49 Acute Management of Cerebral Venous Thrombosis

José M Ferro ¹, Patrícia Canhão ¹

¹ Department of Neurosciences, Serviço de Neurologia, Hospital de Santa Maria, University of Lisboa, Lisboa, Portugal

49.1 Introduction

Thrombosis of the dural sinus and cerebral veins is less common and has a more varied clinical presentation than other types of stroke. CVT is also more difficult to diagnose, as magnetic resonance imaging (MR) and venography are needed to confirm the diagnosis. Furthermore, CVT can be a manifestation of several systemic diseases, a complication of other central nervous system (CNS) disorders, of pregnancy or of the use of drugs with thrombogenic proprieties.

The most frequent symptoms of CVT are headaches, seizures, motor, sensory or language deficits, and altered consciousness. Acute seizures are more frequent in patients with supratentorial parenchymal lesions, sagittal or cortical vein thrombosis and motor or sensory defects.

Symptoms and signs can be grouped in four major syndromes:

• Isolated intracranial hypertension: headache with or without vomiting, papilledema and visual symptoms.
  
• Focal syndrome: focal deficits, seizures or both.
  
• Encephalopathy: multifocal signs, mental status changes, stupor or coma.
  
• Cavernous sinus: diplopia, ocular pain, cheimosis, proptosis, oculomotor palsies

The clinical presentation is influenced by:

• Site and number of occluded sinuses and veins:
  
  
  
  • Cerebral cortical vein thrombosis without dural sinus involvement can cause focal seizures, motor or sensory deficits with or without headache.
    
  • In occlusion of the sagittal sinus, motor deficits, bilateral deficits and seizures are frequent.
    
  • Patients with isolated thrombosis of the lateral sinus often present with isolated intracranial hypertension or isolated headache; aphasia is frequent if the left transverse sinus is involved.
    
  • If the deep cerebral venous system is occluded, the clinical picture is usually more severe, with coma, mental symptoms and bilateral motor deficits.
  
  
• Presence of parenchymal lesions:
  
  
  
  • Patients with parenchymal lesions are more likely to be comatose or to have motor deficits or aphasia and seizures.
  
  
• Age of the patient:
  
  
  
  • Decreased vigilance and mental symptoms are more common in elderly patients.
    
  • Headaches and isolated intracranial hypertension are more frequent in younger patients.
  
  
• Gender: headaches are more common in women.
  
• Interval from onset to presentation:
  
  
  
  • Patients with a chronic or subacute course are more likely to present with isolated intracranial hypertension and to show papilledema.

Concerning prognosis, several recent prospective series and systematic reviews consistently established the current vital and functional prognosis of patients with acute CVT, showing a 15% overall death or dependency rate. The predictors of poor long-term prognosis derived from the ISCVT cohort were:

• Age >37 years.
  
• Male gender.
  
• Glasgow Coma Scale (GCS) score on admission <9.
  
• Mental status disorder.
  
• Deep cerebral venous system thrombosis.
  
• Hemorrhage on CT/MR.
  
• CNS infection.
  
• Malignancy.

This predictive model was validated in two other cohorts.

The acute case-fatality is low (4%). Predictors of mortality at 30 days are depressed consciousness, mental status disorder, thrombosis of the deep cerebral venous system, right hemispherical hemorrhage and posterior fossa lesions. The main cause of death is transtentorial herniation secondary to a large hemorrhagic lesion. Other causes include herniation due to multiple lesions or to diffuse brain edema, status epilepticus, medical complications and pulmonary embolism.

Recanalisation occurs in 40-90% of patients, mostly within the first 4 months, but is not related to outcome. Long-term complications of CVT include seizures, headaches, vision loss, dural arteriovenous fistulae and recurrent venous thrombosis of the brain, extremities or pelvis. Recurrent CVT is rare (2-7%) and also difficult to document, particularly if a previous follow-up MR/MRV is not available. In the Rochester Mayo Clinic series, the likelihood of recurrent venous thrombosis was the same after CVT and lower extremity deep venous thrombosis. Recurrence of CVT was not influenced by warfarin therapy. In children, age at CVT onset (>2 years), persistent venous occlusion, the G20210A mutation and non-administration of anticoagulation predict recurrent CVT or systemic venous thrombosis.

49.2 Confirmation of Diagnosis by Neuroimaging

Confirmation of diagnosis of CVT by neuroimaging implies the visualization of an occluded sinus or vein and of the thrombus. MR combined with MR venography (MRV) is the most sensitive examination technique for the diagnosis CVT. However, even using MR plus MRV, there are some diagnostic difficulties particularly concerning the diagnosis of cortical vein thrombosis, which has a low interobserver reliability. Gradient echo (GRE) T₂* weighted sequences with thrombus susceptibility effect (SE) should always be performed if the working diagnosis of CVT is raised. T2* SE images show the thrombus, including an isolated cortical vein thrombosis, as a hypointense area. Multidetector CT venography (CTV) can be used as an alternative to MRV, with an excellent sensitivity and specificity for the diagnosis of CVT.

49.3 Etiological Investigation

The most frequent causes or associated conditions with CVT are listed in Table 49.1. The relative weight of these causes varies accordingly to world regions. In countries with low Gross National Income, infection, anemia and puerperium-related CVT are more common.

Table 49.1. Common (>5%) causes of cerebrovenous thrombosis [Ferro, 2004; Khealani, 2008].

* among women;

ENT = ear, nose and throat; ISCVT = International Study on Cerebral Vein and Dural Sinus Thrombosis; NA = not available.

More than half of patients have more than one cause for their CVT, while in about 15% no cause can be found despite extensive investigation. Some rules of thumb are suggested during the etiological workup:

Related posts:

Neuroscience Critical Care: Two Experts’ Point of View Acute Spinal Cord Injury: Pathophysiology and Intensive Care Management Monitoring Cerebral Blood Flow and Cerebral Autoregulation: Basic Principles, Techniques, Common Patterns and Interpretation of Results Endocrinology of Acute Brain Injury Monitoring Brain Chemistry by Microdialysis During Neurointensive Care Acute Paraplegias and Quadriplegias of Non-traumatic Cause

Stay updated, free articles. Join our Telegram channel

Join