Sudden Headache and Vomiting in a 33-Year-Old Woman

Roshen Mathew, MBBS; Mathew Abraham, MD, DM


September 12, 2016

The mainstay of treatment for CVT, even in patients with CT evidence of cerebral ischemia or hemorrhage, is anticoagulation. In two retrospective studies of patients with CVT and moderate-sized hematomas, anticoagulation was not associated with increased hemorrhage volume, neurologic deterioration, or a worse outcome. Heparin should be started initially, with a goal of maintaining an activated partial thromboplastin time that is twice the control value. Heparin therapy is gradually transitioned to warfarin, which is then continued for 4-6 months (longer in patients with an identified predisposition to clotting).

Endovascular thrombolytic therapy with urokinase or tissue plasminogen activator may be effective in patients who deteriorate despite adequate anticoagulation with heparin, but this therapy is limited to specialized centers. Surgical intervention, in the form of thrombectomy using a microsnare or rheolytic thrombectomy catheter with local thrombolytic therapy, has been used with variable success in the setting of severe neurologic deterioration.

Adjunctive therapy for seizures, cerebral edema, or co-occurring infections may also be required on a case-by-case basis. Headaches related to increased intracranial pressure may respond to elevation of the head of the bed or to acetazolamide, which decreases CSF production (thereby lowering intracranial pressure). When complicated by visual deterioration unresponsive to these measures, lumboperitoneal shunting or optic nerve sheath fenestration should be considered.[1,2,6]

Complications of CVT may include coma (resulting from status epilepticus, critically elevated intracranial pressure, or impending cerebral herniation) and pulmonary embolism. In patients who are comatose as a result of increased intracranial pressure, prompt intervention is critical. Initial measures include maintaining the patient's head at 30°-40° elevation, keeping the neck in a neutral position to avoid kinking of the jugular veins, and using mannitol or hyperventilation. Additional therapy, such as ventriculostomy and blood pressure titration with vasoactive agents, should be guided by direct monitoring of intracranial pressure.

Pulmonary embolisms occur in up to 11% of cases and may originate from the thrombosed jugular veins or from other sites (such as the legs). This complication carries a high mortality rate.

The prognosis is good for patients with CVT that is recognized early. Full recovery is expected in about 70% of cases. Of the remaining 30% of patients, about one third die and two thirds are left with persistent mild to moderate neurologic deficits. Coma, seizures, or underlying disease have no significant effect on the short-term outcome and should not preclude any type of therapeutic intervention. The long-term recurrence rate of CVT is approximately 20%.

Oral contraceptives are a recognized risk factor for CVT; this is supported by the increasing rate of CVT in women of childbearing age since the introduction of oral contraceptives, with stable rates seen in men of similar age.[2]

In the case presented above, the patient was treated with analgesics and low-molecular-weight heparin, followed by warfarin. She discontinued use of her oral contraceptive pills. The patient recovered completely, with no residual deficits, and she continues to do well on long-term follow-up.


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