Anticoagulation in Traumatic Cerebral Venous Sinus Thrombosis with Concomitant Intracranial Haemorrhage: A Case Report
Ashmi Thomas *
*Correspondence to: Ashmi Thomas.
© 2026 Ashmi Thomas. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received: 17 September 2026
Published: 01 October 2026
DOI: https://doi.org/10.5281/zenodo.23079633
Abstract
Traumatic cerebral venous sinus thrombosis (tCVST) is an uncommon complication of head injury, and management is particularly challenging when traumatic intracranial haemorrhage is also present. We report a 38-year-old man presenting after an assault with headache, dizziness, vomiting and post-traumatic amnesia. CT demonstrated a right occipital-petrous temporal skull fracture with a small traumatic extra-axial haemorrhage. CT cerebral venography subsequently demonstrated right sigmoid sinus thrombosis extending into the terminal internal jugular vein. Following multidisciplinary discussion, anticoagulation was cautiously initiated with low-molecular-weight heparin, with interval imaging planned before transition to longer-term oral anticoagulation.
Case Presentation: A 38-year-old man presented following an assault with headache, dizziness, vomiting, neck pain and incomplete recollection of the event. He was haemodynamically stable, GCS 15/15, and had no focal neurological deficit. Examination demonstrated right haemotympanum. Non-contrast CT showed a longitudinal fracture involving the right occipital and petrous temporal bones, extending towards the jugular foramen, with an associated small posterior fossa extra-axial haemorrhage. CT cerebral venography demonstrated absent opacification of the right sigmoid sinus and terminal internal jugular vein, consistent with traumatic venous thrombosis.
Management: Neurosurgical review recommended conservative management and neurological observation. Because anticoagulation could prevent thrombus propagation but potentially worsen the traumatic haemorrhage, the case was discussed with neurosurgery, haematology and neurology. Anticoagulation was initiated cautiously with tinzaparin. Therapeutic low-molecular-weight heparin was planned for approximately 14 days, followed by repeat CT head imaging to confirm haemorrhagic stability before consideration of a direct oral anticoagulant. Approximately three months of anticoagulation was advised. The patient remained neurologically stable.
Discussion and Conclusion: Traumatic CVST should be considered when a skull fracture crosses or lies adjacent to a dural venous sinus. Symptoms can overlap with uncomplicated head injury, making fracture anatomy and dedicated venous imaging important. When tCVST coexists with intracranial haemorrhage, anticoagulation requires an individualised assessment of the competing risks of thrombus progression and haemorrhagic expansion. Multidisciplinary decision-making, cautious anticoagulation and interval neuroimaging can provide a pragmatic management strategy.
Keywords: traumatic cerebral venous sinus thrombosis; intracranial haemorrhage; anticoagulation; sigmoid sinus thrombosis; skull fracture; traumatic brain injury.
Introduction
Cerebral venous sinus thrombosis is considerably less common than arterial cerebrovascular disease and may occur secondary to several acquired and inherited risk factors. Head trauma represents an important mechanical cause, particularly when skull fractures extend across dural venous sinuses.
Traumatic cerebral venous sinus thrombosis (tCVST) may result from direct endothelial injury, compression of the sinus, altered venous flow or local activation of the coagulation cascade. Fractures involving the occipital and temporal bones are particularly relevant because of their anatomical relationship with the transverse and sigmoid sinuses and jugular bulb.
Diagnosis may be difficult because symptoms such as headache, nausea, vomiting and dizziness overlap considerably with uncomplicated concussion and traumatic brain injury. Furthermore, anticoagulation—the conventional treatment for CVST—poses a therapeutic dilemma when traumatic intracranial haemorrhage is simultaneously present.
We describe a patient with an occipital–temporal skull fracture complicated by right sigmoid sinus and terminal internal jugular vein thrombosis, in whom anticoagulation required careful multidisciplinary assessment because of a concurrent small traumatic extra-axial haemorrhage.
Case Presentation
A 38-year-old man presented to the emergency department following an assault around midnight. He reported that he had consumed alcohol and was unable to fully recall the circumstances surrounding the incident or whether weapons had been used.
Following the injury, he experienced headache, dizziness particularly on standing, neck discomfort and multiple episodes of vomiting. There was no reported chest pain, abdominal pain or respiratory difficulty.
His relevant past medical history included asthma. He was not taking regular anticoagulant or antiplatelet therapy.
On initial assessment, the patient was alert and orientated with a Glasgow Coma Scale score of 15/15. His observations were stable, including a blood pressure of approximately 117/75 mmHg, heart rate of 92 beats/min, respiratory rate of 18 breaths/min and oxygen saturation of 96% on room air.
Neurological examination demonstrated no focal neurological deficit. Cranial nerves were grossly intact, upper- and lower-limb power was 5/5 bilaterally, sensation was preserved and tone was normal.
