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1.3.2 Mechanisms for the progression from acute to chronic pain
The pathophysiological processes that occur after tissue or nerve injury mean that acute pain
may become persistent (Cousins et al, 2000). Such processes include inflammation at the site of
tissue damage with a barrage of afferent nociceptor activity that produces changes in the
peripheral nerves, spinal cord, higher central pain pathways and the sympathetic nervous
system (see Section 1.1).
After limb amputation, reorganisation or remapping of the somatosensory cortex and other
cortical structures may be a contributory mechanism in the development of phantom limb
pain (Flor et al, 1995; Grusser et al, 2004). There is preclinical and clinical evidence of a genetic
predisposition for chronic pain (Mogil, 1999), although one study found that an inherited
component did not feature in the development of phantom pain in members of the same
CHAPTER 1 Descending pathways of pain control may be another relevant factor as patients with efficient
family who all had a limb amputation (Schott, 1986).
diffuse noxious inhibitory control (DNIC) had a reduced risk of developing chronic postsurgical
pain (Yarnitsky et al, 2008 Level III‐2).
Key messages
1. Some specific early anaesthetic and/or analgesic interventions reduce the incidence of
chronic pain after surgery (S) (Level II).
2. Chronic postsurgical pain is common and may lead to significant disability (U) (Level IV).
3. Risk factors that predispose to the development of chronic postsurgical pain include the
severity of pre‐ and postoperative pain, intraoperative nerve injury and psychosocial
factors (U) (Level IV).
4. All patients with chronic postherniorrhaphy pain had features of neuropathic pain (N)
(Level IV).
5 Spinal anaesthesia in comparison to general anaesthesia reduces the risk of chronic
postsurgical pain after hysterectomy and Caesarean section (N) (Level IV).
1.4 PRE-EMPTIVE AND PREVENTIVE ANALGESIA
In laboratory studies, administration of an analgesic prior to an acute pain stimulus more
effectively minimises dorsal horn changes associated with central sensitisation than the same
analgesic given after the pain state is established (see Section 1.1) (Woolf, 1983). This led to the
hypothesis that pain relief prior to surgery may enhance postoperative pain management –
that is, ‘pre‐emptive preoperative analgesia’ (Wall, 1988). However, individual clinical studies
have reported conflicting outcomes when comparing ‘preincisional’ with ‘postincisional’
interventions. In part this relates to variability in definitions, deficiencies in clinical trial design
and differences in the outcomes available to laboratory and clinical investigators (Kissin, 1994;
Katz & McCartney, 2002).
As the process of central sensitisation relates not only to skin incision but also to the extent of
intraoperative tissue injury and postoperative inflammation, the focus has shifted from the
timing of a single intervention to the concept of ‘protective’ and therefore ‘preventive’
analgesia (Kissin, 1994) (see Table 1.4). The differences in these terms relates to the outcomes
being described, because all rely on minimising sensitisation. Pre‐emptive analgesia has been
described above and is measured in terms of pain intensity or related outcomes. Protective
analgesia describes a technique that reduces measures of sensitisation such as hyperalgesia.
12 Acute Pain Management: Scientific Evidence
