Keywords

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FormalPara Keynotes
  1. 1.

    The etiology of persistent “unhappy” knee after a total knee replacement (TKR) is multifactorial, and a multidisciplinary approach is necessary for management.

  2. 2.

    Preemptive and multimodal analgesia should be used to decrease the perioperative pain sensitization to minimize the incidence of chronic pain.

  3. 3.

    Success of management of chronic pain lies in the accuracy of the diagnosis after an extensive evaluation, and most patients with a chronic painful TKR can be managed by a multimodal conservative approach.

  4. 4.

    Revision surgery should be avoided in patients with unexplained pain and without any recognized pathology since they may improve over a period of time and results of revision surgery are inferior and unpredictable.

  5. 5.

    An “unhappy” TKR is a difficult problem to treat, but understanding these principles can turn this “unhappiness” into a successful outcome.

Successful management of a painful total knee replacement (TKR) lies in the accuracy of the diagnosis after an extensive evaluation. This includes a detailed history and physical examination, complimentary laboratory tests, appropriate imaging studies, and microbiological analysis and has been discussed in detail elsewhere [1–3]. Investigations should be swift and expeditiously performed as delay may lead to chronicity of the problem.

Usually explanation is multifactorial, and a multidisciplinary approach is necessary for management. The team should include surgeon, physiotherapists, pain-management physicians, internist, rheumatologists, psychologist, and any consultant specialist on referral basis. A pain specialist should be involved as early as possible in the management of these patients specifically for the prevention of a chronic pain syndrome. Treatment of pain irrespective of etiology is necessary for both quality of life and successful long-term outcomes. Appropriate pain management not only alleviates pain but also reduces the urgency for therapeutic interventions and optimizes psychosocial factors regarding the patient.

The team should include surgeon, physiotherapists, pain-management physicians, internist, rheumatologists, psychologist, and any consultant specialist on referral basis. A pain specialist should be involved as early as possible in the management of these patients specifically for the prevention of a chronic pain syndrome.

36.1 The Importance of Acute Pain Control and Prevention of Chronic Pain

Pain has been defined as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage” [4]. Pain perception has two major components: the sensory-discriminating component, which describes the location and quality of the stimulus, and the affective-motivational component, which underlies the emotional effects of the pain and is responsible for learned avoidance and other behavioral responses [5]. In addition to ethical and humanitarian reasons for minimizing pain, lack of its control can result in anxiety, sleeplessness, and activation of neuroendocrine (sympatho-adrenal) responses. All of these can have deleterious effects on the development of chronic pain. Humoral and neurologic alterations in and around the injury may be responsible for increased postoperative discomfort and disability. Continued activation of nociceptors may initiate reflex motor responses that lead to spasm, stiffness, and myofascial pain. Alteration in blood flow and efferent outflow may be responsible for sympathetically maintained pain and the persistent pain syndromes that can lead to arthrofibrosis, prolonged disability, impaired rehabilitation, and continued dissatisfaction [5]. Thus, early optimal assessment and management of pain during the index surgery can improve patient satisfaction and may prevent development of chronic pain [6, 7].

The two pain perception components are the sensory-discriminating component and the affective-motivational component.

36.2 Molecular Basis of Postoperative Pain

Postoperative pain is mostly nociceptive. Surgery produces an initial afferent barrage of pain signals and generates a secondary inflammatory response, both of which contribute substantially to postoperative pain. The signals have the capacity to initiate prolonged changes in both the peripheral and central nervous system that can lead to amplification and prolongation of postoperative pain [5, 8]. Peripheral sensitization, a reduction in the threshold of nociceptor afferent peripheral terminals, is a result of inflammation secondary to the release of primary mediators such as prostaglandins, cyclooxygenases (Cox I and II), leukotrienes, bradykinins, histamine, and 5-hydroxytryptamine [9]. These physiological primary mediators stimulate the release of peptides such as calcitonin gene-related protein, substance P, and cholecystokinins at the site of injury. Histamine-induced vasodilatation, nerve growth factor release, and reflex sympathetic efferent release of norepinephrine are other processes related to peripheral sensitization. Central sensitization, an activity-dependent increase in the excitability of spinal neurons, is a result of persistent exposure to nociceptive afferent input from the peripheral neurons [10]. Taken together, these two processes contribute to the postoperative hypersensitivity state that is responsible for a decrease in the pain threshold, both at the site of injury (primary hyperalgesia) and in the surrounding uninjured tissue (secondary hyperalgesia) [5, 8, 9] (Fig. 36.1). N-methyl-D-aspartate (NMDA) is a membrane protein that regulates the flow of Na+ and Ca++ into the cell and the outflow of K+ [12]. As intracellular calcium accumulates, a chain of neurochemical and neurophysiologic changes leads to the rapid and independent firing of spinal neurons without stimulation. This process is termed as “spinal wind up,” which is the excitation of the dorsal horn neurons not dependent on transcription of specific genes [13]. Neurotransmission is further modulated by other substances such as gamma-aminobutyric acid (GABA). From here, spinothalamic tracts carry ascending signals, where further central modulation can occur in supraspinal modulatory centers [14] (Fig. 36.2).

