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Perioperative pain management is an important aspect of any plastic surgery practice. As practitioners involved in invasive surgical procedures, plastic surgeons are intimately familiar with acute postoperative pain, chronic pain, and how pain affects our patients, both in the short term and long term. Uncontrolled pain can negatively affect postoperative patient outcomes and a patients’ satisfaction with the surgical experience. Thus, as a primarily referral-based specialty, controlling operative and postoperative pain takes on a greater meaning to provide the patient with the best possible postoperative outcome while maximizing patient satisfaction.
Pain is defined as “an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage”. In an update from commonly held notions, the International Association for the Study of Pain (IASP) states that pain and nociception are different experiences. Pain is an individualized phenomenon that is influenced by an individual’s past experiences, while nociception is a physiologic activity that occurs in the nervous system as a response to noxious stimuli. Lastly, the IASP states that in excess, pain may negatively impact a patient’s functional, social, and psychosomatic wellbeing.
The impact of pain on a patient can be broken down into three categories: physiologic, psychosocial, and postoperative recovery. The physiologic response to pain can lead to impaired ventilation and constipation, higher rates of postoperative nausea and vomiting (PONV), increased rates of deep vein thrombosis (DVT) and urinary retention, and impaired immune response, leading to increased rates of postoperative infections and wound-healing issues. Uncontrolled pain can exacerbate pre-existing psychiatric conditions as well as lead to the development psychosocial issues, as these patients are more likely to isolate themselves from others. In the acute phase, uncontrolled pain can delay discharge from the postanesthesia care unit (PACU) and hospital while increasing the rate of hospital readmissions.
To address these concerns, pain management protocols consisting of multimodal analgesia have been developed across all surgical specialties, with the goal of appropriately managing pain, decreasing opioid consumption, and decreasing patient length of stay. This chapter will focus on the components of an ERAS protocol and present the most recent findings of multimodal analgesia regimens for plastic surgery procedures of the breast.
Opioids have historically been the gold-standard for postoperative pain control, with receptors found in the central nervous system, peripheral nervous system, and enteric nervous system. The primary neurotransmitters involved in the sensation of pain are substance P and glutamate in the central nervous system. Pharmacologic opioids mimic endogenous opioids and, through a complex set of reactions, result primarily in the inhibition of neurotransmitter release and secondarily in the prevention of excitatory signals. As such, opioids have traditionally been popular methods of pain control with oral, intravenous, and patient-controlled analgesia (PCA) routes of administration. Despite their efficacy, opioids have various side effects, including constipation, nausea and vomiting, drowsiness. Furthermore, opioids have proven to be addictive, account for the majority of illicit drug overdoses, and negatively affect patients in terms of quality-of-life and healthcare costs. As the years have passed, it has become more evident that opioids are part of the problem, rather than the solution, to pain control. This has led to efforts to study provider prescribing patterns and standardize perioperative pain management at the institutional level.
To appropriately address postoperative pain and decrease opioid consumption, multimodal analgesia regimens have been created that address the subjective experience of pain, while managing the physiologic and noxious stimuli that lead to pain. These multimodal analgesia protocols have come to be known as “enhanced recovery after surgery” or “ERAS” protocols. The overarching themes between the various ERAS protocols in circulation today are preoperative education, perioperative non-narcotic analgesia, intra-operative local or regional anesthesia, and early postoperative ambulation.
ERAS protocols were originally conceived to decrease patient length of stay during the postoperative phase. To that end, Liu et al . studied 52 patients in a randomized control trial (RCT) to examine the effect that various adjunct anesthetics had on patient length of stay. They found that patients who received local anesthetic met discharge criteria 1.5 days earlier than those who did not. In 1998, Pavlin et al . prospectively analyzed adult outpatient procedures to determine causes of discharge delay. The authors determined that the most important factor in a discharge delay was the method of anesthesia (i.e. general vs. local infiltration vs. nerve block vs. neuraxial anesthesia).
