NM-354
Was it Really a Seizure?
Shah A, Lee H
University of Illinois, plainfield, IL, USA
Seizure-like activity occurs infrequently with general anesthesia and has typically been reported upon induction.2 Sevoflurane has been shown to be more epileptogenic than desflurane or isoflurane. The mechanism for hyperactivity is unclear but might be mediated through kainite receptors.1 Factors associated with sevoflurane induced seizures include high sevoflurane concentration, rapid induction and female gender. However, there is paucity of literature documenting the occurrence of intraoperative seizures while under general anesthesia.
A healthy 80 kg 14 yr old M presents for left distal femoral osteotomy. Uneventful induction of general anesthesia and placement of pre-surgical femoral nerve block (20 ml of 0.25% Bupivacaine). 50 mcg IV fentanyl and 2 mg IV midazolam given prior to incision. General anesthesia maintained with exhaled Sevoflurane 2.3%. There was no hemodynamic response to incision and periosteal dissection. After dissection, the surgical team paused to discuss location of the osteotomy. At this time, the patient developed generalized tonic-clonic shaking with sparing of the LLE and no change in hemodynamics or cardiopulmonary status. Within 30 seconds, the patient was given 50 mg propofol and the movements ceased. EEG or BIS was not available for intra-operative analysis of brain function and continuation of the procedure was estimated to require 2-3 hours of anesthesia. After discussion with the surgical teams, the case was cancelled and the patient emerged uneventfully from general anesthesia. The patient was transferred uneventfully to PICU and further neurological workup was negative.
The unusual presentation of intraoperative tonic clonic movement had us evaluate the possible etiology. Insufficient anesthesia can present as sporadic body movements but there was a lack of tachycardia or hemodynamic instability. Local anesthetic toxicity can cause seizures but the dose given was less than the toxic dose and the onset of symptoms was quite delayed. Drug interactions/withdrawal was possible but not likely given stable vitals (patient later denied drug or alcohol use). The generalized tonic clonic movements resembled descriptions of sevoflurane-induced seizures reported during induction in patients without a seizure disorder. In the absence of hemodynamic instability and burst suppression (isoelectric EEG unlikely at 2% sevoflurane), there was suspicion for new onset seizures due to sevoflurane. This questions the generalized literature of anesthetics as sedatives and indicates ongoing research about the mechanism of action of inhaled anesthetics is needed. Research shows sevoflurane associated hyperactivity might be mediated through kainite receptors in mice but the in vivo mechanism is not fully understood. The ability of intraoperative brain monitoring (EEG, BIS) to detect seizures and how to interpret those results needs to be explored as well.
1.Liang, P. Sevoflurane activates hippocampal CA3 kainate receptors (Gluk2) to induce hyperactivity during induction and recovery in a mouse model, British Journal of Anaesthesia, Nov 2017, Pgs 1047–1054.
2.Mohanram, A. Repetitive generalized seizure-like activity during emergence from sevoflurane anesthesia, Canadian Journal of Anesthesia, Aug 2007, Pgs 657-661.
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