Objectives: The objective of this study was to review the current scientific evidence on the role of Enhanced Recovery After Surgery (ERAS) implementations in reducing postoperative opioid consumption and their potential association with the risk reduction for long-term opioid use, physical opioid dependency, and opioid addiction. Methods: A literature search was conducted using the following medical subject heading keywords: “postoperative pain,” “postoperative pain management,” “multimodal analgesia,” “ERAS,” “Enhanced Recovery,” “opioid-free analgesia,” or “opioid crisis.” Discussion: Identification and management of pre-existing psychosocial factors, comorbid pain entities, and chronic opioid use have a significant impact on the severity of postoperative pain. Different multimodal analgesia approaches have been associated with reduced postoperative pain scores and opioid consumption. Health care providers, patients, and family members should recognize the advantages of opioid-free analgesia techniques in postoperative pain management. As part of ERAS protocols, transitional pain services may consider current therapeutic alternatives for acute and long-term pain management that include minimizing perioperative opioid use and establishing adequate opioid prescription practices.

Regional anesthesia has been considered a great tool for maximizing post-operative pain control while minimizing opioid consumption. Post-operative rebound pain, characterized by hyperalgesia after the peripheral nerve block, can however diminish or negate the overall benefit of this modality due to a counter-productive increase in opioid consumption once the block wears off. We reviewed published literature describing pathophysiology and occurrence of rebound pain after peripheral nerve blocks in patients undergoing orthopedic procedures. A search of relevant keywords was performed using PubMed, EMBASE, and Web of Science. Twenty-eight articles (n = 28) were included in our review. Perioperative considerations for peripheral nerve blocks and other alternatives used for postoperative pain management in patients undergoing orthopedic surgeries were discussed. Multimodal strategies including preemptive analgesia before the block wears off, intra-articular or intravenous anti-inflammatory medications, and use of adjuvants in nerve block solutions may reduce the burden of rebound pain. Additionally, patient education regarding the possibility of rebound pain is paramount to ensure appropriate use of prescribed pre-emptive analgesics and establish appropriate expectations of minimized opioid requirements. Understanding the impact of rebound pain and strategies to prevent it is integral to effective utilization of regional anesthesia to reduce negative consequences associated with long-term opioid consumption.

According to the 2015 National Survey on Drug Use and Health, marijuana continues to be the most common illicit recreational drug used in the US. Cannabis is associated with systemic reactions that potentially affect perioperative outcomes. We have reviewed the most important pharmacological aspects and pathophysiological effects that should be considered during the perioperative management of chronic cannabis/cannabinoids users. The synthetic analogues provide higher potency with increased risk for complications. High cannabinoid liposolubility favors rapid accumulation in fatty tissue which prolongs its elimination up to several days after exposure. The multi-systemic effects of cannabinoids and their pharmacological interactions with anesthetic agents may lead to serious consequences. Low doses of cannabinoids have been associated with increased sympathetic response (tachycardia, hypertension and increased contractility) with high levels of norepinephrine detected 30 min after use. High doses enhance parasympathetic tone leading to dose-dependent bradycardia and hypotension. Severe vascular complications associated with cannabis exposure may include malignant arrhythmias, coronary spasm, sudden death, cerebral hypoperfusion and stroke. Bronchial hyperreactivity and upper airway obstruction are commonly reported in cannabis users. Postoperative hypothermia, shivering and increased platelet aggregation have been also documented.

Current evidence suggests that activation of glial and immune cells leads to increased production of proinflammatory mediators, creating a neuroinflammatory state. Neuroinflammation has been proven to be a fundamental mechanism in the genesis of acute pain and its transition to neuropathic and chronic pain. A noxious event that stimulates peripheral afferent nerve fibers may also activate pronociceptive receptors situated at the dorsal root ganglion and dorsal horn of the spinal cord, as well as peripheral glial cells, setting off the so-called peripheral sensitization and spreading neuroinflammation to the brain. Once activated, microglia produce cytokines, chemokines, and neuropeptides that can increase the sensitivity and firing properties of second-order neurons, upregulating the signaling of nociceptive information to the cerebral cortex. This process, known as central sensitization, is crucial for chronification of acute pain. Immune-neuronal interactions are also implicated in the lesser-known complex regulatory relationship between pain and opioids. Current evidence suggests that activated immune and glial cells can alter neuronal function, induce, and maintain pathological pain, and disrupt the analgesic effects of opioid drugs by contributing to the development of tolerance and dependence, even causing paradoxical hyperalgesia. Such alterations may occur when the neuronal environment is impacted by trauma, inflammation, and immune-derived molecules, or when opioids induce proinflammatory glial activation. Hence, understanding these intricate interactions may help in managing pain signaling and opioid efficacy beyond the classical pharmacological approach.

One of the most common and distressing symptoms after craniotomy is postoperative nausea and vomiting (PONV). PONV could generate delayed postanesthesia care and hospitalization discharge, lower patient satisfaction, and an increase in overall hospitalization costs. The incidence of reported PONV after craniotomy is 22% to 70% without prophylaxis, and a multimodal regimen of medication has been recommended. We conducted a comprehensive literature review of the clinical evidence related to PONV prevention and management after craniotomy. All clinical trials in adult populations relevant to PONV after craniotomy available in English language and indexed in PubMed, Google Scholar and Cochrane Library databases from January 1997 up to September 2018 were retrieved using a combination of free-text words related to PONV in craniotomy. After screening manuscripts identified in the initial search, 23 clinical trials investigating systemic pharmacological intervention versus placebo or active control in patients undergoing craniotomy under general anesthesia met the criteria for inclusion in this comprehensive narrative review. The pathophysiology and mechanisms of PONV after craniotomy could be multifactorial in etiology. Therefore, based on current evidence, PONV management after craniotomy should focus on perioperative patient assessment, surgical, and anesthesia-related risk factors and the selection of systemic pharmacological considerations to reduce its incidence and complications. A multimodal regimen of medication targeting different chemoreceptors in the vomiting center is recommended. Ondansetron and dexamethasone, or their combination, are the most frequently used and effective agents. Further randomized clinical trials comparing different regimens that significantly reduce the incidence of PONV in craniotomy would provide relevant evidence-based data for PONV management in this patient population.

Postoperative nausea and vomiting (PONV) have been widely studied as a multifactorial entity, being of female gender the strongest risk factor. Reported PONV incidence in female surgical populations is extremely variable among randomized clinical trials. In this narrative review, we intend to summarize the incidence, independent predictors, pharmacological and non-pharmacological interventions for PONV reported in recently published clinical trials carried out in female patients undergoing breast and gynecologic surgery, as well as the implications of the anesthetic agents on the incidence of PONV. A literature search of manuscripts describing PONV management in female surgical populations (breast surgery and gynecologic surgery) was carried out in PubMed, MEDLINE, and Embase databases. Postoperative nausea and vomiting incidence were highly variable in patients receiving placebo or no prophylaxis among RCTs whereas consistent results were observed in patients receiving 1 or 2 prophylactic interventions for PONV. Despite efforts made, a considerable number of female patients still experienced significant PONV. It is critical for the anesthesia provider to be aware that the coexistence of independent risk factors such as the level of sex hormones (pre- and postmenopausal), preoperative anxiety or depression, pharmacogenomic pleomorphisms, and ethnicity further enhances the probability of experiencing PONV in female patients. Future RCTs should closely assess the overall risk of PONV in female patients considering patient- and surgery-related factors, and the level of compliance with current guidelines for prevention and management of PONV.