The earliest iterations of ERAS protocols were introduced and put into practice in the field of colorectal surgery during the 1990s and early 2000s. Across the board, ERAS protocols have demonstrated decreased patient length of stay, costs, and opioid use. In a 2009 review article on ERAS in colorectal surgery, authors determined several aspects of care that are critical to a successful ERAS protocol, these include preoperative counseling, local or regional anesthetic blocks, minimization of postoperative opioid use and control of PONV, and early mobilization protocols, much of which have been carried over to plastic surgery ERAS protocols. Multimodal analgesia has proven to be a safe, efficient, and reproducible way to decrease opioid usage in the perioperative setting in various fields, including neurosurgery, hepatobiliary, bariatric, urologic, colorectal, and major oncological resections. Similarly, plastic surgeons have begun incorporating aspects of ERAS protocols into their practices to cut down on excessive opioid prescriptions.
In the effort to remove sources of excess opioids, authors have been studying physician prescribing patterns. The incorporation of ERAS protocols has seen 40%–100% reductions in prescribed perioperative opioids, among various other benefits. When applied to implant-based breast reconstruction, Lombana et al . demonstrated that patient within an ERAS protocol spent significantly less time in the PACU (68.47 min vs. 103.95 min; P = 0.006) than non-ERAS patients and are prescribed significantly less opioids upon discharge ( P = 0.017). Furthermore, analyzing 136 patients undergoing outpatient plastic surgery breast procedures, Wong and Saint-Cyr found that, compared with non-ERAS patients, those within an ERAS protocol consumed 16.6 OMEs versus 23.3 OMEs in the PACU ( P = 0.005) and were prescribed 41.5% less opioids than non-ERAS patients ( P <0.0001). Despite these positive findings, recent data has shown that among non-plastic surgery and plastic surgery procedures, over half of all opioids prescribed are not consumed and a third of patients do not use any opioids in the postoperative phase.
In addition to decreasing patient opioid consumption, ERAS protocols have robust data demonstrating their positive effects on patient pain, length of stay, time to ambulation, and healthcare costs. Regarding healthcare costs, Oh et al . demonstrated costs saving of $4576 per patient when ERAS protocols are used in microsurgical breast reconstruction. Recommendations focus on optimizing patients in each phase of their preoperative, intra-operative, and postoperative course. Interestingly, Shin et al . demonstrated that as a patient’s BMI increases, so too does the benefit they receive from ERAS protocols, with class 1 obesity patient’s experiencing a LOS decrease of 0.99 days ( P = 0.048) and class II+ obesity patients experiencing a LOS decrease of 1.35 days ( P = 0.093). Though the majority of ERAS recommendations are for breast reconstruction, most, if not all, have been carried over to oncoplastic and aesthetic breast procedures. In addition to the previously mentioned benefits, the implementation of ERAS protocols has seen shorter hospital and PACU recovery times, and significant patient cost savings.
Although ERAS studies were first developed to decrease patient length of stay, they have demonstrated decreases in opioid consumption while providing acceptable pain control. This decrease in opioid consumption has subsequently led to a decrease in opioid-related complications. These results have been accomplished through a rigorous examination of all the individual components that go into a patients’ operative course.
In plastic surgery of the breast, most ERAS studies have been incorporated into inpatient breast reconstruction, likely because these operations have a difficult and painful recovery. Thus, the urgent need to develop adequate methods of pain control while preventing opioid over-consumption. Given the importance of ERAS protocols in breast reconstruction, two large systematic reviews analyzed high-quality data to develop a set of comprehensive ERAS recommendation. In conjunction with the ERAS Society, Temple-Oberle et al . strongly recommended incorporation of the following components: preadmission education and optimization; preoperative flap planning; minimization of preoperative fasting and carbohydrate loading; VTE/antimicrobial/PONV prophylaxis; pre/intra-operative analgesia; standard anesthetic protocol; maintaining intra-operative normothermia; goal-directed intra-operative fluid management; postoperative analgesia; early feeding; postoperative flap monitoring; postoperative wound management; early mobilization; and post discharge home support and physiotherapy. Though these recommendations can be applied individually, optimal results are seen with application of multiple aspects.
