JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
thromboembolic events, and improve outcome. 23 Studies have shown that unfractionated heparin or low molecular weight heparin (LMWH) may be safely used in patients without contraindications. 24-26 In the acute phase, current guidelines recommend anticoagulation with adjusted dose unfractionated heparin or weight-based LMWH at full anti- coagulation doses. 21 Continuation of anticoagulation after the acute phase may be necessary to prevent future thrombotic events including recurrent CVT and systemic VTE, which occur in 2% and 5.8% of patients respectively. 27 Based on evidence and recommendations for systemic deep venous thrombosis, oral anticoagulation in provoked CVT should be continued for 3-6 months and 6-12 months in unprovoked CVT with a target INR between 2 and 3. Indefinite anticoagulation should be considered in patients with recurrent CVT and in patients with CVT and severe thrombophilia. 21 In cases with contraindications to anticoagulants, antiplatelet drugs may be considered though there are no data on their efficacy or safety in CVT. Thrombolytic therapy is a treatment option in CVT cases with neurologic deterioration despite anticoagulation treatment. 28 Local thrombolysis employs urokinase or recombinant tissue plasminogen activator directly administered into the site of occlusion with or without mechanical disruption of the thrombus. 29-30 High success rate of rapid recanalization and significant improvement in morbidity and mortality have been noted in clinically severe CVT cases in which local thrombolysis was performed. 28,w30 Additional studies are still needed in order to determine the definitive role of thrombolytics in the management of CVT and the patient population that would ultimately benefit from the therapy. In addition to treatment of CVT, therapy frequently involves management of early complications. Early complications resulting fromCVT include seizures, hydrocephalus, and isolated intracranial hypertension. Antiepileptic drugs (AED’s) may be considered in patients with CVT who have a supratentorial lesion and who present with seizure. 12 Initiation of AED’s may also be reasonable for all patients who present with seizure, as they have a higher risk of recurrent early seizures. Hydrocephalus can be communicating, secondary to decreased CSF outflow, or non- communicating, from hemorrhage into the ventricular system. Neurosurgical consultation is recommended and treatment options include invasive procedures such as ventriculostomy or ventriculoperitoneal shunt. Management of isolated intracranial hypertension includes serial lumbar puncture and acetazolamide. Ophthalmologic consultation is recommended to assist with monitoring of visual fields and papilledema, as prolonged pressure on the optic discs may result in permanent blindness. 21
(Figure 2) was present and visual acuity was normal. Conclusion
CVT remains a clinical diagnosis though advances in neuroimaging have greatly improved its recognition and detection. Acutely, head CT may rule out acute and subacute cerebral causes that share similar presentations. Definitive diagnosis of CVT can be made using MRI in conjunction with MR venography. CT with CT venography is a comparable diagnostic option. If MR and CT venography proves equivocal, cerebral angiography may be considered. Treatment should be promptly initiated once CVT is diagnosed. Anticoagulation is should be recommended inpatientswithout specific contraindications and likely improves clinical outcome. Similar to recommendations for other thrombotic events, continued anticoagulation after the acute phase should be considered to prevent recurrence.
FIGURE 2: Treatment with Anti-coagulation. Improvement in peri-orbital swelling 48 hours after initiation of anticoaulation (top). Exam demonstrates residual CN VI palsy (bottom).
REFERENCES
1. Ferro JM, Canhao P, Stam J, et al. Prognosis of cerebral vein and dural sinus thrombosis: results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT). Stroke 2004; 35:664 2. De Bruijn SF, Stam J, Koopman MM, Vandenbroucke JP. Case-control study of risk of cerebral sinus thrombosis in oral contraceptive users and in carriers of hereditary prothrombotic conditions. The Cerebral Venous Sinus Thrombosis Study Group. BMJ 1998; 316:589. 3. Hillier CE, Collins PW, Bowen DJ, et al. Inherited prothrombotic risk factors and cerebral venous thrombosis. QJM 1998; 91:677. 4. Levi M, Keller T, et al. Infection and inflammation and the coagulation system. Cardiovascular Research 2003; 60: 26-39. 5. Nagai M, Yilmaz CE, Kirchhofer D, et al. Role of coagulation factors in cerebral venous sinus and cerebral microvascular thrombosis. Neurosurgery 2010; 66(3):560-5. 6. Nekludov M, Antovic J, et al. Coagulation abnormalities associated with severe isolated traumatic brain injury: cerebral arterio-venous differences in coagulation and inflammatory markers. J Neurotrauma 2007; 24:174-180. 7. Rother J, Waggie K, van Bruggen N, et al. Experimental cerebral venous thrombosis: evaluation using magnetic resonance imaging. J Cerb Blood FlowMetab 1996;16(6):1353-61. 8. Forbes KP, Pipe JG, Heiserman JE. Evidence for cytotoxic edema in the pathogenesis of cerebral venous infarction. AJNR Am J Neuroradio 2001; 22(3):450-5. 9. Srivastava AK, Kalita J, Haris M, Gupta RK, Misra UK. Radiological and
Follow up
Our patient was started on appropriate antibiotics upon admission. After imaging studies demonstrated cerebral venosinus thrombosis, anticoagulation with un-fractionated heparin was initiated. The patient’s symptoms improved rapidly after initiation of anti-coagulation, including resolution of chemosis (Figure 2). The patient was transitioned to warfarin prior to discharge. Mild impairment of right eye abduction
J La State Med Soc VOL 169 MARCH/APRIL 2017 35
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