Key Takeaways
Cerebral venous thrombosis (CVT) is a rare but life-threatening cause of cerebrovascular accident. This case report highlights the challenges of managing CVT associated with oral contraceptive pills (OCPs) and emphasises the importance of early detection, prompt anticoagulation, and long-term follow-up to optimise patient outcomes. This finding underscores the need for careful risk stratification before prescribing OCPs, particularly in women with thrombotic risk factors.
The Patient and Her History
A previously healthy 32-year-old woman presented to the emergency department in Jeddah, Saudi Arabia, with a 4-day history of persistent headache that had progressively worsened in intensity and was unresponsive to over-the-counter analgesics. The headache was holocranial, with a pressure-like quality, and associated with nausea, intermittent vomiting, and transient episodes of blurred vision. She denied photophobia, phonophobia, or recent febrile illness. A day before admission, she experienced new-onset right-sided weakness and paraesthesia, accompanied by mild dysarthria. There was no history of seizures, head trauma, recent surgery, prolonged immobilisation, or known hypercoagulable disorders. She had no personal or family history of thromboembolic events. Her medical history was unremarkable, except for the use of combined OCPs for the past 2 years for menstrual regulation. She was a non-smoker, had no history of illicit drug use, and denied recent long-haul travels.
Findings and Diagnosis
- Upon examination, her vital signs were within normal limits: Glasgow Coma Scale score of 15 with a blood pressure of 118/76 mm Hg, heart rate of 82 beats/min, respiratory rate of 16 breaths/min, and oxygen saturation of 98% on room air.
- Neurologic assessment revealed mild right-sided hemiparesis (Medical Research Council grade, 4/5), hypoesthesia over the right upper and lower extremities, and mild dysarthria. Cranial nerves were intact, deep tendon reflexes were slightly brisk on the right side, and the plantar response was equivocal bilaterally. Fundoscopic examination showed mild bilateral papilledema.
- Cardiovascular, respiratory, and abdominal examinations were normal.
- Laboratory tests, including complete blood count, renal and liver function tests, coagulation profile, and inflammatory markers, were within normal limits, except for mildly elevated D-dimers at 780 ng/mL (reference range: < 500 ng/mL).
- A thrombophilia workup, including protein C and S levels, antithrombin III, lupus anticoagulant, anticardiolipin antibodies, and factor V Leiden mutation, was sent for evaluation.
- Non-contrast CT of the brain revealed subtle hyperdensity along the superior sagittal sinus, suggestive of a possible thrombus. To further characterise the findings, CT venography was performed, confirming extensive thrombosis of the superior sagittal sinus and right transverse sinus with associated mild venous congestion.
- MRI of the brain with MR venography showed restricted diffusion in the left frontoparietal region, indicating a venous infarct secondary to CVT. No evidence of haemorrhagic transformation was noted.
Therapeutic Interventions
The diagnosis of CVT associated with OCP use was confirmed on the basis of radiologic findings and elevated D-dimer levels. Immediate anticoagulation was initiated with low-molecular-weight heparin, which was later transitioned to an oral vitamin K antagonist (warfarin) with International Normalised Ratio (INR) monitoring. Supportive management included hydration, analgesia for headache control, and acetazolamide to treat increased intracranial pressure due to papilledema.
During hospitalisation, her neurologic symptoms and papilledema gradually improved. The patient was discharged on warfarin with a target INR of 2-3 and discontinue OCPs permanently. She was counselled on alternative non-hormonal contraceptive options and lifestyle modifications and the potential risks of future thrombotic events, especially in the context of hormonal therapy thrombotic risks. A follow-up MRI performed 3 months later showed partial recanalisation of the superior sagittal and right transverse sinuses. Six months later, she remained asymptomatic with complete neurologic recovery, allowing the discontinuation of warfarin under haematologic guidance.
Discussion and Implication
CVT is a rare but potentially life-threatening cause of stroke, accounting for approximately 0.5%-1% of all strokes. Impaired venous drainage leads to increased intracranial pressure and, in severe cases, venous infarction or haemorrhage. CVT predominantly affects young adults, particularly women, due to hormonal factors.
Risk factors include pregnancy and the postpartum period, immobilisation during surgery or long-haul flights, dehydration, thrombophilias, malignancies, haematologic and immunologic disorders, infections, and exogenous hormone use, such as oral contraceptives, which are associated with a fourfold to 13-fold increased risk.
In particular, oestrogen-containing oral contraceptives contribute to a hypercoagulable state through multiple mechanisms, including increased levels of coagulation factors (fibrinogen, factor VII, factor VIII, and factor X), reduced levels of anticoagulant proteins (protein S and antithrombin III), and impaired fibrinolysis.
Despite this known risk, CVT remains under-recognised, often leading to delayed diagnosis and treatment. The clinical presentation is highly variable, ranging from isolated headaches to focal neurologic deficits, seizures, or coma.
In this case, the presence of neurologic deficits prompted further neuroimaging, leading to the timely identification of the underlying pathology of the tumour.
MR venography remains the gold standard for visualising cerebral venous structures and evaluating sinus patency. Non-contrast CT of the brain, although often the first imaging modality performed in suspected stroke cases, has a low sensitivity for CVT, detecting direct signs (hyperdense cortical veins or sinus thrombosis) in only a subset of patients.
Despite historical concerns about anticoagulation in the setting of haemorrhagic infarcts, current guidelines support its use because the primary pathology in CVT is thrombotic occlusion rather than haemorrhage. Emerging data suggest that direct oral anticoagulants may be a viable alternative to warfarin, offering a more convenient and potentially safer profile, although further randomised trials are needed to establish their role in CVT management.
An important aspect of CVT care is long-term follow-up, including the assessment of recanalisation and consideration of anticoagulation duration. Current guidelines recommend anticoagulation for at least 3-6 months in provoked CVT, with longer durations considered in cases with persistent risk factors or recurrent thrombosis.
This article was translated from Univadis Germany using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.