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      A Commonsense Patient-Centered Approach to Multimodal Analgesia Within Surgical Enhanced Recovery Protocols

      1 , 2 , 3 , 4

      Journal of Pain Research

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          Abstract

          “Enhanced recovery” in the context of a surgical patient is both a plan and a goal at the same time. The goal is faster convalescence after surgery with positive outcomes and no complications. The plan takes the form of an enhanced recovery protocol (ERP) or clinical pathway specific to a surgical procedure, a concept pioneered by Professor Henrik Kehlet from Denmark decades ago.1 Over time, this basic concept has evolved and has become arguably too complex. With over twenty elements frequently included in modern ERPs, it is not surprising that consistent implementation and adherence are lacking.2 Not all of these elements are critical, and a study of an ERP for bowel resection has demonstrated that three are particularly important: 1) laparoscopic (minimally invasive) approach; 2) early termination of intravenous fluid; and 3) early mobilization (getting out of bed).3 This last element is critically dependent on effective pain management. Because the objective of achieving analgesia does not exist in a vacuum and must be balanced with the goal of early mobility, today’s standard for pain management in the perioperative period is multimodal analgesia or using more than one analgesic agent with different mechanisms of action.4 While a single analgesic agent has the potential to provide complete postoperative pain management alone, it often comes at a significant cost. Consider these two extremes: continuous spinal anesthesia and opioid-only analgesia. Continuous spinal anesthesia, which may involve an infusion of local anesthetic into the cerebrospinal fluid, is arguably the most effective regional analgesic technique available.5 In the case of lower extremity arthroplasty, a continuous spinal anesthetic will provide complete postoperative pain relief; however, it will also result in complete immobility and prevent the patient from participating in any physical therapy. For the same surgery, opioid-only analgesia may also provide effective pain management, but it may also render the affected patient unconscious, depress respirations, and precipitate nausea, vomiting and constipation, which can also negatively impact postoperative rehabilitation. Additionally, persistent postoperative opioid use has been identified as a common adverse outcome after surgery.6 Given these examples, it is clear why multimodal analgesia has become the cornerstone of all ERPs. Available data suggest that the increasing number of non-opioid analgesic modalities decreases total opioid usage and opioid-related side effects,7 and different patterns of non-opioid analgesic utilization have been identified among anesthesiologists based on the type of surgery and patient factors.8 The scientific mechanisms of postoperative pain have been described elsewhere.9 A practical application of a multimodal analgesic strategy should be patient- and procedure-specific and consider the source, transmission, and processing of the expected surgical pain (Figure 1). We present one commonsense approach using total knee arthroplasty (TKA) as an example below written in a way to facilitate discussions with patients and family members. Figure 1 A simple paradigm for applying a multimodal analgesic strategy taking into consideration the source, transmission, and processing of the expected surgical pain; *= Routine and should be available to all patients unless contraindicated; †=Not routine and given only as indicated. Source of Pain TKA is one of the most common surgical procedures in the United States and reliably generates severe pain in most patients.10 TKA involves removal of the arthritic surfaces of the knee joint and implantation of manufactured prostheses. Localized pain and inflammation are caused by incising and cauterizing skin, subcutaneous layers, and muscle as well as osteotomies (“bone cutting”) of the tibia, femur, and patella and nerve injury. Pain at the surgical site may be relieved by non-steroidal anti-inflammatory drugs (NSAIDs) or the more selective cyclooxygenase-2 inhibitors (e.g., celecoxib), local anesthetics administered around the knee joint, and cryotherapy (i.e. applying ice to affected areas) with or without compression.11 All surgical patients should be eligible for these interventions unless contraindications exist. Transmission of Pain Afferent pain signals are carried from the surgical site to the central neuraxis via peripheral nerves. For certain types of surgery, regional anesthesia techniques (i.e., targeting one area of the body with local anesthetics) can effectively interrupt nerve transmission from the periphery to the spinal cord. These nerve blocks can provide sufficient anesthesia to make general anesthesia unnecessary for some surgeries (e.g., spinal anesthesia for knee replacement or brachial plexus block for hand surgery). Advances in these techniques using perineural or epidural catheters (i.e., regional analgesia) can extend the duration of target-specific pain relief