Anesth Analg 2003;96:1239-1240
© 2003 International Anesthesia Research Society
LETTERS TO THE EDITOR
Is Fast Induction with Sevoflurane Associated with an Increased Anesthetic Risk in Pediatric Patients?
Frank Wappler, MD, and
Petra Bischoff, MD
Department of Anesthesiology, University Hospital Hamburg-Eppendorf, Hamburg, Germany
To the Editor:
We read with great interest the report by Politis et al. regarding endotracheal intubation of children with 8 Vol.% sevoflurane during controlled ventilation (1). However, recent articles suggested that a rapid induction using immediate administration of large dose sevoflurane is associated with an increased risk of serious side effects (2–4) .
Adachi et al. presented for the first time a case of clonic and tonic seizure-like movements of the extremities in a young girl during induction of anesthesia with sevoflurane (2). Two years later, Komatsu et al. reported about two pediatric patients with a history of epilepsy who developed electrical seizures during sevoflurane administration (3). A study in 31 healthy children investigating the effects of inhalational induction with 8 vol.% sevoflurane on brain electrical activity was presented (4). The authors showed that, in a subgroup undergoing controlled ventilation (CV) via a face-mask, 88% of the children developed interictal epileptiform discharges, such as suppression with spikes, rhythmic polyspikes or periodic epileptiform discharges, respectively. In a second subgroup with spontaneously breathing patients, EEG changes occurred in 20% of all cases. Furthermore, EEG discharges affected the autonomic nervous system, leading to a hyperdynamic cardiovascular response. The authors concluded consequently, that administration of large dose sevoflurane in children, especially when using CV with slight hyperventilation, is associated with an increased anesthetic risk.
This raises three relevant questions: First, is the widely used and recommended technique of immediate administration of 8 Vol.% sevoflurane really safe for children? Second, at which threshold concentrations produce sevoflurane EEG changes? And third, do nonconvulsive seizures damage the brain as suggested by Young et al. (5)?
Further neurophysiological studies are needed to investigate the effects of sevoflurane on brain electrical activities. Until more insights into this issue have been found, sevoflurane concentrations used for inhaled induction in pediatric anesthesia should be reduced and hyperventilation by controlled ventilation should be avoided.
References
- Politis GD, Frankland MJ, James RL, et al. Factors associated with successful tracheal intubation of children with sevoflurane and no muscle relaxant. Anesth Analg 2002; 95: 615–20.[Abstract/Free Full Text]
- Adachi M, Ikemoto Y, Kubo K, Takuma C. Seizure-like movements during induction of anaesthesia with sevoflurane. Brit J Anaesth 1992; 68: 214–5.[Abstract/Free Full Text]
- Komatsu H, Taie S, Endo S, et al. Electrical seizures during sevoflurane anesthesia in two pediatric patients with epilepsy. Anesthesiology 1994; 81: 1535–7.[Web of Science][Medline]
- Vakkuri A, Yli-Hankala A, Särkelä M, et al. Sevoflurane mask induction of anaesthesia is associated with epileptiform EEG in children. Acta Anaesthesiol Scand 2001; 45: 805–11.[Web of Science][Medline]
- Young GB, Jordan KG. Do nonconvulsive seizures damage the brain? - Yes. Arch Neurol 1998; 55: 117–9.[Free Full Text]
Response
George D. Politis, MD, and
Mark S. Quigg, MD
University of Virginia Health System, Charlottesville, VA
In Response:
We would like to thank Drs. Wappler and Bischoff for their interesting letter. They accurately and eloquently point out the association of sevoflurane with epileptiform electroencephalographic (EEG) recordings. However, I strongly disagree with their claim that an increased incidence of EEG spike activity during rapid sevoflurane induction should dictate that sevoflurane concentration be reduced and controlled ventilation avoided.
Epileptiform EEG patterns, including rhythmic polyspikes, occur with considerable frequency (20%) even in the absence of controlled ventilation (1) and occur with concentrations of sevoflurane well under 8% (2). If one believes that sevoflurane induced epileptiform activity may lead to brain damage, as Drs. Wappler and Bischoff suppose, then the logical conclusion should be that we should no longer use sevoflurane. Why would it be acceptable to risk brain damage in a lower percentage of patients? Iijima found that epileptiform EEG patterns occurred in 25% of patient receiving between 1–2 MAC isoflurane while receiving 100% oxygen and ventilation to normocarbia (2). Considering that information, would we also need to stop using isoflurane?
Another compelling reason for objecting to Wappler and Bischoff’s argument is the fact that epileptiform activity induced by anesthesia is not necessarily ictal nor epileptogenic. Ictal activity, in both experimental animal models and in humans, shows a predictable sequence of EEG discharges that evolve temporally as the ictal activity progresses (3). Periodic epileptiform discharges, such as those described during sevoflurane anesthesia (1) do not appear to evolve in an equivalent temporal fashion, and do not have the same pathophysiologic basis as ictal discharges encountered in end-stage status epilepticus (3,4) Therefore, the ongoing question of whether nonconvulsive ictal activity in humans induces neuronal damage, as it does in animal models (5), is unlikely to be relevant to the subject of non-ictal epileptiform discharges observed during anesthesia.
The association of anesthetic agents with both seizure activity and with epileptiform EEG patterns is longstanding, with information on enflurane induced electrocortographic seizure activity dating back at least 27 years (6). After a decade of clinical use of sevoflurane, and a considerably longer duration using isoflurane and enflurane, there is no evidence that potent agent induced epileptiform EEG patterns have caused cerebral injury in any patients, even those that had actual clinical seizures. Considering the information we have cited, our reply to Wappler and Bishoff’s questions is that the rapid, smooth, and predictable sevoflurane induction technique that we recently advocated (7) is safe, and that the sevoflurane concentration required to elicit non-ictal epileptiform activity is not particularly relevant because such EEG activity is not associated with the risk of epilepsy, provoked seizures, nor their sequelae.
References
- Vakkuri A, Yli-Hankala A, Särkelä M, et al. Sevoflurane mask induction of anaesthesia is associated with epileptiform EEG in children. Acta Anaesthesiol Scand 2001; 45: 805–11.
- Iijima T, Nakamura Z, Iwao Y, et al. The epileptogenic properties of the volatile anesthetics sevoflurane and isoflurane in patients with epilepsy. Anesth Analg 2000; 91: 989–95.[Abstract/Free Full Text]
- Treiman DM. Generalized convulsive status epilepticus.In: Epilepsy: a comprehensive textbook. Engel J, Pedley TA. Lippincott-Raven, Philadelphia. 1997, 669–680.
- Lothman EW, Bertram EH, Beckenstein JW, et al. Self-sustaining limbic status epilepticus induced by continuous hippocampal stimulation: electrographic and behavioural characteristics. Epilepsy Res 1989; 3: 107–119.[Web of Science][Medline]
- Meldrum BS, Vigorurous RA, Brierly JB. Systemic factors and epileptic brain damage: prolonged seizures in paralyzed artificially ventilated baboons. Arch Neurology 1973; 29: 82–87.[Abstract/Free Full Text]
- Niejadlik K, Galindo A. Electrocorticographic seizure activity during enflurane anesthesia. Anesth Analg 1975; 54: 722–24.[Abstract/Free Full Text]
- Politis GD, Frankland MJ, James RL, et al. Factors associated with successful tracheal intubation of children with sevoflurane and no muscle relaxant. Anesth Analg 2002; 95: 615–20.
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