Page 59 - BSAVA Guide to Pain Management in Small Animal Practice
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BSAVA Guide to Pain Management in Small Animal Practice



        VetBooks.ir  Butorphanol: Butorphanol is a KOP agonist and   in ammatory and analgesic e ects are
           a   P antagonist.  here is con icting evidence,
                                                  unrelated  B  rkman, 199 ; Cashman, 1996;
                                                  Vane and Botting, 1997; Burian and  eisslinger,
           but most anaesthetists agree that butorphanol
           is a good sedative but a poor analgesic. Its        . Prostaglandins act peripherally as
           usefulness as an analgesic is also limited by its   proin ammatory mediators, promoting oedema
           short duration of action, which is about      formation, sensitization of nociceptors and
           minutes in dogs, and probably about 6    hyperalgesia. Proposed central mechanisms of
           minutes in cats. Butorphanol is useful for   action include interference with the descending
           antagoni ing unwanted e ects of   P    nociceptive control system, either mediated by
           analgesics (e.g. dysphoria), while maintaining   a direct e ect on prostaglandin production, or
           some analgesia, and can be titrated to e ect for   by interference with endogenous opioid
           this purpose.                          peptides, the serotoninergic mechanisms or
                                                  NMDA receptors and excitatory amino acids
           Codeine: Codeine is a full MOP agonist and is   (Vanegas et al.,   1  . NSAI s also interfere with
           licensed in dogs in the UK in combination with   the mechanisms of cell adhesion, including
           paracetamol (acetaminophen) for oral   leukocytes, platelets and tumour cells. Speci c
           administration. Codeine has very low oral   mechanisms of interference with cell adhesion
           bioavailability in dogs, but an active metabolite,   and their clinical relevance depend on the class
           codeine 6 glucuronide, is formed after oral   of NSAIDs considered (Cronstein et al., 1994;
           administration, which may provide analgesia.   Ulrich et al.,    6; Silver and Lillich,   16 .
           There is very little research on codeine in cats    hile older NSAI s were C   1 selective or
           and it cannot be recommended in this species.  poorly selective COX inhibitors, modern NSAIDs
                                                  have greater selectivity towards C    , with
                                                  diarylimidazol derivatives (coxibs) currently
           drugs                                  having the greatest selectivity.
           Non steroidal anti in ammatory drugs  NSAI s    C   1 and C     are membrane
           include many drugs used to provide analgesia,   associated en ymes, with C   1 traditionally
           decrease in ammation and control fever.   considered the ‘housekeeping’ isoform
           Licensed products for use in dogs and cats   responsible for physiological production of P s,
           include  carprofen, cimicoxib,  rocoxib,   and C     the inductive isoform whose activity
           ketoprofen, mavacoxib, meloxicam,      is increased in pathological conditions. More
           robenacoxib, and tolfenamic acid. Considering   recent evidence has demonstrated that this
           that acute and chronic and persistent   distinction is simplistic, and both C   1 and
           nociceptive pain have an in ammatory   C     have physiological and pathological
           component in the vast majority of cases,   roles. The quantity and quality of prostanoid
           NSAIDs play a vital role in providing   produced by COXs depends on the tissue and
           perioperative and long-term analgesia. They   the triggering stimulus; thus the nature of the
           are also e ective in treating certain types of   cells present in the in ammatory site a ects the
           cancer pain.                           pro le of P  production   ay  ugford et al.,
                                                      ;  ilson and Chandrasekharan,    4;
           Mechanism of action                    Sessions et al.,      .
           NSAIDs are non-narcotic and their mechanism
           of action consists mainly of peripheral inhibition   Indications, contraindications and
           of the activity of cyclo-oxygenase enzyme   clinical use
            C   1 and C     , and thus of tissue   NSAIDs are weakly acidic, highly protein-
           prostaglandin  P   biosynthesis, but there is   bound compounds, and generally have good
           increasing evidence that NSAIDs may also have   oral bioavailability. Timing of administration
           a central mechanism of action, mostly   with respect to anaesthesia, duration of
           supported clinically by the fact that anti-  treatment, and contraindications are speci c to

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