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Many patients with fibromyalgia (FM) report using cannabis as a strategy to improve pain. Given that pain often co-occurs with symptoms of anxiety and depression (i.e., negative affect) and sleep problems among patients with FM, improvements in these symptoms might indirectly contribute to reductions in pain intensity following cannabis use.The main objective of the study was to examine whether changes in pain intensity following initiation of medical cannabis among FM patients could be attributed to concurrent changes (i.e., reductions) in negative affect and sleep problems.This was a 12-month prospective cohort study among FM patients (n = 323) initiating medical cannabis under the care of physicians. Patients were assessed at baseline and follow-up assessment visits occurred every three months after initiation of medical cannabis. Patients' levels of pain intensity, negative affect, and sleep problems were assessed across all visits.Multilevel mediation analyses indicated that reductions in patients' levels of pain intensity were partly explained by concurrent reductions in sleep problems and negative affect (both p's.001). This remained significant even when accounting for patients' baseline characteristics or changes in medical cannabis directives over time (all p's.05).Our findings provide preliminary insights into the potential mechanisms of action underlying pain reductions among FM patients who are using medical cannabis. Given the high attrition rate (i.e., 75 %) observed in the present study at 12 months, our findings cannot be generalized to all FM patients who are using medical cannabis.

Resumo Justificativa e objetivos: O bloqueio PECS I foi descrito pela primeira vez para cirurgia envolvendo os musculos peitorais. Nenhum estudo clinico randomizado foi realizado em procedimentos envolvendo diretamente os musculos peitorais, como a mamoplastia de aumento submuscular. Nossa hipotese foi de que o bloqueio PECS I diminuiria a dor pos-operatoria nessa populacao. Metodo: Realizamos estudo randomizado, duplo-cego, controlado por placebo em mulheres submetidas a mamoplastia de aumento submuscular. Realizamos o bloqueio PECS I com 0,4 mL.kg-1 de solucao salina a 0,9% de um lado e bupivacaina (0,25%) do outro lado, sendo cada paciente seu proprio controle. Os escores da Escala de Avaliacao Numerica (EAN) de dor (0−10) foram obtidos em repouso e durante movimento. O desfecho primario foi o escore de dor em repouso 30 minutos apos a chegada a SRPA. Para detectar uma diferenca clinicamente significante de 50% na reducao da dor, 14 voluntarias foram incluidas (poder de 90% e alfa Resultados: Na SRPA, tres pacientes nao apresentaram diferenca na dor entre os lados, cinco relataram menos dor no lado do placebo, e seis menos dor no lado da bupivacaina. No grupo bupivacaina, os escores de dor em repouso aos 5, 30 e 60 minutos e 24 horas foram 4,89 (4,23−5,56; IC medio 95%), 3,75 (3,13−4,37), 3,79 (2,93−4,64) e 2,29 (1,56−3,01), respectivamente, enquanto no grupo placebo foram 4,96 (4,32−5,60), 4,00 (3,50−4,49), 3,93 (3,12−4,73) e 2,29 (1,56−3,01), respectivamente. Conclusoes: O bloqueio PECS I em pacientes submetidas a mamoplastia de aumento nao oferece melhor alivio da dor do que o placebo. Portanto, as indicacoes para bloqueio de PECS I na cirurgia de aumento de mama devem ser reconsideradas.

BackgroundData on postoperative outcomes of the COVID-19 patient population is limited. We described COVID-19 patients who underwent a surgery and the pandemic impact on surgical activities.MethodsWe conducted a multicenter cohort study between March 13 and June 192,020. We included all COVID-19 patients who underwent surgery in nine centres of the Province of Québec, the Canadian province most afflicted by the pandemic. We also included concomitant suspected COVID-19 (subsequently confirmed not to have COVID-19) patients and patients who had recovered from it. We collected data on baseline characteristics, postoperative complications and postoperative mortality. Our primary outcome was 30-day mortality. We also collected data on overall surgical activities during this first wave and during the same period in 2019.ResultsWe included 44 COVID-19 patients, 18 suspected patients, and 18 patients who had recovered from COVID-19 at time of surgery. Among the 44 COVID-19 patients, 31 surgeries (71%) were urgent and 16 (36%) were major. In these patients, pulmonary complications were frequent (25%) and 30-day mortality was high (15.9%). This mortality was higher in patients with symptoms (23.1%) compared to those without symptoms (5.6%), although not statistically significant (p = 0.118). Of the total 22,616 cases performed among participating centres during the study period, only 0.19% had COVID-19 at the time of surgery. Fewer procedures were performed during the study period compared to the same period in 2019 (44,486 cases).ConclusionIn this Canadian cohort study, postoperative 30-day mortality in COVID-19 patients undergoing surgery was high (15.9%). Although few surgeries were performed on COVID-19 patients, the pandemic impact on surgical activity volume was important.Trial registrationClinicalTrials.gov Identifier:NCT04458337.

