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Biomedical subjects

J D Ward

Publications and source records attributed to J D Ward.

At least 181 records · Page 10Linked to original sources

Traumatic acute subdural hematoma: major mortality reduction in comatose patients treated within four hours.

To discover which factors contributed to recovery after surgical intracranial decompression, we reviewed the records of 82 consecutive comatose patients with traumatic acute subdural hematoma (ASDH) who were treated in a single center under a uniform protocol. The delay from injury to operation was the factor of greatest therapeutic importance. Patients who underwent surgery within the first four hours had a 30 per cent mortality rate, as compared with 90 percent in those who had surgery after four hours (P less than 0.0001). Other important prognostic variables included results of the initial neurologic examination, sex, multimodality-evoked potentials, and postoperative intracranial pressure (ICP). If all patients with traumatic ASDH were taken directly to hospitals equipped to diagnose and remove the hematoma within four hours of injury, mortality rates could be reduced considerably.

Accidents, Traffic↗

Cervical spinal subdural hematoma.

We report a case of intraspinal subdural hematoma following trauma - a rare entity - with a review of the literature. The location of the hematoma in the cervical spine as described in this report is even more uncommon and was reported only once before. The pathophysiology of this entity is discussed, and the myelographic features are emphasized to facilitate the preoperative diagnosis.

Cervical Vertebrae↗

Craniopharyngioma: Unusual computed tomographic presentation.

Craniopharyngioma usually presents on a computed tomographic (CT) scan as a hypodense or isodense lesion, with calcification, in the suprasellar region. A case with atypical CT findings of a huge, homogeneous, high density, apparently solid, lobulated suprasellar mass is presented. An explanation for the appearance of the tumor is discussed based upon clinical analysis of the tumor contents.

Child↗

Ultrasound measurements of pulse-wave velocity in the peripheral arteries of diabetic subjects.

1. Pulse-wave velocity in both upper and lower limbs has been measured in a series of diabetic and control subjects. Subjects were studied with a Doppler ultrasound system and a real-time frequency analyser. 2. The subjects comprised three groups: (a) diabetic subjects with peripheral neuropathy (43); (b) non-complicated diabetic subjects (8); (c) non-diabetic control subjects (11). Those diabetic subjects with peripheral neuropathy included 12 with non-infected foot ulcers, nine with healed foot ulcers and 22 who gave no history of foot ulceration. All of the diabetic and control subjects had clinically normal peripheral pulses. 3. In the upper limbs the pulse-wave velocity was similar for all groups. By contrast, in the lower limbs pulse-wave velocity was significantly increased (P less than 0.005) in patients with healed or ulcerated feet compared with controls, non-complicated diabetic subjects or diabetic subjects with peripheral neuropathy alone. 4. It is suggested that the increased pulse-wave velocity results from an underlying, diffuse, atherosclerosis. This is not detectable clinically and was found to predominantly affect the lower limb arteries rather than the upper limb vessels. This may be an important aetiological factor in the development of foot ulcers in these patients.

Adult↗

Salbutamol and ketonuria in pregnancy. Case report.

A patient is described who had heavy ketonuria without associated glycosuria during treatment with salbutamol in pregnancy. Blood glucose and ketone concentrations were normal while urine secretion of ketone bodies was increased. This suggests that ketonuria resulted from an altered renal threshold rather than a change in intermediary metabolism. Plasma ketone concentration should be measured before stopping salbutamol on the basis of ketonuria alone.

Adult↗

Electron microscopical studies of vessels in diabetic peripheral neuropathy.

the results of an electron microscopical study of sural nerve biopsies from 11 patients with diabetic neuropathy are presented. Thrombi were seen in six cases in at least one intraneural vessel; nine cases showed hyperplasia of endothelial cells, and in seven out of these nine the hyperplasia was sufficient to occlude completely the lumen of small vessels; six cases showed degenerate pericytes and endothelial cells, and in some cases endothelial cells had been shed from the vessel wall, exposing the blood within the vessel to the underlying basement membrane; in five cases large lipid droplets were seen within endothelial cells. Abnormalities of the vessel wall would result in decreased fibrinolytic activity and a reduction of the antiplatelet aggregating proprties of the vessel. Desquamation of endothelial cells from the vessel wall, with exposure of platelets to underlying collagen, may act as a trigger for thrombus formation, particularly as the blood of diabetic patients is often in a hypercoagulable state. The significance of hyperplasia of endothelial cells is at present unknown but, once established, this too would result in profound alterations of loal blood flow and ischaemia of nerve. Damage to endothelial cells may also allow seepage of haematological constituents into the vessel wall, resulting in its progressive thickening.

