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Cervical spinal cord AVM rupture in parturient.

To JNA Readers: We present a case of a parturient who underwent a caesarian section with epidural anesthesia. Postoperative course was complicated by cervical spinal cord arteriovenous malformation (AVM) rupture with tetraplegia and respiratory insufficiency. We discuss the strategy of conservative therapy, problem of vasospasm, and specificity in puerperal period. The case illustrates the value of using dynamic transcranial Doppler (TCD) monitoring to evaluate, assess, and treat the dramatic changes in neurological status after AVM rupture on cervical level. Assessment and correction of volemic status and cerebral blood flow are important for patients with subarachnoid hemorrhage (SAH). A 36-year-old woman with preeclampsia—arterial hypertension (blood pressure is 170/80mm Hg), hypoproteinemia (42 g/L), and severe edema—had a complicated postoperative period. Against the background of persistent arterial hypertension, neurological symptoms developed on the day of operation. Clinical manifestations included tetraplegia, expressed neck stiffness, and respiratory disorders. A computed tomography scan of her brain showed SAH and significant amount of the blood in basal cistern.1 We determined that in a patient with an intracranial SAH without an identifiable cause, the cause may be spinal. However, emergency magnetic resonance (MR) study was not available at the time. Antihypertensive therapy was corrected; cerebral vasodilatator (Nimodipine) and hypervolemia (160 to 200mL/h of infusion) were used despite initial syndrome of edema. TCD imaging and assessment of vertebral-basilar flow were completed every day. The mean velocity in basilar artery was noted (55 cm/s). There were positive dynamics of neurological recovery at the mild right-side hemiparesis. The treatment and the multimodality monitoring were continued. On the third day, we saw negative changes, progressive of brainstem problems that included swallowing disturbances, dysarthria, phonation disorders, and strabismus. We noted the increase in the rate of velocity in basilar artery (160 cm/s). The patient was considered for MR imaging. The MR films showed a type II AVM at the C2 to C7 levels of the spinal cord, the rupture of AVM, hemorrhages, and severe edema of brainstem (Fig. 1). We continued clinical and laboratory monitoring, TCD imaging, respiratory therapy, infusion program for hypervolemia (200 to 240mL/h), and calcium channel blockers. Osmodiuretic therapy was added. By day 10, there were significant clinical changes, such as, regression of neurological symptoms, normalization of cerebral blood flow, and adequate brainstem perfusion. The neurological outcome of this patient was mild monoparesis in her right arm. After 12 days in the intensive care unit, the patient was transferred to neurology department. Spinal cord AVMs are rare vascular lesions. AVMs of the cervical spinal cord are a small proportion of these.2 They may cause significant neurological symptoms by direct mass effect or venous congestion. Surgery of these lesions may be associated with considerable morbidity and thus a multimodality approach using adequate monitoring and therapy is required. Type II or glomus AVMs typically have multiple arterial feeders and drain into a venous plexus around the spinal cord.3,4 They can be particularly difficult to treat because they are intramedullary, within the spinal cord parenchyma.5 This case illustrates the value of dynamic monitoring of TCD for assessment and therapy of vasospasm in the basilar artery. The commitment to