Curr Orthop Pract. 2016;27(4):360-370.
Perioperative pain management after knee arthroplasty has undergone a conceptual revolution in the last decade. Along with other exciting innovations, including minimally invasive techniques, computer-assisted procedures and a significant stride in tribology, understanding pain modulation and drug action at a molecular level is recognized as the game changer in arthroplasty surgeries. While most patients usually recover and experience pain relief within 3 mo after TKA, about 20% (10–34%) of the patients are left with an unfavorable long-term pain outcome. Fifty-two percent of patients report moderate pain and 16% report severe pain at rest 30 days after TKA, while pain at movement affects as much as 78% of the patients. Inability to adequately control postoperative pain causes undue suffering, inability to participate in fast-track rehabilitation programs, sleep disturbance (44% patients first 3 nights), delayed discharge, and the development of persistent postsurgical pain. The goal of this review article is to give an overview of the fundamental concept of surgical pain, the molecular mechanism of action of different drugs, evolution of the concept of preventive analgesia, and state of the art for current pain management. When combined and standardized, these factors allow arthroplasty surgeons to offer outpatient arthroplasty procedures.
By relieving pain and improving mobility, hip and knee replacement surgeries have successfully alleviated suffering of debilitating conditions such as osteoarthritis, inflammatory arthritis, and avascular necrosis of the femoral head. Improvement in perioperative pain management along with innovations in minimally invasive techniques, computer-assisted procedures, and tribology have improved longevity of the implant and quality of life in patients the world over. Understanding pain modulation and drug action at a molecular level revolutionized postoperative pain management and rehabilitation protocol. Today, most surgeons[1,2] recognize this cultural shift as the game changer in arthroplasty.
While most patients usually recover and experience pain relief within 3 mo after TKA,[3] about 20% (10–34%) of the patients are left with an unfavorable long-term pain outcome. According to Grosu et al.[4]52% of patients report moderate pain and 16% report severe pain at rest 30 days after TKA, while pain on movement occurs in as many as 78% of patients. Inability to adequately control postoperative pain causes undue suffering, inability to participate in fast-track rehabilitation programs, sleep disturbance (44% patients first 3 nights), delayed discharge, and the development of persistent postoperative pain.[5–7] The unexplained painful TKA without problems related to implants continue to be a challenge for the surgeon[5] (55 of 10) and remain a cause of revision surgery.[8]
The goal of this article is to provide an overview of the fundamental concept of surgical pain, the molecular mechanism of action of different drugs, risk factors for acute and chronic pain, evolution of the concept of preventive analgesia, and finally state of the art current pain management. When combined and standardized, these factors allow arthroplasty surgeons to offer outpatient arthroplasty procedures.[9,10]
The complex pain pathway can be briefly summarized as transduction, transmission, modulation and perception .
The surgical incision is the starting point that effects potassium, serotonin, and histamine release from damaged cells, bradykinin (BK) from injured vessels and prostaglandin (PG) from nerve endings (nociceptors). These mediators induce further recruitment of other inflammatory agents like interleukin (IL)-1, IL-6, tumor necrosis factor (TNF)-alpha, Substance-P, Acetylcholine (Ach) among others. Substance-P, a vasoactive neuropeptide is responsible for further release of BK. Histamine from mast cells and serotonin from platelets together then stimulate additional nociceptors. Stimulation of nociceptors results in depolarization of nerve endings, which is carried to the spinal cord via A-delta and C fibers. Neural depolarization reduces excitatory threshold of nociceptors of both the injured area (primary hyperalgesia) and that of noninjured areas (secondary hyperalgesia), and this phenomenon is known as peripheral sensitization.[11–13]
A-delta fibers are myelinated fibers responsible for quickly conducting pain perception and accurately localizing the pain producing area. C-fibers are unmyelinated and slower in conducting pain information from a diffuse area.[14] These fibers mainly terminate at secondary afferent neurons of Rexed laminae 1 and 2 in the dorsal horn of spinal cord. Adjacent interneuron circuits, descending inputs from higher spinal cord, midbrain areas (periaqueductal areas, raphe nucleus, locus coeruleus, reticulo-spinal) and cerebral centers significantly modulate information carried by afferent fibers.
