Hypernatremia as a cause of acute neurological disorder is being recognized with increasing frequency.1-11 Common clinical and metabolic features in infants with fatal outcome were described in the previous paper.12 At autopsy, extensive venous occlusion and subarachnoid, subdural, and intracerebral bleeding were prominent findings. Mechanisms for production of these vascular changes and their relative importance in the clinical picture were not clear. It was not known, for example, to what degree hemorrhagic encephalopathy was an integral manifestation of the underlying metabolic disturbance, or whether these vascular lesions merely represented nonspecific, secondary results of transiently disturbed intracranial-pressure relationships.
Hyperosmolarity, of order of magnitude similar to that encountered in patients (375-400 mOsm/L.), produces comparable clinical alterations in experimental animals.13,14 Within 30 minutes after intraperitoneal injection of hypertonic solutions, cats develop marked tremor, ataxia, muscle twitching, stupor, and occasional convulsions. One cat in three dies within a few hours. In
LUTTRELL CN, FINBERG L, DRAWDY LP. Hemorrhagic Encephalopathy Induced by Hypernatremia: II. Experimental Observations on Hyperosmolarity in Cats. AMA Arch Neurol. 1959;1(2):153–160. doi:10.1001/archneur.1959.03840020027005
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