further into the postoperative period. When this duration matches the expected trajectory of pain resolution after surgery, there may be little need for additional systemic analgesics. For TKA, regional analgesia is well-established as part of the multimodal regimen,4,11 but the trajectory of pain resolution may commonly extend beyond the 3-day duration of most regional analgesic techniques.12 Another important consideration for patients undergoing major surgery is central sensitization. In simple terms, this entails recruitment of neurons at the level of the spinal cord that normally do not transmit pain and results in expansion of the originally painful area (i.e., hyperalgesia). Opioids indirectly stimulate descending inhibitory pathways in the spinal cord that decrease the transmission of painful signals to the brain.13 Gabapentinoids decrease the hyperexcitability of neurons in the spinal cord responsible for central sensitization.14 Ketamine acts on N-methyl-D-aspartate receptors and, in subanesthetic doses, has been recommended for acute postoperative pain management.15 Further, ketamine may also exert beneficial effects in decreasing central sensitization.16 It is our opinion that non-pharmacologic interventions, local anesthetics, and NSAIDs should be administered to all surgical patients who do not have contraindications. However, opioids, gabapentinoids, and ketamine should only be used when indicated. Common factors to consider include patient history, especially comorbid conditions and preoperative analgesic use, preoperative physical function, surgical technique, and the availability of a 24/7 acute pain service that can respond to inadequately treated pain in a timely manner. Processing of Pain Pain processing is both physiological and psychological. By definition, postoperative pain will be an individualized experience.17 Previous studies demonstrate that pain catastrophizing is a risk factor for the development of chronic pain following TKA.18 For some patients with chronic pain undergoing major surgery, combining cognitive-behavioral therapy with physical therapy may improve postoperative outcomes.19 Cognitive-behavioral interventions are time- and labor-intensive and are unfortunately not available everywhere.20 Access to and use of basic patient education available online with regard to postoperative analgesic options and safe opioid management are limited.21,22 A relatively simple intervention of setting patients’ expectations regarding pain after TKA, providing a more detailed pain scale, and educating patients regarding their postoperative pain medications has been shown to decrease the utilization of opioids after surgery.23 In terms of pharmacology, paracetamol or acetaminophen acts centrally and should be given to all surgical patients unless contraindicated. Although its exact mechanisms of action are not completely understood, analgesia may result from activation of descending serotonergic (inhibitory) pain pathways, interfering with prostaglandin synthesis, and interacting with the endocannabinoid system.24 Other systemic analgesics with supraspinal activity include opioids, gabapentinoids, and ketamine.9,11,13,14,16 Putting It All Together The implementation of multimodal analgesia within ERPs is best viewed as a checklist and not a recipe. When following a recipe, each ingredient should be included in a recommended amount and added in a stepwise fashion in order to avoid a culinary disaster. This is not the case with multimodal analgesia. Each analgesic item within an ERP should be considered for the eligible surgical patient; included in the regimen if there are no contraindications and/or there are specific indication; and individualized in terms of dosing and frequency based on the patient’s prior medication use history and comorbid conditions. An example of one institution’s multimodal analgesic regimen included in an ERP for TKA patients is illustrated in Box 1. While the regimen includes multiple interventions and medications, it may be adapted to meet the needs of the individual patients.4 Some patients who are opioid-naïve may not need any scheduled opioid after surgery and will respond to as-need administration only. For all TKA patients, spinal anesthesia is strongly preferred for intraoperative anesthesia25 and will eliminate the need for systemic analgesics during surgery. Patients who take opioids chronically before surgery should continue this regimen in the perioperative period. Patients on medication-assisted treatment for opioid use disorder require special consideration with regard to perioperative pain management.26 Today, the use of opioids for breakthrough pain relief post-TKA has not been eliminated for most patients in the United States even in the setting of robust multimodal analgesia and patient education.23 However, the integration of non-pharmacologic interventions and non-opioid analgesic modalities including regional anesthesia techniques effectively decreases opioid consumption and should be considered routine.4,11,23 Box 1 Sample Perioperative Multimodal Analgesic Regimen Included in an Enhanced Recovery Protocol for Total Knee Arthroplasty Patients Before Surgery Counsel the patient on inpatient fall prevention