Chronic Post-Surgical Pain (CPSP) is defined as chronic pain that develops or increases in intensity after a surgical procedure or a tissue injury and persists beyond the healing process that is for at least three months, after the surgery.1 Its localization is either at the surgical site or projected onto the innervation zone of the nerve supplying the surgical site, or related to the corresponding dermatome, after surgery, or injury to the deep somatic and visceral tissues.
Macrae and Davies were the first to propose that specific criteria should be satisfied in order for chronic pain to be defined as post-surgical.1 These were - the pain must develop after a surgical procedure and must be of at least two months duration with other causes of the pain being ruled out.
The incidence of CPSP has been reported for various surgical procedures in different studies, and ranges from as low as 5% to as high as 85%.2 It has now been included in the International Classification of Diseases (ICD-11) to contribute to its identification, diagnosis, and therapy. The inclusion of CPSP in the ICD-11 is a major step forward that will allow future studies to report the incidence of CPSP more accurately. Furthermore, this raises awareness of this condition as a disease rather than merely a symptom, and the need for specific treatment and management.1 Presently, chronic pain specifier is pain severity rather than pain intensity alone and it encompasses three components, a) pain intensity b) pain-related distress, and c) pain-related interference with daily activities.3
The pathophysiology of chronification of pain includes central (spinal and supraspinal) and peripheral (at the site of injury) sensitization. The inflammatory and the immune response to the axonal and the tissue damage plays the forerunner. The release of neurotransmitters peripherally and centrally, microglial activation, ectopic neural activity, altered activity in the dorsal horn, changes in the supraspinal processing and endogenous, descending pain pathway modulation play vital role in chronification of pain.
Since CPSP develops due to central sensitization, it show characteristics of neuropathic pain. The patients often report atypical clinical symptoms like hyperalgesia (increased painful sensation caused by a noxious stimulus), allodynia (painful sensation caused by a usually non-painful stimulus), and dysaesthesia (unpleasant touch perception or tingling) indicating nerve damage and central sensitization very early after surgery. It is theorized that in CPSP, painful sensations change from acute post-operative pain to complex and mixed pain syndromes comprising of nociplastic, neuropathic or characteristics of both.4 CPSP is known to add to a significant disease burden and decrease the quality of life.3 With the increasing number of surgeries worldwide, the burden of CPSP continues to have a high impact on the health care sector.
Studies suggest that transition from acute to chronic pain by peripheral and central inflammatory and sensitization processes starts as early as 2 weeks of nociceptive input. It is known that early identification of the patients at risk of developing CPSP is an essential step in reducing the pain chronification, hence many attempts are being made to identify the risk factors for the same.
Various risk factors have been recognized for prediction of CPSP. Young age, female gender, type of surgery, preexisting pain, opioid use, duration of surgery being some of them. However, it is important is to understand the interaction of risk factors in a wide range of surgical interventions. Predictive models with greater reliability to predict individual outcomes in the early post-operative period can be useful for the same.
Van Driel et al, in (2022) developed and validated one such early predictive model for CPSP.5 The final predictive model consists of preoperative treatment with opioids, worst pain score (NRS) on post-operative day1(POD1), presence of pruritis within the painful area onPOD1, pain score (NRS) on POD14 and presence of painful cold sensations within the painful area on POD14.
The formal and definitive means of testing is Quantitative Sensory Testing (QST) , however it is time-consuming and not feasible to be used in routine clinical settings, so the bedside QST has been used as an alternative.
CPSP also has an impact on the Quality of life,(QOL) which has been described by numerous studies in an attempt to recognize the risk factors for the same. SF6 is one such validated tool to assess the same.6
5-56% patients with laparoscopic cholecystectomy have a risk of developing CPSP. However, there is no clear relation to the modality of surgery whether open/lap or timing of surgery.7 The development of post-operative pain might be due to tissue or nerve injury or inflammatory changes. The pain due to laparoscopic cholecystectomy can be either incisional (port site), visceral or shoulder tip pain.
It is estimated that in India at a particular time approximately 6-8 % of the population has symptomatic cholelithiasis and need cholecystectomy. Hence, as it forms a large proportion of the surgical procedures, so there is an added need to understand not only its perioperative course but also the late sequalae, CPSP being one such element.