Lidocaine and Bupivacaine Mixtures for Epidural Blockade

Seow, L. T.; Lips, F. J.; Cousins, M. J.; Mather, Laurence E.

doi:10.1097/00000542-198203000-00004

Cited by 59 publications

(9 citation statements)

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“…The practice of mixing short and long-lasting anaesthetic agents with the aim of achieving rapid onset and long duration drug action is based on the premise there is no drug-drug interaction and that both agents behave as if the other agent were not present. Indeed, pharmacokinetic studies of such mixtures have established their safety based on their serum concentrations being in the same range as those of the component drugs injected (Seow et al, 1982). Hall et al (2001) argued that the drug mass (i.e volume × concentration) was probably the most important single determinant of the extent of spread of the epidural administered anaesthetic solution.…”

Section: Resultsmentioning

confidence: 99%

Comparative evaluation of lignocaine and lignocainebupivacaine for lumbo-sacral epidural block in diazepam sedated West African dwarf goats

Lawan¹,

Falade²,

Adetunji³

2019

Sokoto J. Vet. Sc.

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This study compared the onset of neural blockade, onset and duration of analgesia and duration of recumbency produced in five healthy West African Dwarf (WAD) goats by the lumbo-sacral epidural injections of a mixture of 2mg/kg lignocaine 2% solution and 0.95mg/kg bupivacaine 0.5% solution (LBM) and 4mg/kg lignocaine 2% solution. Associated changes in heart rate (HR), respiratory rate (RR) and rectal temperature (RT) were recorded at 10-min intervals in the initial 1 hour. The onset of neural blockade with LBM (9.6±2.7 min) was significantly (p<0.05) longer with LIG (2.8± 0.4 min) the onset (24.8 ± 3.8 min) and duration (113.8± 16.5 min) of analgesia with LBM were significantly (p<0.05) longer than the onset (11.6 ± 2.4min) and duration (68.6 ±14.9min) of analgesia with LIG respectively. The duration of recumbency with LBM (148.0 ± 9.7min) was also significantly (p<0.05) longer with LIG (81.6 ± 6.5). There were no significant differences (p>0.05) in the physiological parameters between the two groups. It was concluded that epidurally administered LBM had a slower onset of neural blockade but longer onset of analgesia, duration of analgesia and duration of recumbency than with LIG in diazepam-sedated goats. The epidural blockade also produced insignificant changes in the mean HR, RR, and RT responses of the experiment to both drug protocols.

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Section: Resultsmentioning

confidence: 99%

Comparative evaluation of lignocaine and lignocainebupivacaine for lumbo-sacral epidural block in diazepam sedated West African dwarf goats

Lawan¹,

Falade²,

Adetunji³

2019

Sokoto J. Vet. Sc.

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“…When normalised for individual doses, blood concentrations oflignocaine and bupivacaine were similar after injection of a combination ofthe two agents and after injection of each drug alone (Seow et al 1982). Since bupivacaine inhibits the hydrolysis of chloroprocaine, blood or plasma concentrations of the latter agent may be increased when 299 a combination of these drugs is administered (Lalka et al 1978;Raj et al 1980).…”

Section: Combining Local Anaestheticsmentioning

confidence: 95%

“…However, the gains (if any) are small and the rationale for using combinations is questionable (Cousins & Bromage 1988;Seow et al 1982).…”

Section: Combining Local Anaestheticsmentioning

confidence: 99%

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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“…There are both disadvantages and advantages of this mixture. A study done as early as 1982 showed the beneficial effect of mixing bupivacaine and lidocaine for epidural anesthesia [19]. Lidocaine has a quicker onset of action, while bupivacaine continues to maintain the anesthetic action for a longer period.…”

Section: Discussionmentioning

confidence: 99%