Recommended Citation
Rehman A, Esbrook E, Burhani S, Bonaguro M, Mehta Patel S. Traumatic Sigmoid Sinus Thrombosis after Mastoid Fracture: Importance of Venous Imaging in High-Risk Skull Fractures. Presented at Scientific Day; May 20, 2026; Milwaukee, WI.
Abstract
Introduction/Background:
Traumatic cerebral venous sinus thrombosis (CVST) is an under-recognized complication of head trauma, particularly in skull fractures overlying dural venous sinuses. Among patients with skull fractures, venous sinus thrombosis is reported in up to 7% of cases and in 41–57% when fractures extend to a dural sinus or jugular bulb on dedicated imaging. We present a case of traumatic sigmoid sinus thrombosis associated with mastoid fracture involving the jugular bulb.
Description:
A previously healthy 15-year-old male presents after being thrown from the hood of a moving vehicle. He experienced a brief loss of consciousness followed by headache, dizziness, nausea, vomiting, amnesia, and right wrist pain. Examination reveals left hemotympanum and decreased hearing without additional focal neurologic deficits. Initial non-contrast CT head and cervical spine show no intracranial hemorrhage. CT temporal bone reveals a left mastoid fracture extending to the jugular bulb. Neurosurgery and otolaryngology are consulted. Given the fracture’s proximity to the sigmoid sinus and persistent headache and dizziness despite supportive management, dedicated venous imaging is obtained. MRI brain shows no hemorrhage or infarct. However, MR venography demonstrates a small nonocclusive thrombus extending from the distal left sigmoid sinus into the jugular bulb. Hematology is consulted, and anticoagulation is initiated following multidisciplinary clearance. The patient remains neurologically stable and transitions to outpatient therapy.
Discussion:
Diagnosis of CVST in the setting of skull fracture is challenging, as non-contrast head CT has limited sensitivity (approximately 30%) for detecting venous thrombosis, particularly in patients without additional focal neurologic deficits. In this case, initial CT head was negative, and the thrombus was identified only after targeted venous imaging prompted by the fracture’s proximity to the jugular bulb and persistent symptoms. This case highlights the need for high suspicion for venous injury in high-risk skull fractures despite reassuring initial imaging. Management is individualized given competing risks of anticoagulation and thrombus propagation, guided by multidisciplinary input. Future research is needed on the utility of detecting CVST in skull fracture, along with specific indications for dedicated venous imaging.
Presentation Notes
Presented at Scientific Day; May 20, 2026; Milwaukee, WI.
Full Text of Presentation
wf_yes
Document Type
Poster
Open Access
Available to all.
Traumatic Sigmoid Sinus Thrombosis after Mastoid Fracture: Importance of Venous Imaging in High-Risk Skull Fractures
Introduction/Background:
Traumatic cerebral venous sinus thrombosis (CVST) is an under-recognized complication of head trauma, particularly in skull fractures overlying dural venous sinuses. Among patients with skull fractures, venous sinus thrombosis is reported in up to 7% of cases and in 41–57% when fractures extend to a dural sinus or jugular bulb on dedicated imaging. We present a case of traumatic sigmoid sinus thrombosis associated with mastoid fracture involving the jugular bulb.
Description:
A previously healthy 15-year-old male presents after being thrown from the hood of a moving vehicle. He experienced a brief loss of consciousness followed by headache, dizziness, nausea, vomiting, amnesia, and right wrist pain. Examination reveals left hemotympanum and decreased hearing without additional focal neurologic deficits. Initial non-contrast CT head and cervical spine show no intracranial hemorrhage. CT temporal bone reveals a left mastoid fracture extending to the jugular bulb. Neurosurgery and otolaryngology are consulted. Given the fracture’s proximity to the sigmoid sinus and persistent headache and dizziness despite supportive management, dedicated venous imaging is obtained. MRI brain shows no hemorrhage or infarct. However, MR venography demonstrates a small nonocclusive thrombus extending from the distal left sigmoid sinus into the jugular bulb. Hematology is consulted, and anticoagulation is initiated following multidisciplinary clearance. The patient remains neurologically stable and transitions to outpatient therapy.
Discussion:
Diagnosis of CVST in the setting of skull fracture is challenging, as non-contrast head CT has limited sensitivity (approximately 30%) for detecting venous thrombosis, particularly in patients without additional focal neurologic deficits. In this case, initial CT head was negative, and the thrombus was identified only after targeted venous imaging prompted by the fracture’s proximity to the jugular bulb and persistent symptoms. This case highlights the need for high suspicion for venous injury in high-risk skull fractures despite reassuring initial imaging. Management is individualized given competing risks of anticoagulation and thrombus propagation, guided by multidisciplinary input. Future research is needed on the utility of detecting CVST in skull fracture, along with specific indications for dedicated venous imaging.
Affiliations
Advocate Christ Medical Center