A case of symptomatic traumatic cerebral vasospasm associated with hyponatremia

The pathogenesis and clinical course of traumatic cerebral vasospasm (TCV) are not yet fully understood. We report a case of delayed symptomatic TCV exaggerated by hyponatremia in spite of minor subarachnoid hemorrhage. A 77-year-old woman was admitted to our hospital with multiple injury caused by a traffic accident. Glasgow coma scale on admission was 8, and CT scan revealed right temporal lobe contusion, thin sub-arachnoid hemorrhage in the right sylvian cistern and right temporal bone fracture. The patient's consciousness level and CT findings improved gradually, but on the 11th day, she suddenly fell into a comatose state. No apparent change was observed on the CT scan, but her serum sodium level was markedly low (113mEq/L). Under the suspicion of hyponatremia induced consciousness disturbance, sodium replacement therapy was commenced. She showed transient neurological recovery, but on day 13, worsening of left hemiparesis and a new low density area on CT were observed. Vasospasms of the right M2 proximal portion were confirmed by cerebral angiogram, so we performed intraarterial papaverine infusion leading to good extension of spastic vessels, but regrettably, there was no neurological recovery. In general, subarachnoid blood plays an important role in the delayed development of cerebral vasospasm, following nor only aneurysmal rupture but also head injury. TCV lends to pass subclinically, but secondary water and electrolyte imbalance may unexpectedly cause TCV to manifest itself clinically. We can confirm that with this patient management of electrolyte balance following head injury was the most important strategy to avoid symptomatic TCV.