The prevalence of persistent postsurgical pain and its neuropathic component varies across surgical procedures. More consistent assessment methodology is recommended for this type of pain.
Persistent ...postsurgical pain (PPSP) is a frequent and often disabling complication of many surgical procedures. Nerve injury–induced neuropathic pain (NeuP) has repeatedly been proposed as a major cause of PPSP. However, there is a lack of uniformity in NeuP assessment across studies, and the prevalence of NeuP may differ after various surgeries. We performed a systematic search of the PubMed, CENTRAL, and Embase databases and assessed 281 studies that investigated PPSP after 11 types of surgery. The prevalence of PPSP in each surgical group was examined. The prevalence of NeuP was determined by applying the recently published NeuP probability grading system. The prevalence of probable or definite NeuP was high in patients with persistent pain after thoracic and breast surgeries—66% and 68%, respectively. In patients with PPSP after groin hernia repair, the prevalence of NeuP was 31%, and after total hip or knee arthroplasty it was 6%. The results suggest that the prevalence of NeuP among PPSP cases differs in various types of surgery, probably depending on the likelihood of surgical iatrogenic nerve injury. Because of large methodological variability across studies, a more uniform approach is desirable in future studies for evaluating persistent postsurgical NeuP.
Phantom pain refers to pain in a body part that has been amputated or deafferented. It has often been viewed as a type of mental disorder or has been assumed to stem from pathological alterations in ...the region of the amputation stump. In the past decade, evidence has accumulated that phantom pain might be a phenomenon of the CNS that is related to plastic changes at several levels of the neuraxis and especially the cortex. Here, we discuss the evidence for putative pathophysiological mechanisms with an emphasis on central, and in particular cortical, changes. We cite both animal and human studies and derive suggestions for innovative interventions aimed at alleviating phantom pain.
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DOBA, IJS, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
Nurse-patient communication in intensive care units is challenged by the fact that patients are voiceless due to intubation and mechanical ventilation. Difficult communication affects nurses ...negatively, and it requires knowledge and expertise to facilitate communication in this complex and technologically tense setting. Augmentative and alternative communication has been suggested as a way of optimising communication; several approaches can be combined in a multi-component intervention. Also, a communication algorithm has been proposed as a way of providing structure in patient communication. To enhance transparency and avoid poorly reported interventions, this paper describes the process, rationale and reflections behind developing a communication intervention called the ICU-COM.
To present the development process of a communication intervention prototype that aims to support and strengthen nurses’ communication with mechanically ventilated patients in an intensive care unit.
The Medical Research Council's framework for developing complex interventions in health was applied. The approach was target-population centred.
The intervention was developed and tailored to four intensive care unit departments at Aarhus University Hospital in Denmark.
Intensive care nurses and various experts, namely, speech-language pathologists, graphic designers, a software company, the local Centre for E-learning and nurse specialists were involved in its development.
An intervention consisting of: 1) a multi-component communication bundle, 2) delivery of the bundle via a teaching session and 3) initial implementation via nurse communication guides was developed. The communication bundle contained: 1) a communication strategy with a BASIS framework and algorithm, 2) a nurse education programme and 3) low-tech and high-tech communication tools.
A systematic approach was applied in the development process. However, the acceptability and feasibility of the intervention is at present unknown.
The role of afferent sensory input in neuropathic pain was examined in 2 groups. Peripheral nerve blocks abolished spontaneous and evoked pain in all patients. Systemic lidocaine was more effective ...in pain due to polyneuropathy than nerve injury. Central sensitization does not act as an autonomous spontaneous pain-generating mechanism. Peripheral sensory input is critical in maintaining pain after peripheral nerve damage.
Central sensitization after peripheral nerve injury may result in ectopic neuronal activity in the spinal cord dorsal horn, implying a potential autonomous pain-generating mechanism. This study used peripheral nerve blockade and systemic lidocaine administration, with detailed somatosensory assessment, to determine the contribution of primary afferent input in maintaining peripheral neuropathic pain. Fourteen patients with neuropathic pain (7 with unilateral foot pain due to peripheral nerve injury and 7 with bilateral pain in the feet due to distal polyneuropathy) underwent comprehensive characterization of somatosensory function by quantitative sensory testing. Patients were then administered an ultrasound-guided peripheral nerve block with lidocaine and intravenous lidocaine infusion in randomized order. The effect of these interventions on spontaneous pain intensity and on evoked cold, warm, pinprick, and brush responses was assessed at each session. All patients had sensory disturbances at baseline. The peripheral nerve block resulted in a complete abolition of ipsilateral pain within 10min (median) in all patients, with lidocaine plasma concentrations being too low to account for a systemic effect of the drug. Intravenous lidocaine infusion reduced the spontaneous pain by 45.5% (±31.7%), and it reduced mechanical and thermal hypersensitivity in most patients who displayed such signs. However, the improvement in evoked hypersensitivity was not related to the effect of the drug on spontaneous pain intensity. This study demonstrated that regardless of the individual somatosensory phenotype and signs of central sensitization, primary afferent input is critical for maintaining neuropathic pain in peripheral nerve injury and distal polyneuropathy.
