BACKGROUND: Brain natriuretic peptide (BNP) is a potent natriuretic and 
vasodilator factor which, by its systemic effects, can decrease cerebral blood 
flow (CBF). In aneurysmal subarchnoid hemorrhage (aSAH), BNP plasma 
concentrations were found to be associated with hyponatremia and were 
progressively elevated in patients who eventually developed delayed ischemic 
deficit secondary to vasospasm. The purpose of the present study was to evaluate 
trends in BNP plasma concentrations during the acute phase following severe 
(traumatic brain injury) TBI.
METHODS: BNP plasma concentration was evaluated in 30 patients with severe 
isolated head injury (GCS<8 on admission) in four time periods after the injury 
(period 1: days 1-2; period 2: days 4-5; period 3: days 7-8; period 4: days 
10-11). All patients were monitored for ICP during the first week after the 
injury.
FINDINGS: The initial BNP plasma concentrations (42+/-36.9 pg/ml) were 7.3 fold 
(p<0.01) higher in TBI patients as compared to the control group (5.78+/-1.90 
pg/ml). BNP plasma concentrations were progressively elevated through days 7-8 
after the injury in patients with diffused SAH as compared to patients with mild 
or no SAH (p<0.001) and in patients with elevated ICP as compared to patients 
without elevated ICP (p<0.001). Furthermore, trends in BNP plasma concentrations 
were significantly and positively associated with poor outcome.
INTERPRETATION: BNP plasma concentrations are elevated shortly after head injury 
and are continuously elevated during the acute phase in patients with more 
extensive SAH and in those with elevated ICP, and correlate with poor outcomes. 
Further studies should be undertaken to evaluate the role of BNP in TBI 
pathophysiology.