Mean hemispheric cerebral blood flow (CBF) and intracranial pressure (ICP) were measured in 19 severely head-injured patients treated with barbiturate coma. The CBF was calculated from the clearance of tracer substance monitored by extracranial scintillation detectors after intravenous administration of xenon-133. In 11 of the patients cerebral arteriovenous oxygen differences were measured simultaneously. In all patients the effects of pronounced hyperventilation were recorded prior to initiation of barbiturate treatment. A normal CBF response to hyperventilation (delta CBF/delta PaCO2 greater than or equal to 1) was obtained in eight patients. In these patients induction of barbiturate coma was accompanied by physiological decreases in CBF and in the calculated cerebral metabolic rate of oxygen (CMRO2); they also exhibited a rapid and lasting decrease in ICP. A decreased or an abolished CO2 reactivity was recorded (delta CBF/delta PaCO2 less than 1) in 11 patients. In 10 of these 11 patients the physiological decreases in CBF and CMRO2 were not obtained during barbiturate treatment and the decrease in ICP was transitory. This study demonstrates a correlation between cerebral vasoreactivity, physiological effects of barbiturate therapy, and clinical outcome.

All complications in a consecutive series of 648 patients subjected to prolonged recording of the ventricular fluid pressure (VFP) during 1982-1986 were registered and analysed. The procedure did not cause permanent symptoms or deficits in any case except for one haemorrhagic complication. Definite infections caused by the VFP recording were found in 4.3% of the 540 patients (83%) surviving their disease or lesion, and in 1.9% in non-survivors. These infections were almost exclusively registered in patients treated with prolonged drainage of hemorrhagic ventricular fluid, while definite infections in other patients were found in only 1.3%. Most infections were caused by Staphylococcus epidermidis and all infections could be treated successfully. Infection did not cause or contribute to the lethal outcome in any case. In 60% of the cases with infectious complications laboratory signs of ventriculitis occurred after a surgical revision of the ventriculostomy. The duration of VFP recording was of subordinate importance for the development of infection. In 13 patients (1.9%) during the studied period a reliable VFP recording was not obtained, a fact that points to the need for alternative methods in a minority of patients with elevated intracranial pressure. It is concluded that complications caused by VFP recording can be kept at an acceptably low frequency in patients without haemorrhagic cerebrospinal fluid demanding long-term drainage.

Mean hemispheric cerebral blood flow (CBF) was studied in 11 comatose brain-injured patients following intravenous administration of xenon-133. Repeated measurements were performed in order to evaluate cerebral vasoreactivity following a decrease in PaCO2. In addition, the effect of induced barbiturate coma was evaluated in patients with intracranial hypertension. The cerebral vasoreactivity and the CBF response following induction of barbiturate coma varied. In patients with normal CO2 reactivity, barbiturate treatment was accompanied by a considerable decrease in CBF as compared to patients with decreased or abolished CO2 response. During barbiturate treatment the intracranial pressure (ICP) became normal in three of four patients with preserved CO2 response, but reached normal levels in only one of five patients with impaired CO2 reactivity. Patients whose ICP became normal recovered. The data suggest a positive correlation between CO2 reactivity and the effect of barbiturate treatment. Furthermore, preserved cerebral vasoreactivity after severe head injury may be of prognostic value.

No abstract

The cases of 127 consecutive patients with subarachnoid hemorrhage (SAH), in whom cerebral panangiography revealed no cause for the bleeding nor any sign of an intraparenchymatous hemorrhage, were reviewed in a study of the long-term prognosis and the possible prognostic factors in this condition. Data for all 127 patients in the study were obtained, with an average follow-up period of 5.4 years. After the 1st week post-SAH, only three rebleeds had occurred. In all, 80% of the patients had returned to full activity, 91% to at least part-time work; if the patients with hypertension were excluded, these figures rose to 86% and 95%, respectively. Decreased wakefulness on admission related to a slightly poorer prognosis, whereas age and red blood cell count in the cerebrospinal fluid had no prognostic significance. Of those patients who, at the end of the 2nd week following the SAH, were fully awake and had not developed any symptoms of delayed cerebral ischemia (87% of all patients admitted), 88% returned to full activity, 97% to at least part-time work. The survival rate for this group, as well as causes of death, seem to be within the range for normal individuals. It should thus be possible to inform these patients (at least the normotensive ones) of the benignity of their condition, directly after normal angiography. Even among the patients who were able to return to full activity, symptoms attributable to the SAH were common: 22% experienced problems such as frequent headaches, vertigo, irritability, and increased fatigability.