Cerebrovascular response in infants and young children following severe traumatic brain injury: a preliminary report.

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 < or = 8 years old (25 were < or = 4 years old) with a Glasgow Coma Score (GCS) on admission of < or = 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 < or = 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 < or = 3) was seen uniformly in children under the age of 1 year and in patients with a CBF of < or = 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 > or = 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 < or = 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.