SeriesTransition from acute to chronic pain after surgery
Introduction
Acute pain is almost ubiquitous after surgery. Fortunately, it can be controlled and mostly resolves within 1 week. It should not cause distress or limit postoperative recovery.1 However, for some patients acute postoperative pain persists beyond the usual time of tissue healing and transitions into a chronic pain state.2, 3, 4, 5, 6
The prevalence of chronic postsurgical pain (CPSP), which is bad enough to cause substantial functional impairment, is approximately 10% after all surgeries (table 1).6 Globally, more than 320 million people have surgery each year, which represents a vast potential for CPSP.25 As a result, CPSP is increasingly recognised as a public health problem, not only because of the discomfort, distress, and disability it causes, but also because past approaches to managing it have contributed substantially to the current opioid crisis.26 The use of opioids for atients who have surgery presents a particularly challenging problem requiring clinicians to balance two competing interests: managing acute pain in the immediate postoperative period and minimising the risks of persistent opioid use after surgery. Finding ways to minimise this risk is particularly salient in light of a growing literature suggesting that patients who have had surgery are at increased risk of chronic opioid use.27 As a result, in 2016, the Joint Commission in the USA began a project to revise its pain standards and address the opioid epidemic.26 In January, 2018, the Commission added an emphasis on the need to actively engage medical staff and hospital leaders to include strategies to decrease opioid use. This included the use of at least one of non-pharmacological modality for pain treatment and access to prescription drug monitoring programmes. There was also a stronger focus on pain assessments of how the pain affects patients' physical function.28
Postsurgical pain is a paradigm for understanding and studying other pain that is also iatrogenic.29, 30 Because CPSP occurs from a planned incision at a specified point in time, it has the potential to be prevented and better controlled. However, there are many factors that contribute to the development and persistence of CPSP, and only some of these are related to the surgery. As with non-surgical chronic pain, psychological and social factors have an important influence. All clinicians—not just surgeons and anaesthetists—should have some knowledge on CPSP and how to manage established cases, which can persist for months or years after the procedure. As with many other chronic conditions, early intervention is likely to improve outcomes and so identifying patients at risk is crucial.
Section snippets
Definition
CPSP is pain that occurs at the site of the incision or related areas of the surgery and persists a month longer than it takes for most injured tissues to fully heal. Consequently, the time of onset has mostly been set between 3 and 6 months.22, 31, 32 Definitions of CPSP also vary as to whether or not other causes of pain, such as disease recurrence after surgery or presence of a pre-existing pain syndrome, are included under the CPSP rubric.32 For example, chronic pain after lumbar spine
Clinical features
The nature of CPSP is often poorly characterised in clinical studies,35 but aching is the most commonly chosen sensory descriptor of persistent pain after a range of different surgical procedures.9 Neuropathic descriptors such as hyperalgesia (heightened sensitivity to painful stimuli), dysaesthesia (an unpleasant, abnormal sense of touch), and allodynia (sensitivity to normally non-painful, often repetitive, stimulation) are frequently used. These descriptors suggest that nerve damage during
Epidemiology: incidence and prevalence
The definitional issues related to chronology and whether recurrence of pre-existing pain is included have hampered definitively establishing the true incidence and prevalence of CPSP. Methodological issues related to data collection have also contributed to this situation. Most studies report on data collected in a single institution or at a national level but this can be problematic, for different reasons.42 Single institution studies use patient-based data from the perioperative period, are
Natural history and prognosis of CPSP
Without large, long-term, prospective studies, the natural history and prognosis of CPSP is hard to predict. On the basis of data in table 1 CPSP does appear to often resolve by the end of the first year. In one study,42 the syndrome was reported to be present 12 months after surgery in 315 (14%) of 3120 patients, being moderate in 12% and severe in 2%. In the aforementioned Tromso study,46 40% of patients reported CPSP an average of 18 months after surgery, and 18% rated it as moderate or
Mechanisms of transition from acute to CPSP
Some molecular mechanisms responsible for the transition of acute to chronic pain and their neurobiological correlates have been identified in animal models of chronic pain.60, 61, 62, 63, 64, 65 The sensory aspects of pain are carried by a bidirectional network of neurons that transmits a variety of noxious signals from peripheral nociceptive Aδ-fibres and C-fibres to the dorsal horn of the spinal cord (SCDH). Here, noxious signals are passed to ascending projection neurons that convey them to
Predictors of CPSP
The ability to predict who is at risk of developing CPSP is clearly important, especially if the risk factors are modifiable. Despite the progress in understanding the transition from acute to chronic pain, the research to date mainly identifies clinical risk factors. This literature is summarised in table 2. To facilitate future research in this field, a standardised approach to data collection of patient-reported and clinical outcomes has been proposed by the Initiative on Methods,
Predictive tools
Because there are multiple, interacting risk factors for developing CPSP, attempts have been made to develop predictive tools that quantify the level of composite risk. Most have been operation specific, but one generic tool evaluated the effect of 14 biomedical and psychosocial items that were derived from a systematic review of the CPSP risk factor literature.106 From a training set of 150 patients, of whom almost half developed CPSP, five of the 14 items were independently predictive of
Prevention of transitional postsurgical pain and CPSP
Some CPSP risk factors are modifiable (eg, body-mass index, preoperative pain, and some comorbidities), especially if surgery is elective, whereas others (eg, demographics, genetics, and pain sensitivity) are not. The very name of CPSP implies the pain is caused by surgery and therefore can be controlled if not prevented.109 Intraoperative nerve injury is a probable contributor to the development of at least some CPSP, but few studies have assessed whether intraoperative nerve handling or
Potential role of a transitional pain clinic
A more pragmatic approach to prevention of CPSP has been the development of transitional pain clinics, which aim to overcome the disconnect between ward-based acute postoperative pain management and outpatient chronic pain management (figure 2). Such a comprehensive and integrated pain service can identify patients at risk of chronic pain through inpatient screening on the basis of established prognostic indicators.3, 4, 6, 33, 39, 54, 55, 117, 118, 119, 120 A further clinic visit of at-risk
Treatment of established CPSP
In a review of CPSP in 2006, numerous potential symptomatic targets were proposed.22 The main two targets for which success has been achieved are the α2 and δ-1 subunit of calcium channels by gabapentin and pregabalin, and the monoamine transporters (which augment descending inhibition) by serotonin norepinephrine reuptake inhibitors such as duloxetine and venlafaxine.123, 124 These drugs are widely used for chronic neuropathic pain but their effects are variable, with the number needed to
Conclusions
CPSP is a growing problem as the population ages and more surgeries are done. Poorly controlled acute postoperative pain is a predictor of CPSP development but the drugs currently available to treat acute pain are mostly ineffective at preventing it. Opioids are too often overused, particularly in the post-discharge period. Preclinical research might yield new drug treatments, but ultimately, CPSP is similar to other chronic pain and therefore requires a comprehensive biopsychosocial approach
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