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Biomedical subjects

J B North

Publications and source records attributed to J B North.

At least 37 records · Page 2Linked to original sources
PubMed1986

Logistics of early management of head and spinal injuries.

The logistics of early management have been studied in a series of 1161 patients with head and/or spinal injuries, who were admitted to hospital in NSW in 1977-78. Special attention has been given to three subgroups: 336 head injuries with records of impaired consciousness before first hospital admission, 355 head injuries later transferred because of deterioration, and 202 serious spinal injuries. It was found that in at least 18% of unconscious head injuries, and a similar percentage of spinal injuries, first aid and transport to hospital were provided by ambulances recorded to have only one trained staff member. In country areas, 41% of unconscious head injuries reached hospital after periods of time exceeding 1 h. For administrative as well as geographic reasons, more than 80% of initially unconscious head injuries and spinal injuries were first admitted to hospitals without neurosurgical and/or spinal services; the majority of cases in both groups, therefore, had to be transferred to other hospitals, often within 6 h of first admission. In the subgroup of cases transferred because of deterioration, mortality increased with distance from a neurosurgical unit. These findings are related to the concept of an integrated regional trauma service.

Ambulances↗
PubMed1983

Phenytoin and postoperative epilepsy. A double-blind study.

A double-blind trial of phenytoin therapy following craniotomy was performed to test the hypothesis that phenytoin is effective in reducing postoperative epilepsy. A significant reduction in the frequency of epilepsy was observed in the group receiving the active drug up to the 10th postoperative week. Half of the seizures occurred in the first 2 weeks and two-thirds within 1 month of cranial surgery. High rates of epilepsy were observed after surgery in patients with meningioma, metastasis, aneurysm, and head injury. Routine prophylaxis with phenytoin (in a dosage of 5 to 6 mg/kg/day) would seem to be indicated, particularly in high-risk patients and, where possible, this treatment should be started 1 week preoperatively. Seizure control is best when therapeutic levels of phenytoin are maintained.

Clinical Trials as Topic↗
PubMed1981

Rapid cerebral vasodilatation in brief hypoxia in anaesthetized animals.

In anaesthetized dogs, cats and rabbits, intracranial pressure was measured continuously during brief or transient hypoxia, induced by (a) lowering inspired O2 to 9--10% for 2--3 min, or (b) giving 2--3 breaths of nitrogen. In almost all instances there was an increase in i.c.p. which started in less than 20 s; this occurred with either spontaneous or controlled ventilation, and whether or not there was also a rise in arterial blood pressure; the time course was similar to that of the arterial chemoreceptor reflex responses of ventilation and blood pressure. Division bilaterally of the sinus and vagus nerves in six cats showed that the intracranial pressure response was not dependent on these chemoreceptor afferent pathways. The results suggest a rapid vasodilatation starting at a time when cerebral arterial oxygen tension is unlikely to be below 7 kPa (50 mmHg). The mechanism remains unexplained.

Anesthesia↗
PubMed1980

Postoperative epilepsy: a double-blind trial of phenytoin after craniotomy.

In a double-blind trial of phenytoin for the prevention of postoperative epilepsy in craniotomy patients, epilepsy was observed in 7.9% (8/101) of patients treated with phenytoin and in 16.7% (17/102) of those receiving placebo. Therapeutic drug levels were associated with a significant reduction in the frequency of epilepsy. Three-quarters of the fits occurred within a month of cranial surgery. High rates of epilepsy have been observed after cranial surgery in patients with meningioma, aneurysm, and head injury with or without intracranial clots, and routine prophylaxis with phenytoin would seem to be indicated in such patients.

Clinical Trials as Topic↗
PubMed1979

Epidural abscess: a hazard of spinal epidural anaesthesia.

Two cases of spinal epidural abscess following prolonged epidural anaesthesia are presented. The clinical features included fever, malaise, and signs of nerve root compression; backache was not marked. Prompt surgical drainage and appropriate antibiotics are required to avoid the costly sequelae of bladder and leg paralysis from spinal cord compression. Both infections were caused by bacterial contamination of catheter, and although this complication is uncommon, it emphasizes that strict asepsis is essential during continuous epidural anaesthesia.