Regarding pain parameters, data has shown that a combination of preoperative education, scheduled perioperative multimodal analgesia, and intra-operative local anesthesia are vital to decreasing opioid consumption and patient pain. The preoperative phase typically consists of education and patient optimization for the surgical experience via various means. The perioperative phase consists of scheduled NSAIDs or COX-2 inhibitors, acetaminophen, gabapentinoids, and/or antispasmodics. The final aspect of comprehensive pain management involves local anesthetic administration, which can be accomplished via peri-incisional injection, surgical site infiltration, regional peripheral nerve blocks, and/or neuraxial anesthesia.
Preoperative education has proven to be an important part of ERAS protocols in plastic surgery. Preoperative education should cover the surgical course, pain expectations, pre-habilitation, and medication and nutritional optimization. Incorporation of such programs are supported by strong, prospective data demonstrating promising effects on patient LOS, pain scores and opioid consumption, medical complications, and overall patient wellbeing. A large systematic review examining preoperative optimization in ERAS protocols, determined that intensive smoking and alcohol cessation programs and preoperative exercise are the most effective measures for decreasing postoperative morbidity and patient LOS. Overall, preoperative optimization should focus on educating the patient on the surgical course, pain management and expectations, and opioid risks and multimodal analgesia, while encouraging weight-loss and alcohol and/or smoking cessation.
Multimodal analgesia regimens are backed by high-level evidence with strong recommendations for their incorporation into ERAS protocols. These regimens are opioid-sparing and seek to address pain though various physiologic angles, by targeting multiple neuronal receptors in various parts of the nervous system. Perioperative non-narcotic analgesia can be broken down into the different drug classes: non-steroidal anti-inflammatory drugs (NSAIDs), cyclo-oxygenase (COX)-2 inhibitors (COXIBs), acetaminophen, gabapentinoids, and antispasmodics.
NSAIDs and COXIBs decrease surgical pain and inflammation by inhibiting the COX system and the production of downstream pain modulators, specifically prostaglandins. NSAIDS have been further refined to selectively inhibit COX-2, a major enzyme involved in the generation of post-injury hyperalgesia. These drugs have been shown to be as effective as nonspecific NSAIDs for pain control, with a lower risk of gastrointestinal (GI) side effects. Although selective COXIBs have been linked with unwanted cardiovascular complications, a large systematic review demonstrated a lower cardiovascular risk-profile of celecoxib compared with non-selective NSAIDs and other COX-2 inhibitors. However, one should exercise caution when prescribing any NSAID or COXIB to patients with high-risk cardiovascular profiles.
Thought to regulate nociception peripherally and centrally via adenosine and serotonin receptors, acetaminophen has proven to be a staple aspect of any ERAS protocol, with an effective analgesic effect and low-risk profile. Although acetaminophen has a relatively low risk-profile, one should be aware of the possibility of hepatic toxicity. Thus, the prescribing physician should practice caution when administering acetaminophen to patients with a history of hepatic dysfunction and caution all patient to avoid consumption of more than 4000 mg/day.
Gabapentinoids were originally developed as anti-convulsants and include gabapentin and pregabalin. These drugs act centrally via calcium-channel binding on neurons and inhibiting the release of pain modulators. They have proven to be useful adjunct medications in ERAS protocols and effective at controlling chronic and acute postoperative pain. These drugs have also shown promise when started preoperatively on a scheduled basis. The final component of multimodal analgesia regimens are antispasmodics. Antispasmodics inhibit postoperative muscle contraction through their antimuscarinic effects and include cyclobenzaprine and methocarbamol. The incorporation of these medications into ERAS protocols has shown promise in reducing length of stay, postoperative pain, and opioid consumption. Please see Table 42.1 for complete dosing and drug information of the various multimodal analgesics discussed above.