Adult↗

Elevated beta-thromboglobulin levels and circulating platelet aggregates in diabetic microangiopathy.

beta-Thromboglobulin levels and platelet-aggregate ratios were determined in blood-samples from healthy control subjects and from diabetic patients with and without microangiopathic complications. Patients with diabetic microangiopathy had significantly elevated beta-thromboglobulin levels and also reversible platelet aggregates. In nine newly treated diabetics blood-glucose control was associated with a significant fall in plasma beta-thromboglobulin. Since beta-thromboglobulin is a platelet-specific protein the results indicate that diabetic microangiopathy is associated with evidence of platelet activation and that this may be influenced by the degree of biochemical control.

Aged↗

The outcome from severe head injury with early diagnosis and intensive management.

In the belief that secondary cerebral compression, hypoxia, and ischemia materially influence the outcome from severe head injury, a standardized protocol was followed in 160 patients, with emphasis on early diagnosis and evacuation of intracranial mass lesions by craniotomy, artificial ventilation, control of increased intracranial pressure, and aggressive medical therapy. Of these patients, 36% made a good recovery, 24% were moderately disabled, 8% were severely disabled, 2% were vegetative, and 30% died. The mortality rate compares favorably with outcomes in similar patients reported from other centers and there has been no increase in the numbers of severely disabled or vegetative patients. It is proposed that vigorous surgical and medical therapy, by preventing or reversing secondary cerebral insults, enables some patients who would have died to make a good recovery without increasing the proportion of severely disabled patients.

Adolescent↗

Significance of intracranial hypertension in severe head injury.

Measurements of intracranial pressure (ICP) were begun within hours of injury in 160 patients with severe brain trauma, and continued in the intensive care unit. Some degree of increased ICP (greater than 10 mm Hg) was present on admission in most cases (82%), and in all but two of the 62 patients with intracranial mass lesions requiring surgical decompression; ICP was over 20 mm Hg on admission in 44% of cases, and over 40 mm Hg in 10%. In patients with mass lesions only very high ICP (greater than 40 mm Hg) on admission was significantly associated with a poor neurological picture and outcome from injury, while in patients with diffuse brain injury any increase in ICP above 10 mm Hg was associated with a poorer neurological status and a worse outcome. Despite intensive measures aimed at prevention of intracranial hypertension, ICP rose over 20 mm Hg during the monitoring period in 64 of the 160 patients (40%). Postoperative increases in ICP over 20 mm Hg (mean) were seen in 52% of the patients who had had intracranial masses evacuated, and could not be controlled by therapy in half of these cases. Even in patients without mass lesions, ICP rose above 20 mm Hg in a third of the cases, despite artificial ventilation and steroid therapy. Of the 48 patients who died, severe intracranial hypertension was the primary cause of death in nearly half and even moderately increased ICP (greater than 20 mm Hg) was associated with higher morbidity in patients with mass lesions and those with diffuse brain injury. Measurement of ICP should be included in management of patients with severe head injury.

Brain Injuries↗

A reassessment of vascular factors in relation to intravascular coagulation.

Sural nerve biopsy was performed in twenty-four diabetic patients, with clinical and electrophysiological evidence of diabetic neuropathy. Material from an autopsy case was also examined. Vessels plugged with fibrin were seen within nerve in nine cases. In three cases fibrin was observed tracking into the vessel wall and in four, older thrombus was observed in vessels. Areas of necrosis in nerve bundles were seen in two of the latter. In two patients there had been a preceding episode of intravascular coagulation. Fibrin deposition within small vessels could well play a part in damaging the diabetic nerve and a disturbance of the balance between deposition and removal by fibrinolysis could explain phasic variation in the symptoms of neuropathy.

Adult↗

Platelet abnormalities in diabetic peripheral neuropathy.

Abnormal platelet function has been demonstrated in 20 patients with diabetic peripheral neuropathy. The results are compared to those obtained from 19 matched diabetic patients with no clinical evidence of complications and 20 matched normal control subjects. Platelets from patients with diabetic neuropathy showed an increased sensitivity to the aggregating agents adenosine diphosphate and adrenaline. Spontaneous platelet aggregation was demonstrated in both groups of diabetic patients.

Adenosine Diphosphate↗