Fig. 36.1
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Role of central hypersensitivity in the development of chronic pain (Adapted with permission from Curatolo et al. [11])

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Fig. 36.2
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Anatomic route for pain modulation [14]

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36.3 The Concept of Preemptive Analgesia and Multimodal Techniques

Preemptive analgesia involves the administration of analgesics before painful stimuli to prevent the establishment of central sensitization and thus the amplification of postoperative pain. It starts before surgery and covers both the period of surgery and the initial postoperative period. Preemptive analgesia prevents (or reduces) pathologic pain that is different from physiologic pain in several aspects: it is excessive (in intensity and spread) and can be activated by low-intensity stimuli (allodynia, hyperalgesia) and hyperpathia [15]. 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. In studies, the dose of morphine needed to prevent central hyperexcitability was one-tenth the dose when given prior to rather than after exposure to a brief noxious electrical stimulation [13]. Decreasing perioperative pain with preemptive techniques improves satisfaction, hastens discharge, spares opioid use (decrease constipation, sedation, nausea, and urinary retention), and may prevent the development of chronic pain.

Multimodal technique is a multidisciplinary approach to pain management with a goal to maximize the synergistic analgesic effect and minimize the side effects of the medications [16]. It takes advantage of the additive or synergistic effects of various analgesics, permitting the use of smaller doses with a concomitant reduction in side effects.

Preemptive analgesia means administration of analgesics prior to surgery in order to have central sensitization and amplification of pain after surgery.

36.4 Techniques of Pain Management

It is important to choose an effective analgesic regimen with minimal side effects to allow timely mobility and optimal functional recovery while decreasing postoperative morbidity and mortality. Although several treatment options involving various combinations of systemic analgesics and/or regional analgesia, with or without opioids, are available for postoperative pain, a gold standard has not been established. Recently, both individual and combined uses of a number of treatment options have been evaluated with respect to post-TKR acute pain control and include daily nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, opioid patient-controlled analgesia (PCA), epidural, oral opioids, periarticular local anesthetics, and peripheral nerve blocks [17–21].

36.5 Preoperative Patient Education

The preoperative patient education is one of the best techniques available to orient patients and their families because it provides information on what will happen to them throughout the whole process and substantially eases the “fear of the unknown.” This is a preemptive technique as the cerebral cortex response can be influenced by educating patients in the preoperative class about a successful pain-management program. Furthermore, the prevention of any onset of severe pain would prevent central sensitization of the cortex which magnifies pain, leading to its chronicity [16]. It should also be shared that pain after TKR persists in about one in eight patients despite an absence of clinical or radiological abnormalities [22].

36.6 Epidural Analgesia

Epidural medications may consist of a local anesthetic, an opioid, or a combination of both. A pure opioid epidural infusion may not provide adequate analgesia, and a pure local anesthetic may provide dense sensory and motor blockade, such that the patient may not be able to walk or void in the early postoperative period [23]. Thus, a combination creates a synergistic analgesic effect that allows lower concentration of each component in the solution. Continuous low-dose infusion has also been advocated as a method to control postoperative pain. Although they provide superior analgesia, they are also associated with technical failures, hypotension, ileus, urinary retention, motor block that limits ambulation, unrecognized compartment syndromes, and spinal hematoma secondary to anticoagulation [23]. Patient-controlled epidural analgesia (PCEA) offers higher analgesic efficacy and lower dose requirements than parenteral patient-controlled analgesia (IV PCA) and provides greater control and patient satisfaction than do either single-dose or continuous infusions. However, despite better pain control, patients still prefer IV PCA because of fewer technical problems, fewer side effects, and more uniform, sustained analgesia with more autonomy [5]. A Cochrane database review concluded that epidural analgesia may be useful after TKR for pain control, but the benefit must be weighed against the frequency of adverse effects [23].

