Commentary Re: “The Onset of Intra-Abdominal Adhesions During Closed-Abdomen Hyperthermic Intraperitoneal Chemotherapy” ( J Laparoendosc Adv Surg Tech A 2016;26:997–1002)

To the Editor:

With a lot of interest, we have read the article by Lotti et al. ¹ entitled: The Onset of Intra-Abdominal Adhesions During Closed-Abdomen Hyperthermic Intraperitoneal Chemotherapy (CAHCT). In a study on consecutive case series, the authors demonstrated an onset of adhesion development during CAHCT in 10 patients with peritoneal carcinomatosis. The authors dynamically monitored early stage of development of fibrinogenic adhesion-like structures between intraperitoneal organs involving the visceral and parietal peritoneum, ¹ which is a very important observation. In our opinion, mechanical trauma by initial adhesiolysis, chemical irritation by cytoreductive surgery, and high temperature impact are the causative factors of fibrin exudation, deposition, and fibrin bond formation between neighboring traumatized structures. Therewith, these fibrin bonds were seen in illustrations after their first division (adhesiolysis).

The authors observed these fibrin bonds during three consecutive control laparoscopic accesses every 15 minutes after the first access (adhesiolysis), when adhesiolysis followed by peritoneal perfusion was performed. ¹ It is not surprising that analogous structures were not observed beyond 45 minutes. Fibrin exudation occurs during the initial reaction of the peritoneal tissue, followed by fibrin deposition and other pathophysiological events in the acute phase of the aseptic inflammatory reaction with initiation of wound healing processes in the peritoneal cavity. These findings perfectly fit with the classical pathogenesis of postsurgical adhesion formation in the abdominal cavity.

We have observed analogous findings in our experimental studies, when, after surgical trauma, fibrinogen from wound exudation formed transient fibrin bonds between neighboring intraperitoneal structures (visceral/peritoneal organs or surfaces) during the first hours after surgery. These transient fibrin bonds were transformed into fibroid adhesions by infiltration of cells, fibroblasts, collagen deposition, and vascularization with further maturation as permanent fibroid adhesions.^2–4

We agree that the authors have demonstrated the onset of intra-abdominal adhesion formation for the first time in patients, but their findings are not the mature postsurgical adhesions. These intraperitoneal structures are fibrin bonds formed by fibrinogen from exudation caused by initial mechanical/chemical/thermal trauma during the acute phase of inflammation. This can be easily proved by a histological examination of these structures. The absence of forming of such structures beyond the 45 minutes, after initial mechanical trauma and chemical procedures, can be as an indirect proof.

Usually, in nonadhesiogenic case, lysis of most of these fibrin bonds occurs during the first hours after surgery by activation of tissue plasminogen activator (tPA) with subsequent adhesion-free wound healing. In high-adhesiogenic cases, tissue ischemia, inflammation, the presence of a foreign body, and other factors can prolongate the existence of these transient fibrin bonds between intraperitoneal structures, because of inhibition of tPA and overexpression of plasminogen activator inhibitors, which together with cellular, immunological, collagen deposition, and other pathophysiological mechanisms enhance formation of severe permanent fibroid adhesions.

We do not support the theory of adhesiogenic property of CO₂ pneumoperitoneum itself,^4,5 the benefits of warm CO₂ pneumoperitoneum environment are under debate, ⁶ whereas the adhesiogenic impact of cytoreductive surgery combined with laparoscopy-enhanced CAHCT needs more investigations.