Generic name | Trade name | Dose (mg) and frequency | Maximum daily dose (mg)** | Contraindications | Adverse reactions |
---|---|---|---|---|---|
Ibuprofen | Motrin, Advil | 400–800 mg PO or IV q6–8 h | 3200 | Prior hypersensitivity reaction, active GI ulcers or bleeding, moderate to severe renal dysfunction, pregnancy, heart dysfunction | GI dysfunction, renal dysfunction, thrombotic events, transaminitis |
Naproxen | Naprosyn | IR: 250–500 mg PO q12hER: 750–1000 mg PO q24h | 1500 | See ibuprofen | See ibuprofen |
Ketorolac | Toradol | IV or IM Load: 15–30 mgMaintenance: 15 mg q6h | IV/IM: 120 | See ibuprofen | See ibuprofen |
Celecoxib | Celebrex | >25 kg: 100–200 mg PO BID | 400 | See ibuprofen, hypersensitivity to sulfa | Hypertension, edema, hepatic/GI/renal dysfunction, skin changes |
Acetaminophen | Tylenol, Panadol, Ofirmev | 325–650 mg PO q4–6 h1000 mg PO q6–8 h * 15 mg/kg IV q6h | 4000 | Prior hypersensitivity reaction, severe hepatic dysfunction | Skin changes, renal/hepatic dysfunction |
Gabapentin | Neurontin | 300–1200 mg PO TID | 3600 | Prior hypersensitivity reaction | Ataxia, dizziness, fatigue, edema, skin changes |
Cyclobenzaprine | Flexeril |
|
|
Hyperthyroidism, arrhythmias, heart failure, heart block, MI, MAOI consumption | Somnolence, xerostomia, dizziness, confusion |
Methocarbamol | Robaxin | 1500 mg PO q6h for 48–72 h, then 1000 mg PO q6h | 6000 | Prior hypersensitivity reaction, renal dysfunction | Somnolence, dizziness, blurry vision, headache, nausea/vomiting, confusion, rash, bradycardia, convulsions, jaundice |
* Senior author prefers to limit acetaminophen consumption to 3000 mg/day to limit toxicity. **Daily dosages are meant for adult patients.
Local anesthetics are an important component of any perioperative pain control regimen, especially in plastic surgery. Commonly used local anesthetics include lidocaine, bupivacaine, ropivacaine, and prilocaine. The indications for each of these differs with regards to desired onset and duration of action. For example, ropivacaine has been shown to have an earlier onset of action but shorter block duration than bupivacaine. Thus, for an intra-operative block in which duration is more important than onset, bupivacaine HCl is often preferred to ropivacaine. Each of these medications can be given with or without epinephrine, attached to a biologic carrier, or in a local anesthetic cocktail. Lastly, method of administration differs depending on the intended effect of the local anesthetic. Outside of peri-incisional local anesthesia, the most common applications for local anesthesia in plastic surgery of the breast are operative site infiltration, regional peripheral nerve blocks, and neuraxial blocks.
Each method of local anesthesia administration can be further divided into sub-categories. Operative site infiltration can take the form of a one-time soft-tissue local infiltration, for example, into the breast parenchyma during a breast reduction, or as an intra-wound catheter for prolonged administration. Regional blocks can be divided by the anatomic regions of the breast and abdomen. Regional blocks that will be discussed in this chapter include PECS1 and PECS2 blocks, serratus anterior plane (SAP) blocks, intercostal nerve blocks, transversus abdominis plane (TAP) blocks, and paravertebral plane (PVB) blocks. Neuraxial blocks can be broken down into epidural anesthesia and spinal anesthesia; due to the relative lack of use within plastic surgery of spinal anesthesia, we will focus on epidural anesthesia.
All local anesthetics are composed of an amide drug of a specific concentration and dosage. Local anesthesia functions by binding to and closing voltage-gated sodium-channels on neuronal cell membranes, preventing depolarization and action potential generation. Pharmacokinetics are influenced by the pKa, lipid solubility, and protein binding of each individual agent. Onset of action is inversely proportional to pKa, i.e., agents with a lower pKa will have a more rapid onset of action, and duration of action is directly proportional to lipid solubility and protein binding. Dosing of local anesthesia is based on a patient’s weight and is unique to each individual agent. The reported maximum dose for lidocaine with epinephrine is 7 mg/kg and 4.5 mg/kg without epinephrine, and between 2 mg and 3 mg/kg for bupivacaine (with or without epinephrine). Regarding duration of action, lidocaine has been shown to provide anesthesia for 1–3 h and bupivacaine for up to 10 h. Please see Table 42.2 for complete local anesthesia dosing guidelines.
