To evaluate the changes in cerebral blood flow (CBF) that occur immediately after head injury and the effects of different posttraumatic lesions on CBF, 61 CBF studies were obtained using the xenon-computerized tomography method in 32 severely head-injured adults (Glasgow Coma Scale score (GCS) less than or equal to 7). The measurements were made within 7 days after injury, 43% in the first 24 hours. During the 1st day, patients with an initial GCS score of 3 or 4 and no surgical mass had significantly lower flows than did those with a higher GCS score or mass lesions (p less than 0.05): in the first 1 to 4 hours, those without surgical mass lesions had a mean CBF of 27 cc/100 gm/min, which rose to 44 cc/100 gm/min by 24 hours. Patients without surgical mass lesions who died tended to have a lower global CBF than did those with better outcomes. Mass lesions were associated with a high global CBF and bihemispheric contusions with the lowest flows. By 24 hours after injury, global blood flow increased in groups that originally had low flows and decreased in those with very high initial flows, such that by 36 to 48 hours, most patients had CBF values between 32 and 55 cc/100 gm/min. Lobar, basal ganglion, and brain-stem blood flow values frequently differed by 25% or more from global averages. Brain-stem CBF varied the most but did not correlate with clinical signs of brain-stem dysfunction. Double studies were performed at two different pCO2 values in 10 patients with various posttraumatic lesions, and the CO2 vasoresponsivity was calculated. Abnormal CO2 vasoresponsivity was found with acute subdural hematomas and defuse cerebral swelling but not with epidural hematomas. In patients without surgical mass lesions, the findings suggest that CBF in the first few hours after injury is often low, followed by a hyperemic phase that peaks at 24 hours. Global CBF values vary widely depending on the type of traumatic brain injury, and brain-stem flow is often not accurately reflected by global CBF values. These findings underscore the need to define regional CBF abnormalities in victims of severe head injury if treatment is intended to prevent regional ischemia.

Fever is common in critically ill neurosurgical patients, especially those with a prolonged length of stay in the ICU or a cranial disease. If hyperthermia worsens the functional outcome after a primary ischemic or traumatic injury, as has been suggested by several studies of stroke patients, treatment of fever is a clinical issue that requires better management.

The influence of anesthetic agents on cerebral blood flow (CBF) was tested in normal rats. CBF is quantified with arterial spinlabeled MRI in rats anesthetized with either an opiate (fentanyl), a potent inhalation anesthetic agent (isoflurane), or a barbiturate (pentobarbital) using doses commonly employed in experimental paradigms. CBF values were found to be about 2. Despite the frequent use of anesthetics in experimental MRI in rats using techniques such as arterial spin labeling (ASL) and blood oxygenation level-dependent (BOLD) signal changes, quantitative assessment of the effect of commonly used anesthetics on cerebral blood flow (CBF) in these protocols is limited (1). Assessment of the effect on CBF of fentanyl, a potent narcotic analgesic agent frequently administered in the clinical neuroanesthesia and neurointensive care setting, is limited even using conventional techniques applied to normal rats (2,3). To this end, we quantified CBF using the continuous ASL method (CASL) in rats administered fentanyl (10 g kg Ϫ1 bolus, then 50 g kg Ϫ1 h Ϫ1 intravenously (IV), during ventilation with N 2 O/O 2 , 2:1) and compared these findings to those observed using isoflurane (1% by inhalation in N 2 O/O 2 , 1:1) or pentobarbital (50 mg kg Ϫ1 h Ϫ1 IV, during ventilation with N 2 /O 2 , 1:1) anesthetic regimens. METHODS Animal ModelThe study protocol was approved by the University of Pittsburgh Animal Care and Use Committee. Twelve mature male Sprague-Dawley rats (332-390 g) were anesthetized with isoflurane and N 2 O/O 2 , 1:1, endotracheally intubated and mechanically ventilated. A femoral arterial catheter and a double lumen venous catheter were surgically inserted for blood sampling, for pressure monitoring, and for administration of agents. Rats were assigned to one of three anesthetic groups for CBF measurements: fentanyl, isoflurane, or pentobarbital (n ϭ 4 per group). Isoflurane was then continued at 1% by inhalation (isoflurane group), or discontinued and either fentanyl (10 g kg Ϫ1 bolus, then 50 g kg Ϫ1 h Ϫ1) or pentobarbital (50 mg kg Ϫ1 h Ϫ1 ) was administered IV. N 2 O/O 2 was continued in fentanyl (2:1) and isoflurane (1:1) groups. Rats were ventilated with N 2 /O 2 , 1:1 in the pentobarbital group. Fentanyl or isoflurane anesthesia was administered with N 2 O because this approach is frequently used in clinical neuroanesthesia (4) and in experimental models (5,6). Similarly, to mirror clinical (7) and laboratory (8) usage, pentobarbital was administered without N 2 O. In the pentobarbital group, N 2 O was replaced with N 2 to match the fraction of inspired oxygen concentration in the isoflurane-anesthetized group. After a 30-min equilibration period, perfusion images were acquired in duplicate. In all studies pancuronium bromide (0.1 mg kg Ϫ1 h Ϫ1) was administered IV for paralysis. Rectal temperature was continually monitored and maintained at 37°C with a heated water blanket. Arterial blood gases and mean arterial blood pressure (MABP) were also monitored throughout the NMR studies. Respiratory t...

To further describe the pathophysiologic processes that occur in infants and young children after severe traumatic brain injury (TBI), we retrospectively reviewed the cerebral blood flow (CBF) values and 6-month Glasgow Outcome Scores (GOS) in 30 children < 8 years old (25 were < 4 years old) with a Glasgow Coma Score (GCS) on admission of < 8. Twelve females and 18 males (mean age 2.1 years, range 1 month to 8 years) underwent 61 CBF studies using stable xenon computed tomography at variable times from admission to 9 days after TBI. In 12 patients, PaCO₂ was manipulated an average of 8.4 torr (range 5–11 torr) and a second CBF study performed to determine CO₂ vasoreactivity (CO₂VR), defined as the percent change in CBF per torr change in PaCO₂. CBF on admission (n = 13) was 25.1 ± 7.7 ml/100 g/min (mean ± SEM) and was < 20 ml/100 g/min in 10 of 13 patients (77%). By 24 h and for up to 6 days after TBI, the mean CBF increased to 55.3 ± 3.4 ml/100 g/min (range 2–95) which differed significantly from the admission CBF value (p < 0.05); a CBF of >70 ml/100 g/min tended to be associated with a good outcome. Poor outcome (GOS ≤ 3) was seen uniformly in children under the age of 1 year and in patients with a CBF of <20 ml/100 g/min any time after TBI. Poor outcome was seen in 85% of children under the age of 24 months, but in only 41% of children ≧ 24 months old. Mean CO₂VR was 2.1 ± 0.6%/torr PaCO₂ and ranged from 0.02 to 5.98%. Mean CO₂VR tended to differ between good and poor outcome children (3.2 ± 0.9 and 1.17 ± 0.2%, respectively) and a CO₂VR of <2% was significantly associated with a poor outcome. Younger age, low CBF in the early period after TBI, and a CO₂VR of <2% was associated with a poor outcome in this subgroup of children. Young children (<24 months) may represent a particular high-risk group with early hypoperfusion after severe TBI. This finding may be a key factor in the pathophysiology and outcome in this age group, and may need to be addressed in our future therapeutic protocols.