Page 169 Acute Pain Management

5. REGIONALLY AND LOCALLY ADMINISTERED

ANALGESIC DRUGS

5.1 LOCAL ANAESTHETICS

Local anaesthetics exert their effect as analgesics by the blockade of sodium channels and
hence impeding neuronal excitation and/or conduction.
5.1.1 Short-duration local anaesthetics

Lignocaine (lidocaine) is the most widely used short‐duration local anaesthetic in acute pain
management. Although the plasma half‐life is approximately 90 minutes, the duration of local
anaesthetic effect depends very much on the site of administration, dose administered and
the presence or absence of vasoconstrictors. Although lignocaine is hydrophilic, it is delivered
in high concentrations and therefore usually diffuses well into nerve bundles, resulting in little
separation of sensory and motor blocking actions (Covino & Wildsmith, 1998).
The use of lignocaine in ongoing acute pain management is usually restricted to the short‐term
re‐establishment of a local anaesthetic infusion block; it is unsuited to long‐term (ie days) use
because of the development of tachyphylaxis or acute tolerance (Mogensen, 1995). For
example, 24‐hour continuous perineural infusions of lignocaine resulted in less effective
analgesia and more motor block than infusions of the long‐acting local anaesthetic agent
ropivacaine (Casati, Vinciguerra et al, 2003 Level II). CHAPTER 5
5.1.2 Long-duration local anaesthetics

The three commonly used long‐duration local anaesthetic agents, bupivacaine,
levobupivacaine and ropivacaine, are structurally related (Markham & Faulds, 1996; McLeod &
Burke, 2001; Casati & Putzu, 2005). Whereas bupivacaine is a racemic mixture of S‐ and R‐
enantiomers, levobupivacaine is the S‐ (or levo) enantiomer of bupivacaine; ropivacaine is
likewise an S‐enantiomer.
The issue with relative potency emerges with lower doses and concentrations of local
anaesthetics. When doses are carefully titrated, a minimum local anaesthetic concentration
(MLAC) can be found at which 50% of patients will achieve a satisfactory analgesic block. In
obstetric epidural analgesia, two separate studies found the MLAC of bupivacaine was 0.6
times that of ropivacaine (Capogna et al, 1999 Level II; Polley et al, 1999 Level II). The motor‐
blocking potency showed a similar ratio of 0.66 (Lacassie et al, 2002 Level II).
When comparing bupivacaine with levobupivacaine, the ‘percentage’ bupivacaine solution is
by weight of bupivacaine hydrochloride, whereas % levobupivacaine solution is for the active
molecule alone (even though presented as the hydrochloride). This means that the molar dose
of equal ‘percentage concentration’ is 13% higher for levobupivacaine (Schug, 2001). The
sensory MLAC potency ratio of levobupivacaine to bupivacaine is 0.98, although if correction is
made for molar concentrations this falls to 0.87 (neither value being different from unity)
(Lyons et al, 1998 Level II). Levobupivacaine has been shown to have slightly less motor‐blocking
capacity than bupivacaine with a levobupivacaine/ bupivacaine potency ratio for epidural
motor blockade of 0.87 (95% CI, 0.77‐0.98) (Lacassie & Columb, 2003 Level II). Another labour
epidural analgesia study has found no difference in MLAC between levobupivacaine and

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