Journal of Pain & Palliative Care Pharmacotherapy. 2014;28:164–166. ISSN: 1536-0288 print / 1536-0539 online DOI: 10.3109/15360288.2014.911797

EUROPEAN PERSPECTIVES ON PAIN AND PALLIATIVE CARE

Subacute Pain After Total Knee Arthroplasty Axel Sauter and Harald Breivik AB STRACT Acute pain during and immediately after total knee arthroplasty (TKA) can be well controlled by spinal anesthesia, local infiltration analgesia, and peripheral nerve blocks; this enables early or fast-track rehabilitation. However, about half of patients have clinically significant pain in the following weeks. Active movements and rehabilitation of joint function, muscle strength, and ability to maintain balance and prevent falls all become more difficult when the joint is painful on movement. Intensive analgesic and antihyperalgesic treatment during the first few weeks after TKA surgery may reduce the risk of chronic pain after this operation, which is itself intended to remove the patient’s chronic osteoarthritis pain. Spinal cord stimulation may be an effective option for patients with mainly neuropathic pain after TKA surgery. This report is adapted from paineurope 2013; Issue 4, ©Haymarket Medical Publications Ltd., and is presented with permission. paineurope is provided as a service to pain management by Mundipharma International, Ltd., and is distributed free of charge to health care professionals in Europe. Archival issues can be accessed via the Web site: http://www.paineurope.com, at which European health professionals can register online to receive copies of the quarterly publication. KEYWORDS arthroplasty, infiltration analgesia, knee, nerve blocks, pain, postoperative, spinal anesthesia

risk of chronic and disabling pain after this type of palliative surgery?

BACKGROUND A significant proportion of patients continue to have severe pain in the weeks and months that follow a total knee arthroplasty (TKA),1 and these often have suboptimal pain treatment. When pain interferes with mobilization and joint movement, the rehabilitation phase is prolonged and painful. Even though many patients will have recovered knee function 1 year after surgery, a significant number still experience pain. Will aggressive attempts to relieve pain and hyperalgesia when present 6 weeks after surgery reduce the

CASE ASSESSMENT An otherwise healthy 68-year-old man had bilateral knee osteoarthritis, severe enough that he agreed to bilateral TKA, one side at a time. After the first TKA, on the right side, spinal anesthesia for surgery and local infiltration of ropivacaine, adrenaline, and ketorolac (that is, local infiltration analgesia) made mobilization out of bed uneventful for 24 hours after surgery.2 However, persistent numbness lateral to the right knee, extending to the dorsal aspects of the foot and all five toes, gradually became painful with tingling paresthesias in the same area. Six weeks after surgery, nonopioid analgesics had no effect on his pain. The pain gradually became more burning in quality and was continuously present. Intensity varied from 3/10 in the morning (numeric rating scale 0–10) to 8–9/10 in the afternoon and evening. Sleeping at night was difficult.

Harald Breivik, MD, DMSc, FRCA, is Emeritus Professor of Anesthesiology, University of Oslo, Oslo, Norway. Alex Sauter, MD, is with the University Hospital, Oslo, Norway. This report is adapted from paineurope 2013; Issue 4, ©Haymarket Medical Publications Ltd., and is presented with permission. paineurope is provided as a service to pain management by Mundipharma International, Ltd., and is distributed free of charge to health care professionals in Europe. Archival issues can be accessed via the Web site: http://www.paineurope.com, at which European health professionals can register online to receive copies of the quarterly publication. Address correspondence to Harald Breivik (E-mail: harald.breivik@medisin. uio.no).

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Hypnotic medications made him drowsy, but did not improve quality of sleep. Six weeks after surgery, examination at the pain clinic revealed hypoesthesia to touch and cold and warm stimuli in the skin area of the common peroneal nerve. In most of the same area, there was cold allodynia (25◦ C) and hyperalgesia with temporal summation of pinprick pain.3 He also had decreased muscle strength on dorsiflexion of the ankle. No other neurological abnormalities were detected. There were no vasomotor or skin color changes as seen with type 2 complex regional pain syndrome. The patient clearly had common peroneal nerve damage, evidently caused by or during the surgical TKA. He now had clear signs of a neuropathic pain condition developing.4 The patient received amitriptyline 25 mg, gradually increasing to 75 mg in the early evening, and pregabalin, gradually increasing from 25 mg every evening to 150 mg twice daily. He could now sleep better at night. He tolerated some drowsiness and dizziness during the day because his constant pain was reduced to 0–2/10 in the morning to 4–5/10 at most in the afternoon and evening. He also received acetaminophen (paracetamol) with codeine at standard dosages, but developed obstinate, laxative-resistant constipation. Therefore, this analgesic medication was discontinued and the patient did not want to risk the same adverse effects with more potent opioids. In the following weeks, paresthesia and the burning pain gradually diminished. Pain was tolerable and physiotherapy and knee-joint rehabilitation was resumed. Six months after surgery, he still had a numb area on his distal leg and ankle dorsiflexion was still weak, requiring an ankle support. His antihyperalgesic medications were gradually weaned, but he continued with amitriptyline 25 mg and pregabalin 75 mg in the late afternoon when pain was bothering him. The patient underwent staged bilateral total knee arthroplasty. Analgesic medication was discontinued and the patient did not want to risk the same adverse effects with more potent opioids. In the following weeks, paresthesia and the burning pain gradually diminished. Pain was tolerable and physiotherapy and knee-joint rehabilitation was resumed. Six months after surgery, he still had a numb area on his distal leg and ankle dorsiflexion was still weak, requiring an ankle support. His antihyperalgesic medications were gradually weaned, but he continued with amitriptyline 25 mg and pregabalin 75 mg in the late afternoon when pain was bothering him.

