Post cholecystectomy pain syndrome: Letter to Editor

Bruno Bordoni

doi:10.1515/sjpain-2024-0001

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Post cholecystectomy pain syndrome: Letter to Editor

Bruno Bordoni

Published/Copyright: March 7, 2024

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From the journal Scandinavian Journal of Pain Volume 24 Issue 1

Dear Editor,

I have read with interest the article by Lee and colleagues, and I congratulate them for their publication [1]. The article highlighted some possible reasons that lead to post cholecystectomy pain (PCP) syndrome after laparoscopic cholecystectomy, evaluating 200 patients undergoing surgery. The gallbladder is removed with instruments inserted into the abdomen through small incisions (three or four of approximately 5 mm), a minimally invasive approach created by Muhe in 1986 (see Reynolds W Jr., The first laparoscopic cholecystectomy. JSLS. 2001 Jan–Mar;5(1):89–94). Despite a minimal duration of the surgical intervention (approximately within an hour) and the discharge from hospital quickly, this surgery is not without risks, such as chronic pain in the surgery area or in the surrounding areas [1]. Pain or related symptoms may appear days or years after surgery. The reasons highlighted by the research derive from visceral dysfunctions (new onset pancreatitis, gastritis, sphincter of Oddi dysfunction) or of somatic origin. The latter symptoms (in 54% of patients) derive from the presence of abdominal myofascial pain syndrome (AMPS), such as the localization of trigger points [1]. I would like to make some clarifications of the article published by Lee.

PCP is not well understood. The patient may have acute exacerbations and recurrent hospital admissions, as well as chronic pain/symptoms [1]. One of the causes of PCP that was not taken into consideration in Lee’s article is the formation of adhesions and scar tissue. The latter can give rise to symptoms, such as dysfunction of the pancreatic sphincter (pain and pancreatitis), due to cicatricial papillary stenosis, or persistent abdominal pain in the choledochal region commonly deriving from intestinal scars/adhesions [2,3]. Adhesions form when different tissues/layers do not move properly after trauma or surgical injury. On the one hand, the patient must not stress the area involved by the surgery, while on the other hand, an inflammation of the tissues involved by the surgery is the physiological response to obtain tissue repair [4]. The latter two conditions can lead to the formation of adhesions, which will be innervated and vascularized over time [4]. This new tissue (hyperplasia) can become one of the causes of PCP, stimulated by simple movement and/or movements of the viscera. Adhesions are commonly found after surgery and often cause pain or symptoms that cannot be easily described by the clinician [4]. The hyperplastic tissue can be mistaken for the presence of trigger points and AMPS, because with palpation they are painful and hard structures and can induce symptoms. The fact that there is no resolution of the symptoms with injection of drugs for hypothetical trigger points is the possible answer that the symptoms were not of muscular origin [5].

Another point of the article that could be improved is the concept of “Viscerosomatic convergence is a phenomenon of central and peripheral sensitisation” [1]. Convergence is not a phenomenon, and it is not a central and peripheral sensitization. The theory of viscerosomatic reflexes describes spinal facilitation, probably due to aberrant afferent/efferent activation patterns, temporarily or chronically altering the electrical and metabolic environment of synaptic contact. Once established, this alteration could self-generate. The physiological reality is more complex. According to a new vision or distributed nociceptive system, nociceptive processing that can derive from visceral or somatic stimuli is distributed bilaterally in the medulla crossing Rexed laminae [6]. The afferent information via the axons of the dorsal root ganglion, when entering the spinal cord, divides, with ascending and descending branches coursing into Lissauer’s tract, sending off collateral pathways and creating multiple synapses at multiple levels [7]. The spinal neurons involved partly process the nociceptive afferents before the same information reaches the supraspinal pathways. Once information reaches the supraspinal neurons, more cerebral areas are activated bilaterally, making the efferent response not easy to decipher [6,7]. Our understanding of pain processing is still a mystery [8].

To conclude, one of the causes of PCP is the presence of adhesions between tissues, and the painful symptomatology of PCP is still a question without a precise answer, and it is not so simple to identify an adhesion or trigger points on the abdomen.

References

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Received: 2023-12-29

Revised: 2024-01-26

Accepted: 2024-01-26

Published Online: 2024-03-07

This work is licensed under the Creative Commons Attribution 4.0 International License.

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