Abstract

The mechanism limiting the tolerance to repeated subarachnoid hemorrhages was analysed experimentally. Blood introduced by an extracorporeal femorointrathecal shunt or by injection, into five different sites of the cranio-spinal system in living and dead dogs, produced a progressive increase in the steady state CSF pressure after each subsequent bleed. The pressure increase was quantitatively related to the amount of blood entering the system. A comparison of the respective effects of injections of whole blood and of erythrocytes indicated that the red blood cells were the component which induced an increase in the outflow resistance by clogging the pathways of the cerebrospinal fluid. The increase in outflow resistance with each bleed resulted in a stepwise rise in pressure to a level incompatible with survival. The lethal volume of bleed was specific for each site of hemorrhage: namely for brain parenchyma 8.1 ml, lateral ventricle 16.2 ml, cisterna chiasmatica 17.7 ml, cisterna magna 30 ml, and spinal subarachnoid space 55 ml. The assumption that death might be a random event was discarded, the failure of vital functions being considered to be the result of the high intracranial pressure. Mock bleeds using intrathecal infusions of saline suggested that spatial decompensation rather than cumulative ischemic effects caused death.

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