Neurotransmitters of the majority of interneurons are gama-aminobutyric acid (GABA) and glycine both of which are inhibitory in action. The main excitatory amino acid is alpha amino-3-hydroxy-5-methyl-4-isozole propionic acid (AMPA/kinate receptor) located at the post-synaptic to primary afferent fibers. It is important to note that N-methyl-D-aspartate (NMDA) receptors are postsynaptic to interneurons and the AMPA/kinate and substance-P must be activated prior to NMDA receptor activation.[11,15] The first event at a molecular level in the dorsal horn is release of excitatory amino acids like glutamate and aspartate from primary afferent fiber nerve endings (Figure 2). They bind to AMP/kinate receptors leading to the opening of ion channels and depolarization of second order neurons. These voltage sensitive events remove a magnesium plug responsible for keeping NMDA receptors in an inactive state. Glycine binding also takes place to finally activate NMDA receptors.
Now a complex cascade of events occurs, which includes marked release of intracellular calcium, which then activates phospholipase-A2, enhances PG production and increases production of substance-P. NMDA activation also causes release of nitric oxide (NO). Both PG and NO diffuse extracellularly to induce primary afferent neurons and release excitatory neurotransmitters. It is believed that once the cascade of events is initiated, the blockade of peripheral nociceptor input fails to completely stop dorsal horn neurons from firing. This wind-up phenomenon leads to clinical sequelae of hyperalgesia, muscle spasm, allodynia, increased sympathetic tone, and subsequent decrease in blood flow.[16–18] Higher doses of analgesics such as opiates are required to suppress the pain, and hence NMDA receptors are implicated in the development of opiate tolerance. This also explains why long standing pain syndrome fails to improve even after surgical intervention and correction of primary anatomic abnormality. This is responsible for chronic pain and pain syndrome even after successful TKR in some patients who have had severe long-term osteoarthritis pain. NMDA receptors also are held responsible for the complex phenomenon of central sensitization (ability of benign and low-threshold stimuli to activate second order neurons) if afferent nerve stimulation is intense and of sufficient duration.[4,11–13,15]
After extensive modulation at the dorsal horn, the second-degree afferent from the dorsal spinal cord ascends one to two levels before crossing to other side, ascending as a crossed spinothalamic tract. These tracts end in the thalamus, and third order neurons start from here to end in the cerebral cortex. It is where that second degree of modulation takes place, also known as central nociceptive processing.[6,11,15,16] On the way there are projections to periaqueductal gray matter (PAG), which is specialized for pain localization. The spinoreticular tract is another ascending tract that has a synapse at the brainstem reticular formation, before terminating in the thalamus and hypothalamus. This tract is particularly responsible for the emotional aspect of pain. Descending tracts through PAG and rostral ventromedial medulla inhibit pain transmission due to presence of high concentrations of opioid receptors and endogenous opioids.
A large area of cerebral cortex known as the "pain matrix" is activated during acute pain activation, which includes the somatosensory area (S1 and S2), insular, anterior cingulate cortex as well as thalamus. Thalamus modulation is responsible for sensory discriminative processing, whereas the cerebral cortex produces emotional and affective responses. This explains why pain perception is affected by factors such as cognition (e.g. distraction or catastrophizing), mood, beliefs, and genetics.
Conventional pain management is unimodal and additive in nature. In other words, it usually involves administration of opioids (injectable) with or without nonsteroidal antiinflammatories as required. This often requires higher doses of opioids, with its potential side effects and the administration of drugs being dependent on nursing staff usually gets delayed. To overcome this, patient-controlled analgesia (PCA) gained worldwide acceptance by both patients and surgeons.
