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|Year : 2015 | Volume
| Issue : 6 | Page : 832-833
Dural venous sinus thrombosis after head injury
Harjinder S Bhatoe
Director Neurosciences, Max Super Specialty Hospital, New Delhi, India
|Date of Web Publication||20-Nov-2015|
Harjinder S Bhatoe
Director Neurosciences, Max Super Specialty Hospital, New Delhi
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Bhatoe HS. Dural venous sinus thrombosis after head injury. Neurol India 2015;63:832-3
Dural venous sinus thrombosis (DVST) usually follows hypercoagulable states such as pregnancy, puerperium, and use of oral contraceptives. It also occurs following intracranial infections, severe dehydration, and coagulopathies. Li et al., have conducted a commendable study in reporting 40 such patients. Thus far, DVST has been a rarely reported sequel to traumatic brain injury (TBI), reportedly having a mortality between 4% and 30%. The available literature comprises only a few case reports and small series. In a specific group of patients with blunt injury to the head and with skull fracture extending to the jugular bulb, the incidence was reported to be 19.5%. Penetrating craniocerebral injuries, depressed or compound skull fractures, or tangential, nonpenetrating injuries to the vertex may directly damage the superior sagittal sinus or its bridging veins and produce an interhemispheric subdural hematoma. The vein linking the vein of Labbe to the lateral sinus and the veins draining the temporal lobes into the petrosal sinuses are also susceptible to injury.
The pathogenesis of sinovenous occlusion following head injury is uncertain, and a parallel with Virchow's triad probably holds true in this situation. Superior sagittal sinus thrombosis following closed head injury may be attributable to endothelial damage and intramural hemorrhage at the site of the entry of draining veins. Injury to the endothelium of venous sinuses, rupture of sinusoids, extension of thrombosis from injured emissary veins, and compression of the sinus due to any cause may result in DVST. Post-head injury coagulopathy probably plays an important role in the pathogenesis of DVST, especially if one considers the release of procoagulants such as thromboplastin following TBI. Hemorrhage into the Pacchionian granules may be an initiating event. Pre-existing coagulopathy may be a factor in predisposing patients with TBI to DVST.
The clinical profile is generally nonspecific, with features of raised intracranial pressure, seizures, and worsening of sensorium. A syndrome of gait ataxia, headache, and vomiting following blunt occipital head trauma may be associated with thrombosis of the sigmoid sinus. Also, it is important to identify and screen patients at risk of developing DVST following TBI. A known history of coagulopathy, consumption of oral contraceptives in women, fracture crossing the anatomical course of the sinuses, craniocerebral missile injury, and onset of coagulopathy following TBI are the risk factors for DVST.
The diagnosis of DVST requires a high index of suspicion in a patient with TBI who develops altered sensorium, seizures, and raised intracranial pressure, often without overt imaging evidence of an intracranial hematoma. Generally, the involvement is that of the lateral sinus, the sigmoid sinus, or the superior sagittal sinus. Although thrombotic occlusion of deep veins following TBI is extremely rare, occlusion of the vein of Galen has been described after head injury. Diagnosis of traumatic DVST requires a specific protocol-based imaging to observe the venous sinuses. This includes computed tomography (CT) and magnetic resonance imaging (MRI) within 24 hours of onset of symptoms, including diffusion-weighted imaging (DWI), magnetic resonance venography (MRV), as well as the conventional sequences. Contrast CT may show a classic inverted delta sign in case of superior sagittal sinus thrombosis. MRI is diagnostic, and the appearances on the scan depend on the changes in hemoglobin. In the acute phase, the thrombosed sinus appears isointense on T1-weighted images and hyperintense on T2-weighted images [Figure 1]a, [Figure 1]b, and [Figure 2]. Follow-up MRV is important to document recanalization of the occluded sinus. There may be associated subdural hematoma of the falx or the tentorium.
|Figure 1: (a) MRV showing thrombotic occlusion of the superior sagittal sinus and the straight sinus. (b) MRI (mid-sagittal, T1-weighted) showing thrombotic occlusion of the superior sagittal sinus, the straight sinus, and the vein of Galen|
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|Figure 2: MRI (axial, T1-weighted) showing thrombotic occlusion of the lateral sinus on the right side|
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Should these patients with TBI and DVST be treated with anticoagulation? Continuous urokinase infusion has been tried earlier. Anticoagulation can be a double-edged sword, wherein the benefits in the form of recanalization are aptly matched by a higher incidence of intracerebral hemorrhage. Although low-molecular-weight heparin has been used, it has been observed that most of these patients have recanalization of the thrombosed sinus without anticoagulation therapy.
DVST needs a high index for suspicion for prompt diagnosis, and Li et al., and Almandoz et al., have suggested a workable protocol in suitable patients for a high positive yield. Management essentially involves measures to reduce intracranial pressure, sinus thrombectomy, and surgical decompression whenever indicated.
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[Figure 1], [Figure 2]
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