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Laboratory Investigation:
J. M. Cuellar, R. C. Dutton, J. F. Antognini, and E. Carstens
Differential effects of halothane and isoflurane on lumbar dorsal horn neuronal windup and excitability
Br. J. Anaesth. 2005; 0: aei107v1 [Abstract] [PDF]
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[Read E-letter] Avoid the transition from acute to chronic pain.
Alfred P J Lake   (11 May 2005)

Avoid the transition from acute to chronic pain. 11 May 2005
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Alfred P J Lake,
Consultant in Anaesthesia and Pain Management
Glan Clwyd Hospital, Rhyl, Denbighshire LL18 5UJ

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Re: Avoid the transition from acute to chronic pain.

Wind-up, on which the authors report, is the progressive increase in c-fibre evoked nociceptive neuronal responses, both directly and indirectly, in the dorsal horn of the spinal cord which results in the creation of a facilitated state and an exaggerated response to subsequent noxious stimuli.

Peripheral injury occurring in association with surgery is itself a repeated noxious stimulation through acute tissue damage and the development of inflammation. The resultant characteristic excitation of spinal cord dorsal horn cells, also called central sensitisation, is the magnification and prolongation of the response to subsequent sensory stimuli in the wide dynamic range (WDR) neurones mediated through the key regulator the N-methyl-D-aspartate (NMDA) receptor in post-synaptic location (1) with opioids, anaesthetic agents and NMDA antagonists having differential effects related to their sites of action (2,3).

The acute pain associated with surgery is the initiation of an extensive, persistent, nociceptive and behavioural cascade which can lead to the development of chronic pain following surgery (4) which remains an ongoing significant problem about which we, as anaesthetists, could do something useful. Unfortunately, by working hard to deliver the light balanced anaesthesia which is designed today to deliver rapid recovery, we may have disregarded the fundamental importance of abolishing noxious reflexes at the spinal level where volatile anaesthetics predominantly act.

Inhalational anaesthetics affect spinal cord processing and may modulate the response to noxious stimuli by suppressing transmission of nociception through modification of the activity of NMDA receptors; GABA agonist action may explain the inhibitory effects of inhalational (and intravenous) anaesthetic agents on spinal sensitisation. Each volatile anaesthetic agent has been known for some time to have its own pattern of action not quite identical to the others (5).

The introduction of the concept of balanced anaesthesia may have, inadvertently, created a problem and now we must move on to ensure that balance is delivered not only with respect to sleep, analgesia and relaxation but also to include the suppression of spinal sensitisation (6).

The key is to provide an anaesthetic of sufficient depth, the 0.8 – 1.2 MAC delivered to the rats as reported in the study could not in all likelihood be expected to suppress wind-up. Indeed, the level of anaesthesia required to prevent the post-injury state of facilitated processing or wind up (MAC-FAC) may not be achievable with inhalational agents alone but can be with the addition of preoperative intrathecal opiate at a cost of little physiologic compromise (7) which, with the avoidance of agents that may have a detrimental effect (8) could mitigate the development of chronic pain.

Administration of the inhalational agent at a higher concentration than is usual practice has already been shown to reduce postoperative pain in patients receiving isoflurane undergoing bariatric surgery (9).

To avoid the transition from acute perioperative to chronic persistent pain must become the anaesthetist’s goal (10).

1. Doubell TP, Mannion RJ, Woolf CJ. The dorsal horn: state-dependent sensory processing, plasticity and the generation of pain. In: Wall PD, Melzack R, eds. Textbook of Pain, 4th edn. Edinburgh: Churchill Livingstone, 1999: 165-181.

2. Woolf CJ, Bennett GJ, Doherty M, Dubner R, Kidd B, Koltzenburg M, et al. Towards a mechanism-based classification of pain? Pain 1998; 77: 227-229.

3. Dickenson AH. A cure for wind up: NMDA receptor antagonists as potential analgesics. Trends Pharmacol Sci 1990; 11: 307-309.

4. Macrae WA: Chronic pain after surgery. Br J Anaesth 2001; 87: 88- 98

5. O’Connor TC, Abram SE. Inhibition of nociception-induced spinal sensitization by anesthetic agents. Anesthesiology 1995; 82: 259-266.

6. Lake APJ. Balanced Anaesthesia 2005: Avoiding the transition from acute to chronic pain. S Afr J Anaesth Analg 2005; 11: 14-18.

7. Abram SE, Yaksh TL. Morphine, but not inhalation anesthesia, blocks post-injury facilitation. Anesthesiology 1993; 78: 713-721.

8. Lake APJ, Hugo S. Barbiturate hyperalgesia revisited. Reg Anesth Pain Med 2004; 29: 70-71.

9. Gurman GM, Popescu M, Weksler N, Steiner O, Avinoah E, Porath A. Influence of the cortical electrical activity level during general anaesthesia on the severity of immediate postoperative pain in the morbidly obese. Acta Anaesthesiol Scand 2003; 47: 804-808

10. Kehlet H, Dahl JB. Anaesthesia, surgery and challenges in postoperative recovery. Lancet 2003; 362: 1921-1928.

Conflict of Interest:

None declared