Although MIA was proven to be safe and effective for a heterogeneous group of patients with adrenal disorders, the prevalence of CPSP has not been reported widely. In this cohort study the prevalence of CPSP following MIA was 14.9%. The presence of CPSP was correlated with a significantly lower HRQoL.
Acosta et al. found a prevalence of 8% chronic back pain in twelve open and 6% in seventeen laparoscopic bilateral adrenalectomies for hypercortisolism.11 Walz et al. observed an incidence of 8.5% of temporary hypoesthesia and/or relaxation of the abdominal wall after PRA.12 A study by Bruintjes et al. showed a prevalence of CPSP of 5.7% following laparoscopic donor nephrectomy in relatively healthy live kidney donors. They also showed a significantly lower HRQoL in patients with CPSP on all subscales of the RAND-SF36, except role limitation due to emotional problems.13
Perioperative nerve injury seems to play an important role in the development of neuropathic pain, but nociceptive and inflammatory processes are also involved.14 We found sixteen patients (33%) with a combination of CPSP and symptoms of hypoesthesia. This is in accordance with the study by Johansen et al., who reported a strong association between sensory abnormalities and persistent pain, increasing with higher pain intensities.15 These findings may indicate that direct neuronal injury is a potential factor for developing CPSP, since nerve damage can result in central sensitization, which is linked to the development of CPSP.16 Preventing central sensitization may provide a mechanism-based approach by blocking nociceptive input using regional anesthesia or through direct antihyperalgesic medical therapy, subsequently reducing the chance to develop CPSP.
After multivariable regression analysis young age was a significant predictor of CPSP. This predictor has been described for other surgical procedures than adrenalectomy, such as video-assisted thoracoscopy or thoracotomy,17 breast cancer surgery,18 and hysterectomy.19 The etiology is not well-understood, but may be the result of a reduction in peripheral nerve functioning that occurs with increased age.20
When looking at pain severity, patients with a higher VAS-score had significantly lower scores on several domains of the RAND-SF36. This means that the presence of more severe pain results in a significantly lower HRQoL. CPSP can lead to functional limitations and psychological distress in patients. Therefore, identifying the risk factors and applying a preventive strategy may help to decrease the incidence of CPSP and the resulting lower HRQoL. Possible preventive strategies include modification of the surgical technique, adequate pain control throughout the perioperative period, and preoperative psychological intervention focusing on psychosocial and cognitive risk factors.21
The main strength of this study is that we specifically investigated the prevalence of CPSP after MIA as a primary outcome, which was not done before. Furthermore, this study includes a large patient number from an expert centre, with a relatively high response rate compared with other small-scale phone or e-mail surveys.22 This allowed us to perform multivariate logistic regression analyses to identify independent predictors of CPSP.
We acknowledge a few limitations in our study. First, patients with a variety of indications for surgery, disease-related symptoms and differences in comorbidity were compared. This could have an influence on preoperative and postoperative HRQoL between patients and may influence their recovery after surgery, with or without the presence of CPSP. Second, our data could be subject to a certain degree of recall bias, which can cause an overestimation of the true prevalence of CPSP, since patients with pain are more likely to respond. Third, the prevalence of preoperative pain was 24.5% in patients that subsequently reported CPSP. Although the questionnaire regarding CPSP was specific to only answer “yes” if the pain could be related back to their adrenalectomy, it is possible that patients with pre-existing pain reported “yes” as well. This could have resulted in an overestimation of the true prevalence of CPSP. Finally, no structured preoperative HRQoL data were present in our population.
In conclusion, in this study we have shown a substantial prevalence of CPSP following MIA. The presence of CPSP was significantly correlated with a lower HRQoL. When present, CPSP should be identified in a timely manner, since adequate management by pharmacotherapy, appropriate pain interventions, surgery and/or psychological management, can improve the pain and the physical and social functionality of patients. Furthermore, in the absence of evidence for effective treatment in established chronic pain, prevention should be the key strategy. Future trials should focus on etiology and prevention of CPSP after MIA.