Aneurysmal Subarachnoid Hemorrhage Complicated by Central Neuronal Hyperventilation (P4.318)

Objective: NA Background: Few Cases have reported central neuronal hyperventilation (CNH) secondary to infiltrative malignancy or autoimmune disease. The lesion is usually located at the pontine tegmentum and interrupts the fibers between the respiratory centers in the pons and those in the medulla. Design/Methods: We report a case of 57 year-old female with multiple comorbidities who was admitted to the neurocritical care unit after intra-operative rupture of a 4mm distal basilar aneurysm while being electively coiled. An external ventricular drain (EVD) was placed due to early signs of ventriculomegaly. The postoperative exam showed progressive encephalopathy, left more than right hemiplegia, progressive tachypnea (rate and depth) despite being on assisted mode ventilation leading to severe hypocapnia (12.8 mmhg) and compensatory renal acidosis (Bicarbonate = 8.5 mmol/L) to maintain normal PH. Attempt to sedate the patient led to severe metabolic acidosis. Intraventricular nicardipine was started and the patient ventilator settings were changed to bi-level pressure control. Transcranial Doppler (TCD) showed markedly improved vasospasms. The patient respiratory rate and to a lesser extent, the tidal volumes improved after several days. Sedation was weaned off successfully. EVD was successfully weaned off and removed. Results: TCD and CT angiogram showed sever basilar artery vasopspasm while MRI done later showed bilateral tegmental midbrain ischemia. Conclusions: One case has reported acute central neuronal hyperventilation following left thalamic bleed while another reported chronic neuronal hyperventilation that was attributed to old bilateral lacunar thalamic strokes by exclusion. Our case is the first to report central neuronal hyperventilation following aneurysmal subarachnoid hemorrhage that complicated by bilateral tegmental midbrain strokes. While respiratory centers are known to exist in the medulla and pons, more recent articles have described networks that regulate breathing extending to the midbrain peri-acquiductal grey and possibly the thalami. Our unique case supports this hypothesis. Study Supported by: NA Disclosure: Dr. Abd Elazim has nothing to disclose. Dr. Hussein has nothing to disclose. Dr. Hamed has nothing to disclose. Dr. Sawalha has nothing to disclose. Dr. Torbey has nothing to disclose. Dr. Greene-Chandos has nothing to disclose.