The pectoral nerves (PECS) I block, first described in 2011 for surgery involving the pectoralis muscle, has principally been used for breast cancer surgery. No formal evaluation of its differential motor- and sensory-blocking abilities has been reported. We hypothesize that the PECS I block will produce a motor block of the pectoralis muscles with diminished upper limb adduction strength as measured with a handheld dynamometer. We conducted a PECS I block in a randomized placebo-controlled trial in six healthy subjects who received 0.4 mL·kg−1 of 0.9% saline (placebo) on one side and bupivacaine (0.25% with 1:400 000 epinephrine) on the other. We measured both upper limb adduction strength with a dynamometer and sensory skin levels over the thorax. The mean (standard deviation [SD]) adductor strength evaluated before the block was 119.4 (20.7) Newtons (N). After the PECS I block with bupivacaine, the mean (SD) strength of 54.2 (16.3) N was compared with 116.0 (30.4) N in the placebo group (difference in means 61.8 N; 95% confidence interval [CI], 27.8 to 95.8 N; P = 0.005), showing a 54.6% (95% CI, 43.6 to 65.6%) reduction in adductor strength. There was no difference in dermatomal skin sensory testing between the placebo and bupivacaine sides. This study shows that a PECS I block produces motor blockade as shown by reduced upper limb adductor strength without any overlying dermatomal sensory loss. www.clinicaltrials.gov (NCT03040167) 2 February 2017.

Introduction/Aim: The objectives of this systematic review and meta-analysis were to examine the relative frequency and risk factors (patient, surgical, medical, clinical) for prolonged opioid therapy among surgical and trauma patients. Methods: Studies published in English and French between 1998 and April 2018 examining risk factors for prolonged (3–6 months) or chronic (>6 months) opioid use after surgery/trauma were included. Literature search: seven databases were queried, empirical studies were identified via direct and back citation search, grey literature was also included. A minimum of two independent reviewers assessed studies for inclusion, extracted data and assessed studies quality. Results: Thirty-five out of 10,003 screened articles were included. The median relative frequency of prolonged (50.9%) and chronic (58.5%) opioid therapy among pre-event patients already on opioid therapy was much higher compared to pre-event opioid naïve patients (4.1% and 2.6%, respectively). Tobacco use, depressive disorder and antidepressants use were significant risk factors for prolonged and/or chronic opioid therapy among pre-event opioid naïve patients. Tobacco use, depressive disorder and history of migraines were risk factors for prolonged opioid therapy among pre-event opioid-treated patients. Discussion/Conclusions: Prevention initiatives to reduce the risk of prolonged opioid therapy after surgery or trauma should target specific health behaviors and psychiatric disorders; these interventions should be tailored based on patients’ pre-event opioid status.

We report a case of awake paralysis due to residual neuromuscular blockade (NMB) in the intensive care unit (ICU) in a patient following fast-track cardiac surgery. As a result of this case, we performed a prospective quality assurance audit to investigate the incidence of residual paralysis in the ICU in a similar population of cardiac surgery patients. A 73-yr-old woman (69 kg) underwent coronary artery bypass surgery under anesthesia induced with intravenous sufentanil 25 µg, midazolam 5 mg, ketamine 25 mg, and rocuronium 100 mg (followed by two additional 50-mg doses during surgery) and maintained with sevoflurane. Postoperatively in the ICU, the patient was initially sedated with propofol (50 mg·hr−1) but failed to awaken 90 min after its cessation. As train-of-four neurostimulation showed residual paralysis, she was re-sedated. Neostigmine 3 mg and glycopyrrolate 0.6 mg were administered, and she was extubated 30 min later. During this episode of residual paralysis, the patient was conscious and reported explicit memory of the events. She was discharged on day 7 without psychological distress related to her postoperative awake paralysis. We subsequently performed a prospective audit in 50 consecutive patients to determine the timing of NMB dosing and to quantify the incidence of residual paralysis after fast-track cardiac surgery. Of the 50 patients studied, 24 (48%) had received an NMB during the last hour of surgery and 33 (66%) had evidence of residual paralysis during the immediate postoperative period. Postoperative residual paralysis after fast-track cardiac surgery was common in our institution and likely contributed to the reported case of postoperative awake paralysis. We suggest that an NMB not be administered after intubation in fast-track patients. If given, however, it must be well communicated to the ICU team upon ICU admission. We further recommend routine assessment of neuromuscular function before sedation is weaned prior to extubation.

