The treatment of hypotension in traumatized patients with head injuries is paramount and sequential slow inflation of the pneumatic antishock garment can be used in such patients without apparent ill effect to the brain when the initial intracranial pressure is 20 mm Hg or below. Further study is needed to determine the safety of the device in head injured patients with elevated intracranial pressures.

Adolescent↗