Abstract

Purpose Ceftriaxone related nonconvulsive status epilepticus is least suspected and unusual complication especially patients with renal insufficiency (Pre admission Creatinine 140 microMol/L). Methods We reviewed the clinical and electroencephalographic (EEG) characteristics of a patient presented with delirium due to UTI and renal failure in whom developed alteration of consciousness without convulsions associated with continuous epileptiform EEG activity while being treated with ceftriaxone. Results and conclusion Patient was given Ceftriaxone as treatment for UTI and treatment for electrolyte imbalance. Patient started having decreased responsiveness and altered level of consciousness. The EEG showed continuous or intermittent bursts of generalized, high-voltage, 1–2 Hz sharp wave activity or sharp and slow wave activity that resembled triphasic waves but completely differentiated from triphasic waves. It was not possible to obtain EEG few days after ceftriaxone discontinuation and level of consciousness improved and patient transferred to nursing home with continue AED (dilantin). Epoch 1 is EEG after first dose of ceftriaxone and Epoch 2 is 2nd day after discontinuation of ceftriaxone. It is usually not correlated with the use of ceftriaxone and it is hard to speculate. After evaluating all possible common causes, only thing correlated with this patient was ceftriaxone. Also continued epileptiform activity in presence of dilantin and Lorazepam infusion. The temporal relationship between the start of ceftriaxone therapy and the manifestation of NCSE as well as the withdrawal of ceftriaxone and the improved consciousness within 48 h indicated that ceftriaxone was a causative agent. It has been proposed to be mediated by competitive antagonism of γ-aminobutyric acid (GABA) in brain, which is the principal inhibitory neurotransmitter in the brain, could lead to a low neuronal threshold for neuronal excitation. Cephalosporins can cause nonconvulsive status epilepticus in setting of poor renal elimination. The clinical picture is difficult to differentiate from that of metabolic encephalopathy unless an EEG is obtained. Physicians should be aware of this potentially dangerous complication.

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