Young patient with thunderclap headache, seizure activity, and fixed eye deviation.

Abstract

A 39-year-old female with a history of iron deficiency anemia presented to the emergency department (ED) with a 3-hour history of severe headache followed by acute-onset projectile non-bilious, non-bloody vomiting, acute mental status change, and seizure-like activity. The onset of the headache was spontaneous and described as the worst headache of her life. Vomiting and seizure-like activity began several hours after the onset of headache, and emergency medical services (EMS) were called at that time. The patient was found to be unresponsive by EMS. Upon arrival to the ED, the physical examination was notable for fixed left eye deviation, intermittent withdrawal from noxious stimuli, and spells of sustained clonus in the lower extremities greater on the left than the right. The patient was given 2-mg intravenous lorazepam with minimal improvement in the tonic–clonic activity. The patient was hemodynamically stable and had an oxygen saturation of 98% on room air. Initial laboratory test results were significant for anemia (hemoglobin = 5.2 g/dL, hematocrit = 21%) and elevated platelets (426.5). Computed tomography (CT) of the head, CT angiogram of the head and neck, CT venogram of the head, and urgent neurology consult were obtained immediately after arrival to the ED. The patient continued to decline after CT and was intubated for airway protection. Imaging was suggestive of acute venous sinus thrombosis extending from the superior sagittal sinus to the right cranial jugular vein with no definite intracranial hemorrhage (Figures 1 and 2) and bilateral segmental and subsegmental pulmonary emboli (Figure 3). This case describes a typical presentation of cerebral venous sinus thrombosis (CVST). CVSTs are more commonly seen in women aged 30–50 years.1 Commonly, sinus thrombosis can lead to subarachnoid hemorrhage with a subsequent “thunderclap” headache that can lead to neurological symptoms.3 Neurology evaluated the patient in the ED, and the patient was taken to the operating room for an aspiration thrombectomy and started on a continuous heparin infusion. The patient had gradual improvement of symptoms after 1 week of inpatient care in the neurology intensive care unit. At discharge, she was started on indefinite anticoagulation and levetiracetam for seizure prophylaxis. Further workup showed no evidence of hypercoagulability, no recent trauma, and no oral contraceptive use. CVST is defined as occlusion of dural sinuses leading to decreased venous flow, an increase in intracranial pressure, decreased cerebral perfusion pressures, and dilation of the cerebral veins. Continued hypoperfusion can result in ischemic tissue damage, resulting in acute neurologic symptoms such as seizures, headaches, altered mental status, and increased intracranial pressure. Without treatment, the thrombus can damage vessel walls, increasing the chances of vessel rupture, leading to subarachnoid hemorrhages and decreased cerebrospinal fluid outflow.1 Common risk factors for CVSTs include recent trauma, malignancy, thrombophilia, infection, obesity, oral contraceptive use, and increased estrogen states such as pregnancy.2