Invited commentary to: “Spontaneous splenic rupture during pringle maneuver in liver resection for hepatic abscess”

Abstract

Trauma is the most frequent cause for splenic rupture, which typically occurs along the peritoneal attachments of the splenic convexity or at the splenic hilum after deceleration trauma or as avulsion fractures of the spleen after direct lateral impact to the left lower ribcage. Spontaneous splenic ruptures are described as complications after infectious or neoplastic afflictions of the splenic parenchyma (5). Intraoperative splenic injury usually occurs at the splenic insertion of the splenocolic ligament, especially if the left colonic flexure is not detached from the spleen. The case reported by Kling et al. is indeed a rare case of spontaneous splenic rupture that has been reported in a similar setting only once (1). The site of rupture does not present like an intraoperative splenic injury, but was attributed by the authors to an increased intrasplenic pressure after Pringle's maneuver for a left lateral liver resection. Control of the hepatic inflow by Pringle 's maneuver is one of the measures to decrease bloodloss during major liver resection (2). While the consequences of Pringle 's maneuver on systemic and pulmonary macro hemodynamic parameters have been studied in humans (3), little is known about the impact of Pringle 's maneuver on the splanchnic, especially splenic circulation. Delva et al. demonstrate that Pringle 's maneuver causes a significant increase in systemic peripheral vascular resistance and consequently an increase in blood pressure and a decreased cardiac index (3). The authors here hypothesize that splenic venous congestion during Pringle 's maneuver was the cause for the rupture. In the only comparable case published by Baradaran et al. (1) that ve-