Abscess↗
PubMed1976

Painful ophthalmoplegia following treated squamous carcinoma of the forehead. Orbital apex involvement from centripetal spread via the supraorbital nerve.

Intraneural and perineural spread of squamous carcinoma from the face to the cranial cavity is an important cause of delayed cranial nerve palsies after local excision of a skin tumour. As exemplified in reports of two cases, signs of this type of centripetal spread of squamous cell tumour along the branches and trunk of the supraorbital nerve are (i) severe unremitting orbital and forehead pain with associated hypoaesthesia, (ii) palpable or radiological evidence of thickening of the nerve at the supraorbital notch and (iii) evolution of ophthalmoplegia, blindness, and sensory loss in the first division of the trigeminal nerve. Appearance of severe supraorbital neuralgia months or years after excision of a skin tumour from the forehead should alert the clinician to extension of tumour cells along the supraorbital nerve. This may enable him to institute timely treatment before a complete orbital apex syndrome has developed.

Aged↗
PubMed1976

Response of ventilation and of intracranial pressure during rebreathing of carbon dioxide in patients with acute brain damage.

A study of the ventilatory response to rising CO2 in 43 patients with acute brain damage, using a rebreathing method, has revealed several instances of abnormally low responsiveness. The increased responsiveness previously reported in chronic brain damage was not observed in these patients by this method. The incidence of a very low response to CO2 tended to be associated with hyperventilation and brain-stem damage, but the numbers were insufficient to define a statistical relationship. There was no association between responsiveness to CO2 and either bilateral forebrain damage or periodic breathing. Studies of changes in intracranial pressure with rising CO2 suggest that such a rebreathing test might provide a simple means of confirming the presence or absence of cerebrovascular response to changing CO2.

Brain Injuries↗
PubMed1976

Effect of intermittently raised intracranial pressure on breathing pattern, ventilatory response to CO2, and blood gases in anesthetized cats.

In anesthetised cats, breathing pattern, blood gases, and ventilatory response to CO2 were recorded before and during intermittent 10-minute episodes of hydrostatically raised intracranial pressure. The first effect on breathing was a stimulation which was followed at higher pressures by irregularity, depression, and periods of apnea; hyperventilation at high intracranial pressure (ICP was rare. Raised ICP did not consistently depress the ventilatory response to CO2 until ventilation during airbreathing was already depressed; therefore, we cannot experimentally justify applying this test clinically to detect incipient ventilatory depression. When hypoxemia developed during raised ICP, it was compatible with the degree of hypoventilation due to central depression of breathing; thus, there was no evidence of a neurally mediated effect on the lungs, causing defective gas exchange.

Animals↗
PubMed1975

Effects of increased arterial pressure on blood flow in the damaged brain.

The effect of induced arterial hypertension on cerebral blood flow and intracranial pressure was measured before and after the production of a standard cryogenic brain lesion in 10 anaesthetized, ventilated baboons. Before injury the animals were divided into a group with intact autoregulation, having more than 20% increase in cerebrovascular resistance during arterial hypertension, and a group with impaired autoregulation, in which the change in cerebrovascular resistance was much less. The cryogenic injury produced a rapid rise in intracranial pressure and a reduction of cerebral blood flow in the affected hemisphere. Despite this, there was an increase in cerebrovascular resistance during arterial hypertension in all animals after brain injury, accompanied by a further significant rise in intracranial pressure. It is suggested that this response is unlikely to represent normal physiological autoregulation and caution should be exercised in interpreting it as such in the course of studies of cerebral blood flow in patients with acute brain damage.

Animals↗
PubMed1974

Post-hyperventilation apnoea in patients with brain damage.

A study of 100 subjects has confirmed that brief voluntary hyperventilation commonly causes apnoea in patients with supramedullary lesions, but not in healthy people. Apnoea was related to drowsiness rather than to the extent of the lesion; it was unrelated to the measured reduction in end-tidal carbon dioxide tension.

Adolescent↗