Abstracts

Rationale: Nonconvulsive status epilepticus(NCSE) is a heterogenous disorder with variable etiology and multiple subtypes, which can be defined as a condition with a prolonged state of impaired consciousness or altered sensorium associated with continuous paroxysmal activity or electrographic discharges on the EEG. Among various etiologies of NCSE, we could somewhat easily see patients with NCSE having underlying CKD. So, we tried to analyze etiologies of NCSE in chronic kidney disease patients. Methods: We retrospectively reviewed 80 patients between Feb 2013 and April 2017 diagnosed with NCSE in our hospital who were admitted to our Neurology department and selected 18 patients with NCSE who had underlying chronic kidney disease. Etiologic factors, EEG, Brain MRI, CSF study(if done), treatment and prognosis were analyzed. NCSE was diagnosed by EEG findings based on Kaplan’s NCSE EEG criteria. Results: Mean age of the patients was 65 (ranging from 44 to 79). Male to female ratio was 5:13. CKD stages of the patients were 3 in 2 patients, 4 in 4 patients, and 5 in 14 patients. EEG findings showed typical absence type in 2 patients, atypical absence type in 4 , and rhythmic delta/theta activity in 12. Causative conditions include drugs (5 patients, 27.7%), AKI on CKD (4, 22.2%), hypoglycemia (1, 5%), post-op state (2, 11.1%), CNS infection (1, 5%), other infections (2, 11.1%), and cryptogenic (1, 5.6%). 13 patients underwent antiepileptic treatment and rest of five patients were treated with controlling precipitating factors without AED medication. No one recovered from 1st line AED therapy. 8 patients underwent 2nd line AED therapy. Among them, 2 patients couldn't even start the treatment when considering the 3rd line therapy, because of sudden death due to cardiac arrest. 5 patients underwent benzodiazepine continuous therapy. Nine patients were fully recovered, two were partially improved, another two did not have any change during admission (including 1 patient with refusal of treatment by family members), and 5 expired. Conclusions: As well known, epileptogenic activity of beta-lactam antibiotics is described as a competitive antagonism of the inhibitory neurotransmitter known as gamma-aminobutyric acid(GABA). And impaired renal clearance leads to increased antibiotic concentrations that may reach neurotoxic levels. The mechanism of uremia induced NCSE still needs to be more researched, but can be explained by imbalances of neurotransmitter amino acids within the brain. By activation of excitatory NMDA receptors and inhibition of inhibitory GABA receptor, uremia can result in seizures. About 22.5% of all NCSE patients had underlying CKD in our hospital. The result that toxic (especially drugs) and uremic conditions consisted most of the proportion of the etiology was characteristic in our study. 13 patients recovered from NCSE, and five expired due to exacerbation of underlying condition. Approximately 72.2% showed favorable prognosis (full or partial recovery). Thus, in case of unexpected mental change in CKD patient, we should suspect NCSE, carry out EEG, figure out causative factors and start management actively along with controlling underlying comorbidities on diagnosis. Funding: none