PCA is an interesting, attractive, appealing, and effective concept that involves patients in pain control management. The PCA uses a microprocessor controlled infusion device that can deliver a continuous baseline dose. It is programmed for additional, small, and repetitive doses with a lock-out period (5–10 min) after each demand dose. The program also decides maximal total dose to be delivered per hour. Lock-out time needs calibration in the beginning. Setting the lock-out time too short allows the patient to self-administer additional medication (overdose) whereas a prolonged lock-out interval fails to give adequate analgesia.[4,19,20]
PCA remains a popular and reasonably[21] viable option; however, it has certain flaws. (1) The chances of overmedication with potential adverse effects such as nausea, vomiting, respiratory depression, ileus, urinary retention, pruritus, hypotension, bradycardia, hyperalgesia and cognitive changes can occur. (2) Despite the ease of administration and titratability, parenteral opioids typically do not provide adequate analgesia for total joint replacement patients, particularly during movement with ambulation. Movement evoked pain (MEP) is 95% to 226% more intense than pain at rest (PAR), awakens the patients from sleep, is not reduced by opiates, and is a potential risk of persistent postsurgical pain syndrome (PPSP).[4,22] (3) By activation of NMDA receptors in the central nervous system, opioids induce a complex phenomenon of hyperalgesia by paradoxically lowering the pain threshold. This, in turn, rapidly escalates greater opioid requirements (overdose) in an attempt to reduce pain after surgical procedures with unacceptable side effects. This phenomenon may be minimized by limiting opioids and maximizing nonopioid drugs.[23]
Transdermal PCA utilizes ionotophoresis technology to deliver drug (fentanyl) through the skin by use of an external electrical field.[24–26] This includes a needle-free credit-card-size system that is applied to the patient's upper arm or chest for 24 hr. The system utilizes on demand delivery dose of 40 microgram of fentanyl for 10 min up to six doses an hour with a maximum dose of 80.
Multimodal analgesia is a multidisciplinary approach to pain management that takes advantage of synergistic effects of various analgesics with different mechanisms of action (Figure 1) to achieve maximal control of pain with minimal side effects.[27] A multimodal pain protocol consists of patient education, pre-emptive oral pain medications preoperatively, preference to regional anesthesia, peripheral nerve block, and intraoperative modalities like periarticular infiltration of a cocktail of drugs and finally a standardized postoperative rehabilitation program. Because many of the negative effects of analgesic therapy are related to parenteral opioids, limiting their use is a major principle of multimodal analgesia.[2,19,28]
Pain perception has two major components: the sensory discriminating component and affective-motivational component, which underlies the emotional effects of the pain and is responsible for learned avoidance and other behavioral responses. MMP control begins with patient education in the form of preoperative interactions with patients and relatives to draw a realistic goal, to explain various steps the patient would undergo, the likely things to happen, and the supportive care available. This decreases anxiety and the "fear of the unknown" and hence improve cooperation and decrease in pain score and overall better patient satisfaction.[29,30]
This involves the administration of analgesics before painful stimuli to prevent peripheral and central sensitization. This starts before surgery, during surgery, and the initial period after surgery. Preemptive analgesia[1] is more effective only when the treatment used is adequate to break the vicious cycle of noxious stimuli recruiting more and more neural pathways. The interventions, therefore, must produce a dense blockade of appropriate duration to block the transmission of noxious afferent information from the peripheral nervous system to the spinal cord and the brain.[31] Scientific communities have attempted multiple modifications in the pursuit of uniformly acceptable multimodal pain control regimens in the last few years. This includes fixed-dose versus titrated-dose of opioids in PCA, single-dose versus continuous-epidural analgesia, single-shot versus continuous peripheral nerve blocks (femoral, sciatic, or adductor nerve block), and periarticular soft-tissue infiltration of drugs.
The various drugs employed are acetaminophen, cyclooxygenase (COX) inhibitors, opioids (and their derivatives), gabapentinoids, dexamethasone, and others.
Acetaminophen. Acetaminophen is a nonopioid, non-NSAID analgesic. Its action is predominantly by inhibiting prostaglandin synthesis in the central nervous system, which possibly plays a role in preventing central sensitization syndrome. These attributes make it an integral part of most multimodal postoperative pain regimens. Oral acetaminophen continues to be most commonly prescribed route; however, its intravenous administration is very effective and reduces postoperative opioid consumption.[32] In an adult weighing more than 50 kg the 1 g of intravenous paracetamol can be administered four times a day. However, in those weighing over 50 kg, the safe dose is 15 mg/kg with a maximal dose of 60 mg/kg a day.
NSAIDS and COX-2 Inhibitors. NSAIDs operate by binding and inhibiting COX 1 and 2 involved in the conversion of arachidonic acid to prostaglandins, which truncates the inflammatory mediator cascade. By inhibiting reduction of PG synthesis both peripherally and centrally, NSAIDS not only prevent peripheral tissue sensitization and secondary hyperalgesia effect on the uninjured tissues but also minimizes central sensitization.
