A prospective and consecutive series of 225 patients with severe head injuries who were managed in a uniform way was analyzed to relate outcome to several clinical variables. Good recovery or moderate disability were achieved by 56% of the patients, 10% remained severely disabled or vegetative, and 34% died. Factors important in predicting a poor outcome included the presence of intracranial hematoma, increasing age, abnormal motor responses, impaired or absent eye movements or pupil light reflexes, early hypotension, hypoxemia or hypercarbia, and elevation of intracranial pressure over 20 mm Hg despite artificial ventilation. Most of these predictive factors were assessed on admission, but a subset of 158 patients was identified in whom coma was present on admission and was known to have persisted at least until the following day. Although the mortality in this subset (40%) was higher than in the total series, it was lower than in several comparable reported series of patients with severe head injury. Predictive correlations were equally strong in the entire series and in the subset of 158 patients with coma. A plea is made for inclusion in the definition of "severe head injury" of all patients who do not obey commands or utter recognizable words on admission to the hospital after early resuscitation.

In a previous paper, the authors showed that mannitol causes cerebral vasoconstriction in response to blood viscosity decreases in cats. The present paper describes the changes in intracranial pressure (ICP) and cerebral blood flow (CBF) after mannitol administration in a group of severely head-injured patients with intact or defective autoregulation. The xenon-133 inhalation method was used to measure CBF. Autoregulation was tested by slowly increasing or decreasing the blood pressure by 30% and measuring CBF again. Mannitol was administered intravenously in a dose of 0.66 gm/kg; 25 minutes later, CBF and ICP were measured once again. In the group with intact autoregulation, mannitol had decreased ICP by 27.2%, but CBF remained unchanged. In the group with defective autoregulation, ICP had decreased by only 4.7%, but CBF increased 17.9%. One of the possible explanations for these findings is based on strong indications that autoregulation is mediated through alterations in the level of adenosine in response to oxygen availability changes in cerebral tissue. The decrease in blood viscosity after mannitol administration leads to an improved oxygen transport to the brain. When autoregulation is intact, more oxygen leads to decreased adenosine levels, resulting in vasoconstriction. The decrease in resistance to flow from the decreased blood viscosity is balanced by increased resistance from vasoconstriction, so that CBF remains the same. This might be called blood viscosity autoregulation of CBF, analogous to pressure autoregulation. Vasoconstriction also reduces cerebral blood volume, which enhances the effect of mannitol on ICP through dehydration of the brain. When autoregulation is not intact there is no vasoconstriction in response to increased oxygen availability; thus, CBF increases with decreased viscosity. With the lack of vasoconstriction, the effect on ICP through dehydration is not enhanced, so that the resulting decrease in ICP is much smaller. Such a mechanism explains why osmotic agents do not change CBF but decrease ICP in normal animals or patients with intact vasoconstriction, but do (temporarily) increase CBF in the absence of major ICP changes after stroke.

✓ The authors have analyzed their experience with intracranial pressure (ICP) monitoring in 207 patients over a 4-year period. Patients with either high-density or low-density lesions on computerized tomography (CT) at admission had a high incidence (53% to 63%) of intracranial hypertension (ICP persistently over 20 mm Hg). In contrast, patients with normal CT scans at admission had a relatively low incidence of ICP elevation (13%). Among these patients, three features were found to be strongly associated with the development of intracranial hypertension: 1) age over 40 years; 2) systolic blood pressure under 90 mm Hg; and 3) motor posturing — unilateral or bilateral. When two or more of these features were noted at admission, the incidence of intracranial hypertension was 60%, as compared to 4% when only one, or none, of these features were present. Thus, the patients at high risk for developing intracranial hypertension after severe head injury are those with abnormal CT scans at admission, and those with normal CT scans who demonstrate two or more of the above-mentioned adverse features. Based on these criteria, only 16% of this series of patients with normal CT scans would have qualified for monitoring. In addition to the three clinical features noted above, multimodality evoked potential (MEP) studies were also found to be strong predictors of ICP elevation in the normal CT scan group, with a 75% incidence of intracranial hypertension in patients with disseminated deficits. There was no statistically significant correlation between the Glasgow Coma Scale score, eye movements, pupillary reaction, hypoxia, or anemia at admission and subsequent ICP elevation in the group with normal CT scans. In this series, an intraventricular catheter was used as the sole monitoring device in 91% of the cases. In the remaining 9%, subarachnoid screws were employed, either alone, or upon failure of the ventriculostomy. While no mortality was directly ascribed to the monitoring process, there was a 7.7% complication rate (infection 6.3% + hemorrhage 1.4%). Eighty-five percent of the infections occurred in patients who had been monitored for 5 days or more, while no infections were noted in those monitored for less than 3 days. Used judiciously, this technique can be valuable in the monitoring and treatment of the brain-injured patient.

The effects of two levels of fluid-percussion brain injury on cerebral blood flow (CBF) and pial arteriolar diameter were investigated in cats. Regional CBF was measured using the radioactive microsphere technique. Experimental brain injury resulted in changes in arterial blood pressure, CBF, and pial arteriolar diameter that were related to the severity of the injury. Low-level injury (1.88 +/- 0.11 atm, mean +/- standard error of the mean) resulted in a slight transient increase in CBF which had returned to preinjury levels by 30 minutes. High-level injury (2.68 +/- 0.19 atm) resulted in larger, statistically significant (p less than 0.01) increases in whole-brain CBF, decreases in cerebrovascular resistance, and increases in pial arteriolar diameter 1 minute postinjury. One hour after injury, CBF had returned to preinjury levels while cerebral perfusion pressure was significantly (p less than 0.01) reduced. There was no evidence of reduced CBF in any region studied. Pial arterioles dilated during the posttraumatic hypertensive period and then returned to control diameters within 1 hour after injury. Changes in the diameter of pial arterioles were significantly correlated with posttraumatic changes in CBF.

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.