Not the site you
are looking for?
Traumatic Dural Venous Sinus Thrombosis-Still an Enigma?
Deepak Agrawal, A K Mahapatra
Department of Neurosurgery, Neurosciences center, All India Institute of Medical Sciences, New Delhi-110029,
Review Article
INTRODUCTION
Intracranial dural venous sinus thrombosis remains a poorly understood condition with unpredictable course and outcome. The first description of dural sinus thrombosis was made by Ribes, who in 1825 reported on a 45-year old man with malignancy, headache, seizures and delirium. Postmortem examination revealed superior sagittal sinus, transverse sinus, straight sinus, and cortical vein thrombosis. Overall, since 1942, fewer than 250 cases of intracranial venous sinus thrombosis have been reported.
EPIDEMIOLOGY
The incidence of dural venous sinus thrombosis has been reported to be up to 4% with penetrating trauma and to be extremely rare with closed head injuries.1 The mortality ranges from 5.5%-50%.2 Even amongst the survivors, 15%-25% demonstrate lasting abnormalities.
PATHOPHYSIOLOGY
Dural venous sinus thrombosis has been described in association with trauma in a number of entities, including penetrating and closed head injuries, cranial fractures, disseminated intravascular coagulopathy, and after neurosurgical and non-neurosurgical operations. With penetrating trauma, thrombosis occurs due to trauma to the sinus or compression of the sinus from adjacent structures. Extension of the thrombosis from the scalp injuries or injured emissary veins has also been described. Although dural venous sinus thrombosis has been described in association with both mild and severe head injuries,1 the mechanism of dural venous sinus thrombosis with closed head injury remains unknown till date.
CLINICAL FEATURES
Signs and symptoms of dural venous sinus thrombosis are numerous, with a variable time course. Thrombosis of the nondominant sinus may remain asymptomatic. Symptoms include headache, stroke, visual loss, seizures and pulmonary embolus.2 Headache is found in approximately 75% of cases and is thought to result from elevated intracranial pressure.3 Protracted vomiting, increases intracranial pressure, hydrocephalus and papilloedema are particularly described with thrombosis of the sigmoid and transverse sinuses.4
INVESTIGATIONS
CT, MRI and angiography are all used to assist in the diagnosis of dural sinus and cerebral vein thrombosis. CT images of the brain may be normal in 10%-20% of the patients with venous thrombosis. Findings may include hemorrhagic or nonhemorrhagic venous infarcts, cerebral edema, small ventricles, hydrocephalus, contrast enhancement of the tentorium and falx, thrombosed cortical veins (cord sign), a dense triangle sign representing fresh thrombus in the posterior SSS or sigmoid sinus (fig 1), and an empty delta sign on contrast studies that represents enhancement of collateral veins in the SSS wall surrounding a nonenhancing thrombus. The ‘empty delta sign’ may be confused with the ‘pseudodelta’ sign, the latter seen on unenhanced CT scans and caused by parafalcine interhemispheric hemorrhage or posterior parafalcine subarachnoid hemorrhage after head injury. Angiographic findings include partial or complete nonopacification of venous sinuses and veins (Fig 2), dilated cortical collateral veins and corkscrew appearance, increased cerebral circulation time, and reversal of flow away from the obstructed sinus or vein.2 MRI and MR angiography (Fig 3) present noninvasive means of assessing the presence of thrombosed sinuses and veins and are currently considered investigations of choice in cases of suspected dural venous sinus thrombosis.2
MANAGEMENT
Treatment of dural venous sinus thrombosis in the setting of closed head injury remains difficult. Treatment options include cerebral dehydrating agents, steroids, acetozolamide, cerebrospinal fluid, drainage, barbiturates, decompressive craniectomy, sinus thrombectomy, heparin /warfarin, urokinase and tissue plasminogen activator. Since the thrombosis leads to the formation of hemorrhagic infarctions, there has been much concern over the use of anticoagulation in the treatment of superior sagittal sinus thrombosis.3 Einhaupal performed the only randomised, blinded study of adjusted dose heparin in patients with venous sinus thrombosis and concluded that treatment with heparin was not only safe, but also beneficial, even in the setting of intracerebral hemorrhage.5 Typically anticoagulation is reserved for those with early, partial or propagating thrombosis without evidence of hemorrhagic venous infarction. In patients with progressive neurological decline, treatment must be instituted to prevent progression of the thrombus, and in severe cases, treatment is directed at restoring flow through the sinuses. More aggressive treatment, including endovascular thrombolysis or surgical thrombectomy, is reserved for those patients with serious neurological sequelae. Thrombolysis has been performed either percutaneously (via the femoral vein) or by a small craniotomy over the SSS and directly injecting thrombolytic drugs such as urokinase into the sinus. In general, a conservative treatment regime that may be used includes an initial administration of 100,000 units urokinase during 30-45 minutes and than an infusion in the range of 40,000 to 60,000 units per hour is preferred. This regime must be adjusted based on the patients’ neurological condition and response to treatment. Following thrombolysis patients are usually kept anticoagulated for at least six months.5
CONCLUSIONS
While neurological changes following head trauma may result from concussion or more life threatening injuries such as subdural or epidural hematomas, intracerebral hemorrhage, arterial dissection, and diffuse axonal injury, venous sinus thrombosis should be considered when other etiologies are eliminated. Only prompt identification and treatment can help in avoiding secondary complications that can at times be life threatening.
REFERENCES
1. Kuether TA, O'Neill O, Nesbit GM, Barnwell SL. Endovascular treatment of traumatic dural sinus thrombosis: case report. Neurosurgery 1998;42:1163-1167.
2. D'Alise MD, Fitchel F, Horowitz M. Sagittal sinus thrombosis following minor head injury treated with continuous urokinase infusion. Surg Neurol 1998;49:430-435.
3. Ferrera PC, Pauze DR, Chan L. Sagittal sinus thrombosis after closed head injury. Am J Emerg Med 1998;16:382-385.
4. Brors D, Schafers M, Schick B, Dazert S, Draf W, Kahle G. Sigmoid and tranverse sinus thrombosis after closed head injury presenting with unilateral hearing loss. Neuroradiology 2001;43:144-146.
5. Einhaupl KM, Villringer A, Meister W. Heparin treatment in venous sinus thrombosis. Lancet 1991;338:597-600.
LEGEND
Fig 1:
Fig 2: Angiogram showing superior sagittal sinus thrombosis
Fig 3: T2-weighted MRI, axial section of the same patient showing the thrombosis as an abnormal hypointense signal within the left sigmoid sinus (white arrow), consistent with the presence of deoxyhemoglobin.