Acute subarachnoid hemorrhage

Discussion

The diagnosis of CVST is typically made on the basis of radiological studies because the large spectrum of clinical manifestation makes clinical diagnosis of CVST difficult. Headache, focal seizures, focal motor or sensory deficits, and mental obtundation are the most commonly described symptoms.5

Both our cases presented with headache of sudden onset, neck stiffness, seizures, and imaging evidence of SAH, simulating a ruptured intracranial aneurysm. The correct diagnosis of CVST can be more difficult if it is associated with SAH, which is unusual with CVST.1,2 As with our first patient, who initially was admitted under neurosurgery as a potential case of aneurysmal bleed, initial imaging showed localized SAH without underlying parenchymal involvement.

The exact pathogenesis of SAH associated with CVST remains unknown. The most believable explanation is the extension of the venous hemorrhagic infarct into the subarachnoid spaces.1 In the absence of parenchymal sign of venous infarct (as in our patient one), SAH could be due to venous hypertension, secondary to back pressure due to blocked cerebral venous system that can lead to rupture of dilated, fragile, thin-walled, cortical veins resulting in bleeding into the subarachnoid space.1

An important practical issue needs to be addressed here. Clinical and imaging picture of patients with CVST and SAH can mimic aneurysmal SAH. An observation in the case reports and case series,3-7 regarding the distribution of SAH, is the difference in radiological findings between CVST and SAH from arterial origin due to aneurysmal bleed. Each has a characteristic pattern. Localized SAH in CVST is confined to parasagittal or dorsolateral cerebral convexity (cSAH), and sparing the basal cisterns. These findings should prompt the physician to look for non-aneurysmal causes of SAH by requesting additional vascular imaging of dural venous sinuses. Both of our cases showed cSAH in the brain imaging at presentation. Because of varied clinical spectrum, diagnosis of CVST is challenging in some clinical situations and is typically made by vascular imaging available at that time.

Digital subtraction angiography, an invasive procedure, was widely accepted in the past, as the gold standard for CVST diagnosis. In the present era, MRI combined with MRV is the single most sensitive and effective diagnostic method for CVST.8 In our cases, we used this investigative tool, because it is non-invasive, more convenient, and more reliable. The CT venography is considered a good alternative to MRI + MRV, and found to have both sensitivity and a specificity of 75-100% depending on the sinus and vein involved.8

The other differential diagnosis of cSAH is cerebral amyloid angiopathy, reversible cerebral vasoconstriction syndrome, large-vessel stenotic atherosclerosis, and posterior reversible encephalopathy syndrome.6 There is a high incidence of spontaneous intracerebral bleeding within the venous infarct, and this concern created the controversy of using anticoagulation for many years. On other hand, withholding anticoagulation puts the patient at risk of developing ongoing occlusion of additional cortical veins and sinuses resulting in more extension of venous infarcts.9 Anticoagulation with heparin is generally considered the mainstay of treatment of CVST, supported by a few small clinical trials,9 and found to be beneficial and safe even in the presence of hemorrhagic infarction (Level of evidence B).10 Now, most clinical experts are agreed that full anticoagulation should be started in patients with CVST as soon as the diagnosis is confirmed. We found anticoagulation safe and favorable with good clinical outcome in our 2 patients. Endovascular thrombolysis and decompressive hemicraniectomy are also available as more invasive treatment options for CVST. The first one is reserved for severe cases, not responding to full anticoagulation, while the other can be used as a life saving procedure in patients with large hemorrhagic venous infarct causing cerebral herniation.9

In conclusion, CVST is a potentially life threatening but treatable condition. Careful radiological as well as clinical analysis is important for the correct and early diagnosis of this condition. When SAH, is confined to cerebral convexity and sparing the basal cisterns, the strong and prompt suspicion of underlying CVST should be made to avoid any unnecessary delay in the management.