Amide drug (concentration range) * and technique concentration range | Spinal | Caudal/lumbar epidural | Peripheral | Subcutaneous |
---|---|---|---|---|
|
1–2.5 | 5–7 † | 5–7 † | 5–7 † |
|
0.3–0.5 | 2–3 † | 2–3 † | 2–3 † |
|
0.3–0.5 | 2–3 † | 2–3 † | 2–3 † |
|
NR | 5–7 †,‡ | 5–7 †,‡ | 5–7 †,‡ |
* Concentrations are displayed in mg percent. Example, a 1% solution contains 10 mg/mL, a 2% solution contains 20 mg/mL.
† The higher dose is recommended only with the co-administration of epinephrine 1:200,000. Maximum epinephrine dose for adults under general anesthesia with volatile agents is 2–3 mcg/kg.
Although plain local anesthetic has proven to be an effective anesthetic, steps have been taken to improve duration of anesthesia, and, in effect, pain control. Due to the relatively short duration of action of plain bupivacaine, liposomal bupivacaine has emerged as an attractive alternative, with anesthesia duration reported for up to 72 h as a TAP block. After an initial release of bupivacaine, liposomes increase the solubility of bupivacaine for gradual release to provide prolonged anesthesia. Liposomal bupivacaine has shown great promise in various aspect of plastic surgery, with results demonstrating a decrease in patient LOS, opioid consumption, and pain. However, data is conflicting surrounding its regular use as a local anesthetic.
In addition to its high cost, some studies have suggested the non-superiority of liposomal bupivacaine to plain bupivacaine as a TAP block. In addition, there is a lack of consensus regarding the onset of action of liposomal bupivacaine. Due to the ambiguity regarding an “anesthetic gap” with the administration of liposomal bupivacaine, some authors mix plain bupivacaine with liposomal bupivacaine, to provide immediate anesthesia while the patient is recovering in the PACU. It should be noted that to preserve the efficacy of liposomal bupivacaine when mixing liposomal bupivacaine with plain bupivacaine or diluting within a solution, there are specific guidelines that should be adhered to. According to the manufacturers of liposomal bupivacaine, 20 cc of 2.6% liposomal bupivacaine can be diluted in a maximum of 280 cc of NS or lactated Ringer’s solution and the ratio of milligrams of bupivacaine HCl to liposomal bupivacaine cannot exceed 1:2. Thus, up to 150 mg of bupivacaine HCl can be combined with a 20 cc vial of 2.6% liposomal bupivacaine. Because of the high price of liposomal bupivacaine and the conflicting data regarding its efficacy, some authors have begun making evidence-based anesthetic cocktails.
For centers that do not allow or provide liposomal bupivacaine, the use of alternate blocks can be considered for regional blocks. These cocktails commonly contain agents that will address noxious stimuli and postoperative inflammation. Three common additions to local anesthesia include ketorolac (non-steroidal anti-inflammatory drug), dexmedetomidine (selective alpha 2-adranergic agonist), and dexamethasone (synthetic glucocorticoid). The addition of these components to plain local anesthesia has demonstrated positive effects on opioid consumption and postoperative pain, with recent findings suggesting equivalency of local anesthetic cocktails to liposomal bupivacaine.
Care should be taken when administering dexamethasone to diabetics and ketorolac to patients with a history of bariatric surgery, renal issues, or stomach ulcers. However, in a large multi-specialty systematic review, ketorolac did not demonstrate a significant increase in postoperative hematoma rates. Lastly, there has been some consideration toward utilizing intra-operative botulinum-A (BTX-A) toxin to prevent postoperative muscle spasm of the pectoralis major muscle. In a systematic review looking at the use of BTX-A in subpectoral implant placement, Winocour et al . found improvement in patient postoperative pain when 75–100 units of BTX-A is injected into the pectoralis major muscle.
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