ObjectiveTo evaluate the effectiveness of a subanaesthetic single-dose ketamine (SDK) as an adjunct to opioids for acute pain in emergency department (ED) settings.DesignSystematic review and ...meta-analysis.MethodsA systematic search was performed in MEDLINE, Embase, Scopus and Web of Science through March 2022. Randomised controlled trials (RCTs) that investigated SDK as an adjunct to opioids in adult patients for any painful condition in ED settings were selected. Two reviewers screened studies, extracted data and assessed study quality. Data were pooled using random-effects models. The primary outcome was mean pain intensity score measured at baseline, >0–15 min, >15–30 min, >30–45 min, 60 min, 90 min and 120 min. Secondary outcomes included need for rescue analgesia, adverse events and patient satisfaction. Results were reported as mean differences (MDs) and risk ratios. Statistical heterogeneity was calculated using the I2 statistic.ResultsEight RCTs were included (n=903). Studies were judged to be at moderate to high risk of bias. Mean pain intensity scores were significantly lower 60 min after study drug administration favouring adjuvant SDK (MD −0.76; 95% CI −1.19 to −0.33), compared with opioids alone. There was no evidence of differences in mean pain intensity scores at any other time point. Patients who received adjuvant SDK were less likely to require rescue analgesia, no more likely to experience serious side effects and had higher satisfaction scores, compared with opioids alone.ConclusionsAvailable evidence suggests adjuvant SDK can have an effect on lowering pain intensity scores. Although reduction of pain scores was not clinically significant, the combination of reduced pain intensity and reduced opioid requirements suggest the results could be clinically important and support the potential utility of SDK as an adjunct to opioids to treat acute pain in adult ED patients. However, current evidence is limited and higher quality RCTs are needed.PROSPERO registration numberCRD42021276708.
Objective
Although axons within neuromas have been shown to produce inappropriate spontaneous ectopic discharges, the molecular basis for pain in patients with neuromas is still not fully understood. ...Because sodium channels are known to play critical roles in neuronal electrogenesis and hyperexcitability, we examined the expression of all the neuronal voltage‐gated sodium channels (Nav1.1, Nav1.2, Nav1.3, Nav1.6, Nav1.7, Nav1.8, and Nav1.9) within human painful neuromas. We also examined the expression of two mitogen‐activated protein (MAP) kinases, activated p38 and extracellular signal‐regulated kinases 1 and 2 (ERK1/2), which are known to contribute to chronic pain, within these human neuromas.
Methods
We used immunocytochemical methods with specific antibodies to sodium channels Nav1.1, Nav1.2, Nav1.3, Nav1.6, Nav1.7, Nav1.8, and Nav1.9, and to activated MAP kinases p38 and ERK1/2 to study by confocal microscopy control and painful neuroma tissue from five patients with well‐documented pain.
Results
We demonstrate upregulation of sodium channel Nav1.3, as well as Nav1.7 and Nav1.8, in blind‐ending axons within human painful neuromas. We also demonstrate upregulation of activated p38 and ERK1/2 MAP kinases in axons within these neuromas.
Interpretation
These results demonstrate that multiple sodium channel isoforms (Nav1.3, Nav1.7, and Nav1.8), as well as activated p38 and ERK1/2 MAP kinases, are expressed in painful human neuromas, indicating that these molecules merit study as possible therapeutic targets for the treatment of pain associated with traumatic neuromas. Ann Neurol 2008;64:644–653
In this randomized, double-blind, placebo-controlled crossover study, we investigated whether a peripheral nerve block could temporarily eliminate phantom and stump pain after amputation. Amputees ...with constant postamputation pain were included and randomized to receive a nerve block with lidocaine 2% with adrenaline or saline in a crossover design. Spontaneous phantom and stump pain and evoked responses were assessed at baseline and at fixed time-points until 120 minutes after lidocaine or saline injection. The primary outcome was the difference in absolute change between worst pain intensity, either phantom or stump pain, at baseline and at 30 minutes after lidocaine or saline injection. Twelve amputees were randomized and 9 patients were included in the analysis. The absolute change in median worst pain intensity between lidocaine and saline injection was -2.0 (interquartile range, -4.0 to 0.0) (n = 9, P = 0.12). Nine of 9 patients reported at least some pain relief after lidocaine injection compared with only 2 of 9 patients after saline injection (P = 0.02). Phantom pain intensity was significantly reduced after lidocaine compared with saline injection (P = 0.04), whereas there was no significant change in stump pain intensity between the 2 interventions (P = 0.17). In all 9 amputees, evoked responses were eliminated after lidocaine injection. Thus, our findings suggest that afferent input from the peripheral nervous system plays an important role in postamputation pain.
