Abstract Or112: Brain Oxygen and ICP Optimization in Severe post Cardiac Arrest (BOOSCA)

Abstract

Background: Cerebral edema after resuscitation from cardiac arrest (CA) may elevate intracranial pressure (ICP) and lower brain tissue oxygen (PbtO2) levels, causing secondary brain injury. We initiated a clinical protocol for invasive ICP and PbtO 2 monitoring and management in selected CA patients. Research Question: What specific radiographic and clinical criterial can be used to select post-resuscitation patients for invasive ICP and PbtO 2 monitoring, and does medical therapy mitigate high ICP (>22mmHg) and low brain oxygen (<20mHgHgHH)? Aim: Characterize the initial experience of selected post-CA patients with early radiographic edema managed with ICP/PbtO 2 monitoring. Approach: Right frontal Raumedic PTO catheters were placed in patients with abnormal head CT (loss of gray-white differentiation, narrowed cisternal spaces at the tentorium, diffuse loss of sulci), and early EEG suppression ratio >70%. We excluded patients radiographically herniated, lacking cranial nerve reflexes, requiring systemic anticoagulation, or not desiring aggressive care. Monitors were placed during TTM, prior to rewarming, and elevated ICP and low PbtO 2 managed with a clinical algorithm. Results: Ten monitored patients included 6 women and 4 nonwhite people of mean age 40 (±13) years; 8/10 had noncardiac etiology of arrest. The ICP was elevated in 10/10 patients, requiring treatment with head positioning, sedation, cerebral perfusion pressure optimization, temperature management, osmotherapy, mild hyperventilation, and barbiturates. PbtO 2 was <20mmHg in 8/8 patients, requiring treatment with increased FiO 2 or PEEP, fluids, vasopressors, inotropes, prone positioning, and ventilator changes. Of 10 patients with elevated ICP, 2 progressed to brain herniation, 2 rearrested and died, 6 were “successfully” managed with nonsurgical therapies, and 2 (20%) survived and made a good functional recovery. Prognostic MR imaging was often delayed due to monitoring, and temperature management often prolonged due to ICP elevation. No complications of ICP monitor insertion or maintenance were noted. Conclusions: All qualifying patients had dangerous elevations of ICP and low PbtO 2 . These abnormalities often responded to non-surgical therapy, and in 2/10 cases resulted in good functional outcomes. Intracranial hypertension and brain hypoxia after cardiac arrest are treatable, and might reduce secondary neurological injury leading to better outcomes.