Journal: Can J Anesth 54(8): 657-661, 2007. 22 References
Reprint: Veterans Affairs Medical Center, Anesthesia Service, 5000 W. National Avenue, Milwaukee, WI 53295 (PS Pagel, MD)
Faculty Disclosure: Abstracted by R. Klotz, who has nothing to disclose.
Sevoflurane-induced seizures are most often described during mask induction when high concentrations of agent are administered concomitant with alveolar hyperventilation. The occurrence of seizure-like activity during emergence has been rarely reported, with only four previous cases noted in peer -reviewed literature. In this article, the authors describe a healthy patient who developed several episodes of generalized tonic-clonic seizure-like activity during and immediately after emergence from sevoflurane anesthesia.
A 29-year-old male, with a history of obesity and tobacco abuse, presented for elective left inguinal hernia repair under general anesthesia. Previous anesthetics were uneventful. The patient was medicated preoperatively with midazolam 3 mg IV and general anesthesia was induced with propofol 2 mg/kg and fentanyl 1 mcg/kg IV. A #5 laryngeal mask airway was easily placed, and anesthesia was maintained with sevoflurane in oxygen under spontaneous ventilation. End-tidal sevoflurane concentrations were maintained between 1.8 and 2.6% (0.9 to 1.3 minimum alveolar concentration [MAC]). End-tidal carbon dioxide (ETCO2) concentrations were maintained between 47 and 53 mmHg with tidal volumes between 300 to 350 mL during spontaneous ventilation. Oxygen saturation remained greater than 98%.
Sevoflurane was discontinued upon completion of the procedure. As the patient began to emerge from anesthesia, with an end-tidal concentration of sevoflurane of 0.8% (0.4 MAC), generalized tonic-clonic seizure-like activity without focal abnormalities or apparent initial site or temporal progression occurred without purposeful movement or response to verbal commands or painful stimuli. Propofol 30 mg IV resulted in immediate cessation of seizure activity. The sevoflurane concentration was briefly increased. Sevoflurane was again discontinued, but generalized seizure-like activity recurred. Midazolam 2 mg IV was administered and the seizure activity temporarily subsided. Propofol 2 mg/kg and succinylcholine 1 mg/kg IV were then administered, the LMA removed, and an endotracheal tube was placed. The patient suffered another tonic-clonic event during transport and two additional episodes upon arrival in the ICU. Tonic-clonic activity was suppressed with bolus doses of midazolam 2 mg IV and an infusion of propofol. A loading dose of phenytoin 10 mg/kg IV was administered and a 1 mg/kg/8 hr maintenance phenytoin infusion was begun.
A CT scan of the head was unremarkable. No further seizure-like activity occurred during the remainder of the hospitalization. The propofol infusion was discontinued and the patient weaned from the ventilator the following morning. After extubation, the patient displayed normal mental and neurological status and had no recollection of perioperative events. The patient was released from the hospital on postoperative day two, with continuation of chronic oral phenytoin treatment. A cranial MRI performed 6 weeks after discharge was unremarkable, and phenytoin therapy was discontinued.
A recently published investigation identified high alveolar sevoflurane concentration, short delay to the onset of anesthesia, and female gender as important risk factors for the development of epileptiform EEG activity during anesthetic induction with sevoflurane in healthy patients. The mechanisms responsible for seizure-like activity during emergence from sevoflurane anesthesia remain to be defined. Low blood-gas solubility that allows for rapid elimination of sevoflurane after discontinuation may also represent a risk factor. The role of alveolar hypoventilation and hypercarbia remain to be determined.
The authors conclude that further investigation into the etiology of seizure-like activity associated with emergence from sevoflurane is warranted. |
