USE OF HYPERTONIC (3-PERCENT)SALINE ACETATE INFUSION IN THE TREATMENTOF CEREBRAL EDEMA - EFFECT ON INTRACRANIAL-PRESSURE AND LATERAL DISPLACEMENT OF THE BRAIN/
Ai. Qureshi et al., USE OF HYPERTONIC (3-PERCENT)SALINE ACETATE INFUSION IN THE TREATMENTOF CEREBRAL EDEMA - EFFECT ON INTRACRANIAL-PRESSURE AND LATERAL DISPLACEMENT OF THE BRAIN/, Critical care medicine, 26(3), 1998, pp. 440-446
Objective: To determine the effect of continuous hypertonic (3%) salin
e/acetate infusion on intracranial pressure (ICP) and lateral displace
ment of the brain in patients with cerebral edema. Design: Retrospecti
ve chart review. Settings: Neurocritical care unit of a university hos
pital. Patients: Twenty seven consecutive patients with cerebral edema
(30 episodes), including patients with head trauma (n = 8), postopera
tive edema (n = 5), nontraumatic intracranial hemorrhage (n = 8), and
cerebral infarction (n = 6). Intervention: Intravenous infusion of 3%
saline/acetate to in crease serum sodium concentrations to 145 to 155
mmol/L. Measurements and Main Results: A reduction in mean ICP within
the first 12 hrs correlating with an increase in the serum sodium conc
entration was observed in patients with head trauma (r(2) = .91, p = .
03), and postoperative edema (r(2) = .82, p = .06), but not in patient
s with nontraumatic intracranial hemorrhage or cerebral infarction. In
patients with head trauma, the beneficial effect of hypertonic saline
on ICP was short-lasting, and after 72 hrs of infusion, four patients
required intravenous pentobarbital due to poor ICP control. Among the
21 patients who had a repeat computed tomographic scan within 72 hrs
of initiating hypertonic sa line, lateral displacement of the brain wa
s reduced in patients with head trauma (2.8 +/- 1.4 to 1.1 +/- 0.9 [SE
M]) and in patients with postoperative edema (3.1 +/- 1.6 to 1.1 +/- 0
.7). This effect was not observed in patients with nontraumatic intrac
ranial bleeding or cerebral infarction. The treatment was terminated i
n three patients due to the development of pulmonary edema, and was te
rminated in another three patients due to development of diabetes insi
pidus. Conclusions: Hypertonic saline administration as a 3% infusion
appears to be a promising therapy for cerebral edema in patients with
head trauma or postoperative edema. Further studies are required to de
termine the optimal duration of benefit and the specific patient popul
ation that is most likely to benefit from this treatment.