Postoperative Pain Control and Rehabilitation in Revisional Foot and Ankle Surgery

Postoperative Pain Control and Rehabilitation in Revisional Foot and Ankle Surgery

Sheung Wai Law, Tun Hing Lui


Foot and ankle revision surgery generally takes longer operative time to complete than the primary foot surgery and is often more challenging with greater risk of complications. The postoperative pain control and rehabilitation is a challenging task; pain response is a protective mechanism, but at some point, it may be counterproductive, limiting the progress of rehabilitation and affecting the outcome.

The International Association for the Study of Pain defines pain as “an unpleasant experience that involves conscious awareness of noxious sensations, with hurting and aversive feelings associated with actual or potential tissue damage or described in terms of such damage.” Perioperative pain is perceived by patients as one of the most unpleasant aspects of surgical procedures. Postoperative pain management in revision foot and ankle surgery is a complex issue, and understanding the acute and chronic pain mechanism is important in instituting effective therapeutic regimens. As all pain cannot be completely eliminated during subsequent phases of treatment especially during the early phase of rehabilitation, however, a reasonable level of pain control is required for effective rehabilitation and to prevent disuse atrophy.

Acute postoperative pain is a complex physiological reaction to tissue injury with surgical intervention. Revision surgery has a higher chance of getting postoperative pain with prolonged period of rehabilitation. Until recently, surgeons did not recognize the importance of management of postoperative pain. Pain control is a mandatory part of a comprehensive surgical plan, which will affect the ultimate functional outcome since inadequate postoperative pain management may cause chronic pain, which will affect the postoperative rehabilitation course resulting in long-term impairment and disability.

Pathophysiology of Postoperative Pain

The physiology of acute operative pain can be thought of as a distinct pathway beginning with the noxious stimulus and ending with perception (Figure 35.1). In the absence of sustained stimulation, the consequent physiology leading to perceptic does not occur. In more basic terms, the pain stops when the stimulus is removed. However, through both peripheral and central sensitization, this linear pathway can be transformed into a chronic cycle without a beginning or endpoint.

Figure 35.1 Physiology of postoperative pain pathway.

Surgery produces tissue injury with consequent release of histamine and inflammatory mediators, such as bradykinin, substance P, prostaglandins, neurotransmitters (eg, serotonin), and neurotrophins (eg, nerve growth factor). Noxious stimuli are then transduced by peripheral nociceptors, transmitted by A-delta and C nerve fibers from peripheral visceral and somatic sites to the dorsal horn of the spinal cord (see Figure 35.1).

These stimuli are transmitted to higher centers through the spinothalamic and spinoreticular tracts, where they induce suprasegmental and cortical responses to ultimately produce the perception of and affective component of pain. Sensitization of peripheral nociceptors may occur upon noxious stimuli and is marked by a decreased threshold for activation. This may lead to functional changes in the dorsal horn of the spinal cord that may later cause postoperative pain to be perceived as more painful than it would otherwise have been and result in central sensitization.

There is a disproportionate excitatory signal from peripheral and central sources “opening the gate” and leading to noxious processing. Centrally at the dorsal horn, excitatory signals from C fibers displace magnesium ions from N-methyl-d-aspartate (NMDA) receptors and open calcium channels at other excitatory synapses. A “wind-up” phase results in the postsynaptic neurons as excitatory neuropeptides and amino acids accumulate within the synapse.

Central sensitization is induced by peripheral excitatory signals (particularly from the C fibers), and it cycles to increase peripheral effects. Axonal reflexes lead to a secondary hyperalgesia where the perceived area of pain increases. A reflex develops within the activated peripheral nerve and spinal cord to cause activation and sensitization along the entire distal extent of the peripheral nerve, not just the branches of the injured tissue. Through this mechanism, nociceptors in the surrounding area of the injured tissue become activated (Figure 35.2).

Figure 35.2 Interaction of peripheral and central sensitization in amplification of pain.

Figure 35.3 Possible role of central hypersensitivity in the pathophysiology of chronic pain.