The COX-1 isoenzyme, ubiquitous in gastric mucosa, platelets, kidneys, and liver, is involved in maintaining normal organ function, such as mucosal blood flow and barrier function in the stomach, and in mediating platelet aggregation. Hence, use of nonselective NSAIDS before surgery potentially increases bleeding (by decreasing platelet aggregation), gastritis, and peptic ulcer disease, renal impairment, and poor wound healing. NSAIDs are, therefore, relatively contraindicated in patients who are anticoagulated with warfarin, unfractionated and low molecular weight heparin (LMWH), Factor Xa inhibitor (rivaroxaban), direct thrombin inhibitors (dabigatran and fondaparinaux).
COX-2 isoenzyme, typically present at a lower level in these organs, is produced primarily in inflamed tissues. COX-2 selective inhibitors lack platelet inhibition and adverse gastrointestinal effects; however, its long-term use has fallen out of favor due to its unfavorable risk of cardiovascular side effects. Published literature demonstrated that use of COX-2 inhibitors (celecoxib and rofecoxib) as preemptive analgesia significantly reduces pain scores as compared to placebo at 1, 2, and 24 hr after surgery.[33]It is further established that use of COX-2 significantly reduces consumption of opioids (referred as opioid sparing), produces faster time to physical rehabilitation, reduces nausea and vomiting, provides better sleep patterns, and has greater patient satisfaction after surgery.[34,35] Alexander et al.[36]showed that a single dose of preoperative diclofenac or ketorolac reduced morphine consumption by 29% compared to placebo with an additional decrease in postoperative nausea, vomiting, and pruritus in patients undergoing joint arthroplasty. Ketorolac and diclofenac are nonselective NSAIDs with potent analgesic effects that can be given intravenously, intramuscularly, orally and topically without respiratory or central nervous system depression effects. It is shown that a single dose of preoperative diclofenac or ketorolac reduced morphine consumption by 29% compared to placebo with an additional decrease in postoperative nausea, vomiting, and pruritus in patients undergoing joint arthroplasty.[36,37]
Glucocorticoids. Glucocorticoids are known for their potent antiinflammatory properties. It is established that a single preoperative dose of long-acting glucocorticoids like dexamethasone and methylprednisolone are effective in preventing postoperative nausea and vomiting.[38–40] Additionally, dexamethasone has been shown to reduce postoperative dynamic pain.[41,42] Koh et al.[43] concluded that dexamethasone as part of a multimodal regimen reduced postoperative emesis and pain without an increased risk of wound complications.
Opioids. Opioid analgesics have long been, and continue to be, part of the surgeon's armamentarium for the treatment of postoperative pain. Opiates exert their effect by binding to three principal opioid receptors viz. mu, kappa and delta.[13] Opiates or their synthetic derivatives (meperidine or fentanyl) are metabolized in the liver and their onset of action largely depends on lipid solubility. Lipid soluble agents such as meperidine and fentanyl have rapid action but are of short duration because they cross the blood brain barrier easily. In presence of renal impairment, morphine and meperidine are avoided while fentanyl, hydromorphone, and oxycodone (which have minimal renal excretion) are preferred.
Oral opioids are available in immediate-release and controlled-release formulations. The former are effective in relieving moderate to severe pain, but require administration every 4 hr. Interruption in timely administration offers suboptimal pain control particularly in the night. The Acute Pain Management Guidelines developed by the Agency for Healthcare Policy and Research[40] recommend a fixed dosing schedule for all patients requiring opioid medications for more than 48 hr postoperatively. The adverse effects of oral opioid administration are considerably less than those of intravenous administration and are mainly gastrointestinal in nature.
Morphine is metabolized to its active metabolite morphine-6-glucuronide (M6G) in the liver and has a half-life of between 2 and 5 hr, and is excreted in the urine. In patients with renal impairment (estimate glomerular filtration rate <60 mL/min/1.73 m2) there is a risk of respiratory depression because of accumulation of M6G. Morphine may cause significant biliary and urinary tract spasm with few cardiovascular effects.
