The relationship between cerebrospinal fluid creatine kinase and morphologic changes in the brain after transient cardiac arrest.

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Abstract
Recent studies show that the increase in creatine kinase (CK) in lumbar spinal fluid (CSF) can effectively predict the outcome of cerebral ischemia after cardiac arrest. Maximum CSF-CK concentrations in 40 patients who died more than 3 days after successful cardiopulmonary resuscitation were related to the histologic brain damage. The level of consciousness was assessed in all patients during the time of survival. Neuronal necrosis was determined semiquantitatively according to a scoring system in sections from the frontal cortex, thalamus, hippocampus and the cerebellum. A curvilinear relationship was found between maximum CSF-CK and extent and magnitude of defined histologic brain damage. Maximum CSF-CK activity was found 48-72 h after the anoxic episode. No cerebral damage was found when maximum CSF-CK remained below 4 U[units]/l. The frontal cortex was less severly damaged than the other regions examined. CSF-CK increased to between 4-10 U/l in patients without damage to the frontal cortex but with slight-to-severe damage of the other regions. In deeply comatose patients, the CSF-CK activity always exceeded 10 U/l and neuronal necrosis was found in all regions. Approximately 1/2 of the patients had a diffuse loss of nerve cells in the cerebral cortex and hippocampus, while the other half had a patchy necrosis. The former patients generally had a rapid rise and fall in CSF-CK, with a peak at 48 h, while the latter group had a delayed rise and fall, with a maximum value at 72 h. This difference may be due to a delayed necrosis of nerve cells caused by a no-reflow phenomenon in the latter group. Despite a selective vulnerability in certain parts of the brain, and a delayed necrosis of nerve cells in some patients, maximum CK activity in the lumbar CSF accurately and reliably measures the extent of the permanent brain damage and the functional outcome after cerebral ischemia.