and expected pain trajectory. Assess each patient’s medical and substance abuse history, pain medication history, drug allergies, and intolerances to analgesic medications. Give acetaminophen 1000 mg and celecoxib 400 mg by mouth if no contraindications exist. Insert an adductor canal catheter under ultrasound guidance in the regional anesthesia induction area (“block room”); add infiltration between the popliteal artery and capsule of the knee (IPACK) block if the surgeon does not routinely perform local infiltration analgesia at the end of surgery. If applicable, continue the patient’s chronic outpatient analgesics on the day of surgery and postoperatively. For the chronic pain or opioid-tolerant patient, consider giving a single dose of gabapentin 300–600 mg by mouth (lower dose in elderly and renal insufficiency). During Surgery Recommend and perform spinal anesthesia (local anesthetic only) unless refused by the patient or contraindicated (then proceed with general anesthesia). For the patient who does not receive spinal anesthesia, intravenous opioids may be administered as needed based on reactivity to painful stimuli. For the opioid-tolerant patient who receives general anesthesia, consider intraoperative low-dose ketamine infusion (0.5 mg/kg bolus followed by 0.25 mg/kg/hr infusion). Encourage surgeons to perform local infiltration analgesia (ropivacaine 0.2% 150 mL with epinephrine 2.5 mcg/mL and ketorolac 30 mg) before closure; if not an option, perform IPACK block preoperatively. After Surgery Provide routine cryotherapy with or without compression based on institutional practice. Prescribe scheduled acetaminophen 1000 mg by mouth every 6 hrs unless contraindicated (reduce the dose in patients with impaired liver function). Prescribe scheduled celecoxib 200 mg by mouth twice a day for up to 5 days then continue as needed (avoid if history of gastric ulcer or renal insufficiency). Short-acting oxycodone may be prescribed on a scheduled basis 5–10 mg every 6 hrs for the first 1–2 days after surgery; replace with the patient’s preoperative opioid regimen when applicable. For breakthrough pain relief, prescribe short-acting oxycodone tablets (e.g., 5 mg) by mouth and hydromorphone intravenously (e.g., 0.2 mg) every 4 hrs as needed. Initiate perineural infusion of ropivacaine 0.2% (basal rate 6 mL/hr; patient-controlled bolus 5 mL, lockout 30 min) via adductor canal catheter immediately after surgery. Provide daily monitoring of the patient’s pain experience, achievement of functional goals, and overall recovery through hospital discharge and adjust medications and interventions as needed. Counsel the patient on outpatient opioid use and safe storage following discharge and recommend provision of a tapering schedule for prescribed outpatient opioids based on the patient’s prior 24 hr opioid use; continue non-pharmacologic interventions and non-opioid analgesics on an as-needed basis. For the patient taking opioids chronically before surgery, communicate the discharge analgesic plan with the outpatient prescribing physician. In order to be successful, ERPs must be accepted by both healthcare practitioners and patients. Ethical concerns have been raised about the “weaponization” of ERPs with the goal of eliminating all postoperative opioids even in patients on long-term opioids. We appreciate that an important goal of ERPs should be to minimize the need for postoperative opioids whenever possible and practical through effective multimodal analgesia. However, we assert that the intended goal of ERPs, particularly for severely painful surgical procedures (e.g., total joint replacement), is incorporation of “opioid-sparing” rather than “opioid-eliminating” pain management strategies.27 Opioids as a class of analgesic drugs continue to have a role in postoperative pain management, and the reality is that many patients presenting for surgery today are already on long-term opioids preoperatively. These patients may rightfully fear “oligoanalgesia” due to the deliberate underutilization of opioids in the perioperative period. The ethical application of ERPs emphasizes that pain is a subjective experience, and all ERPs should continue to promote personalized pain medicine in the hospital postoperatively and post-discharge. A recent article describing a multidisciplinary patient-specific opioid prescribing and tapering protocol after lower extremity arthroplasty suggests a reasonable goal of return to baseline opioid use after recovery from surgery.28 In conclusion, there has been tremendous progress in the field of acute perioperative pain medicine. Effective pain management to facilitate early mobility is a critical element of modern ERPs for surgical patients. The use of multimodal analgesia has decreased the over-reliance on opioids for postoperative pain relief with regional anesthesia techniques targeting the specific site of pain and systemic non-opioid and non-pharmacologic interventions expanding coverage across the complex network of pain mechanisms. While opioids have yet to be eliminated from the postoperative period, and may well never be, the effectiveness of multimodal analgesia is well proven and has become the standard for perioperative pain management.