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DISCUSSION A significant number of patients experience persistent pain after TKA, and signs of neuropathy often accompany their pain. The number of elderly people in need of TKA is expected to increase dramatically in Europe as well as in the United States as the population ages.5 It is likely that physicians can reduce the risk of chronic pain with optimal treatment of acute pain during the first few days after TKA, and even more so by specific antihyperalgesic drugs that diminish neuropathic pain mechanisms during the weeks after TKA. If supported by evidence, this will be a strong argument for allocating appropriate resources for acute and subacute pain management, preferably by a specific subacute pain service as an adjunct to the acute pain service that all surgical hospitals must have.6 Appropriate pain management and rehabilitation of function during and after joint replacement enables fast-track rehabilitation and is highly beneficial to quality of life.

REFERENCES [1] [2] [3] [4] [5]

Pinto PR, McIntyre T, et al. J Pain Res. 2013;6:691–703. Breivik H, Sauter A. Scand J Pain. 2012;3:44–45. Martinez V, Fletcher D, et al. Anesth Analg. 2007;105:815–821. Haroutiunian S, Nikolajsen L, et al. Pain. 2013;154:95–102. Kurtz SM, Ong KL, et al. J Bone Joint Surg Am. 2007;89(Suppl 3):144–151. [6] Breivik H, Curatolo M, et al. How to implement an acute postoperative pain service: an update. In: Breivik H, Shipley M, eds. Pain: Best Practice & Research Compendium. London: Elsevier; 2007:xx–xx.

COMMENTARY FROM SWITZERLAND Alain Borgeat This case illustrates one ofthe major problems occurring after surgery, the issue of postoperative chronic pain syndrome. Neuropathic pain in the area of the common peroneal nerve can be caused by surgery, tourniquet, some regional blocks, or a combination of all these factors. Electroneuromyography may have been helpful in this case, not only to localize the site of damage, but also to provide some clues about recovery. The Alain Borgeat, MD, is Professor and Head of the Department of Anesthesiology, Balgrist University Hospital, Zurich, Switzerland.

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treatment of this patient is standard and reflects what would have been done in my institution. Light physiotherapy to avoid muscle atrophy may also have been useful. Severe preoperative pain—as in this case—is one of the most recognized risk factors for the occurrence of postsurgical pain syndrome after total joint arthroplasty.1 Other factors include preoperative depression and anxiety. A perioperative multimodal analgesic treatment regimen including regional catheters, nonsteroidal anti-inflammatory drugs (NSAIDs), paracetamol, and α 2 -agonists, with ketamine if needed, may have been warranted. It is well known that opioids have limited value in this context.2 Severe nerve damage (neurapraxia or neurotmesis) requires a long recovery. There is no treatment to speed up recovery, although functional electrical stimulation has shown promising results in animals.

REFERENCES [1] Liu SS, Buvanendran A, et al. Int Orthop. 2012;36:2261–2267. [2] McNicol ED, Midbari A, et al. Cochrane Database Syst Rev. 2013;(8):CD006146. DOI: 10.1002/14651858.CD006146. pub2.

COMMENTARY FROM SWEDEN Narinder Rawal Intraoperative nerve damage to peroneal and tibial nerves can occur during TKA but most cases can expect to recover completely.1,2 Most nerve injuries do not cause neuropathic pain; in one study it was shown that although 90% of nerves were injured, only 5% caused neuropathic pain.2 A recent review showed that the neuropathic component in persis-

tent postsurgical pain (PPSP) varies with the type of surgery, after TKA it was only about 6%.1 Although the neuropathic component in this patient’s pain appears high, other risk factors for PPSP such as psychosocial, environmental and patient-related genetic factors also need to be considered. Studies have shown improved pain, function, and quality of life after TKA; however, up to 20% of patients are dissatisfied, mainly due to PPSP.3 A survey of more than 1000 patients reported a 53% incidence of PPSP after TKA with average pain scores of 3–5/10, these patients had significantly lower healthrelated quality of life scores.3 The underlying etiology of PPSP is still unclear.1,2 Injury to peripheral nerves during surgery or ongoing inflammation have been stipulated as primary causal factors. Mechanisms for increased acute pain leading to PPSP are speculative but may involve either peripheral or central sensitization. The intensity of perioperative pain has been identified as a key risk factor in some studies; however, no single factor seems to play a significant role. The American Society of Anesthesiologists practice guidelines for multimodal management of postoperative pain can be recommended, these include wound infiltration with a long-acting local anesthetic, paracetamol, NSAIDs, and calciumchannel blockers.4

REFERENCES [1] Haroutiunian S, Nikolajsen L, et al. Pain. 2013;154:95–102. [2] Kalso E. Br J Anaesth. 2013;111:9–12. [3] Liu SS, Buvanendran A, et al. Region Anesth Pain Med. 2012;37:415–422. [4] American Society of Anesthesiologists Task Force on Acute Pain Management. Anesthesiology. 2012;116:248–273.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

Narinder Rawal, MBBS, MD, PhD, is a Professor at Department of Anes¨ thesiology and Intensive Care at University Hospital in Orebro, Sweden.

Journal of Pain & Palliative Care Pharmacotherapy

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Subacute pain after total knee arthroplasty.

Acute pain during and immediately after total knee arthroplasty (TKA) can be well controlled by spinal anesthesia, local infiltration analgesia, and p...
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