36.7 Peripheral Nerve Blocks/Selective Sensory Blocks

The trend of early ambulation and discharge as well as same-day initiation of physical therapy has popularized the concept of peripheral nerve blocks. This trend has been aided by the technical advances in needles, catheters, nerve stimulation, and ultrasound detection of nerves. They minimize exposure to opioids and are ideally suited for patients sensitive to opioid-induced ileus, respiratory depression, and pruritus. Postoperatively, patients reported lower pain scores at rest and morphine consumption decreased for up to 8 h after transfer to the floor with placement of a femoral or femoral/sciatic block when compared to sham blocks [24]. Thus, advantages include effective postoperative analgesia, lower opioid consumption, improved rehabilitation, lower complications, and higher patient satisfaction [25]. Peripheral nerve block and catheter options include femoral with or without sciatic, lumbar plexus, adductor canal, and fascia-iliaca compartment blocks and have been discussed in detail elsewhere [19, 24, 25]. The role of selective sensory block for TKR is a relatively new concept under study [26].

36.8 Periarticular Injections

Periarticular injections and catheters have been shown to be safe and effective and have reduced the requirement of parenteral narcotics significantly compared to oral or intravenous opioids [16, 21]. The injections and catheters often use a combination of local anesthetics, steroid, epinephrine, NSAID, long-acting opioid, and antibiotic [16]. They are often used to compliment epidural and nerve blocks.

36.9 Opioids and Non-opioids Medications

When used preemptively as well as postoperatively, multiple opioid and non-opioid medications used in a multimodal way can significantly reduce postoperative pain scores, total opioid use and thus most of the adverse side effects, and length of hospital stay with patients having TKR. These include immediate- and controlled-release opioid formulations; tramadol; COX I, II, and III inhibitors; acetaminophen; steroids; anticonvulsants (gabapentin, pregabalin, carbamazepine); antidepressants (amitriptyline); NMDA antagonists (ketamine and dextromethorphan); and α2-agonists (clonidine, dexmedetomidine) and have been discussed in detail elsewhere [16–33].

36.10 Chronic Pain After TKR

Some patients still have persistent chronic knee pain after a TKR, and their management can be difficult. The surgeon should be aware of both the common and rare underlying causes (Table 36.1) and should formulate a customized management algorithm [1–3] (Fig. 36.3). Depending on the etiology, management consists of three basic options: conservative approach, reoperations not needing an exchange of prosthetic components, and reoperations with exchange of at least one prosthetic component. For patients without any mechanical or infectious etiology, revision surgery often leads to suboptimal and unpredictable outcomes and should be avoided when possible [34, 35]. Mont et al. surgically explored the knees of 27 patients with debilitating pain after TKR without an identifiable cause; only 41 % resulted in an excellent or good result [35]. On the other hand, management of these patients conservatively has shown promising outcomes. In a prospective study of 116 patients, 15 had unexplained pain at the end of 1 year after TKR but were satisfied at the 5-year follow-up [22]. Another study of 622 TKRs found 24 to have unexplained pain, of which 55.5 % demonstrated improvement at the 5-year follow-up [36]. Moreover, in a randomized trial with 60 refractory painful TKRs, a single intra-articular botulinum toxin A injection provided significant short-term improvements in pain, global assessment scores, and function [37]. Thus, reassurance should be provided to the patient that improvement is possible after a conservative treatment. The details of surgical management have been discussed in detail elsewhere [1–3] and are beyond the scope of this chapter.

Table 36.1 Causes of pain after a TKR [1–3]
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Fig. 36.3
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Management algorithm for painful total knee replacement

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36.11 Neuropathic Pain

Neuropathic pain can be defined as pain caused by a lesion or dysfunction of the central or peripheral nervous systems. Neuropathic pain encompasses dysesthesia (abnormal sensation), allodynia (pain associated with normally non-noxious stimulus), hyperalgesia (increased response to a normally mildly noxious stimulus), and spontaneous pain. Treatment of neuropathic pain benefits from a multimodal approach because traditional opioid medications are not as effective – in fact, opioids should be used as second-line agents to treat neuropathic pain [38]. The various pharmacologic options to treat neuropathic pain have been shown in Table 36.2 [39]. As an adjuvant to neuropathic pain medication, alternative approaches such as topical capsaicin, transdermal lidocaine, ketamine, or fentanyl patches can help with poorly controlled neuropathic pain. Regular massage of the scar or the painful site may help and thereby prevent neglect of the joint and subsequent stiffness.

