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BJA Advance Access originally published online on February 20, 2004
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British Journal of Anaesthesia, 2004, Vol. 92, No. 4 504-511
© 2004 The Board of Management and Trustees of the British Journal of Anaesthesia

Clinical Investigations

Agitation and changes of Bispectral IndexTM and electroencephalographic-derived variables during sevoflurane induction in children: clonidine premedication reduces agitation compared with midazolam{dagger}

I. Constant*,1, Y. Leport1, P. Richard1, M.-L. Moutard2 and I. Murat1

1 Service d’Anesthésie-Réanimation, Hopital d’enfants Armand Trousseau, Assistance-Publique, Hôpitaux de Paris, Paris VI University, France. 2 Service de Neurologie pédiatrique, Hopital Saint Vincent de Paul, Assistance-Publique, Hôpitaux de Paris, France*

*Corresponding author. E-mail: isabelle.constant@trs.ap-hop-paris.fr
{dagger}Presented in part at the annual meeting of the European Society of Anaesthesiologists, Nice, France, April 6–9, 2002.

Background. This double-blind randomized study was undertaken to assess agitation, Bispectral IndexTM (BISTM) and EEG changes during induction of anaesthesia with sevoflurane in children premedicated with midazolam or clonidine.

Methods. Children were allocated randomly to receive rectal midazolam 0.4 mg kg–1 (n=20) or oral clonidine 4 µg kg–1 (n=20) as premedication. Rapid induction of anaesthesia was achieved with inhalation of sevoflurane 8% in nitrous oxide 50%–oxygen 50%. After tracheal intubation, the children’s lungs were mechanically ventilated and the inspired sevoflurane concentration was adjusted to achieve an end-tidal fraction of 2.5%. The EEG and BISTM were recorded during induction until 10 min after tracheal intubation. The EEG was analysed using spectral analysis at five points: baseline, loss of eyelash reflex, 15 s before the nadir of the BISTM (BISnadir), when both pupils returned to the central position (immediately before intubation), and 10 min after intubation.

Results. Agitation was observed in 12 midazolam-treated and five clonidine-treated patients (P=0.05). At baseline, EEG rhythms were slower in the clonidine group. Induction of anaesthesia was associated with similar EEG changes in the two groups, with an increase in total spectral power and a shift towards low frequencies; these changes were maximal around the end of the second minute of induction (BISnadir). When the pupils had returned to the central position, fast EEG rhythms increased and BISTM was higher than BISnadir (P<0.05). In both groups, agitation was associated with an increase in slow EEG rhythms at BISnadir.

Conclusions. Compared with midazolam, clonidine premedication reduced agitation during sevoflurane induction. During induction with sevoflurane 8% (oxygen 50%–nitrous oxide 50%), the nadir of the BISTM occurred at the end of the second minute of inhalation. Agitation was associated with a more pronounced slowing of the EEG rhythms at BISnadir compared with inductions in which no agitation was observed. The BISTM may not follow the depth of anaesthesia during sevoflurane induction in children.

Br J Anaesth 2004; 92: 504–11


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