摘要
In the study by Tan et al. [1], the authors identified several independent risk factors for chronic postsurgical pain (CPSP) after breast cancer surgery, and developed a risk prediction model to predict CPSP. The authors rigorously evaluated the pre-operative and intra-operative risk factors for CPSP. However, only the severity of pain and opioid consumption in the postoperative period were reported, and the assessment of postoperative risk factors was limited to 72 h following surgery. It is unlikely that all patients who report persistent pain in the early postoperative phase, for example, within 2–4 weeks, will develop CPSP at 4 months. However, it is important to identify the factors that make subacute postoperative pain become chronic. One such risk factor is acute neuropathic pain after surgery. Recently, a prospective cohort study found that the presence of neuropathic pain characteristics (pruritus and an unpleasant cold feeling in the painful area) within 2 weeks following surgery were independent risk factors for CPSP [2]. Likewise, scar hyperesthesia at 6 weeks after cosmetic augmentation mammoplasty increased the odds of CPSP [3]. The risk of nerve injuries is high during breast surgery and this may lead to acute postsurgical neuralgia. As a result of acute neuropathic pain, peripheral and central sensitisation start in the transition phase of the postoperative period, leading to CPSP. In addition, secondary hyperalgesia around the wound area is an indicator of central sensitisation and may be a predictor of CPSP. However, the authors did not assess the neuropathic component of pain, nor secondary hyperalgesia, in the postoperative period. Not all acute neuropathic pain leads to CPSP, but the risk is likely high. Other contributing factors for CPSP that were missing were postsurgical chemotherapy and psychosocial changes that occur after cancer surgery. Severe acute postoperative pain has consistently been linked with the development of CPSP. However, the authors did not find a significant association between severity of postsurgical pain and CPSP in a multivariable analysis. It has been shown that, in addition to the intensity of acute postoperative pain, it is the duration of severe pain during the first 24 h postoperatively, and the speed of resolution of pain during the first five postoperative days, that impact the occurrence of CPSP [4, 5]. As a result, pain trajectories other than pain intensity may be predictive of developing chronic postoperative pain. Whether the above-mentioned postsurgical events are predictors or effect modifiers/mediators for CPSP after breast surgery, they cannot be ignored, and further studies are required.