New regulations are in place at the federal and provincial levels in Canada regarding the way medical cannabis is to be controlled. We present them together with guidance for the safe use of medical cannabis and recent clinical trials on cannabis and pain. The new Canadian regulations on the use of medical cannabis, the provincial regulations, and the various cannabis products available from the Canadian Licensed Producers were reviewed from Health Canada, provincial licensing authorities, and the licensed producers website, respectively. Recent clinical trials on cannabis and pain were reviewed from the existing literature. Health Canada has approved a new regulation on medical marijuana/cannabis, the Marihuana for Medical Purposes Regulations: The production of medical cannabis by individuals is illegal. Health Canada, however, has licensed authorized producers across the country, limiting the production to specific licenses of certain cannabis products. There are currently 26 authorized licensed producers from seven Canadian provinces offering more than 200 strains of marijuana. We provide guidance for the safe use of medical cannabis. The recent literature indicates that currently available cannabinoids are modestly effective analgesics that provide a safe, reasonable therapeutic option for managing chronic non-cancer-related pain. The science of medical cannabis and the need for education of healthcare professionals and patients require continued effort. Although cannabinoids work to decrease pain, there is still a need to confirm these beneficial effects clinically and to exploit them with acceptable benefit-to-risk ratios.

12109 Background: The Quebec Cannabis Registry (QCR) was launched in 2015 to allow physicians to prescribe medical cannabis (MC) in the province of Quebec, Canada. This study aimed to investigate the safety and effectiveness of MC in cancer patients using pharmacovigilance data prospectively collected for up to 24 months. Methods: Patients were enrolled in the QCR between May 2015 and October 2018 and followed every 3 months. Study outcomes included adverse events (AE), pain severity and interference (Brief-Pain Inventory), wellbeing (Revised-Edmonton Symptom Assessment Scale) and overall health scale (EQ5D5L) at baseline and at each follow-up (F-UP). Significance of changes over time were assessed using repeated-measures ANOVA. Results: Out of the 2991 patients enrolled in the QCR, 358 (12.8%) were cancer patients (mean age 57.7 (± 14.6); 171 (47.8%) males). The main cancer types were breast (16.2%), lung (11.7%), leukemia (11.5%) and colorectal (11.2%). MC was prescribed primarily for pain (72.1%), anxiety (4.7%), nausea (4.5%), anorexia (3.9%), and insomnia (3.1%). A total of 13 patients (3.6%) reported AE with only three being serious (one unrelated to MC: stroke; and two possibly related: diarrhea, from CBD oil overdose and pneumonia from smoking MC). Mean scores significantly (p < 0.05) improved between baseline and 3 months F-UP for pain severity (4.8 ± 1.5 vs 4.1 ± 1.8), pain interference (4.6 ± 1.8 vs 3.8 ± 1.7), and the overall health scale (60 ± 21 vs 71 ± 18). Well-being scores also significantly improved between baseline and 6 months F-UP (4.4 ± 2.1 vs 3.5 ± 2.8). Conclusions: Population-based data shows that cancer patients can benefit safely and effectively from MC as a complementary treatment, when prescribed and monitored under medical-nursing supervision.

