Phenytoin exerts a beneficial effect by reducing seizures only during the first week after severe head injury.

To examine the relationship between serum glucose and the outcome of patients suffering from head injury, the authors retrospectively reviewed the clinical course of 169 patients admitted for treatment to Harborview Medical Center (a regional trauma center). All patients underwent craniotomy for evacuation of intracranial hematoma and/or placement of a subarachnoid bolt for intracranial pressure monitoring under general anesthesia. Patients with a Glasgow Coma Scale (GCS) score of 8 or less had significantly higher serum glucose levels than patients with GCS scores of 12 to 15 (mean +/- standard error of the mean 192 +/- 7 mg/dl vs. 130 +/- 8 mg/dl or 10.7 +/- 0.4 mmol/liter vs. 7.2 +/- 0.4 mmol/liter) (p less than 0.0001). Patients who subsequently remained in a vegetative state or died had significantly higher glucose levels both on admission and postoperatively than patients who had good outcome or moderate disability (217 +/- 12 mg/dl vs. 167 +/- 6 mg/dl or 12.1 +/- 0.7 mmol/liter vs. 9.3 +/- 0.3 mmol/liter on admission, and 240 +/- 16 mg/dl vs. 156 +/- 5 mg/dl or 13.3 +/- 0.9 mmol/liter vs. 8.9 +/- 0.3 mmol/liter postoperatively) (p less than 0.0001). Among the more severely injured patients (GCS score less than or equal to 8), a serum glucose level greater than 200 mg/dl (11.1 mmol/liter) postoperatively is associated with a significantly worse outcome (p less than 0.01). The authors conclude that severely head-injured patients frequently develop hyperglycemia and the elevated serum glucose level may aggravate ischemic insults and worsen the neurological outcome in such patients.

A small number of patients with an apparently minor head injury will develop a life-threatening intracranial hematoma that must be rapidly detected and removed. To assess the risk of a significant intracranial neurosurgical complication after apparently minor head injury, the authors collected data prospectively on 610 patients who had sustained a transient posttraumatic loss of consciousness or other neurological function and who had a Glasgow Coma Scale (GCS) score of 13, 14, or 15 in the emergency room. Skull x-ray films were obtained in 583 patients, 66 of whom (10.8% of the study population) had cranial fractures. Eighteen of the 610 patients (3.0%) required a neurosurgical procedure. Three acute subdural hematomas, one epidural hematoma, and one traumatic intracerebral hematoma required craniotomy. Of the 66 patients who had skull fracture, 7.6% required a craniotomy for intracranial hematoma. Thirteen (19.7%) of the 66 patients with skull fracture required an operative procedure as compared to five (1.0%) of the 517 patients without skull fracture. Two patients with a normal GCS score of 15 and normal skull x-ray films subsequently underwent operative treatment. The cost of three alternative management schemes for these patients was estimated. A 50% reduction in cost of management could be effected by the use of computerized tomography (CT) scans (or possibly skull x-ray films) in determining which of the patients who are alert at the time of presentation should be admitted for observation. Several other conclusions can be drawn from this study. First, an initial GCS score between 13 and 15 does not necessarily indicate that a patient has sustained a trivial head injury, since 3% of such patients will require an operative procedure despite an initially normal level of alertness. Second, an abnormal skull x-ray film increases by a factor of 20 the probability that a patient will need neurosurgical treatment. Third, it is very unusual for patients who have a GCS score of 15 and a normal skull x-ray film to have a significant neurosurgical complication. Fourth, the alternative management schemes that depend on selective use of skull films and CT scans may significantly reduce the cost of caring for patients with minor head injury.

This study describes a closed cranial window technique that allows the observation and measurement of rat pial arterioles and venules in situ. The resolving power of this system is 1–2 μm. Using this sensitive technique, we characterized the responses to 7% carbon dioxide inhalation and adenosine in arterioles (10–70 μm) and venules (15–100 μm). During carbon dioxide inhalation, larger arterioles (>40μm) dilated more than smaller arterioles (<20 μm). There was limited vasoreac-tivity of pial venules during CO2 inhalation. Dilation of arterioles was initially observed with an adenosine concentration of 10−8 M. Almost a twofold increase in diameter was noted at 10−3 M. In contrast to the effect of CO2 inhalation, the degree of dilation with topical application of adenosine was not size dependent. Pial venules did not respond to adenosine. The technique for observation of pial vessels using the closed cranial window and for measurement of vessel diameter by video camera system microscopy is a powerful tool for studying in vivo the cerebral circulation in the rat.