Chronic post-surgical pain

Abstract

Chronic post-surgical pain (CPSP) is one of the most common and serious complications after surgery. There is no universally agreed definition of CPSP; however, the working definition proposed by Macrae and Davies is commonly used (Fig. 1). CPSP is associated with increased analgesic use, restriction of activities of daily living, significant effects on quality of life, and increased health-care utilization. More than 4 million people undergo surgery every year in the UK, so CPSP poses a significant economic and health-care burden. Not all studies are consistent about the incidence of CPSP; there are wide variations between different surgical procedures (Table 1). Some of this variability is likely to result from lack of clarity in the definition of CPSP, small sample sizes, poor questionnaire response rates, and selection bias. Nerve injury during surgery has been implicated in the development of CPSP; some (but not all) patients with CPSP have neuropathic pain. Inflammatory and immune reactions after damage to axons results in release of neurotransmitters that act locally and in the spinal cord to produce hypersensitivity and ectopic neural activity; this contributes to central sensitization (Fig. 2). Central sensitization occurs when repetitive nociceptive stimuli result in altered dorsal horn activity and amplification of sensory flow; this can lead to persistent nervous system changes, for example, death of inhibitory neurones, their replacement with excitatory afferent neurones, and microglial activation. These changes lead to evoked and spontaneous symptoms associated with neuropathic pain, for example, allodynia and hyperalgesia. CPSP is reported in more than 50% of patients who have surgery associated with nerve and tissue damage, for example, mastectomy, thoracotomy, and amputation. Despite this, there is no simple relationship between nerve injury during surgery and the development of CPSP. There is no association between intercostal nerve damage assessed at the time of thoracotomy by nerve conduction studies and the development of chronic pain 3 months later. Paradoxically, rib resection, which results in more intercostal nerve damage, is associated with a reduced incidence of post-thoracotomy neuralgia. Similarly, although damage to the intercostobrachial nerve has been implicated in the development of CPSP after mastectomy, many patients with objective signs of nerve injury (such as numbness) do not develop chronic pain. In addition, in other surgical procedures associated with nerve damage, not all patients with CPSP have neuropathic pain, for example, among thoracic surgery patients with CPSP, only half had significant neuropathic symptoms identified by a validated questionnaire. Patients with chronic pain after surgical procedures such as hip arthroplasty and hysterectomy do not demonstrate sensory loss, suggesting that mechanisms other than nerve injury are responsible for ongoing pain in these patients. Therefore, any link between nerve damage during surgery and the development of CPSP is complicated. Not all patients with nerve damage develop CPSP, and those who do develop CPSP do not necessarily have neuropathic pain. Some operations not associated with nerve damage can result in CPSP. Although the mechanisms behind the development of CPSP have yet to be fully elucidated, a number of risk factors have been identified. As our understanding of the pathophysiology, risk factors, and prevention of CPSP expands, the traditional focus of the anaesthetist on managing acute perioperative pain should include identifying and managing patients at risk of developing CPSP.