Fentanyl is a synthetic opiates with a half-life of 2 to 3 hr which demonstrates rapid onset of action due to lipid solubility but for shorter duration because of redistribution. It has excellent cardiovascular safety profile. It is available as transdermal patches (25, 50, 75 or 100 μg/h), which last for 72 hr, transoral formulations, intrathecal and epidural. It is useful for PCA analgesia, with typical 4-hour doses of 200 to 400 μg depending on weight of patient and tolerance.
Oxycodone: Controlled-release formulation of oxycodone demonstrates excellent and sustained pain relief over an extended period of up to 72 hr and is associated with less sedation, vomiting, or sleep disturbances.
Codeine is probably the most widely prescribed oral opiate that differs from other opiates in having a ceiling effect at 60 mg. It has a relatively low incidence of euphoria and thus perhaps a lower abuse potential; however, nausea and vomiting are common side effects. Its semisynthetic derivative hydrocodone is more potent with lesser side effects and is commonly prepared in combination with ibuprofen.
Tramadol is another synthetic analog of codeine. Besides being a weak μ-receptor agonist, it blocks serotonin and norepinephrine reuptake similar to tricyclic antidepressants. It has excellent oral bioavailability with a half-life of 4 to 6 hr. Tramadol has gained popularity because of the low incidence of adverse effects, specifically respiratory depression, constipation, and potential for abuse.
Gabapentinoids (Pregabalin and Gabapentin). Pregabalin and its predecessor gabapentin were first developed as anticonvulsant medications. They have shown promising results in neuropathic pain by acting on the voltage gated calcium channels in the central nervous system through alpha 2-delta ([alpha]2-[delta]) subunit thereby decreasing neurotransmitter release. Neuropathic pain is a complex phenomenon recognized in as high as 12.7% of patients after TKA. Use of pregabalin in the perioperative period reduces neuropathic pain, minimizes opioid consumption, and lessens sleep disturbance.[44,45] They also demonstrate synergistic effects with COX-2 inhibitors in clinical studies. The adverse side effects of gabapentinoids include dizziness and somnolence with long-term use.
Ketamine. Ketamine is a noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonist that may play a critical role in the intensity of perceived postoperative pain and preventing central sensitization. Ketamine has opioid-sparing effects but no reduction in opioid-related adverse effects. In patients undergoing knee arthroplasty, a low-dose infusion of ketamine (3 μg/kg per minute intraoperatively and 1.5 μg/kg per minute for 48 hr postoperatively) reduced morphine requirements and decreased the time to achieve 90 degrees of active flexion.[29] Intravenous ketamine can be used in conjunction with femoral nerve blocks or epidural analgesia after total knee arthroplasty. It can also be infiltrated into the wound.
Hypotensive regional anesthesia (spinal, epidural, or combined) gained rapid popularity over general anesthesia because it avoids central nervous system depression and by modest reduction in arterial blood pressure it also contributes to reduced surgical blood loss and decreases risk of deep venous thrombosis (DVT) and thromboembolism. Furthermore, it has less cardiac and respiratory depression. Besides neuraxial anesthesia allows postoperative pain management by appropriately titrating the dose of opioids with local anesthetics.
Neuraxial and Regional Anesthesia. Spinal and epidural opioids provide superior analgesia compared with systemic opioids. The onset and duration of neuraxial opioids are determined by the lipophilicity of the drug. For example, lipophilic opioids, such as fentanyl, provides a rapid onset of analgesia (10–15 min), is effective for shorter duration (2–4 hr), has limited spread within the cerebrospinal fluid (and hence less respiratory depression), and gas rapid clearance and resolution. Conversely, hydrophilic opioids, including morphine and hydromorphone, have a longer duration of action (18–24 hr) but are associated with a greater frequency of side effects, such as pruritus, nausea, and vomiting, as well as delayed respiratory depression.[46] Patients given a single dose of extended release epidural morphine[47] have demonstrated 48-hour period of analgesia.
