Page 69 - BSAVA Guide to Pain Management in Small Animal Practice
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BSAVA Guide to Pain Management in Small Animal Practice
VetBooks.ir with nociceptive bre function returning last. using speci c combinations of volume and
concentration, to cause segmental anaesthesia,
he pro le of di erential recovery depends on
therefore a ecting only the nerves bathed by
the concentration and the anaesthetic molecule
used, with lower concentrations having less the local anaesthetic. The result is a ‘belt’ of
e ect on motor function, and some anaesthesia, with minimally a ected sensory
anaesthetics (bupivacaine, levobupivacaine and and motor function cranially and caudally to the
ropivacaine) presenting a more evident site of administration. The local anaesthetic is
di erential e ect on motor and sensory bres removed from the epidural space mostly by
during the o set period Aguirre et al., 1 . venous drainage and systemic absorption,
Duration of action of local anaesthetics distribution in the epidural fat and
depends mostly on their protein binding, with transmeningeal uptake, but also by exiting the
increased protein binding resulting in longer spinal canal via the intervertebral foramen.
duration of action, because of a slower clearance The larger the volume of drug administered, the
from the administration site. Unfortunately, a high longer the duration of action Burm, 1989;
degree of protein binding also results in more Feldman et al., 1997; Clement et al., 1999; Rose
anaesthetic binding to non speci c sites in the et al., 7; Rata c ak Enselme et al., 7;
tissue adjacent to the nerve to be anaesthetized, onohoe and Pandit, 1 ; Siafaka, n.d. .
with a slower onset of action. Administration of
larger doses will prolong the duration of action, Subarachnoid ‘spinal’ administration
and also result in a faster onset. Addition of The site of action and the disposition of local
vasoconstrictors (generally adrenaline anaesthetics administered in the subarachnoid
1 1 1 prolongs the duration of space (spinal, subarachnoid or intrathecal
action of local anaesthetics by decreasing their anaesthesia are considerably di erent from
clearance, and the e ect is more relevant for those of epidurally administered anaesthetics,
those with a short duration of action (i.e. as the anaesthetic is administered within the
prilocaine, lidocaine . hile most local cerebrospinal uid CS . he sites of action for
anaesthetics at clinical doses cause vasodilation, drugs injected in the subarachnoid space are
ropivacaine causes vasoconstriction, which both the spinal cord and the nerve roots. Since
all neural structures are exposed to the local
explains its longer duration of action (Aguirre et anaesthetic, they are all a ected by the block,
al., 1 ; Becker and Reed, 6 .
resulting in sensory, motor and autonomic
Epidural administration blockade. To some extent, this could be
considered a ‘temporary chemical cordectomy’,
hen administered epidurally, the main site of although the extent of penetration into the
action of local anaesthetics is the nerve roots spinal cord and nerve roots will depend on the
leaving the spinal cord, where the meninges amount and concentration of drug used.
taper o and the anaesthetic can easily reach The disposition of drugs administered
the nerve. Part of the local anaesthetic, intrathecally is still poorly understood, but
especially if administered at high concentrations, possible mechanisms could be epidural
will penetrate the meninges and reach the di usion, spinal cord di usion, and bulk
spinal cord. The arachnoid membrane accounts removal by CSF turnover. Regardless of the
for 9 of the resistance to drug migration. exact mechanism, the duration of action of
Transmeningeal uptake may also be promoted intrathecal anaesthetics is considerably shorter
by addition of vasoconstrictors, which reduce than epidural administration and depends on
systemic absorption, therefore maintaining a the total amount of drug administered and, to
high concentration of drug in the epidural space some extent, on its concentration, with lower
that drives the uptake. he e ect is less concentrations having a shorter e ect
pronounced for ropivacaine, because of its (Clement et al., 1999; Rose et al., 7;
intrinsic vasoconstrictor e ect. he preferential Sarotti et al., 11; Sarotti et al., 1 ; e
extramedullary site of action can be exploited, ennaro et al., 14 .
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