Case Presentation: We present a 25-year-old female with history of antithrombin III deficiency, recurrent PEs and DVTs due to medication noncompliance, currently on therapeutic anticoagulation with Lovenox who presented to the ED with a headache. Patient was recently discharged from an outside hospital 4 days prior after being admitted for chest pain, headache and lightheadedness. At that time she underwent CTA chest, CTH and LP which were all unremarkable. On presentation to ED 4 days later, she complained of severe, sharp, positional headache that worsened with laying down. Physical exam was without any focal deficits. Vitals were stable, CBC and CMP unremarkable. Her headache was thought to be secondary to post lumbar puncture. She was treated with Toradol and Tylenol and discharged.10 hours later patient was brought to ED via EMS with AMS. She was tachycardic, tachypneic and unresponsive to painful stimuli with a tonic posturing. She was treated with Ativan and Keppra and was then intubated for airway protection. Per pharmacy records, she filled her Lovenox 4 days ago. Labs were significant for metabolic acidosis with pH 7.29, lactate 12.8 and WBC count 21.9. CTH non-contrast was negative. UDS was positive for benzodiazepine and marijuana. Patient was started on broad-spectrum antibiotics and admitted to ICU. 9 hours after admission she became tachycardic and hypotensive. Exam showed fixed pupils and absent corneal, gag, cough reflex. Emergent CT head obtained showed diffuse cerebral edema, right frontal infarct and concern for superior sagittal sinus DVT. Stroke team and Neurosurgery were emergently consulted. CTA head and neck CT perfusion scan showed markedly attenuated intracranial arterial vasculature, diffuse cerebral edema and global hypoperfusion.Given the extent of cerebral edema, ischemic strokes on CT and poor prognosis, surgical intervention was deemed not to improve outcome. Brain death testing was performed at the patient was pronounced dead the following day.

Discussion: Cerebral venous thrombosis is a rare disorder with an annual incidence ranging from 0.22 to 1.57 per 100,000. Most CVT cases have been linked with acquired or inherited prothrombic conditions, oral contraceptives, pregnancy, puerperium, infection, head injury, and malignancy. It can manifest as a number of neurological symptoms; however, headache is the most frequent symptom and has found to be present in almost 89% of the patients. The diagnosis of CVT requires a high level of clinical suspicion. Urgent neuroimaging is important to make the diagnosis. American Heart Association and the European Federation of Neurological Societies guidelines recommend MRI/MRV as the preferred imaging modality, whereas CT/CT venogram is an acceptable option when MRI is not available..Treatment is aimed at recanalizing the occluded veins/sinus and initiation of anticoagulation with unfractionated heparin or LMWT.

Conclusions: Early recognition is important as CVT can lead to elevated ICP, cerebral edema, and brain herniation. Headache being the most common and often only presenting symptom can make the diagnosis challenging. Headache could precede other symptoms by days or weeks as seen in our patients’ case. Our patient was a young female with history of antithrombin III deficiency which put her at high risk for CVT. With the help of this case we want to highlight the importance of keeping CVT in mind as a cause of persistent headache in a patient with associated risk factors