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5. There are no consistent differences between ropivacaine, levobupivacaine and bupivacaine
when given in low doses for regional analgesia (epidural and peripheral nerve blockade) in
terms of quality of analgesia or motor blockade (U) (Level II).
6. Cardiovascular and central nervous system toxicity of the stereospecific isomers
ropivacaine and levobupivacaine is less severe than with racemic bupivacaine (U) (Level II).
7. Lipid emulsion is effective in resuscitation of circulatory collapse due to local anaesthetic
toxicity, however uncertainties relating to dosage, efficacy and side effects still remain and
therefore it is appropriate to administer lipid emulsion once advanced cardiac life support
has begun and convulsions are controlled (N) (Level IV).
The following tick box represents conclusions based on clinical experience and expert
opinion.
Case reports following accidental overdose with ropivacaine and bupivacaine suggest that
resuscitation is likely to be more successful with ropivacaine (U).
5.2 OPIOIDS
5.2.1 Neuraxial opioids
Opioid receptors were described in the spinal cord of the rat in 1976 (Pert et al, 1976) and the
CHAPTER 5 these animals (Yaksh & Rudy, 1976). Opioid analgesia is spinally mediated via presynaptic and
same year a potent analgesic effect of directly applied intrathecal morphine was reported in
postsynaptic receptors in the substantia gelatinosa in the dorsal horn (Yaksh, 1981). Spinal
opioid receptors are 70% mu, 24% delta and 6% kappa (Treman & Bonica, 2001), with 70% of all
mu and delta receptors being presynaptic (predominantly small primary afferents) and
commonly co‐located, and kappa receptors being more commonly postsynaptic.
Antinociception may be further augmented by descending inhibition from mu‐opioid receptor
activation in the periaqueductal area of the brain, which may be potentiated by neuraxial
opioids. In addition to this, a local anaesthetic action has been described for pethidine
(meperidine), which may contribute to the clinical effect when administered intrathecally (Jaffe
& Rowe, 1996). The first clinical use of intrathecal morphine was for analgesia in cancer patients
(Wang et al, 1979).
Neuraxial opioids may cause respiratory depression, sedation, nausea, vomiting, pruritus,
urinary retention and decreased gastrointestinal motility. Depending on type and dose of the
opioid, a combination of spinal and systemic mechanisms may be responsible for these
adverse effects. Many of these effects are more frequent with morphine and are to some
extent dose related (Dahl et al, 1999 Level I; Cole et al, 2000 Level I). Late onset respiratory
depression, which is believed to be a result of the cephalad spread of opioids within the
cerebrospinal fluid, is also seen more commonly with hydrophilic opioids such as morphine
(Cousins & Mather, 1984).
Intrathecal opioids
The lipid solubility of opioids largely determines the speed of onset and duration of intrathecal
analgesia; hydrophilic drugs (eg morphine) have a slower onset of action and longer half‐lives
in cerebrospinal fluid with greater dorsal horn bioavailability and greater cephalad migration
compared with lipophilic opioids (eg fentanyl) (Bernards et al, 2003).
126 Acute Pain Management: Scientific Evidence
