TY - JOUR
T1 - Treatment of refractory intracranial hypertension with 23.4% saline
AU - Suarez, Jose I.
AU - Qureshi, Adnan I.
AU - Bhardwaj, Anish
AU - Williams, Michael A.
AU - Schnitzer, Mark S.
AU - Mirski, Marek
AU - Hanley, Daniel F.
AU - Ulatowski, John A.
PY - 1998
Y1 - 1998
N2 - Objective: To evaluate the effect of intravenous bolus administration of 23.4% saline (8008 mOsm/L) on refractory intracranial hypertension (RIH) in patients with diverse intracranial diseases. Design: Retrospective chart review. Setting: A neurosciences intensive care unit in a university hospital. Patients: We present eight patients and a total of 20 episodes of increased intracranial pressure (ICP) resistant to standard modes of therapy. Five patients had subarachnoid hemorrhage, one patient had traumatic brain injury, one had a brain tumor, and another had spontaneous basal ganglia hemorrhage. Seven patients had intraventricular catheters, and one had a subarachnoid pressure screw placed. We monitored continuously mean ICP, serum sodium concentrations, mean arterial pressure, cerebral perfusion pressure (CPP), central venous pressure, and urine output before and after the administration of hypertonic saline (HS). Post mortem examination of the brain was performed in two patients. Intervention: Intravenous bolus administration of 30 mL of 23.4% saline. Measurements and Main Results: There was a significant (p < .05) decrease in ICP from a median of 41.5 mm Hg before HS to 17 mm Hg at 1 hr, 16 mm Hg at 2 hrs, and 14 mm Hg at 3 hrs after HS administration. In 80% of cases, ICP decreased by >50% of the pretreatment value over a duration of 21.2 ± 10.3 mins. ICP decreased to <20 mm Hg in 65% of all cases and the mean time for it to again exceed 20 mm Hg was 6.3 ± 4.9 hrs. There was a significant improvement in CPP, from 64.7 ± 19 (so) mm Hg before HS to 85.6 ± 18 mm Hg (1 hr) and 83 ± 18 mm Hg (3 hrs) after HS. There were no significant differences in the other variables measured. The post mortera examinations showed no white matter changes or subdural collections. Conclusions: This preliminary case series suggests that the intravenous bolus administration of 23.4% saline reduces ICP and augments CPP in patients with resistant increased ICP. This reduction can be maintained for several hours while other therapeutic measures are being considered. The patient population most likely to respond to this therapy needs to be further defined. Although more research is needed, this treatment is promising as a new modality for RIH because of its ICP-lowering effect without intravascular volume depletion.
AB - Objective: To evaluate the effect of intravenous bolus administration of 23.4% saline (8008 mOsm/L) on refractory intracranial hypertension (RIH) in patients with diverse intracranial diseases. Design: Retrospective chart review. Setting: A neurosciences intensive care unit in a university hospital. Patients: We present eight patients and a total of 20 episodes of increased intracranial pressure (ICP) resistant to standard modes of therapy. Five patients had subarachnoid hemorrhage, one patient had traumatic brain injury, one had a brain tumor, and another had spontaneous basal ganglia hemorrhage. Seven patients had intraventricular catheters, and one had a subarachnoid pressure screw placed. We monitored continuously mean ICP, serum sodium concentrations, mean arterial pressure, cerebral perfusion pressure (CPP), central venous pressure, and urine output before and after the administration of hypertonic saline (HS). Post mortem examination of the brain was performed in two patients. Intervention: Intravenous bolus administration of 30 mL of 23.4% saline. Measurements and Main Results: There was a significant (p < .05) decrease in ICP from a median of 41.5 mm Hg before HS to 17 mm Hg at 1 hr, 16 mm Hg at 2 hrs, and 14 mm Hg at 3 hrs after HS administration. In 80% of cases, ICP decreased by >50% of the pretreatment value over a duration of 21.2 ± 10.3 mins. ICP decreased to <20 mm Hg in 65% of all cases and the mean time for it to again exceed 20 mm Hg was 6.3 ± 4.9 hrs. There was a significant improvement in CPP, from 64.7 ± 19 (so) mm Hg before HS to 85.6 ± 18 mm Hg (1 hr) and 83 ± 18 mm Hg (3 hrs) after HS. There were no significant differences in the other variables measured. The post mortera examinations showed no white matter changes or subdural collections. Conclusions: This preliminary case series suggests that the intravenous bolus administration of 23.4% saline reduces ICP and augments CPP in patients with resistant increased ICP. This reduction can be maintained for several hours while other therapeutic measures are being considered. The patient population most likely to respond to this therapy needs to be further defined. Although more research is needed, this treatment is promising as a new modality for RIH because of its ICP-lowering effect without intravascular volume depletion.
KW - Cerebral edema
KW - Hypertonic solutions
KW - Intracranial hypertension
KW - Neurointensive care
KW - Saline
KW - Serum sodium
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U2 - 10.1097/00003246-199806000-00038
DO - 10.1097/00003246-199806000-00038
M3 - Article
C2 - 9635664
AN - SCOPUS:0031798403
SN - 0090-3493
VL - 26
SP - 1118
EP - 1122
JO - Critical care medicine
JF - Critical care medicine
IS - 6
ER -