E H Major1, P O'Connor, B Mullan. 1. Regional Intensive Care Unit, Royal Victoria Hospital, Grosvenor Road, BT12 6BA, Belfast, Northern Ireland, UK, e.major@qub.ac.uk.
Abstract
BACKGROUND: In recent years hypertonic saline has attracted increasing interest in the treatment of traumatic intracranial hypertension, and has a number of documented and theoretical advantages over other hyperosmolar agents. To date, no consensus has been achieved on the safest and most effective HTS concentration for administration. AIMS: The purpose of this paper was to evaluate the efficacy of intravenous bolus administration of highly concentrated (30 %) hypertonic saline (HTS) in the treatment of refractory intracranial hypertension secondary to traumatic brain injury. METHODS: Patients were treated with an intravenous bolus of 10 ml of 30 % hypertonic saline. Multiple physiological parameters were measured throughout, including intracranial pressure, mean arterial pressure, cerebral perfusion pressure, pulse and inotrope/pressor requirements. Laboratory investigation pre and post HTS administration included: arterial pH, pCO2, HCO3, base excess; serum biochemistry measurements of sodium, potassium, chloride, urea and creatinine; and coagulation studies. RESULTS: TBI patients saw a rapid and significant reduction in ICP from a baseline value of 28 ± 5.31 to 18.44 ± 6.17 mmHg at 1 h post HTS, a statistically significant reduction that was maintained for up to 7 h. This response was maintained even with repeated HTS administration, which was also associated with an augmented cerebral perfusion pressure from a baseline of 58.0 ± 6.48 to 76.33 mmHg within 1 h of HTS administration. CONCLUSION: No associated harmful biochemical or haematological abnormalities were noted. In conclusion, highly concentrated 30 % HTS appears to be both effective and safe in the management of refractory intracranial hypertension.
BACKGROUND: In recent years hypertonicsaline has attracted increasing interest in the treatment of traumatic intracranial hypertension, and has a number of documented and theoretical advantages over other hyperosmolar agents. To date, no consensus has been achieved on the safest and most effective HTS concentration for administration. AIMS: The purpose of this paper was to evaluate the efficacy of intravenous bolus administration of highly concentrated (30 %) hypertonicsaline (HTS) in the treatment of refractory intracranial hypertension secondary to traumatic brain injury. METHODS:Patients were treated with an intravenous bolus of 10 ml of 30 % hypertonicsaline. Multiple physiological parameters were measured throughout, including intracranial pressure, mean arterial pressure, cerebral perfusion pressure, pulse and inotrope/pressor requirements. Laboratory investigation pre and post HTS administration included: arterial pH, pCO2, HCO3, base excess; serum biochemistry measurements of sodium, potassium, chloride, urea and creatinine; and coagulation studies. RESULTS: TBI patients saw a rapid and significant reduction in ICP from a baseline value of 28 ± 5.31 to 18.44 ± 6.17 mmHg at 1 h post HTS, a statistically significant reduction that was maintained for up to 7 h. This response was maintained even with repeated HTS administration, which was also associated with an augmented cerebral perfusion pressure from a baseline of 58.0 ± 6.48 to 76.33 mmHg within 1 h of HTS administration. CONCLUSION: No associated harmful biochemical or haematological abnormalities were noted. In conclusion, highly concentrated 30 % HTS appears to be both effective and safe in the management of refractory intracranial hypertension.
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