Introduction
The development of chronic pain after surgery is an important and often overlooked problem. Chronic postsurgical pain (CPSP) can dramatically impair quality of life, limit postoperative rehabilitation, and strain patient–physician relationships.
The incidence of CPSP varies widely by study and surgical procedure, but can range from low estimates of 5% to as high as 85%. CPSP after abdominal surgeries specifically have been reported to range from 19% for emergent laparotomy, 5%–32% after hysterectomy, 10%–52% after inguinal hernia repair, and 5%–42% after cholecystectomy.
The exact pathophysiology of CPSP is poorly understood but is theorized to be the result of maladaptive and persistent pain sensitization. Preexisting pain syndromes, surgical site complications, and recurrence of the primary disease process should be ruled out and a spatiotemporal relationship to surgery is required to diagnose CPSP.
Management primarily focuses on prevention through effective perioperative analgesia and minimization of surgical trauma. Once established, CPSP management should target inciting pain mechanisms, which can be diverse. For instance, abdominal surgery may result in chronic visceral pain from injury to the organs themselves or from the development of scarring and adhesions postoperatively. Conversely, abdominal wall pain may represent referred pain from intraabdominal sources or may be the result of an abdominal wall neuroma or nerve compression.
A comprehensive approach is crucial and includes physical and psychological therapies in addition to multimodal pharmacotherapy. A range of interventions and surgical procedures have been reported for patients who do not improve with conservative therapies.
Etiology and Pathogenesis
The mechanistic underpinnings of CPSP are poorly understood. Development of CPSP is presumed to be multifactorial, representing the complex interplay from surgical, genetic, psychological, and perioperative factors. , Chronic pain may arise from a background of acute postsurgical pain or may develop later after an asymptomatic period.
Intraoperative nerve injury is associated with the development of CPSP. Surgeries with nerve damage, deliberate or inadvertent, demonstrate the highest prevalence of CPSP. , Accordingly, many patients exhibit signs and symptoms consistent with neuropathic pain, such as hyperalgesia and sensory disturbances. However, not all CPSP is neuropathic and not all patients with known nerve damage go on to develop chronic pain.
As with all chronic pain syndromes, CPSP is thought to be due to aberrant peripheral and central sensitization. , Surgery inherently imparts tissue damage upon surrounding tissues. As part of the adaptive response to this injury, peripheral and central sensitization can develop. These neuroplastic changes induce a state of hypersensitivity intended to protect during times when the risk for injury is greatest. As the surgical site heals, inflammation resolves and the noxious stimuli are removed, the upregulation of peripheral and central neurons usually returns to baseline. However, in a subset of patients, pain sensitization persists. , In some cases, this may be due to ongoing nociceptive activation. For instance, implanted mesh or excessive scarring can compress or stretch nerves, eliciting ongoing pain signals. In other cases, however, there may not be an obvious source of ongoing inflammation. In these instances, inadequate inhibitory pain pathways may prevent the appropriate downregulation of pain sensitization.
Although the exact mechanisms that lead to CPSP are not yet known, there are well-described risk factors that shed insight into the pathogenesis ( Table 15.1 ). The most consistent risk factor to develop chronic postoperative pain is pain itself. The presence of preoperative pain and the duration and intensity of postoperative acute pain are strong risk factors for CPSP. Pain is also strongly affected by psychological conditions. Anxiety, depression, and pain catastrophizing are predictive of CPSP, and chronic pain in general.
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Clinical Features
The clinical presentation of CPSP can be highly variable. Chronic pain most commonly arises from uncontrolled or high intensity acute postoperative pain. However, patients can present months later after an intervening asymptomatic period, sometimes termed the honeymoon period. Neuropathic pain findings are common in CPSP, such as allodynia, hyper- or hypoalgesia, or dysesthesia in both somatic and visceral structures. ,
CPSP may present with visceral pain features including diffuse, poorly localized pain that is often crampy, colicky, and achy in nature. The diffuse distribution is the result of visceral convergence in which relatively few afferent fibers innervate each visceral organ and then converge on overlapping spinal dorsal horn neurons. Visceral pain tends to be highly associated with autonomic features including nausea, vomiting, sweating, pallor as well as functional bowel and bladder disorders.
Pain is generally described at the surgical site but can also be referred or remote somatic areas. Abdominal wall pain may be the result of referred visceral pain due to somato-visceral convergence or may be the result of pain originating in the abdominal wall structures as a result of surgical injury, such as the ilioinguinal nerve during hernia repair. Carnett’s test may differentiate abdominal wall pain from visceral pain. It is performed by palpating the area with the patient supine and abdomen relaxed. The patient is then asked to tighten the abdominal muscles (by lifting their head and shoulder off the bed), and the area is palpated again. Abdominal wall pain will be increased when the abdominal muscles are contracted, whereas intraabdominal sources of pain will decrease from guarding by rigid overlying musculature.
As always, clinicians should maintain a high suspicion accompanying comorbidities and mood disorders, particularly anxiety and depression, which are commonly reported in CPSP patients.
Diagnosis
The diagnostic criteria for CPSP have evolved since the first description in 1999 by Crombie et al. Table 15.2 displays the established diagnostic criteria as well as recently proposed modifications.
