A 29-year-old woman sits forward on the stretcher, pressing both hands against a headache that began as a dull pressure three days ago and now pulses behind her eyes. She has vomited twice and says the room briefly went gray when she stood up. Her husband reports one brief episode of “staring and shaking” this morning; she is now awake but slow to answer. The CT images are loading, and the next decision has not yet been made.

— What’s your move? Read on.

Before you read
  • What imaging study confirms the diagnosis?
  • When should anticoagulation begin—even if intracranial blood is present?

When to Think of It

Think CVT with a new progressive or thunderclap headache, papilledema, seizure, unexplained intracranial hemorrhage, focal deficit that does not fit an arterial territory, encephalopathy, or headache plus a prothrombotic state: pregnancy/postpartum, estrogen exposure, malignancy, infection, inflammatory disease, dehydration, or inherited thrombophilia.

Sick or Not Sick

Sick versus not sick hinges on neurologic threat: altered mental status, recurrent seizures, declining consciousness, focal deficit, large venous infarct/hemorrhage, or signs of herniation. The key call is whether the patient needs immediate airway/seizure/ICP support and neurocritical-care involvement while confirmatory venous imaging is obtained.

The First Fifteen Minutes

  • ABCs, glucose, cardiac monitor, two IVs, focused neurologic examination, pregnancy test, CBC/platelets, CMP, PT/INR, aPTT, and type and screen.
  • If actively seizing or seizure lasts ≥5 minutes → lorazepam 0.1 mg/kg IV, usual adult maximum 4 mg per dose; may repeat once, because benzodiazepines rapidly terminate cortical electrical activity. If no IV access → midazolam 10 mg IM. Dose limits vary; verify institutional seizure protocol.
  • If ongoing seizure after benzodiazepine → levetiracetam 60 mg/kg IV, maximum 4,500 mg (common ED loading dose; check local protocol), because it suppresses recurrent neuronal firing with few interactions.
  • If markedly hypertensive with suspected intracranial hypertension → treat cautiously; nicardipine 5 mg/h IV infusion, increase by 2.5 mg/h every 5–15 minutes, maximum 15 mg/h, because controlled reduction limits further pressure injury without abruptly reducing cerebral perfusion. Avoid reflexive normalization.
  • If impending herniation or severe deterioration → 3% hypertonic saline 2–3 mL/kg IV bolus (institutional protocols vary) or mannitol 0.5–1 g/kg IV if hemodynamically and renally appropriate, because osmotic therapy lowers brain water. Check sodium, osmolality, renal function, and local neurocritical-care protocol.
  • Once CVT is confirmed—or strongly suspected after venous imaging—and there is no absolute contraindication → start therapeutic anticoagulation: enoxaparin 1 mg/kg SC every 12 hours or unfractionated heparin 80 units/kg IV bolus followed by 18 units/kg/h infusion, because anticoagulation prevents thrombus propagation and new venous infarction. Intracranial hemorrhage from CVT is not, by itself, a reason to withhold anticoagulation; coordinate with neurology/neurosurgery.

Definitive Care & Disposition

Obtain MRI brain with MR venography or CT venography; a normal noncontrast CT or D-dimer does not exclude CVT. Admit confirmed CVT to a monitored bed; ICU for coma, mass effect, recurrent seizures, hydrocephalus, or herniation risk. Continue heparin/LMWH, then transition to an oral anticoagulant when stable; typical treatment is at least 3–6 months, longer for persistent thrombophilia or recurrent thrombosis. Treat provoking infection, stop estrogen exposure, involve hematology for selected thrombophilia evaluation, and reserve catheter-directed thrombolysis or thrombectomy for deterioration despite anticoagulation in an experienced center.

How This One Kills

The dangerous error is dismissing a progressive headache as migraine after a normal noncontrast CT. Venous infarction and hemorrhage may develop while the patient is still conversational; waiting for papilledema, paralysis, or coma forfeits the window for anticoagulation and neurocritical-care intervention.
The Differential — What Else Looks Like This
  • Migraine — stereotyped prior episodes with normal neurologic examination and no progressive course; confusing it with CVT delays venous imaging.
  • Subarachnoid hemorrhage — abrupt maximal-at-onset headache with meningeal features; confusing it with CVT may lead to incomplete venous evaluation after a negative initial CT.
  • Idiopathic intracranial hypertension — papilledema and headache, but usually no focal deficit, seizure, or venous infarct; confusing the two misses anticoagulation.
  • Arterial ischemic stroke — deficit in a recognizable arterial territory; treating CVT as arterial stroke alone misses the need for anticoagulation and venous imaging.

The Second-Day Story

Older adults, postpartum patients, and partially treated patients may present only with fatigue, confusion, isolated nausea, or a slowly progressive headache. Anticoagulation, analgesics, or seizures can blur the examination, and papilledema may be absent early. The combination of a new persistent headache plus any seizure, visual symptom, focal sign, or prothrombotic exposure should lower the threshold for CT venography or MR venography.
Back to Our Patient
Back to the 29-year-old woman: her progressive headache, visual obscurations, seizure, and estrogen exposure trigger recognition of CVT, while her postictal slowing and seizure make her neurologically high risk. CT venography shows superior sagittal sinus thrombosis with a small hemorrhagic venous infarct; after seizure control and airway reassessment, therapeutic anticoagulation is started despite the hemorrhagic component because the blood resulted from venous congestion. She is admitted to the neuro-ICU for serial examinations, seizure monitoring, and intracranial-pressure surveillance, with later transition to outpatient anticoagulation.
Patient Presentation to Attending
How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling
“This is a 29-year-old woman with three days of progressive pressure-like headache, vomiting, transient visual dimming, and a witnessed brief seizure, now awake but postictal and slow to respond. She uses an estrogen-containing contraceptive and has no prior migraine history, fever, neck stiffness, trauma, or persistent focal deficit. She is protecting her airway, but has mild bilateral papilledema and a GCS of 14. Noncontrast CT shows a small parasagittal hemorrhagic lesion, and CT venography demonstrates superior sagittal sinus thrombosis. My assessment is high-risk cerebral venous thrombosis with venous infarction and seizure; I’ll continue neurologic and airway monitoring, treat recurrent seizure with benzodiazepine followed by levetiracetam, start therapeutic heparin after neurology discussion, and admit her to the neuro-ICU.”

Study Directive

  • Draw the venous drainage system and label the superior sagittal, transverse, sigmoid, straight, and cavernous sinuses from memory.
  • Practice a 60-second CVT risk-factor and red-flag history on three headache cases.
  • Compare CT venography, MR venography, and noncontrast CT in a short written algorithm.
  • Memorize therapeutic enoxaparin and UFH dosing, then verify them in your institutional anticoagulation protocol.
  • Review one neurocritical-care case involving CVT with hemorrhagic venous infarction and state why anticoagulation was still used.

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