How should I diagnose and manage traumatic transverse sinus thrombosis in a patient with a recent head injury (e.g., basilar skull or temporal bone fracture) who develops new headache, vomiting, papilledema, focal neurologic deficits, seizures, or signs of raised intracranial pressure, and how can I differentiate it from non‑traumatic cerebral venous sinus thrombosis?

Traumatic Transverse Sinus Thrombosis: Diagnosis and Management

Diagnosis

In patients with head trauma and skull fractures involving the temporal or occipital bone, obtain CT venography (CTV) immediately to detect traumatic transverse/sigmoid sinus thrombosis, as this is the most sensitive acute imaging modality and skull fractures extending to venous sinuses carry a 41% risk of thrombosis. 1, 2

Clinical Presentation

• Headache is the most common symptom (90% of cases), typically diffuse and progressive over days to weeks 1, 3
• Focal neurological deficits including hemiparesis, aphasia, or other cortical signs may occur from venous ischemia 1, 3
• Papilledema and diplopia (sixth nerve palsy) from increased intracranial pressure are key diagnostic clues 1, 3, 4
• Seizures occur in 40% of patients, both focal and generalized 3
• Altered mental status, particularly with deep venous system involvement 3
• Unilateral hearing loss and tinnitus may be presenting symptoms, especially with sigmoid sinus involvement 5

Imaging Strategy

Primary imaging: CTV is the most useful acute study for suspected traumatic venous injury, particularly when skull fractures involve dural sinuses or jugular bulb/foramen 1. Look for:

• Abnormally decreased contrast opacification of the dural venous sinus
• "Empty delta" sign indicating acute thrombosis
• Exclude extrinsic compression from epidural hemorrhage 1

Secondary imaging: MRI with MR venography is more sensitive than CT overall but is slower and has more safety concerns in acute trauma 1, 3. Use MRV as second-line or for follow-up imaging 1

Concurrent head CT should be obtained to assess for:

• Hemorrhagic venous infarction (posterior temporal hemorrhagic areas ipsilateral to affected sinus) 2
• New or progressive structural brain changes 1
• Basilar skull fractures in temporal or occipital regions 2

Laboratory Evaluation

• D-dimer may be elevated but normal levels do not exclude CVST, especially with limited clot burden 3
• Obtain CBC, chemistry panel, PT, and aPTT 3
• Do not delay imaging based on D-dimer results if clinical suspicion is high 3

Management

Traumatic transverse/sigmoid sinus thrombosis follows a benign clinical course in most cases and does not require anticoagulation, unlike non-traumatic CVST. 6

Conservative Management (Preferred for Traumatic CVST)

• Observation without anticoagulation is appropriate for unilateral transverse/sigmoid sinus thrombosis in trauma patients 6
• The 2024 World Neurosurgery study found that 96.4% of traumatic CVST involved unilateral transverse or sigmoid sinus, with no attributable venous infarcts, thrombus propagation, or increased mortality compared to trauma patients without CVST 6
• Complete recanalization occurred in 28% of patients on follow-up imaging without anticoagulation 6

When to Consider Anticoagulation

Use anticoagulation selectively in traumatic CVST only when:

• Significant neurological deficits develop despite conservative management 2, 5
• Evidence of thrombus propagation on serial imaging 5
• Bilateral sinus involvement or deep venous system thrombosis 1

Anticoagulation protocol (when indicated):

• Start with intravenous heparin infusion 5, 7
• Bridge to warfarin to achieve therapeutic INR 5, 7
• Duration: typically 2 weeks IV heparin followed by oral anticoagulation 5

Surgical Management

Decompressive craniectomy is reserved for:

• Refractory intracranial hypertension despite medical management 8
• Massive venous infarction with significant mass effect 8
• Note: Outcomes with surgical intervention are variable; one case showed excellent outcome while another showed no improvement 8

Thrombectomy/thrombolysis has limited evidence in traumatic CVST and carries hemorrhagic risk in trauma patients 8

Distinguishing Traumatic from Non-Traumatic CVST

Key Differentiating Features

Traumatic CVST:

• Always associated with skull fracture extending to dural sinus or jugular bulb/foramen 1, 2
• Predominantly unilateral transverse/sigmoid sinus involvement (96.4%) 6
• Benign clinical course without anticoagulation 6
• No thrombus propagation or venous infarcts in most cases 6
• Occurs acutely following head injury 2, 5

Non-Traumatic CVST:

• Risk factors: oral contraceptives, pregnancy, thrombophilia, prothrombotic conditions, dehydration 1, 3
• More variable sinus involvement including superior sagittal sinus (most common), deep venous system 1
• Requires anticoagulation as first-line treatment 1
• Higher risk of thrombus propagation and venous infarction without treatment 1
• Isolated headache without focal findings occurs in 25% of cases 1

Clinical Pitfalls to Avoid

• Do not dismiss symptoms as simple post-traumatic headache when basilar skull fractures involve temporal or occipital bone—obtain CTV 2
• Do not assume posterior temporal hemorrhage is traumatic contusion; it may represent hemorrhagic venous infarction from sinus thrombosis 2
• Do not routinely anticoagulate traumatic CVST as you would non-traumatic CVST; management should be distinct 6
• Do not diagnose idiopathic intracranial hypertension without MR venography to exclude CVST when diplopia and papilledema are present 4
• Failure to detect traumatic sinus thrombosis may explain unexpected clinical deterioration and increased intracranial pressure 2