The role of ketamine in the current practice of paediatric anaesthesia

Since its introduction in 1965, ketamine has maintained a place among the useful drugs of the paediatric anaesthetist. While ketamine did not become the panacea that some hoped it might, its role has evolved such that it fills several niches in the clinical practice of paediatric anaesthesia and remains the subject of clinical investigation in a variety of areas. Ketamine has been discussed in detail in two excellent review articles (White, Way & Trevor 1982; Reich & Silvay 1989). In recent years investigators have attained a greater understanding of the pharmacological characteristics of ketamine. It has been shown to be a noncompetitive antagonist of the central nervous system receptors of the excitatory amine N-methybaspartate ( h i s et al. 1983; Thomson, West & Lodge 1985). While this effect is probably the most important mechanism of action, opioid and other neuronal system receptors may also be involved. Ketamine undergoes biotransformation in the liver into several metabolites, among them the pharmacodynamically active norketamine. The conjugated metabolites are excreted mainly in the urine. Although the pharmacokinetics of ketamine are similar in children and adults (Grant et al. 1983; Hartvig, Larsson & Joachimsson 1993), children have anaesthetic recovery times that are briefer than those of adults (Grant et al. 1983) and dose requirements that vary inversely with age (Lockhart & Nelson 1974). Ketamine has many attributes in clinical practice. It supports heart rate, blood pressure, and cardiac output, primarily through central stimulation of the sympathetic nervous system. Ketamine supports chest wall muscle tone and maintains the functional residual capacity (FRC) of the lung. MuscuIar tone of the upper airway is supported so that the airway is usually maintained. Ketamine has bronchodilating effects, which are probably due to central sympathetic stimulation. It is an anaesthetic and analgesic of rapid onset when administered intravenousIy, intramuscularly, or by absorption through mucous membranes. Ketamine is inexpensive, is easily stored, and does not require special apparatus for administration. Ketamine has undesirable effects as well. It depresses contractility of the isolated heart. It can decrease spontaneous respiratory rate. Airway protective reflexes are dysfunctional during ketamine anaesthesia so that pulmonary aspiration of pharyngeal contents is not prevented. Pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) are sometimes increased by ketamine, as is intracranial pressure (ICP). Unpleasant emergence phenomena, including bad dreams and hallucinations, appear to be infrequent in children (Hollister & Bum 1974; Sussman 1974). Such reactions are usually not observed when ketamine is used as an induction agent followed by another anaesthetic of long duration or as a maintenance anaesthetic in combination with a benzodiazepine. Recovery from ketamine anaesthesia can be prolonged following higher doses and when additional anaesthetics are used. It is this combination of attributes and faults that defines ketamine’s current role in paediatric anaesthetic practice. Its cardiovascular stability and ability to be administered intramuscularly make it a versatile induction agent for patients with congenital heart disease (Koch 1988). It could be hypothesized that the sympathetic stimulation inight cause dynamic obstruction of the right ventricular outflow tract in patients with tetralogy of Fallot; however, this has not been demonstrated to be a problem. Anaesthetic induction with either intravenous ketamine accompanied by a muscle relaxant and controlled ventilation (Laishley et al. 1986) or intramuscular ketamine accompanied by oxygen administration (Greeley et al. 1986) in children with tetralogy of Fallot or other cyanotic heart lesions is