The landmark paper discussed in the chapter, published by 2008 by Mallet et al., reports on the mechanisms of action of acetaminophen for pain treatment. Acetaminophen, also known as paracetamol (N-acetyl-para-aminophenol), has analgesic and antipyretic properties and has superior tolerance, compared to non-steroidal anti-inflammatory drugs, making it appropriate for widespread use in patients. However, despite many years of use worldwide and numerous studies, acetaminophen’s mechanism of action is still uncertain. The article by Mallet et al. is a landmark paper because it reconciled many observations made at the time to propose a plausible mechanism of action of acetaminophen in pain treatment.

Background and Objectives General anesthesia for breast surgery may be supplemented by using a regional anesthetic technique. We evaluated the efficacy of the first pectoral nerve block (Pecs I) in treating postoperative pain after breast cancer surgery. Methods A randomized, double-blind, dual-centered, placebo-controlled trial was performed. One hundred twenty-eight patients scheduled for unilateral breast cancer surgery were recruited. A multimodal analgesic regimen and surgeon-administered local anesthetic infiltration were used for all patients. Ultrasound-guided Pecs I was performed using bupivacaine or saline. The primary outcome was the patient pain score (numerical rating scale [NRS]) in the recovery unit 30 minutes after admission or just before the morphine administration (NRS ≥4/10). The secondary outcomes were postoperative opioid consumption (ie, in the recovery unit and after 24 hours). Results During recovery, no significant difference in NRS was observed between the bupivacaine (n = 62, 3.0 [1.0–4.0]) and placebo (n = 65, 3.0 [1.0–5.0]) groups (P = 0.55). However, the NRS was statistically significantly different, although not clinically significant, for patients undergoing major surgeries (mastectomies or tumorectomies with axillary clearance) (n = 29, 3.0 [0.0–4.0] vs 4.0 [2.0–5.0], P = 0.04). Morphine consumption during recovery did not differ (1.5 mg [0.0–6.0 mg] vs 3.0 mg [0.0–6.0 mg], P = 0.20), except in the major surgery subgroup (1.5 mg [0.0–6.0 mg] vs 6.0 mg [0.0–12.0 mg], P = 0.016). Intraoperative sufentanil and cumulative morphine consumption up to 24 hours did not differ between the 2 groups. Three patients experienced complications related to the Pecs I. Conclusions Pecs I is not better than a saline placebo in the presence of multimodal analgesia for breast cancer surgery. However, its role in extended (major) breast surgery may warrant further investigation. Clinical Trial Registration This study was registered at ClinicalTrials.gov, identifier NCT01670448.

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El dolor es el motivo de consulta principal en reumatologia. Mas del 50% de los dolores cronicos afectan al aparato musculoesqueletico. La evaluacion es una etapa fundamental de la atencion de cualquier paciente con dolor. Ante un dolor agudo, se basa en la autoevaluacion unidimensional de la intensidad dolorosa, que debe repetirse para poder adaptar rapidamente el tratamiento. En caso de dolor cronico, sintomatico de una afeccion cronica o autonomizada (dolor como enfermedad), la evaluacion es mas compleja y pluridimensional. Intervienen los componentes sensorial, emocional, cognitivo y conductual; de igual manera, intervienen el contexto familiar y el sociolaboral. La evaluacion bien conducida y precisa permite establecer una relacion empatica con el paciente. En el dolor cronico, guia el tratamiento al separar los diversos componentes del dolor y estimar el valor de cada uno. Asi, orientara hacia algunos tratamientos medicamentosos o hacia tecnicas antalgicas no medicamentosas. La evaluacion debe repetirse para ajustar el tratamiento, con mayor frecuencia en un dolor agudo y con regularidad en un dolor cronico, en el que el valor de los componentes puede modificarse con el paso del tiempo.

La evolucion de los conocimientos sobre las bases neurofisiologicas del dolor ha permitido captar mejor la complejidad del fenomeno doloroso, muy frecuente en reumatologia. La fisiopatologia del dolor conduce a distinguir clasicamente tres tipos principales: los dolores nociceptivos, caracterizados por una estimulacion anormal de los nociceptores perifericos en un sistema nervioso normal; los dolores neuropaticos, caracterizados por una lesion del sistema nervioso, central o periferico, que induce los fenomenos dolorosos, y los dolores no clasificados o disfuncionales, que no dependen de una estimulacion periferica de los nociceptores ni de una lesion definida del sistema nervioso. Por otra parte, las lesiones perifericas, por ejemplo articulares, pueden producir una hiperexcitabilidad de los nociceptores y, de forma secundaria, una hiperexcitabilidad central medular. Ademas, la dicotomia entre estos tipos de dolor no siempre es real, y buena parte de ellos, sobre todo en reumatologia, son mixtos; pueden asociar, por ejemplo, un componente nociceptivo y otro neuropatico. Un mejor conocimiento de la fisiopatologia de los dolores permite determinar dianas terapeuticas y adaptar mejor el tratamiento.