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          Most cited references 23

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          • Article: not found

          Pain terms: a list with definitions and notes on usage. Recommended by the IASP Subcommittee on Taxonomy.

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            • Record: found
            • Abstract: not found
            • Article: not found

            Basic opioid pharmacology: an update

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              Pain catastrophizing as a risk factor for chronic pain after total knee arthroplasty: a systematic review

              Significance A moderate level of evidence was obtained for pain catastrophizing as an independent predictor of chronic post-surgical pain following total knee arthroplasty (TKA); Lack of uniformity in data capture, particularly in pain outcome measures, precludes meta-analysis and underscores the need for consensus regarding standardized reporting of chronic pain outcomes; Future directions for research include larger study samples, improved covariate adjustment (especially for analgesic use, depression, and anxiety), adoption of consensus guidelines on outcome measures for clinically relevant chronic pain, optimal thresholds for pain catastrophizing levels that predict adverse pain outcomes, and assessment of interventions aimed to reduce the negative effects of pain catastrophizing symptoms on chronic pain outcomes. Introduction With the aging population and mounting obesity epidemic, rates of TKA have increased dramatically in the last two decades such that TKA now constitutes one of the most common and costly medical procedures in the US and Canada.1–3 Although studies employing survivorship and surgeon-based measures have generally reported TKA success rates exceeding 80%,4 these measures do not account for post-surgical pain following TKA such that chronic pain remains a major health burden for many patients.5 Specifically, studies utilizing patient-based outcome measures have indicated that 6%–30% of patients continue to experience chronic pain in the months and years after TKA.6–10 This critical gap in recovery outcomes has prompted investigators to search for modifiable risk factors for chronic pain outcomes after TKA surgery. Converging evidence from the literature on non-surgical chronic pain suggests that pain disability does not result solely from the severity of the pain, but rather, is largely influenced by patients’ interpretation and adjustment to their pain.11–13 In particular, pain catastrophizing has emerged as an important factor in chronic pain onset, severity, and duration, and may represent an independent predictor of poor treatment outcomes including the development of chronic pain after surgery.14 Pain catastrophizing is a multidimensional construct comprising elements of rumination (ie, an anxious preoccupation with pain and the inability to inhibit pain-related thoughts and fears), magnification (ie, the tendency to amplify the significance of pain with respect to implications for one’s global health), and helplessness (ie, despair surrounding perceived inability to control one’s pain experience).15 Accordingly, high levels of pain catastrophizing have been shown to predict high levels of acute and persistent pain after various surgeries.16,17 Further, a recent systematic review of psychological risk factors for pain in total knee and hip arthroplasty included catastrophizing as a potential risk factor, although the search strategy employed was somewhat limited leading to the omission of key studies.18 Although prospective studies have emphasized the role of pain catastrophizing as a risk factor for poor pain outcomes following surgical procedures including TKA,19 the majority of research has employed the outcome of acute pain (ie, 0.05; Table 4). Neither of these studies reported odds ratios (ORs) with confidence intervals (CIs) for the TKA patients, masking potential trends and precluding future meta-analysis. Further, pre-operative anxiety emerged as an important predictor in both final models; however, the authors did not publish univariate or stepwise results from their logistic models. Thus, it remains unclear whether pain catastrophizing would have conferred a significant risk before depression and anxiety were added as covariates, which could again indicate collinearity of these constructs. Another small scale study (S2; n=55) assessed the impact of pain catastrophizing on a dichotomized definition of pain defining the presence of non-zero pain at 24 months follow-up as the primary outcome. The authors used two instruments to assess their outcome of non-zero pain: 1) the Short-Form MPQ–Pain Rating Index (PRI), which asks participants to rate adjectives that describe qualitative aspects of pain on a 4-point scale, and 2) the MPQ–VAS. Because the data were skewed, the authors employed Mann–Whitney U tests and receiver operating characteristic (ROC) curve analysis to assess the impact of catastrophizing on non-zero pain presence. The model using the adjective-based measure of non-zero pain (ie, MPQ–PRI), showed that both the total PCS score (PCS-T) and the rumination subscore (PCS-R) were significant predictors of the outcome (PCS-T, P=0.028, area under the curve =0.71; PCS-R, P=0.043, area under the curve =0.70). When the MPQ–VAS score was employed, however, the effect of catastrophizing lost significance (P’s from 0.56 to 0.71; Table 4). It is likely that the MPQ–PRI constitutes a more sensitive measure of variation among individuals with low-level