Case: Subacute pain after total knee arthroplasty
With Dr Axel Sauter, Professor Harald Breivik and Professor Narinder Rawal | 19 Mar 2015 | Print
Professor Harald Breivik is emeritus professor of anaesthesiology, Universitetet i Oslo, Norway, as well as editor-in-chief of the Scandinavian Journal of Pain; Professor Alain Borgeat is head, department of anaesthesiology, Uniklinik Balgrist, Zurich, Switzerland; and Professor Narinder Rawal is from the Department of Anaesthesiology and Intensive Care, Örebro University Hospital, Sweden.
A significant proportion of patients continue to have severe pain in the weeks and months that follow a total knee arthroplasty (TKA), 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 one year after surgery, a significant number still experience pain. Will aggressive attempts to relieve pain and hyperalgesia when present six weeks after surgery reduce the risk of chronic and disabling pain after this type of palliative surgery?
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.
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, non-opioid 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. 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, 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. 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.
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 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.
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 US as the population ages.
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 sub-acute pain service as an adjunct to the acute pain service that all surgical hospitals
Appropriate pain management and rehabilitation of function during and after joint replacement enables fast-track rehabilitation and is highly beneficial to quality of life.
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