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Thiopental infusion in the treatment of intracranial hypertension complicating fulminant hepatic failure

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Intracranial hypertension complicating fulminant hepatic failure has a mortality in excess of 90% in the presence of renal failure if not rapidly responsive to mannitol and ultrafiltration. Based on data which suggest that barbiturates can be of value in controlling the intracranial hypertension of head injury, intravenous thiopental was assessed in 13 patients with fulminant hepatic failure. All had developed acute renal failure complicated by intracranial hypertension unresponsive to other modes of therapy and were likely by all published criteria to have little chance of survival. The dosage of thiopental was adjusted incrementally until intracranial pressure, measured by extradural transducers, fell to within normal limits or adverse hemodynamic changes occurred. The intracranial pressure was reduced, in each case, by 185 to 500 mg (median: 250 mg) thiopental given over 15 min, and in eight cases continuing infusion achieved stable normal intracranial pressure and cerebral perfusion pressure. Five of the patients made a complete recovery and there were only three deaths from intracranial hypertension. Side effects were few and included minor hypotension controlled by dose reduction. The response of otherwise intractable intracranial hypertension and the 38% survival rate are remarkable for a group of patients with such a poor prognosis.
Title: Thiopental infusion in the treatment of intracranial hypertension complicating fulminant hepatic failure
Description:
Intracranial hypertension complicating fulminant hepatic failure has a mortality in excess of 90% in the presence of renal failure if not rapidly responsive to mannitol and ultrafiltration.
Based on data which suggest that barbiturates can be of value in controlling the intracranial hypertension of head injury, intravenous thiopental was assessed in 13 patients with fulminant hepatic failure.
All had developed acute renal failure complicated by intracranial hypertension unresponsive to other modes of therapy and were likely by all published criteria to have little chance of survival.
The dosage of thiopental was adjusted incrementally until intracranial pressure, measured by extradural transducers, fell to within normal limits or adverse hemodynamic changes occurred.
The intracranial pressure was reduced, in each case, by 185 to 500 mg (median: 250 mg) thiopental given over 15 min, and in eight cases continuing infusion achieved stable normal intracranial pressure and cerebral perfusion pressure.
Five of the patients made a complete recovery and there were only three deaths from intracranial hypertension.
Side effects were few and included minor hypotension controlled by dose reduction.
The response of otherwise intractable intracranial hypertension and the 38% survival rate are remarkable for a group of patients with such a poor prognosis.

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