Observations on hexachlorophene-induced paralysis in the cat and its antagonism by hypertonic urea.

Cats given HCP (20 mg/kg) orally each day developed hindlimb paralysis and greatly elevated CSFP (174 mm saline; 19 mm in controls) in 3 to 5 days. "Status spongiosis" was seen in white matter only in sections of brain and cord. There was no dilation of cerebral ventricles, or damage to their ependymal linings or to the arachnoid villi. The neurological picture excluded any but a terminal effect upon cranial nerve function. There appeared to be no damage to neurons, and recovery of survivors was complete within 6 weeks after cessation of HCP administration. Elevated CSFP in paralyzed anesthetized cats was quickly lowered by an average of 256 mm by slow iv administration of 30% urea (2 g/kg in 10% invert sugar). Unanesthetized cats similarly paralyzed were able to stand and walk for up to 4 hr after this treatment. Neither acetazolamide nor prednisolone alone had any effect, nor did coadministration with urea enhance the effect of urea. The HCP lesion does not appear to be inflammatory in origin, nor does it seem to involve ventricular obstruction or overproduction of cerebrospinal fluid. The reappearance of paralysis about 4 hr after osmotic diuresis, which corresponds with the elimination of urea, suggests that prolonged iv infusion with urea or a similar osmotically active substance may have significant clinical value in the management of HCP poisoning.