Table 36.2 Common medications for the treatment of neuropathic pain
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36.12 Neuromas

When nerve ends are injured, occasionally ineffective and unregulated nerve regeneration occurs especially in close proximity to scars. When painful neuromas arise around the knee that are debilitating, a trial of conservative therapy is attempted for at least 6 months [40]. When conservative management (cortisone injections and topically delivered NSAIDs) fails, and surgery is considered to address the neuroma, patient selection is a priority in order to achieve good outcomes. Patients must respond favorably to a preoperative local anesthetic block or patch in order to predict outcome for surgical management of a neuroma [41]. Selective denervation is the procedure of choice for most surgeons, during which nerves supplying a neuroma are transected. Patient satisfaction rates reach up to 86 %, but patients need to be made aware of a 40 % minor complication rate including hypersensitivity from collateral sprouting of the normal, proximal stump due to nerve growth factor release [40, 41]. This is a self-limiting issue and responds well to desensitization therapy within 6 weeks.

36.13 Complex Regional Pain Syndrome (See Chap. 24)

Complex regional pain syndrome (CRPS) represents a constellation of signs including pain, swelling, stiffness, and skin changes, such as dusky discoloration and atrophy [42]. Type I (reflex sympathetic dystrophy syndrome) occurs after injury without nerve damage and accounts for 90 % of patients with CRPS following TKR. Type II (causalgia) follows a distinct nerve injury. A prospective study reported prevalence to be as high as 21, 13, and 12.7 %, respectively, at 1, 3, and 6 months after TKR [43]. Risk factors for the development of CRPS include preoperative pain and distress [43]. Successful treatment of this entity remains dominated by conservative management by a multidisciplinary team and mostly include a combination of physical therapy, pharmacological agents, and lumbar sympathetic blockage. Pain specialists sometimes need to use alternative pain treatments, and psychologists may be effective in addressing the distress, anxiety, and depressive thoughts experienced in CRPS. Through the help of neuroimaging, connection between central sensory/motor processing and peripheral and sympathetic mechanisms has been shown in CRPS [44]. As a result of this theory, development of programs have been introduced to manage CRPS including mirror visual feedback therapy, graded motor imagery, and graded exposure programs [45]. The most important determinant of successful treatment of CRPS is early diagnosis followed by immediate commencement of therapy. TKR complicated by CRPS has demonstrated to have similar outcomes to uncomplicated TKR at 54 months, when diagnosis and intervention occurs early [46]. This does not always occur, however, and diagnosis has been shown to be delayed as much as 30 months after onset of symptoms [47].

36.14 Physical Therapy

Physiotherapy for a patient in CRPS should be gentle and focused on preventing joint contractures, improving voluntary motor control, and controlling edema through massage. Aggressive therapy should be avoided as patients with CRPS have exaggerated response to any stimulus (painful and non-painful) and may exacerbate the condition. In addition to traditional physiotherapy techniques, other techniques have also proven effective (Table 36.3) [45, 48–50] (see Chaps. 37 and 39).

Table 36.3 Physical therapy options for complex regional pain syndrome (CRPS) [45, 48–50]
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36.15 Pharmacological Agents

Control of pain is essential for participation in physical therapy as well as ability to restore functionality in patients with CRPS. Medications attempt to modify the sympathetic and non-sympathetic symptoms of CRPS. The most common medications are acetaminophen, NSAIDs (e.g., celecoxib or meloxicam), steroids, and medications typically used for neuropathic pain (Table 36.2). An early referral to a pain-management team is essential to ensure adequate treatment [51].

36.16 Sympathetic Blockade

Lumbar sympathetic blockade can be performed with a local anesthetic and corticosteroids. It is typically performed one to two times per week with an average of 4–5 blocks required to permanently relieve symptoms. For short-term relief, a continuous epidural catheter can be placed to facilitate physical therapy [52]. Sympathetic blockade has demonstrated to be a key diagnostic and effective therapeutic modality in management of CRPS after TKR [53]. A surgical lumbar sympathectomy can be performed if the patient gets only limited relief from continuous catheter placement.