Long-Term Impact of Acute Pain

The development of central and/or peripheral sensitization after traumatic injury or surgical incision can result in the amplification of acute pain. Inadequate pain control following revision foot and ankle surgery has the potential to create complications, readmissions, and unnecessary procedures with costly diagnostic tests and imaging. The patient who is in significant pain is less likely to be satisfied with decreased mobilization and higher risk for developing into chronic pain.

Chronic postsurgical pain is a largely unrecognized problem, which may occur in 10% to 50% of postoperative patients (depending on type of surgery) with 2% to 10% of these patients experiencing severe chronic postsurgical pain.1 Poorly controlled acute postoperative pain or acute pain is an important predictive factor in the development of chronic pain. The transition from acute to chronic pain can occur very quickly and with long-term behavioral and neurobiologic changes. Early intervention for pain control is then important for prevention of postsurgical pain.

The severity of acute postoperative pain may be an important predictor in the development of chronic postsurgical pain; a causal relationship between severity of acute postoperative pain and subsequent central poststroke pain has not been definitively established, and other factors such as psychological and underlying pain experience may be more important in predicting the development of chronic postsurgical pain. Tissue and nerve damage produce central hypersensitivity as a result of central nervous system plasticity. The psychological distress of chronic pain condition further contributes to central hypersensitivity, thereby producing further amplification of pain.

Strategies of Perioperative Pain Management

Preventing the establishment of altered central processing by analgesic treatment may, in the short term, result in the reduction of postprocedural or traumatic pain and accelerated recovery. In the long-term, the benefits may include a reduction in the development of chronic pain and an improvement in the patient’s quality of recovery and satisfaction. Pain management should therefore begin prior to surgery and be continued throughout the patient’s entire surgical journey. The focus of preventive analgesia is not on the relative timing of analgesic interventions but on attenuating the impact of the peripheral nociceptive barrages associated with noxious preoperative, intraoperative, and/or postoperative stimuli. By interrupting the transmission of the peripheral nociceptive barrages to the spinal cord throughout the perioperative period, a preventive approach aims to block the induction of central sensitization, resulting in less intense postoperative pain and lower analgesic requirements. The severity of pre- and postoperative pain influences the development of chronic postsurgical pain, and there is evidence that early analgesic interventions reduce the incidence of chronic pain after surgery.

Preemptive Analgesia

This term refers to the delivery of analgesic intervention(s) before the first surgical incision. The rationale is to stop (or obtund) the transmission of the intense nociceptive barrage to the brain that occurs with the onset of surgery. In theory this should prevent sensitization of the neural pathways and reduce the requirement for subsequent postoperative analgesia.

Preemptive analgesia is defined as an analgesic intervention started before the noxious stimulus arises to block peripheral and central pain transmission. This preemptive intervention is possible, primarily, in the context of surgical intervention; ideally, one in which the patient has no or minimal pain prior to the intervention. The rationale is to stop (or obtund) the transmission of the intense nociceptive barrage to the brain that occurs with the onset of surgery. In theory, this should prevent sensitization of the neural pathways and reduce the requirement for subsequent postoperative analgesia. It includes an attempt to block pain transmission prior to the injury (incision), during the noxious insult (surgery itself), and following the injury and throughout the recovery period.

Preventive Analgesia

Preventive analgesia aims to provide a longer duration of effective analgesia in the perioperative period (hours to several days). This includes:

  1. Attempt to give medications prior to surgical incision.
  2. Administration of medications during the intraoperative or intraprocedural period.
  3. Administration of medications during the intraoperative and postoperative period.

There is evidence that successful analgesic interventions in this initial perioperative window have a beneficial effect on postoperative pain or on analgesic consumption that exceeds the expected duration of action of the drug. NMDA receptor antagonist drugs show preventive analgesic effects. For some procedures the use of ketamine at induction reduces postoperative morphine consumption. Preventive analgesia is demonstrated when postoperative pain and/or analgesic use are reduced beyond the duration of action of the target drug and the observed effects are not direct analgesic effects of the target drug.

Pharmacologic Approach

Oct 22, 2022 | Posted by in ORTHOPEDIC | Comments Off on Postoperative Pain Control and Rehabilitation in Revisional Foot and Ankle Surgery
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