Severe Cerebral Vasospasm and Infarction After Minor Head Trauma.

Cerebral vasospasm is commonly reported following traumatic brain injury (TBI) and traumatic subarachnoid hemorrhage (tSAH). However, severe vasospasm after TBI with minimal, focal tSAH is rare and often forgotten. A 62-year-old woman experienced an evident mechanical fall with head injury, but with no loss of consciousness or abrasions to the head or neck. She was being treated for hypertension and a previous unprovoked pulmonary embolism with trandolapril, hydrochlorothiazide, and dabigatran. She initially presented with confusion, vomiting, and urinary incontinence. Glasgow Coma Scale was 14. She had no fever, meningismus, or focal neurological deficits on presentation. There were no prodromal symptoms, thunderclap headaches, or changes in cognition in the weeks or days leading to the head injury. Initial computed tomography (CT) and magnetic resonance imaging showed minimal convexal tSAH and minimal intraventricular hemorrhage (Figure 1). Magnetic resonance angiography (MRA) was normal. She was hyponatremic (Na, 126mmol/L) and had leukocytosis (white blood cell count, 21.6 × 10/L), attributed to urinary tract infection, which quickly normalized to 10.6 × 10/L 4 days following her admission. Blood cultures were negative. She was treated for delirium secondary to hypovolemia and a presumed urinary tract infection. A follow-up CT scan on day 7 showed expected evolution/stabilization of her bleed. Her delirium resolved by day 8, and the patient was prepared for discharge. However, on day 10, the patient developed left hemiparesis, left homonymous hemianopsia, and neglect. CT/CT angiography (CTA) revealed a right parietal infarct and diffuse, bihemispheric vasospasm with no topographical relationship to the focal tSAH (Figure 2). No proximal or distal aneurysms were seen. A thorough infectious and inflammatory workup was negative at that time. The patient was treated with milrinone 20mg in 80ml normal saline infused at 0.75mg/kg/min, nimodipine 60mg by mouth every 4 hours, and magnesium sulfate 5 g/250ml saline over 5 hours. Response to treatment was monitored with serial transcranial Doppler ultrasounds and CTAs. The transcranial Doppler ultrasounds were interpreted by a single radiologist using sonographic criteria. The CTAs were read by two separate radiologists, who used coronal, sagittal, maximum intensity projection, and three-dimensional reformatted images and volumetric measurements. Vasospasm resolved by day 21, at which time the patient was completely compos mentis but had persistent neurological deficits relevant to her infarct. She was transferred to inpatient rehabilitation and achieved independence for basic activities of daily living. Cerebral vasospasm is a reported complication of TBI and tSAH. Its incidence appears to correlate with the severity of bleeding, and it is rarely reported following a relatively small subarachnoid hemorrhage. In our patient, TBI and tSAH were relatively minor and focal. It was therefore unexpected for her to suffer such severe bilaterally diffuse cerebral vasospasm. An intracranial or systemic