As the use and abuse of drugs increases, the likelihood of an anesthesiologist encountering addicted patients perioperatively also will increase. Addicted patients may present for anesthetic care in a variety of circumstances: in obstetrics for labor or cesarian sections, in trauma for emergency surgeries, in lifesaving situations, and in everyday elective surgeries. Therefore, it is important for anesthesiologists to know about the most common illicit drugs being used, their clinical presentation and side effects, and to know what anesthetic options would be beneficial or detrimental for these patients.

Background The mechanism of action of acetaminophen remains unclear. One hypothesis involves an interaction with the serotoninergic system. Antagonists to serotonin (5-HT)3 receptors (setrons) have antiemetic properties. Therefore, co-administration of acetaminophen and a setron could lead to a decrease or a loss of acetaminophen analgesic effects. The aim of this study was to demonstrate such an interaction. Methods Paratron is a prospective, randomized, controlled, double-blind, parallel group trial. All children aged 2–7 years (n = 69) scheduled for a tonsillectomy ± adenoidectomy received intraoperative acetaminophen with ondansetron or droperidol. Pain scores [Children's Hospital of Eastern Ontario Pain Scale (CHEOPS)], morphine consumption and the incidence of post-operative nausea and vomiting (PONV) were measured for 24 h following surgery. Results Pain scores were not different at all times between the groups but median morphine consumption (μg) in recovery was 322.5 [interquartile range (IQR) 0.0–500.0] and 0 (IQR 0-0) in the ondansetron (n = 35) and droperidol (n = 34) groups, respectively (p = 0.004). The percentages of patients who received morphine titration were 57.1% and 20.6% in the ondansetron and droperidol groups, respectively (p = 0.008). No significant difference was found for PONV. Conclusions An interaction between acetaminophen and ondansetron is suggested, with children receiving three times more morphine during pain titration in the recovery room. More studies are necessary to evaluate whether this finding is clinically relevant enough to preclude the simultaneous perioperative administration of both drugs in the future.

The two most studied endocannabinoids are anandamide (AEA), principally catalyzed by fatty-acid amide hydrolase (FAAH), and 2-arachidonoyl glycerol (2-AG), mainly hydrolyzed by monoacylglycerol lipase (MGL). Inhibitors targeting these two enzymes have been described, including URB597 and URB602, respectively. Several recent studies examining the contribution of CB1 and/or CB2 receptors on the peripheral antinociceptive effects of AEA, 2-AG, URB597 and URB602 in neuropathic pain conditions using either pharmacological tools or transgenic mice separately have been reported, but the exact mechanism is still uncertain. Mechanical allodynia and thermal hyperalgesia were evaluated in 436 male C57BL/6, cnr1KO and cnr2KO mice in the presence or absence of cannabinoid CB1 (AM251) or CB2 (AM630) receptor antagonists in a mouse model of neuropathic pain. Peripheral subcutaneous injections of AEA, 2-AG, WIN55,212-2 (WIN; a CB1/CB2 synthetic agonist), URB597 and URB602 significantly decreased mechanical allodynia and thermal hyperalgesia. These effects were inhibited by both cannabinoid antagonists AM251 and AM630 for treatments with 2-AG, WIN and URB602 but only by AM251 for treatments with AEA and URB597 in C57BL/6 mice. Furthermore, the antinociceptive effects for AEA and URB597 were observed in cnr2KO mice but absent in cnr1KO mice, whereas the effects of 2-AG, WIN and URB602 were altered in both of these transgenic mice. Complementary genetic and pharmacological approaches revealed that the anti-hyperalgesic effects of 2-AG and URB602 required both CB1 and CB2 receptors, but only CB2 receptors mediated its anti-allodynic actions. The antinociceptive properties of AEA and URB597 were mediated only by CB1 receptors.