Though epidural anesthesia (EA) is preferred by some clinicians, the limitations are failed or dislodged catheters. Epidural catheters used for analgesia also lead to motor blockade (quadriceps weakness necessitating use of knee immobilizer), numbness in contralateral limb, urinary retention, and chances of epidural hematoma if clexane or fondaparinaux is concomitantly used for DVT prophylaxis. It is important to note that the typical side effects of opioids are much more common (and more prolonged) after neuraxial administration compared with all other routes. For example, in a large series, the frequency of pruritus, nausea and vomiting, and respiratory depression was 37%, 25%, and 3%, respectively, with an intrathecal morphine injection.[48] Therefore, patients who exhibit sensitivity to an opioid when administered systemically should not receive that agent neuraxially.
Peripheral Nerve Block (PNB). Use of nerve stimulator and ultrasound have facilitated accurate localization of the neural structure and thereby significantly improved their safety and success rate. Recently, single-dose and continuous peripheral nerve block techniques (femoral, sciatic, and adductor canal block) have drawn attention in joint replacement surgery because of its ability to provide quality of analgesia similar to those of continuous epidural analgesia but with fewer side effects (reduced incidence of arterial hypotension or urinary retention) besides being compatible with anticoagulants.[49–52]
After total knee arthroplasty, patients receiving epidural analgesia or continuous femoral block reported lower pain scores, better knee flexion, faster ambulation, and shorter hospital stays than did patients who received intravenous PCA morphine. However, continuous femoral block was the preferred analgesic technique in each study because fewer technical problems and fewer side effects were noted compared with the epidural and PCA approaches. Recent literature notes that 90% of patients undergoing minimally invasive primary hip or knee replacement were ready for discharge from the hospital within 48 hr if continuous peripheral nerve block is combined with multiple scheduled analgesics.[2,53]
Neurologic dysfunction and intravascular injection are the primary concerns associated with peripheral blockade. However, in a large series involving more than 50,000 peripheral blocks, there were six seizures, and 12 patients (0.02%) reported postoperative nerve injury. Most neurologic complications were transient.[54]
Lumbar plexus block can be achieved by psoas approach, femoral approach, or fascia iliaca approach. Psoas approach blocks the femoral nerve along with lateral femoral cutaneous nerve and obturator nerve rendering it preferable in hip replacement surgeries. For knee replacement, femoral approach and fascia iliaca approaches are sufficient. The patient is positioned supine and a linear transducer (8–14 MHz) is placed just below inguinal ligament and moved slightly medial or lateral to identify the femoral artery (Figure 3). If it cannot be seen, tilting the transducer craniocaudal helps artery visualization or a color Doppler can be used. Then the femoral nerve is located lateral to the artery as hyperechoic triangular or oval shape on the iliopsoas muscle under fascia lata. The needle is placed 1 cm lateral to the nerve, and after negative aspiration 15–25 mL of a local anesthetic drug is injected. If a nerve stimulator is used, the presence of patellar or quadriceps twitch between 0.3–0.5 mA confirms appropriate positioning of the needle.
Figure 3.
Sequential steps of peripheral nerve block.
A sciatic nerve block results in anesthesia of the skin of the posterior aspect of the thigh, hamstring, and biceps femoris muscles, part of the hip and knee joint, and the entire leg below the knee with the exception of the skin of the medial aspect of the lower leg. A sciatic nerve block can be given by posterior or anterior approach. In the classic posterior approach, the patient is placed in a lateral decubitus position with slight forward tilt. Needle insertion is 4–5 cm caudal and perpendicular to the midpoint of the line connecting the greater trochanter and posterior superior iliac spine (Figure 3). A 10-cm (4-in) stimulating needle is advanced until either a tibial or peroneal motor response is elicited, then 20–30 mL of a local anesthetic is incrementally injected. The nerve stimulator may be used to deliver an initial current intensity of 1.5 mA to visualize twitches of either tibial or peroneal motor response (hamstring, calf, foot, or toe twitches). The stimulating current is gradually decreased until twitches are still seen or felt at 0.2 to 0.5 mA, which typically occurs at a depth of 5 to 8 cm. At this low current intensity, any observed motor response is from the stimulation of the sciatic nerve rather than direct muscle stimulation (false twitch). After negative aspiration for blood, 15 to 20 mL of local anesthetic is injected slowly.
