Vascular Remodeling of Visceral Arteries Following Interruption of the Splenic Artery During Liver Transplantation

Abstract

Splenic artery (SA) ligation can be performed during liver transplantation (LT) to avoid portal hyperperfusion, which is involved in the pathogenesis of both small‐for‐size and SA syndrome. The SA can also be used as an inflow for arterial reconstruction. Exceptionally, SA interruption or agenesis has been associated with positive remodeling of collateral arteries supplying the spleen via the left gastric artery (LGA), short gastric vessels, and the gastroepiploic arcade (GEA), with subsequent severe upper gastrointestinal (GI) bleeding. To determine incidence, magnitude, predictors, and clinical implications of vascular remodeling after SA interruption during LT, we identified 465 patients transplanted in the period 2007‐2017 who had the SA ligated or interrupted at LT. Among them, 88 had a computed tomography angiography suitable for evaluation of vascular remodeling after LT. The presence of prominent gastric arterial collaterals and the increase in LGA and GEA diameter were evaluated on 2‐dimensional axial images and multiplanar reconstructions. Of the 88 patients, 28 (31.8%), 32 (36.4%), and 22 (25.0%) developed gastric collateralization graded as mild, moderate, or severe. Of the patients for whom comparison with pre‐LT imaging was possible (n = 54), 51 (94.4%) presented a median 37% and 55% increase in LGA and GEA diameter, respectively. Severe gastric collateralization was associated with lower body mass index (odds ratio, 0.84; 95% confidence interval [CI], 0.71‐0.98; P = 0.03), whereas a GEA caliper measurement increase was positively correlated with Model for End‐Stage Liver Disease score (r2 = 0.12; 95% CI, 0.65‐4.15; P = 0.008). Out of 465 patients, 2 (0.43%) had severe episodes of arterial upper GI bleeding, possibly exacerbated by vascular remodeling. In conclusion, vascular remodeling after SA interruption during LT is frequent and can aggravate GI bleeding during follow‐up.

Vascular Remodeling of Visceral Arteries Following Interruption of the Splenic Artery During Liver Transplantation

“…An advanced pre-LT liver disease with increased portal hypertension can be assumed in those patients who developed severe gastric collateralization. Here, we show a reduction in vascular remodeling of the nonsevere collateralized patients over time, data that were not reported by Patrono et al (2) The post-LT progressive reduction (5) of visceral hyperflow/hypertension due to pre-LT portal hypertension could explain the reduction in visceral artery diameter. In our opinion, a CT evaluation of splanchnic remodeling could describe not only the pathogenetic mechanisms elicited by SA ligation but also persistent post-LT portal hypertension.…”

“…Patrono et al (2) recently published an article that described their experience in splenic artery (SA) ligation to prevent portal hyperperfusion and arterial hypoperfusion. For the first time, the authors tried to evaluate the impact of these procedures on post-LT vascular remodeling and outcomes.…”

“…(3,4) In 8 patients, we had complete digital imaging records: in 5 patients, the SA was ligated for SA aneurysms, and in 3 patients, it was sectioned for arterial anastomosis. We reviewed the computed tomography (CT) images (before LT and 1-24 months after LT) of these patients using the criteria outlined by Patrono et al (2) Among the patients who developed vascular remodeling (7/8 patients), 5 developed severe collateralization with indications of pre-LT portal hypertension (Table 1). After the initial increase, the diameters of the left gastric artery (LGA) and the gastroepiploic arcade (GEA) of the 5 patients with severe collateralization remained stable, whereas the diameters tended to reduce over time in the nonsevere patients ( Fig.…”

“…Post-LT vascular remodeling occurred within the same vascular district that underwent profound changes in pre-LT portal hypertension, even though the first is due to arterial hypervascularization. Patrono et al (2) reported a higher Model for End-Stage Liver Disease-sodium score and lower platelets in patients affected by severe collateralization.…”

Reply

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We read with interest the letter by Dondossola et al concerning our article. (1) The authors' data seem to confirm our hypothesis that patients suffering from severe portal hypertension are more prone to develop vascular remodeling. These data also suggest that a dynamic evaluation of vascular remodeling over time could be used as an accessory tool to diagnose persistent portal hypertension after liver transplantation (LT).

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