Background: Acute postoperative pain is common. Nearly 20 per cent of patients experience severe pain in the first 24 h after surgery, a figure that has remained largely unchanged in the past 30 years. This review aims to present key considerations for postoperative pain management.Methods: A narrative review of postoperative pain strategies was undertaken. Searches of the Cochrane Library, PubMed and Google Scholar databases were performed using the terms postoperative care, psychological factor, pain management, acute pain service, analgesia, acute pain and pain assessment.Results: Information on service provision, preoperative planning, pain assessment, and pharmacological and non-pharmacological strategies relevant to acute postoperative pain management in adults is presented, with a focus on enhanced recovery after surgery pathways.Conclusion: Adequate perioperative pain management is integral to patient care and outcomes. Each of the biological, psychological and social dimensions of the pain experience should be considered and understood in order to provide optimum pain management in the postoperative setting.

Summary: Pain diagnosis and management would benefit from the development of objective markers of nociception and pain. Current research addressing this issue has focused on five main strategies, each with its own advantages and disadvantages. These encompass: (i) monitoring changes in the autonomic nervous system; (ii) biopotentials; (iii) neuroimaging; (iv) biological (bio‐) markers; and (v) composite algorithms. Although each strategy has shown areas of promise, there are currently no validated objective markers of nociception or pain that can be recommended for clinical use. This article introduces the most important developments in the field and highlights shortcomings, with the aim of allowing the reader to make informed decisions about what trends to watch in the future.

Summary: Background: Nearly half of adult patients undergoing surgery experience moderate or severe postoperative pain. Inadequate pain management hampers postoperative recovery and function and may be associated with adverse outcomes. This multidisciplinary consensus statement provides principles that might aid postoperative recovery, and which should be applied throughout the entire peri‐operative pathway by healthcare professionals, institutions and patients. Methods: We conducted a directed literature review followed by a four‐round modified Delphi process to formulate recommendations for organisations and individuals. Results: We make recommendations for the entire peri‐operative period, covering pre‐admission; admission; intra‐operative; post‐anaesthetic care unit; ward; intensive care unit; preparation for discharge; and post‐discharge phases of care. We also provide generic principles of peri‐operative pain management that clinicians should consider throughout the peri‐operative pathway, including: assessing pain to facilitate function; use of multimodal analgesia, including regional anaesthesia; non‐pharmacological strategies; safe use of opioids; and use of protocols and training for staff in caring for patients with postoperative pain. Conclusions: We hope that with attention to these principles and their implementation, outcomes for adult patients having surgery might be improved.

Endogenous pain modulation, as tested by the conditioned pain modulation (CPM) protocol, is typically less efficient in patients with chronic pain compared with healthy controls. We aimed to assess whether CPM is less efficient in patients with painful diabetic polyneuropathy (DPN) compared with those with nonpainful DPN. Characterization of the differences in central pain processing between these 2 groups might provide a central nervous system explanation to the presence or absence of pain in diabetic neuropathy in addition to the peripheral one. Two hundred seventy-one patients with DPN underwent CPM testing and clinical assessment, including quantitative sensory testing. Two modalities of the test stimuli (heat and pressure) conditioned to cold noxious water were assessed and compared between patients with painful and nonpainful DPN. No significant difference was found between the groups for pressure pain CPM; however, patients with painful DPN demonstrated unexpectedly more efficient CPM_HEAT (−7.4 ± 1.0 vs −2.3 ± 1.6; P = 0.008). Efficient CPM_HEAT was associated with higher clinical pain experienced in the 24 hours before testing (r = −0.15; P = 0.029) and greater loss of mechanical sensation (r = −0.135; P = 0.042). Moreover, patients who had mechanical hypoesthesia demonstrated more efficient CPM_HEAT (P = 0.005). More efficient CPM among patients with painful DPN might result from not only central changes in pain modulation but also from altered sensory messages coming from tested affected body sites. This calls for the use of intact sites for proper assessment of pain modulation in patients with neuropathy.

We aimed to investigate the genetic associations of neuropathic pain in a deeply phenotyped cohort. Participants with neuropathic pain were cases and compared with those exposed to injury or disease but without neuropathic pain as control subjects. Diabetic polyneuropathy was the most common aetiology of neuropathic pain. A standardised quantitative sensory testing protocol was used to categorize participants based on sensory profile. We performed genome-wide association study, and in a subset of participants, we undertook whole-exome sequencing targeting analyses of 45 known pain-related genes. In the genome-wide association study of diabetic neuropathy (N = 1541), a top significant association was found at the KCNT2 locus linked with pain intensity (rs114159097, P = 3.55 × 10⁻⁸). Gene-based analysis revealed significant associations between LHX8 and TCF7L2 and neuropathic pain. Polygenic risk score for depression was associated with neuropathic pain in all participants. Polygenic risk score for C-reactive protein showed a positive association, while that for fasting insulin showed a negative association with neuropathic pain, in individuals with diabetic polyneuropathy. Gene burden analysis of candidate pain genes supported significant associations between rare variants in SCN9A and OPRM1 and neuropathic pain. Comparison of individuals with the “irritable” nociceptor profile to those with a “nonirritable” nociceptor profile identified a significantly associated variant (rs72669682, P = 4.39 × 10⁻⁸) within the ANK2 gene. Our study on a deeply phenotyped cohort with neuropathic pain has confirmed genetic associations with the known pain-related genes KCNT2, OPRM1, and SCN9A and identified novel associations with LHX8 and ANK2, genes not previously linked to pain and sensory profiles, respectively.