Hyperperfusion Syndrome in Small-for-Size Livers

Abstract

Background: Portal hyperperfusion in small-for-size livers might seriously impair postoperative liver regeneration. Using an experimental model, we investigated splenectomy as a measure to reduce portal blood flow and its impact on postoperative recovery following extended liver resection. Method: Wistar rats underwent partial (90%) hepatectomy with or without splenectomy under temporary inflow occlusion (30 min). In addition to 10-day survival rate, laser Doppler flowmetry of hepatic blood flow and fluorescence microscopic analysis of hepatic microcirculation were performed to assess the effect of splenectomy on initial microvascular reperfusion of liver remnants. Results: While postischemic perfusion failure was comparable between both groups, portal blood flow was significantly reduced after simultaneous splenectomy (3.5 ± 0.4 vs. 5.4 ± 0.4 ml/min). Moreover, red blood cell velocity and volumetric blood flow were reduced in splenectomized animals. These animals experienced lower AST levels (421 ± 36 vs. 574 ± 73 U/l) and a significantly increased survival rate, reaching 6.6 ± 1.3 vs 2.6 ± 0.8 days. Conclusion: Simultaneous splenectomy significantly reduced the risk for postoperative hyperperfusion syndrome in small-for-size livers. Shear-stress-induced liver injury was diminished due to a significant reduction of portal venous blood flow, which positively influenced postoperative regeneration resulting in significantly higher survival.

Interleukin-6 inhibits oxidative injury and necrosis after extreme liver resection

“…Murine and rat models of excessive liver resection show a high mortality rate similar to that of humans and appear to be valid models to understand this important question. 7,[22][23][24] The presence of TUNEL-positive cells after extensive hepatectomy has been interpreted as evidence for apoptotic pathways to liver death 7 ; however, TUNEL staining is nonspecific. TUNEL-positive cells occur with apoptosis, but also with necrosis or Fig.…”

“…15 Administration of glucose, alternative resection methods, procedures that reduce portal flow, and inhibitors of nuclear factor kappaB such as A20 can improve survival after extreme hepatectomy, [22][23][24] although the precise mechanisms are unclear. As well, inhibition of receptor for advanced glycation end products after 85% hepatectomy increases survival, apparently through a pathway involving nuclear factor kappaB and dendritic cell activation.…”

Splenectomy improves survival by increasing arterial blood supply in a rat model of reduced-size liver

“…With the increasing practice of living-donor liver transplantation and the enlargement of the resectable liver mass, the small-for-size syndrome has emerged as an important clinical problem [8]. The ongoing debate on the causes of the small-for-size syndrome mainly focuses on portal hyperperfusion with high intravascular shear stress [9][10][11]. To avoid liver failure by portal hyperperfusion, techniques for reduction of portal inflow, such as portal-caval and mesocaval shunts, splenic artery ligation, and splenectomy have been established [12][13][14].…”

“…As a consequence, the extent of spleen-derived blood perfusion is an important factor in determining portal inflow pressure. Glanemann et al could demonstrate that simultaneous splenectomy with extended partial hepatectomy in rats reduces the PVBF by approximately 44% compared with nonsplenectomized animals [11].…”

A 3D porous media liver lobule model: the importance of vascular septa and anisotropic permeability for homogeneous perfusion

“…in the case of fibrosis, cirrhosis [15,16], hepatocellular carcinoma [17], steatosis [18], portal hypertension [19,20]), as well as surgery-induced effects (e.g. small-for-size liver syndrome [21][22][23] after partial hepatectomy). For example, cirrhosis is known to alter and deteriorate the liver's microvessel structure leading to higher vascular resistances, which could be modelled by changing structure-related parameters such as the permeability.…”