Mannitol crosses the blood-brain barrier in Reye’s syndrome

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Although cerebral edema was noted at autopsy in the first reported victims of Reye’s syndrome1 (RS) in 1963, it was not until 1975 that the morbid role of intracranial hypertension in this syndrome became clear2, 3 and that survival depends on its control.4

Monitoring intracranial pressure (ICP) is now standard in the management of moderate and severe cases of RS,5 with mannitol the osmotic diuretic of choice.2–14 However, studies of the serum and cerebrospinal fluid (CSF) concentrations of mannitol in RS therapy raise serious questions about the prolonged and indiscriminate use of this drug.

Materials and methods

Four patients with RS confirmed by liver biopsy were treated by a standard protocol.6 Each patient fulfilled the clinical and laboratory diagnostic criteria for RS,15 and both light and electron microscopy findings in the liver biopsy specimens were consistent with RS.

Once the patient reached clinical Stage II,16 aggressive, definitive therapy was commenced consisting of nasotracheal intubation, neuromuscular paralysis with pancuronium bromide, controlled ventilation to maintain a PaCO2 of 25 ± 2 mm Hg and a PaO2 of 100–150 mm Hg, sedation with morphine sulfate, placement of an intraventricular catheter to monitor ICP and sample CSF, arterial and Swan-Ganz catheterization, and induced hypothermia to 31 C.5 An EEG was obtained as soon as possible after the start of therapy and repeated daily. Fluid intake was restricted to 1200–1400 cc/m2/day. Intracranial hypertension was managed initially by manual hyperventilation whenever the ICP exceeded 20 mm Hg as a plateau wave; if 2 . . .



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