ObjectiveTo examine the risk factors for new chronic opioid use in elderly patients who underwent hip fracture surgery.DesignProspective population-based cohort study.Setting and participantsUsing ...Danish nationwide health registries, we identified all opioid non-user patients aged ≥65 years who had undergone hip fracture surgery from 2005 to 2016 and were alive within the first year following surgery.Main outcome measuresNew chronic opioid use defined by the dispensing of at least two prescription opioids within two of the last three quarters during the first year following surgery.ResultsWe identified 37 202 opioid non-user patients who underwent hip fracture surgery. Of these, 5497 (15%) developed new chronic opioid user within 1 year of surgery. Risk factors for new chronic opioid use were Body Mass Index (BMI) of <18.5 (adjusted OR (aOR) 1.22, 95% CI 1.09 to 1.36), BMI of 25.0–29.9 (aOR 1.12, 95% CI 1.04 to 1.21) and BMI of ≥30 (aOR 1.57, 95% CI 1.40 to 1.76) with BMI 18.6–24.9 as reference, a pertrochanteric/subtrochanteric fracture (aOR 1.27, 95% CI 1.20 to 1.34) with femoral neck fracture as reference, preoperative use (vs no-use) of non-steroidal anti-inflammatory drug (aOR 1.68, 95% CI 1.55 to 1.83), selective serotonin reuptake inhibitor (aOR 1.42, 95% CI 1.32 to 1.53), antidepressants (aOR 1.36, 95% CI 1.24 to 1.49), antipsychotics (aOR 1.21, 95% CI 1.07 to 1.35), corticosteroids (aOR 1.54, 95% CI 1.35 to 1.76), statins (aOR 1.09, 95% CI 1.02 to 1.18), antibiotics (aOR 1.32, 95% CI 1.22 to 1.42), antiosteoporosis drugs (aOR 1.33, 95% CI 1.19 to 1.49) and anticoagulatives (aOR 1.24, 95% CI 1.17 to 1.32). Presence of cardiovascular comorbidities, diabetes, gastrointestinal diseases, dementia, chronic obstructive pulmonary disease or renal diseases was further identified as a risk factor.ConclusionIn this large nationwide cohort study, we identified several risk factors associated with new chronic opioid use after hip fracture surgery among patients who were alive within the first year following surgery. Although not all factors are modifiable preoperative, this will allow clinicians to appropriately counsel patients preoperatively and tailor postoperative treatment.
The gene SCN9A is responsible for three human pain disorders. Nonsense mutations cause a complete absence of pain, whereas activating mutations cause severe episodic pain in paroxysmal extreme pain ...disorder and primary erythermalgia. This led us to investigate whether single nucleotide polymorphisms (SNPs) in SCN9A were associated with differing pain perception in the general population. We first genotyped 27 SCN9A SNPs in 578 individuals with a radiographic diagnosis of osteoarthritis and a pain score assessment. A significant association was found between pain score and SNP rs6746030; the rarer A allele was associated with increased pain scores compared to the commoner G allele (P = 0.016). This SNP was then further genotyped in 195 pain-assessed people with sciatica, 100 amputees with phantom pain, 179 individuals after lumbar discectomy, and 205 individuals with pancreatitis. The combined P value for increased A allele pain was 0.0001 in the five cohorts tested (1277 people in total). The two alleles of the SNP rs6746030 alter the coding sequence of the sodium channel Nav1.7. Each was separately transfected into HEK293 cells and electrophysiologically assessed by patch-clamping. The two alleles showed a difference in the voltage-dependent slow inactivation (P = 0.042) where the A allele would be predicted to increase Nav1.7 activity. Finally, we genotyped 186 healthy females characterized by their responses to a diverse set of noxious stimuli. The A allele of rs6746030 was associated with an altered pain threshold and the effect mediated through C-fiber activation. We conclude that individuals experience differing amounts of pain, per nociceptive stimulus, on the basis of their SCN9A rs6746030 genotype.
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