Transcutaneous pCO2 and Seizures in the Epilepsy Monitoring Unit: Associations with Markers of Seizure Severity (S14.003)

OBJECTIVE: Transcutaneous pCO2 (TCpCO2) may be an indicator of risk for Sudden Unexpected Death in Epilepsy (SUDEP). BACKGROUND: SUDEP is the single largest direct epilepsy-related cause of death, and theories include central or obstructive apneas leading to hypoxemia and hypercapnia and cerebral shutdown. Studies have shown oxygen desaturation <70[percnt], and increases in End-tidal CO2. TCpCO2 is a different technology, is less cumbersome, and its use during seizures has not yet been reported. METHODS: The Tosca500 (Radiometer America, Inc) was used in the epilepsy monitoring unit to continuously measure SaO2, heart rate and TCpCO2 in patients at high risk for cardiopulmonary distress during seizures and those undergoing intracranial EEG monitoring. We retrospectively reviewed data from 12 patients who underwent TCpCO2 recording. Seizure type, electro-clinical seizure duration, and the presence of post-ictal generalized electrographic suppression (PGES) were also assessed. PGES was defined as post-ictal EEG suppression <10uV, ending when 15/30 seconds of cerebral activity reached 蠅10uV. RESULTS: Peri-ictal TCpCO2 data were reliable in 15 seizures: 7 GTCs, 3 complex partial, 2 hemiclonic, 2 subclinical and 1 tonic seizure. The average peak increase in TCpCO2 was 8±7.3mmHg, with 7 seizures associated with a 蠅20[percnt] elevation. TCpCO2 typically peaked several minutes after electrographic offset. Hemiclonic and GTC seizures were also associated with oxygen desaturations and tachycardia, and were left temporal in onset. PGES occurred in 2 GTCs. Seizure duration (p=0.009), seizure type (p=0.029) and PGES (p=0.02) were significantly correlated with ΔTCpCO2 (Spearman correlation). In multivariate analysis using these three variables, only PGES was significantly associated with ΔTCpCO2 (p=0.004). CONCLUSIONS: TCpCO2 elevation was associated with PGES and may denote greater severity and duration of seizure activity. Further study and direct comparison with ETCO2 is required to better understand the cause of hypercapnea, and the potential of this novel modality in identifying SUDEP risks. Disclosure: Dr. Chong has received personal compensation for activities with Eisai Inc. as a consultant. Dr. Patel has nothing to disclose. Dr. Ahmed has nothing to disclose. Dr. Khan has nothing to disclose. Dr. Still has nothing to disclose. Dr. Marzouk has nothing to disclose. Dr. Friedman has received personal compensation for activities with the Epilepsy Study Consortium as a consultant. Dr. Devinsky has received personal compensation in an editorial capacity for Epilepsy & Behavior.