The vexing problem of post-amputation pain: What is the optimal perioperative pain management for below-knee amputation?

Abstract

Phantom pain, defined as intense throbbing or burning pain in the missing distal limb, is a common affliction after amputation. First described in 1872 by Ambroise Pare, the phenomenon is a common occurrence in 60–80% of amputees. Although some reports suggest abatement of phantom pain after a few years, others affirm it is longlasting. In addition to phantom pain, the unfortunate patient may also experience pain in the residual leg (stump pain) for reasons such as osteomyelitis, excessive scar tissue, or neuroma formation. In numerous pharmacotherapy trials, opioids, ketamine, anticonvulsants, and tricyclic antidepressants have provided only inconsistent relief. Intense pre-amputation pain is likely to be associated with the development of long-term phantom pain. In the 1970s, this observation led researchers to hypothesize that pain created a permanent imprint in the dorsal horn and in the pain-processing regions of the central nervous system. A number of investigations were undertaken to reduce afferent input to the dorsal horn preoperatively and thus lessen the memory of pain in the central nervous system. The results of these trials, summarized below, have taught us a great deal about pain processing and have advanced knowledge in the field of regional analgesia. Nevertheless, pre-emptive analgesia yielded inconsistent results and does not appear to have made significant headway in reducing the vexing problem of long-term post-amputation pain. The conclusion, based on new insights from animal and neuroimaging studies into the mechanism of phantom pain, is that reorganization in the somatosensory cortex is at least as important as events in the periphery. Reorganization may also occur at the dorsal horn and at the thalamic level and may be influenced by peripheral input. The mechanism of phantom limb pain remains obscure. It has the clinical characteristics of a neuropathic pain syndrome with a complex interplay between peripheral and central components, and it displays considerable variability among individuals. For example, when brachial plexus anesthesia was administered to prevent peripheral input from the amputation stump, both phantom pain and cortical reorganization were eliminated in 50% of upper-limb amputees, whereas the phantom pain remained unchanged in the remaining 50% of subjects. In order to attenuate the undesirable cortical reorganization, both sensory stimulation therapy and centrallyacting drugs, such as ketamine and gabapentin, have been proposed as preemptive therapies that could be used in the perioperative period for patients identified at high risk for phantom pain. What criteria should we use to determine those at highest risk? The observational study in this issue of the Journal is the first to suggest that pre-amputation use of prescribed opioids may be a risk factor for developing phantom pain. Since a landmark clinical trial published in 1988 by Bach et al., anesthesiologists have been interested in the role of perioperative neuraxial blockade as a pre-emptive treatment for phantom pain. Patients with vascular disease scheduled for amputation were randomized to receive either epidural bupivacaine for three days preand postprocedure or an epidural with placebo infusion plus conventional morphine analgesia postoperatively. After 6 months, the incidence of phantom limb pain was significantly lower in the epidural-treated group than in the morphine group. In 1994, this finding was confirmed in another randomized trial where an epidural was P. K. Morley-Forster, MD (&) Department of Anesthesia and Perioperative Medicine, St. Joseph’s Health Centre, University of Western Ontario, 268 Grosvenor St., London, ON N6A 4V2, Canada e-mail: pat.morley-forster@sjhc.london.on.ca