F. Munar et al., Cerebral hemodynamic effects of 7.2% hypertonic saline in patients with head injury and raised intracranial pressure, J NEUROTRAU, 17(1), 2000, pp. 41-51
The aim of the present study was to investigate the acute effects of 7.2% h
ypertonic saline (HS) on intracranial pressure (ICP), cerebral and systemic
hemodynamics, serum sodium, and osmolality in 14 patients with moderate an
d severe traumatic brain injury (Glasgow Coma Scale less than or equal to 1
3) and raised ICP (>15 mm Hg) within the first 72 h postinjury. After CO2 r
eactivity and autoregulation were tested, each patient received a 15-min in
fusion of 7.2% HS (1,232 mEq/L, volume 1.5 mL/kg). ICP, serial hemodynamics
, cerebral blood flow (CBF) estimated from cerebral arteriovenous oxygen co
ntent difference (AVDO(2)), and laboratory variables, including serum osmol
ality, electrolytes, urea, and creatinine were collected before infusion (T
-0) and at 5, 30, 60, and 120 min after (T-5, T-30, T-60, T-120). Urine out
put was measured 2 h before infusion and at T-120. While CO2 reactivity was
preserved in all patients, autoregulation was preserved in only four. ICP
decreased to about 30% of base line (p = 0.0001) during the whole study per
iod. During the first hour after infusion, cerebral perfusion pressure (p l
ess than or equal to 0.04) and cardiac index (CI; p less than or equal to 0
.01) increased, while systemic vascular resistance index fell (p less than
or equal to 0.05). Heart rate increased (p less than or equal to 0.04) duri
ng the first 30 min. Pulmonary artery occlusion pressure (PAOP) increased (
p = 0.004) at T-5. There were no significant changes in mean arterial blood
pressure (MABP), urine output, and estimated CBF. A significant positive c
orrelation (r = 0.75; p = 0.02) between ICP and serum osmolality was found
at T-5. The administration of 7.2% HS in patients with traumatic brain inju
ry significantly reduces ICP without significant changes in relative global
CBF (expressed as 1/AVDO(2)), increases CI and transiently increases PAOP,
without changing MABP and urine output. The correlation between changes in
osmolality and ICP supports the hypothesis that HSS may in part decrease I
CP by means of an osmotic mechanism.