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.

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.

Chronic pain is an important problem after critical care admission. Estimates of the prevalence of chronic pain in the year after discharge range from 14% to 77% depending on the type of cohort, the tool used to measure pain, and the time point when pain was assessed. The majority of data available come from studies using health-related quality of life tools, although some have included pain-specific tools. Nociceptive, neuropathic, and nociplastic pain can occur in critical care survivors, but limited information about the aetiology, body site, and temporal trajectory of pain is currently available. Older age, pre-existing pain, and medical co-morbidity have been associated with pain after critical care admission. No trials were identified of interventions to target chronic pain in survivors specifically. Larger studies, using pain-specific tools, over an extended follow-up period are required to confirm the prevalence, identify risk factors, explore any association between acute and chronic pain in this setting, determine the underlying pathological mechanisms, and inform the development of future analgesic interventions.

SummaryPain is a common and distressing symptom experienced by intensive care patients. Assessing pain in this environment is challenging, and published guidelines have been inconsistently implemented. The Pain Assessment in INTensive care (PAINT) study aimed to evaluate the frequency and type of physician pain assessments with respect to published guidelines. This observational service evaluation considered all pain and analgesia‐related entries in patients’ records over a 24‐h period, in 45 adult intensive care units (ICUs) in London and the South‐East of England. Data were collected from 750 patients, reflecting the practice of 362 physicians. Nearly two‐thirds of patients (n = 475, 64.5%, 95%CI 60.9–67.8%) received no physician‐documented pain assessment during the 24‐h study period. Just under one‐third (n = 215, 28.6%, 95%CI 25.5–32.0%) received no nursing‐documented pain assessment, and over one‐fifth (n = 159, 21.2%, 95%CI 19.2–23.4)% received neither a doctor nor a nursing pain assessment. Two of the 45 ICUs used validated behavioural pain assessment tools. The likelihood of receiving a physician pain assessment was affected by the following factors: the number of nursing assessments performed; whether the patient was admitted as a surgical patient; the presence of tracheal tube or tracheostomy; and the length of stay in ICU. Physician‐documented pain assessments in the majority of participating ICUs were infrequent and did not utilise recommended behavioural pain assessment tools. Further research to identify factors influencing physician pain assessment behaviour in ICU, such as human factors or cultural attitudes, is urgently needed.

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Burn injury can be a devastating traumatic injury, with long-term personal and social implications for the patient. The many complex local and disseminating pathological processes underlying burn injury’s clinical challenges are orchestrated from the site of injury and develop over time, yet few studies of the molecular basis of these mechanisms specifically explore the local signaling environment. Those that do are typically destructive in nature and preclude the collection of longitudinal temporal data. Burn injury therefore exemplifies a superficial temporally dynamic pathology for which experimental sampling typically prioritizes either specificity to the local burn site or continuous collection from circulation. Here, we present an exploratory approach to the targeted elucidation of complex, local, acutely temporally dynamic interstitia through its application to burn injury. Subcutaneous microdialysis is coupled with ultraperformance liquid chromatography–mass spectrometry (UPLC–MS) analysis, permitting the application of high-throughput metabolomic profiling to samples collected both continuously and specifically from the burn site. We demonstrate this workflow’s high yield of burn-altered metabolites including the complete structural elucidation of niacinamide and uric acid, two compounds potentially involved in the pathology of burn injury. Further understanding the metabolic changes induced by burn injury will help to guide therapeutic intervention in the future. This approach is equally applicable to the analysis of other tissues and pathological conditions, so it may further improve our understanding of the metabolic changes underlying a wide variety of pathological processes.

General anaesthesia for obstetric surgery has distinct characteristics that may contribute towards a higher risk of accidental awareness during general anaesthesia. The primary aim of this study was to investigate the incidence, experience and psychological implications of unintended conscious awareness during general anaesthesia in obstetric patients. From May 2017 to August 2018, 3115 consenting patients receiving general anaesthesia for obstetric surgery in 72 hospitals in England were recruited to the study. Patients received three repetitions of standardised questioning over 30 days, with responses indicating memories during general anaesthesia that were verified using interviews and record interrogation. A total of 12 patients had certain/ probable or possible awareness, an incidence of 1 in 256 (95%CI 149-500) for all obstetric surgery. The incidence was 1 in 212 (95%CI 122-417) for caesarean section surgery. Distressing experiences were reported by seven (58.3%) patients, paralysis by five (41.7%) and paralysis with pain by two (16.7%). Accidental awareness occurred during induction and emergence in nine (75%) of the patients who reported awareness. Factors associated with accidental awareness during general anaesthesia were: high BMI (25-30 kg.m -2 ); low BMI (<18.5 kg.m -2 ); out-of-hours surgery; and use of ketamine or thiopental for induction. Standardised psychological impact scores at 30 days were significantly higher in awareness patients (median (IQR [range]) 15 (2.7-52.0 [2-56]) than in patients without awareness 3 (1-9 [0-64]), p = 0.010. Four patients had a provisional diagnosis of post-traumatic stress disorder. We conclude that direct postoperative questioning reveals high rates of accidental awareness during general anaesthesia for obstetric surgery, which has implications for anaesthetic practice, consent and follow-up.

Burn injury is associated in the skin, with increased levels of leptin and fractalkine. Signalling by these cytokines leads to macrophage accumulation and hypersensitivity to heat and mechanical stimuli. AbstractBurn injury is a pathology underpinned by progressive and aberrant inflammation. It is a major clinical challenge to survival and quality of life. While burn injury's complex local and disseminating pathological processes ultimately stem from local tissue damage, to date relatively few studies have attempted to characterise the local inflammatory mediator profile.Here, cytokine content and associated transcriptional changes were measured in rat skin for three hours immediately following induction of a scald-type (60 o C, 2 minutes) burn injury model. Leptin (p = 0.0002) and fractalkine (p = 0.0478) concentrations were significantly elevated post-burn above pre-burn and control site values, coinciding with the development of burn site oedema and differential expression of leptin mRNA (p = 0.0004). Further, gene sequencing enrichment analysis indicated cytokine-cytokine receptor interaction (p = 1.45x10 -6 ). Subsequent behavioural studies demonstrated that, following subcutaneous injection into the dorsum of the paw, both leptin and fractalkine induced mechanical allodynia, heat hyperalgesia and the recruitment of macrophages. This is the first report of leptin's elevation specifically at the burn site and the first report of fractalkine's elevation in any tissue post-burn which, together with the functional findings, calls for exploration of the influence of these cytokines on pain, inflammation and burn wound progression. Additionally targeting these signalling molecules represents a therapeutic potential as early formative mediators of these pathological processes.