Abstracts

Rationale: Mild Therapeutic Hypothermia (MTH) is thought to provide neuroprotection after cardio-pulmonary arrest (CPA). At our institution a MTH cooling protocol is instituted following CPA. A Neurology consult and continuous video EEG (cVEEG) are often obtained in these patients. Initial clinical trials defined a 24 hour duration of MTH, followed by a rewarming period, as the appropriate clinical treatment. However, some inflammatory processes and cerebral edema related to cerebral anoxic injury occur or persist beyond a 24 hour window, which could result in clinical and neurophysiological deterioration after rewarming in some patients. Methods: We reviewed consecutive cases from the University of Colorado Hospital between April, 2011 and March, 2012 and identified patients who underwent MTH after CPA and had cVEEG's done. Patients were cooled for 24 hours and rewarmed over approximately 12 hours. CVEEG's were recorded during the cooling phase and continued for at least 12 hours post warming. Results: There were a total of 27 patients with cVEEG's who underwent MTH following CPA. Three patients were identified who had deterioration in their EEG's following rewarming. During cooling, the EEG's showed generalized suppression or burst suppression in these patients. Case 1: 79 year old female whose cVEEG initially improved after rewarming, demonstrating a continuous pattern with moderate slowing. At 64 hours post-arrest, the cVEEG deteriorated to generalized periodic epileptiform discharges followed by burst-suppression. Case 2: 52 year old male whose cVEEG initially improved after rewarming demonstrating moderate slowing with continuity and reactivity. At 48 hours post-arrest, his cVEEG background deteriorated to burst suppression then severe suppression. Case 3: 55 year old male whose cVEEG initially improved after rewarming and was continuous and reactive, but at 66 hours post-arrest deteriorated to burst-suppression with subsequent progressive suppression. There were no clear medical changes or complications to account for the deterioration in these patients' EEG's. All 3 patients died. Conclusions: In these 3 cases, there was improvement in the EEG after rewarming followed by deterioration to a malignant EEG pattern. This deterioration may indicate further progression of underlying secondary injury processes following anoxic brain injury. Our results highlight the potential importance of the cVEEG during MTH and the benefit of continuing it following the rewarming phase. Further neurophysiologically based studies may also help determine if MTH applied longer than 24 hours may offer an additional neuroprotective effect in some CPA patients.