pain because it prompts participants to consider different aspects of their pain experience, of importance in studies with extended follow-up intervals where floor effects can make relations difficult to detect. Nonetheless, caution should be exercised when interpreting these results given the small sample size, non-parametric analyses, failure to adjust for any covariates, and failure to adjust for multiple analyses, all of which increase the likelihood of false-positive findings. Finally, we identified a mid-sized (n=140) US case–control study (S5) that used TKA treatment failure (insufficient pain reduction) at 6 months follow-up as the case definition. The authors also used the PCS to measure preoperative pain catastrophizing, but chose to dichotomize this predictor variable according to high vs low catastrophizers. High catastrophizers were arbitrarily defined as those individuals in the highest tertile of obtained scores, corresponding to PCS scores ≥16, and all others were designated as low catastrophizers. It is noteworthy that the PCS manual provides cut-off scores for problematic pain catastrophizing; the selected threshold of ≥16 constitutes the cut-off score for the 41st percentile.34 Treatment failure was operationalized both in terms of 1) 1 year follow-up, the larger, more methodologically-rigorous study (S6) found an effect of catastrophizing on pain intensity, whereas the smaller unadjusted study (S2) found mixed results for an effect on non-zero pain, a divergence that likely reflects sensitivity differences in pain measures used. Thus, while length of follow-up may not interact with the strength of relation between pain catastrophizing and chronic pain outcomes, a floor effect may occur due to fewer chronic pain cases and/or general reductions in pain intensity with time. Discussion The objective of this systematic review was to provide a synthesis of the evidence to date on pain catastrophizing as a prospective risk factor for chronic pain (ie, persisting ≥3 months) after TKA. Overall, five out of the six identified studies were able to detect some effect of pain catastrophizing on chronic pain outcomes using at least one outcome measure. Although large-scale data were not available, two mid-sized multivariate cohort studies (S3 and S6) found a positive effect of pain catastrophizing on chronic pain intensity following TKA surgery independent of baseline demographics, pain levels, and psychological factors. Whereas, two mid-sized multivariate case–control analyses (S3 and S4) failed to replicate such an effect when clinically-meaningful pain thresholds were employed as case definitions and additional adjustment was made for anxiety and depression, another multivariable case–control study found that high pain catastrophizers had dramatically increased odds of TKA-treatment failure with respect to chronic pain outcomes (S5). A lagged analysis (S1) found that pain catastrophizing remained a stable predictor of future pain severity over 1 year follow-up, and a small unadjusted (S2) study found a measurable effect of catastrophizing on non-zero pain 2 years postoperatively. These data provide a moderate level of evidence that high pain catastrophizing is a risk factor for chronic pain following TKA. A major shortcoming in all identified studies was failure to report and adjust for analgesic use in multivariate models. It is possible that high pain catastrophizers had lower adherence to pain medications, perhaps due to heightened concerns regarding potential side-effects, which in turn may have led to poorer pain control at follow-up, thus confounding the investigated relations. Another important consideration that remains to be resolved is whether other psychological constructs (such as anxiety and depression), which are known to be related to pain catastrophizing, were measured and included as covariates in the model predicting chronic pain. For example, the global pain rating parameter estimate for pain catastrophizing in the lagged analysis (S1) lost significance after further inclusion of depression in the model, although nighttime pain remained significant after inclusion of depression. Further, the two non-significant case–control analyses that used clinically meaningful outcomes (S3 and S4) adjusted for anxiety and depression, although their potential impact on catastrophizing estimates was not reported. These studies suggest that depression and anxiety may be more relevant exposures, and to the extent that these are causally related to development of chronic pain, there are well-established treatments for both. In contrast, pain catastrophizing remained an independent predictor after controlling for anxiety (S3) and/or depression (S3, S4) in the two prospective multivariable cohort studies, which together constitute the highest level of evidence available to date. Taken together, we currently lack sufficient evidence to conclude which risk factor(s) among the many related psychological constructs (eg, pain catastrophizing, anxiety, and depression) contribute uniquely to chronic pain after TKA. In general, pain catastrophizing levels remained stable over follow-up, whereas pain levels gradually diminished, on average (Table 4). However, length of follow-up did not appear to modify the effect of catastrophizing on chronic pain outcomes measured, with no clear pattern of significance/non-significance observed as follow-up intervals increased. Rather, detection of a pain catastrophizing effect appeared to depend more on adequate power. Thus, the primary consideration in studies with lengthy follow-up periods (ie, >1 year) should