Chronic post-surgical pain: an under-recognized problem

5 May 2015  |  Print

Chronic post-surgical pain: an under-recognized problem

Chronic post-surgical pain (CPSP) is highly prevalent and frequently severe, and yet is often neglected.[1] How has this happened? It may simply be that we do not yet understand it well enough to manage it effectively – the physiological mechanisms that underlie CPSP are poorly characterized.[2] Furthermore, the treatment options are limited, not least because CPSP is usually at least partly neuropathic.[3]

However, the pain associated with CPSP can be severe in around 2-10% of cases,[4] and this can have highly significant implications for quality of life. It is therefore essential that physicians involved in the management of pain grasp the gravity of CPSP and act appropriately to minimize the risk. Here, we discuss some of the key questions relating to this condition

How frequent is CPSP?

The incidence of CPSP varies greatly between different types of procedure.[3] For example, following amputation surgeries, incidences of 50-85% have been reported. Similarly, mastectomy is associated with high rates of CPSP, with incidences in the region of 20-50%.[3] These are concerning figures, even though these procedures are not among the most common types of surgery undertaken. However, even some of the most frequently performed procedures are associated with alarmingly high rates of CPSP:[3]

  • Cardiac surgery, 30-55%
  • Hernia repair, 5-35%
  • Hip replacement, 12%
  • Cesarean section, 6%

What causes CPSP?

Although the pathophysiological mechanisms that underlie the development of CPSP are not well understood, peripheral and central sensitization are thought to play a key role.[2]

After a surgical procedure, inflammatory mediators are released by damaged tissues, and this triggers an inflammatory cascade. As a result, pain receptors often have a reduced threshold and increased responsiveness to subsequent input in the damaged tissue – a phenomenon known as ‘peripheral sensitization’.[2]

A similar process can also occur more centrally as a result of the so-called ‘afferent barrage’ induced by the activation of pain receptors during and after surgery. This ‘central sensitization’ involves an alteration in the responsiveness of central neurons, for example in the spinal cord. It results in a variety of properties – such as increased responsiveness to activation, reduced threshold, expanded receptive fields, and spontaneous activity – that can contribute to increased pain after surgery.[2]

These processes may initially have a protective function and help to promote healing. It is only when they become maladaptive that harmful consequences occur. Inhibition of peripheral and central sensitization may therefore inhibit the processes responsible for the development of CPSP.[2]

What are the risk factors for CPSP?

Prediction of CPSP is important to allow healthcare professionals to tailor their management of surgical patients and thereby decrease the risk of chronic pain. Factors associated with CPSP typically fall into one of three categories:

  1. Patient-related factors:
    • Preoperative pain history – A number of studies have shown that preoperative pain is significantly related to CPSP. For example, in a meta-analysis of 32 studies examining predictors of CPSP after total knee arthroplasty, pre-operative pain was the most commonly observed factor.[5]
    • Psychological vulnerability – This may include a number of different elements, including depression, anxiety and negative pain-coping strategies. In a meta-analysis of 29 studies on this issue, 16 studies (55%) reported a statistically significant association between anxiety or pain catastrophizing and CPSP.[6]
    • Genetic factors – It is likely that genetic polymorphisms play some role in susceptibility to CPSP. For example, specific alleles of a neuronal potassium channel and of a protein involved in receptor trafficking have each been independently linked with chronic pain.[7,8]
  2. Surgical factors:
    • Experience of the surgical unit – A study comparing chronic symptoms following mastectomy among women operated in a high-volume versus low-volume surgical unit found that chronic pain was less common in the former (43% vs 56%, respectively; p<0.05).[9] This implies that better surgical procedures in the more experienced unit may have reduced the risk of CPSP.
    • Surgical technique – The way that a surgery is performed can have a major impact on pain outcomes. For example, in a study of hernia repair procedures, division of nerves during the surgery was clearly correlated with the development of CPSP.[10]
  3. Early post-surgical warnings:
    • Acute post-operative pain – Both initial pain intensity and pain resolution during the first five post-operative days have been shown to independently predict for the development of CPSP 6 months post-surgery.[11]
    • Detection of neuropathic pain characteristics – It is important that these are detected early so that appropriate management strategies can be implemented. However, post-surgical pain is typically less well diagnosed than neuropathic pain.[12]

Conclusions

CPSP is common but under-recognized issue. Although further work is required to better understand its pathophysiology, there are a number of well-characterized risk factors. These have now been collated into an easy-to-use risk index for the prediction of CPSP, based on key factors such as preoperative pain, post-surgical acute pain and co-morbid stress symptoms.[13]

If we can better identify at-risk patients and then manage these patients appropriately, we can improve our chances of preventing CPSP.

References:

  1. 1. Andreae MH, Andreae DA. Regional anaesthesia to prevent chronic pain after surgery: a Cochrane systematic review and meta-analysis. Br J Anaesth 2013;111:711-720.
  1. 2. Clarke H, Woodhouse LJ, Kennedy D, Stratford P, Katz J. Strategies Aimed at Preventing Chronic Post-surgical Pain: Comprehensive Perioperative Pain Management after Total Joint Replacement Surgery. Physiother Can 2011;63:289-304.
  1. 3. Macrae WA. Chronic post-surgical pain: 10 years on. Br J Anaesth 2008;101:77-86.
  1. 4.Kehlet H, Jensen TS, Woolf CJ. Persistent postsurgical pain: risk factors and prevention. Lancet 2006;367:1618-1625.
  1. 5. Lewis GN, Rice DA, McNair PJ, Kluger M. Predictors of persistent pain after total knee arthroplasty: a systematic review and meta-analysis. Br J Anaesth 2014 [Epub ahead of print].
  1. 6. Theunissen M, Peters ML, Bruce J, Gramke HF, Marcus MA. Preoperative anxiety and catastrophizing: a systematic review and meta-analysis of the association with chronic postsurgical pain. Clin J Pain 2012;28:819-841.
  1. 7. Costigan M, Belfer I, Griffin RS, et al. Multiple chronic pain states are associated with a common amino acid-changing allele in KCNS1. Brain 2010;133:2519-2527.
  1. 8. Nissenbaum J, Devor M, Seltzer Z, et al. Susceptibility to chronic pain following nerve injury is genetically affected by CACNG2. Genome Res 2010;20:1180-1190.
  1. 9. Tasmuth T, Blomqvist C, Kalso E. Chronic post-treatment symptoms in patients with breast cancer operated in different surgical units. Eur J Surg Oncol 1999;25:38-43.
  1. 10. Alfieri S, Rotondi F, Di Giorgio A, et al. Influence of preservation versus division of ilioinguinal, iliohypogastric, and genital nerves during open mesh herniorrhaphy: prospective multicentric study of chronic pain. Ann Surg 2006;243:553-558.
  1. 11. Althaus A, Arránz Becker O, Neugebauer E. Distinguishing between pain intensity and pain resolution: using acute post-surgical pain trajectories to predict chronic post-surgical pain. Eur J Pain 2014;18:513-521.
  1. 12. Martinez V, Attal N, Vanzo B, et al. Adherence of French GPs to chronic neuropathic pain clinical guidelines: results of a cross-sectional, randomized, “e” case-vignette survey. PLoS One 2014;9:e93855
  1. 13. Althaus A, Hinrichs-Rocker A, Chapman R, et al. Development of a risk index for the prediction of chronic post-surgical pain. Eur J Pain 2012;16:901-910.

 

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