Local Anaesthetic Plasma Levels in Children

Eyres, R. L.; Kidd, Joseph N.; Oppenheim, R. C.; Brown, T. C. K.

doi:10.1177/0310057x7800600312

Cited by 72 publications

(29 citation statements)

References 8 publications

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“…Plasma concentrations in infants and children following caudal injection of lignocaine, mepivacaine and bupivacaine were similar or slightly lower than those in adults given similar doses on an mgt kg basis (Ecoffey et al 1984(Ecoffey et al , 1985Eyres et al 1978Eyres et al , 1983Mazoit et al 1988;Takasaki 1984). In infants the free fraction of bupivacaine (average = 0.16) was markedly higher than that reported in adults (average = 0.04) [Mazoit et al 1988].…”

Section: Agementioning

confidence: 91%

Clinical Pharmacokinetics of Epidural and Spinal Anaesthesia

Burm

1989

Clinical Pharmacokinetics

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Epidural and spinal anaesthesia results from the interaction of local anaesthetics with nerve structures, primarily those located within the subarachnoid space. Local anaesthetics can reach the sites of action along various distribution pathways. Uptake into extraneural tissues (in particular epidural fat) and systemic absorption compete with neural tissue distribution and thereby affect the clinical potency and duration of action. Consequently, epidural doses must be much higher than spinal doses. The systemic absorption of lignocaine (lidocaine), bupivacaine and etidocaine following lumbar epidural administration has been shown to be biphasic, with a rapid initial absorption phase followed by a much slower absorption phase. Initial absorption rates of lignocaine and bupivacaine following subarachnoid injection are much slower, but the late absorption rates are similar to those after epidural administration. The tissue distribution characteristics of various amide-type agents are similar, because more extensive plasma binding offsets the greater tissue affinity of the more lipophilic compounds bupivacaine and etidocaine. The amide-type agents are predominantly eliminated by hepatic metabolism, except prilocaine, which is also metabolised elsewhere in the body. Ester-type agents are rapidly hydrolysed in blood and liver and are eliminated much faster than amide-type agents. The blood concentrations attained depend primarily upon the dose administered. The addition of adrenaline (epinephrine) reduces the peak plasma drug concentrations; similarly, the age of the patient, disease states and drug interactions may alter the pharmacokinetics to various extents. Because of the low dose requirements, systemic toxicity is not a problem during spinal anaesthesia. During epidural anaesthesia, however, the safety margin is relatively small, and systemic toxicity is very likely to occur after inadvertent intravascular injection of an epidural dose.

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Section: Agementioning

confidence: 91%

Clinical Pharmacokinetics of Epidural and Spinal Anaesthesia

Burm

1989

Clinical Pharmacokinetics

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“…Thus the present result clearly shows that propofol in combination with alfentanil offers an alternative method for tracheal intubation in situations where the use of suxamcthonium is not recommended and onset time or the duration of action of nondepolarizing neuromuscular blocking agents may be too long. However, rapid uptake and potentially toxic plasma levels of lidocaine were found in children under 3 years of age after topically applied lidocaine to the larynx and trachea (17). In adults the corresponding figure after propofol 2.5 m g .…”

Section: Intubating Conditionsmentioning

confidence: 97%

Tracheal intubation after induction of anaesthesia with propofol, alfentanil and lidocaine without neuromuscular blocking drugs in children

Hiller¹,

Klemola²,

Saarnivaara³

1993

Acta Anaesthesiol Scand

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In a double-blind study, intubating conditions and haemodynamic responses were assessed in two age-groups of 45 ASA I-II children, with mean ages of 2.4 and 6.3 years, premedicated with oral midazolam and atropine. The children were randomly allocated to one of three groups: alfentanil 20 micrograms.kg-1 + lidocaine 1 mg.kg-1 (Alf20 + Lign); alfentanil 20 micrograms.kg-1 (Alf20); or alfentanil 40 micrograms.kg-1 (Alf40), followed by propofol 3.5 mg.kg-1 in the children aged 1-3 years and 3.0 mg.kg-1 in the older children. Intubating conditions, 40 s after the administration of propofol, were assessed as good, moderate or impossible on the basis of jaw relaxation, ease of insertion of the endotracheal tube and coughing during intubation. In the younger age group the frequencies of good, moderate or impossible intubating conditions were 87, 13 and 0% in the Alf40, 40, 60 and 0% in the Alf20 (P < 0.05 compared to the Alf40 group) and 53, 47 and 0% in the Alf20 + Lign group. In the older age group the corresponding frequencies were 60, 33 and 7% in the Alf20 + Lign, 47, 53 and 0% in the Alf20 and 47, 40 and 13% in the Alf40 group. All the drugs prevented any increase in arterial pressure and heart rate after tracheal intubation. The QTc interval of the ECG was always in the normal range. Clinically important bradycardia did not occur. In conclusion, the best intubating conditions occurred after propofol 3.5 mg.kg-1 and alfentanil 40 micrograms.kg-1 in the younger age group.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Therefore, local anaesthetics can induce a variety of toxic effects in several types of tissue particularly in the brain, heart, and skeletal muscle. [8] In adults, toxic effects on the CNS are common but in children, effects on the heart are common. [8] While the main site of both the clinically desirable and toxic effects of local anaesthetics are thought to be exerted at the voltage-gated sodium channel, many alternative sites, such as a disruption of components of oxidative phosphorylation, have also been considered.…”

Section: Discussionmentioning

confidence: 99%

“…[8] In adults, toxic effects on the CNS are common but in children, effects on the heart are common. [8] While the main site of both the clinically desirable and toxic effects of local anaesthetics are thought to be exerted at the voltage-gated sodium channel, many alternative sites, such as a disruption of components of oxidative phosphorylation, have also been considered. In children, especially neonates and infants, the risk of reaching toxic levels might be greater due to an altered pharmacokinetic of local anaesthetics.…”

Section: Discussionmentioning

confidence: 99%

“…[9] Risk of toxicity can be increased by changes in absorption, for example when acidosis occurs in sick children, or by an alteration of the level of binding to components of blood, such as albumin, a1acid Glycoprotein and red blood cells. [8][9][10] Additionally, rates of liver metabolism are reduced in children due to a deficiency of enzymes belonging to the Cytochrome P450 family, especially during the first 36 months of life. Toxicity of anaesthetics also depend on the hepatic extraction ratio which itself depends on liver perfusion.…”

Section: Discussionmentioning

confidence: 99%

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