be ensuring adequate numbers of cases or sufficient sensitivity in outcome measures to detect minor variability in low-grade pain. Nevertheless, without statistical analysis of large-scale data that models baseline catastrophizing on repeated pain measures over time, an interaction effect of follow-up time on the investigated relationship cannot be completely dismissed. We observed substantial heterogeneity in studies with respect to study designs, analyses employed, multivariate adjustments, measures used, and outcome reporting. Of particular importance, each study we identified employed a different outcome measure for pain. The failure to adopt standardized outcome measures of pain intensity as well as a relevant cut-off for clinically-meaningful pain precludes direct comparison of results and limits opportunities for meta-analysis. Authors did not typically report stepwise results of multivariate models or univariate parameter estimates to aid the reader in understanding the impact of collinearity. Furthermore, the identified studies did not report specific parameter estimates or confidence intervals for non-significant findings, limiting their interpretation and further precluding meta-analysis of small sample data. For instance, although three studies used logistic regression to assess the impact of pain catastrophizing on pain outcomes (S3, S4, S5), only the study with significant results (S5) presented ORs and CIs. Assessment of exposure was more consistent, with five of six studies employing the PCS. However, the one study that dichotomized patients as high vs low pain catastrophizers (a potentially valuable clinical distinction) failed to provide data on the validity of their threshold. To improve future data capture, the field would benefit from the adoption of the Initiative on Methods, Measurement, and Pain Assessment in Clinical Trials consensus guidelines for standardized reporting of clinically relevant pain outcomes in RCTs, which have direct relevance to both cohort and case–control studies as well.19,35–37 Multivariable adjustment should include analgesic use (type, dose), depression, and anxiety, in addition to traditional clinical risk factors. Further, investigation of the optimal PCS cut-off for ‘high pain catastrophizers’ in predicting adverse post-surgical pain outcomes (ROC analysis) would both set the stage for its inclusion in disease complexity measures in future investigations and would be of high clinical relevance as a practical screening tool. Finally, studies should report parameter and confidence estimates for non-significant findings so that future investigators may pool their data for powerful meta-analyses. Strengths and limitations of our systematic review deserve comment. Strengths of our review include a comprehensive and replicable research strategy with two independent raters and quality assessment of all articles by three independent raters, as well as a systematic approach to evidence synthesis on the predictive value of catastrophizing on chronic post-TKA pain. A limitation of our review is that the identification and selection of relevant articles may have been influenced by publication bias (ie, underreporting of non-significant findings). Further, due to the heterogeneity in data capture and reporting across the included studies, a quantitative meta-analysis was not possible. Although further well-controlled and large-scale data would be valuable, the current evidence provides moderate support that pain catastrophizing is an important risk factor for chronic pain following TKA surgery. Given that pain catastrophizing constitutes a modifiable response to threat among other populations of chronic pain patients38–40 and to the extent that it is a causal risk factor, interventions aimed at reducing pain catastrophizing symptoms41 may translate to improved pain outcomes of TKA. As rates of TKA continue to increase with the aging population and rising obesity epidemic,1,3 further clarification of the prognostic value of various pain catastrophizing levels holds promise to close the gap in TKA recovery outcomes.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                JPR
                jpainres
                Journal of Pain Research
                Dove
                1178-7090
                24 December 2019
                2019
                : 12
                : 3461-3466
                Affiliations
                [1 ]Department of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine , Stanford, CA, USA
                [2 ]Anesthesiology and Perioperative Care Service, Veterans Affairs Palo Alto Health Care System , Palo Alto, CA, USA
                [3 ]Department of Public Health & Community Medicine, Tufts University School of Medicine , Boston, MA, USA
                [4 ]Department of Diagnostic Sciences, Tufts University School of Dental Medicine , Boston, MA, USA
                Author notes
                Correspondence: Edward R Mariano Anesthesiology and Perioperative Care Service, VA Palo Alto Health Care System , 3801, Miranda Avenue (112A), Palo Alto, CA94304, USATel +1 650 849-0254Fax +1 650 852-3423 Email emariano@stanford.edu
                Article
                238772
                10.2147/JPR.S238772
                6935269
                © 2019 Mariano and Schatman.

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                Page count
                Figures: 1, References: 28, Pages: 6
                Categories
                Editorial

                Anesthesiology & Pain management

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