Examination demonstrated cervical spinal tenderness and pain on movement of the head. Facial examination demonstrated left infraorbital bruising and an abrasion of the upper lip. Otoscopic examination subsequently demonstrated blood within the right external auditory canal with evidence of haemotympanum.
Investigations
Initial non-contrast CT imaging of the head demonstrated a longitudinal fracture through the right occipital bone extending into the right petrous temporal bone.
The fracture was associated with right-sided haemotympanum and air/fluid within the mastoid air cells. Surgical emphysema was present within the right upper neck.
A small linear hyperdensity was identified posterior to the right cerebellar hemisphere adjacent to the occipital fracture. This was initially considered to represent a small traumatic extra-axial haemorrhage, although acute venous thrombosis was included in the differential diagnosis.
Importantly, the fracture extended towards the right jugular foramen, creating concern regarding injury to the adjacent venous structures.
Given the anatomical relationship of the fracture to the venous sinus and the indeterminate hyperdensity on the initial CT, CT cerebral venography was performed.
This demonstrated absent contrast opacification of the right sigmoid sinus and terminal right internal jugular vein, confirming thrombosis. The remaining major intracranial venous sinuses demonstrated satisfactory contrast opacification.
The final radiological diagnosis was therefore traumatic right sigmoid sinus thrombosis extending into the terminal internal jugular vein associated with an occipital–temporal skull fracture.
Management
The case was discussed with the regional neurosurgical service. Given the patient’s preserved neurological status and absence of significant mass effect or neurological deterioration, no acute neurosurgical intervention was considered necessary.
He was admitted locally for neurological observations.
Because the venous thrombosis occurred in association with a traumatic skull fracture and a small concurrent intracranial haemorrhage, initiation of therapeutic anticoagulation required careful consideration of the competing risks of thrombus propagation versus haemorrhagic expansion.
Advice was sought from haematology and neurology in addition to neurosurgery.
Following multidisciplinary discussion, anticoagulation was recommended. The patient initially received prophylactic-dose tinzaparin, followed by a planned escalation to therapeutic low-molecular-weight heparin using a split-dose regimen.
The proposed strategy consisted of therapeutic tinzaparin for approximately 14 days, followed by repeat CT head imaging to assess stability of the traumatic intracranial haemorrhage. Provided that imaging demonstrated no significant haemorrhagic progression, conversion to a direct oral anticoagulant was planned.
A total anticoagulation duration of approximately three months was recommended, with specialist follow-up.
The patient underwent continued neurological observation. During subsequent review he remained alert with GCS 15/15 and no focal neurological deficit. He continued to experience headache and intermittent dizziness, prompting further clinical assessment and interval imaging because anticoagulation had been initiated.
ENT follow-up was also arranged because of persistent reduction in hearing associated with the traumatic haemotympanum.
Discussion
This case illustrates three important aspects of traumatic CVST.
First, the anatomical course of a skull fracture can provide an important clue to an underlying venous sinus injury. In this patient, the fracture involved the occipital and petrous temporal bones and extended towards the jugular foramen. This placed the sigmoid sinus and jugular venous outflow directly adjacent to the traumatic injury.
Second, traumatic CVST may be clinically difficult to distinguish from uncomplicated traumatic brain injury. Headache, vomiting and dizziness are common following head trauma and do not independently establish venous thrombosis. In this case, the relationship of the fracture to the venous structures and the abnormality identified on the initial CT prompted dedicated venous imaging, which established the diagnosis.
Third, treatment becomes particularly challenging when CVST occurs alongside traumatic intracranial haemorrhage. Anticoagulation can reduce thrombus propagation and facilitate recanalisation but theoretically risks expansion of traumatic haemorrhage. Consequently, treatment requires individualised assessment incorporating neurological status, stability and size of the intracranial haemorrhage, location and extent of thrombosis and interval radiological findings.
In this patient, multidisciplinary discussion resulted in a staged anticoagulation strategy, beginning cautiously with low-molecular-weight heparin and incorporating repeat neuroimaging before conversion to longer-term oral anticoagulation.
The case therefore emphasises that traumatic CVST should be actively considered when fractures cross or closely approach a dural venous sinus, particularly the transverse or sigmoid sinus. Early CT or MR venography in appropriately selected patients may prevent delayed diagnosis.
Conclusion
Traumatic cerebral venous sinus thrombosis is an important complication of skull fractures involving structures adjacent to the dural venous sinuses. A fracture extending through the occipital and petrous temporal bones towards the jugular foramen should raise suspicion for sigmoid sinus or jugular venous injury.
This case demonstrates the value of dedicated venous imaging after suspicious findings on initial trauma CT and highlights the therapeutic challenge posed by simultaneous venous thrombosis and traumatic intracranial haemorrhage. Early multidisciplinary involvement and carefully monitored anticoagulation with interval neuroimaging can facilitate an individualised management strategy.
Learning points