An adductor canal block targets the saphenous nerve (sensory only branch of the femoral nerve) in adductor canal. The saphenous nerve travels between the medial border of the vastus medialis muscle and the medial border of the adductor muscles, along the femoral artery and courses from lateral to medial beneath the sartorius muscle. Being a purely sensory block, it relieves pain and also spares the quadriceps muscle thereby facilitating physiotherapy, rehabilitation, and early independent ambulation.
The patient lies supine with the knee slightly flexed and leg externally rotated. A high-frequency, linear array ultrasound probe is placed in the anteromedial thigh to first localize the femoral artery and trace it distally where it gives off genicular artery (Figure 3). Doppler scanning may be used in difficult situations to trace the femoral artery caudally from the inguinal crease. Once the femoral artery is identified, the needle is inserted in-plane in a lateral-to-medial orientation, and advanced toward the femoral artery. The needle tip is placed just medial to the artery in the adductor canal, underneath the sartorius muscle. The saphenous nerve is identified along the genicular artery. If nerve stimulation (0.5 mA) is used, the passage of the needle through the sartorius or adductor muscles and into the adductor canal usually is associated with the patient reporting a paresthesia in the saphenous nerve distribution. After confirming needle placement and negative aspiration, 15 mL of local anesthetic drug is injected.
Periarticular infiltration in TKA is a technique in which a cocktail of drug combination is injected into the periarticular soft tissues such as posterior capsule, medial and lateral collateral ligaments, quadriceps mechanism, and peripatellar tissue at the end of the surgery (Figure 4). Though there is no standardized protocol, it usually is a combination of long-acting local anesthetic drug along (bupivacaine, ropivacaine) with steroids, morphine, and epinephrine. Steroids prevent local inflammation. Morphine blocks the three opiate receptors and epinephrine prolongs the action of local anesthesia by decreasing its absorption via its alpha-2 adrenergic effect. Injection of the mixture is avoided in the posterolateral corner to prevent inadvertent injury to the peroneal nerve (Figure 4).
Figure 4.
Infiltration of cocktail of drugs in periarticular soft tissues.
Recent studies[55–62] found that periarticular injection significantly improved pain relief from 24 hr to 1 wk and straight leg raise in the early postoperative period. In addition, the meta-analysis of opioid consumption through PCA also corresponded well with the outcome of pain score, which showed that periarticular injection consumed significantly less PCA during the first 24 hr postoperatively. The meta-analysis showed that more patients could do active straight leg raise in the injection group than that in noinjection group from postoperative 1 day to discharge day. Ropivacaine has the similar efficiency to bupivacaine but is longer acting and has fewer complications in the nervous and cardiovascular systems.[52] Some prefer leaving an indwelling catheter tube before joint closure for postoperative analgesia.
All patients received Pregabalin 150 mg the night before and celecoxib 400 mg orally 2 hr before surgery with a sip of water. Intravenous dexamethasone (8 mg) is given for antiinflammatory effects and to minimize nausea and vomiting. A cocktail of drug mixture (Figure 5) is injected after component implantation into the posterior aspect of the joint capsule, medial and lateral collateral ligaments, soft tissue around the quadriceps tendon, and patellar tendon, fat pad, and synovium. Rationale of ropivacaine is its longer action and superior cardiovascular and neurotoxic profile. Morphine relieves pain by acting on morphine receptors present in the articular activity and addition of adrenaline slows release of ropivacaine into the vascular system.
Authors preferred protocol.
A standard postoperative regimen included acetaminophen, celecoxib, and pregabalin along with morphine/fentanyl or tramadol as rescue drugs (Figure 5). Onandesterone 4 mg is used to control vomiting in the postoperative period and pantoprazole 40 mg daily is given for gastrointestinal prophylaxis until discharge. Liberal ice-pack application, limb elevation, and pneumatic compression device of both legs are other measures to reduce swelling. Standard DVT prophylaxis is followed, active straight-leg raising and range of motion is encouraged from the same day. The patient is discharged usually on the third postoperative day after gaining 80 to 90 degrees of flexion and can walk independently with support for at least 50 feet.
A fundamental understanding of different modes of pain control techniques along with limitation of each technique is the first vital step towards effective control of postoperative pain. Close observation for potential side effects of any drug is the next most important thing. We must move forward toward a more holistic, interdisciplinary, multimodal approach to pain medicine. Educating patients about a realistic goal is the cornerstone of pain management.
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