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that patients often relate the onset of their pain to an acute injury, drawing attention to the
need to prevent the progression from acute to chronic pain (Blyth et al, 2003 Level IV).
The association between acute and chronic pain is well‐defined, but few randomised
controlled studies have addressed the aetiology, time course, prevention or therapy of the
transition between the two pain states. Acute pain states that may progress to chronic pain
include postoperative and post‐traumatic pain (see below and Section 9.1), acute back pain
(see Section 9.4) and herpes zoster (see Section 9.6.2).
Chronic pain is common after surgery (see Table 1.2) (Kehlet et al, 2006; Macrae, 2008) and
represents a significant source of ongoing disability, often with considerable economic
consequences. Such pain frequently has a neuropathic element. For example, all patients with
chronic postherniorrhaphy pain had features of neuropathic pain (Aasvang et al, 2008 Level IV).
CHAPTER 1 There is some evidence that specific early analgesic interventions may reduce the incidence of
Neuropathic pain may be seen early in the postoperative period (see Section 9.1.1).
chronic pain after surgery. Epidural analgesia initiated prior to thoracotomy and continued
into the postoperative period resulted in significantly fewer patients reporting pain 6 months
later compared with patients who had received intravenous (IV) PCA opioids for postoperative
analgesia (45% vs 78% respectively) (Senturk et al, 2002 Level II). There was no statistically
significant difference in the incidence of chronic pain between patients given pre‐emptive
epidural analgesia (initiated prior to surgery) and patients in whom epidural analgesia was
commenced after surgery – 39.6% vs 48.6% (Bong et al, 2005 Level I). In patients undergoing
colonic resection, continuous perioperative epidural analgesia led to a lower risk of developing
persistent pain up to 1 year after surgery compared with IV analgesia (Lavand'homme et al,
2005 Level II).
Spinal anaesthesia in comparison to general anaesthesia reduced the risk of chronic
postsurgical pain after Caesarean section (Nikolajsen et al, 2004 Level IV) and hysterectomy (OR:
0.42; CI 0.21 to 0.85) (Brandsborg et al, 2007 Level IV). The latter study found no difference in risk
between abdominal and vaginal hysterectomy.
An infusion of ropivacaine into the site of iliac crest bone graft harvest resulted in significantly
less pain in the iliac crest during movement at 3 months (Blumenthal et al, 2005 Level II).
Local anaesthetic wound infiltration reduced the proportion of patients with persistent pain
and neuropathic pain 2 months following intracranial tumour resection (Batoz et al, 2009
Level II).
Preincisional paravertebral block reduced prevalence and intensity of pain 12 months after
breast surgery (Kairaluoma et al, 2006 Level II). Perioperative use of gabapentin or mexiletine
after mastectomy reduced the incidence of neuropathic pain at 6 months postoperatively,
from 25% in the placebo to 5% in both treatment groups (Fassoulaki et al, 2002 Level II). Similar
protective results were achieved by the same group by the use of a eutectic mixture of local
anaesthetics alone (Fassoulaki et al, 2000 Level II) or in combination with gabapentin (Fassoulaki
et al, 2005 Level II).
Deliberate neurectomy (of the ilioinguinal nerve) for inguinal hernia repair reduced the
incidence of chronic postsurgical pain (from 21% to 6%) (Malekpour et al, 2008 Level II), although
this was not seen in an earlier study (Picchio et al, 2004 Level II).
See Section 1.5 below for more examples of the use of pre‐emptive and preventive analgesic
interventions in attempts to reduce the risk of persistent pain after surgery, and Sections 9.1.2
to 9.1.3 for more details on prevention of phantom pain after limb amputation and other
postoperative pain syndromes.

10 Acute Pain Management: Scientific Evidence