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Purpose <p>Approximately 1–7% of patients develop persistent lymphatic ascites after liver transplantation. This study describes the diagnosis and treatment of lymphatic ascites in patients post liver transplantation, refractory to conservative therapy.</p> Materials and Methods <p>A review of the prospectively collected database was conducted to identify patients who received interventions for persistent lymphatic ascites following liver transplantation. Patient demographics, baseline characteristics, imaging findings, procedural details, and follow-up information were gathered.</p> Results <p>Four adult patients after orthotopic liver transplantation with chylous ascites (CA) and 4 pediatric patients after split liver transplantation with hepatic lymphorrhea (HL) were included in this study. CA patients were characterized by elevated triglycerides (1010&#xa0;mg/dL, 442–1769), and HL patients were characterized by low serum albumin ascites gradient (SAAG &lt; 1.1) and low triglycerides. In 3/4 patients with CA, dynamic contrast MR lymphangiography and intranodal lymphangiography demonstrated obstruction of the central lymphatic system. The mesenteric lymphatics were then embolized with either <i>n</i>-BCA glue or lipiodol. One-fourth patients had stenosis of the portal vein anastomosis, which was balloon dilated using a transjugular approach. All 4 patients reached resolution of ascites at a median of 27&#xa0;days. In 3/4 patients presenting with HL, liver lymphangiography demonstrated extravasation of the contrast. That was embolized with either glue or lipiodol. One-fourth patient demonstrated no extravasation but significant lymphangiectasia. In all patients, there was a resolution of ascites at a median of 14&#xa0;days after intervention.</p> Conclusion <p>Three mechanisms of post-transplantation lymphatic ascites were identified: portal venous hypertension due to iatrogenic obstruction; obstruction of central lymphatics resulting in congestion of the mesenteric lymphatic system and mesenteric lymphatic leak; and liver lymphorrhea. Identification of the mechanism of ascites allowed for successful percutaneous treatment in all patients.</p> Graphical Abstract <p></p>

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Persistent Lymphatic Ascites After Liver Transplantation: Identification of the Underlying Mechanism of Ascites Permits Successful Percutaneous Treatment

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月23日

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  • Alexey Gurevich,
  • Priscilla Stecher,
  • Peter L. Abt,
  • Maarouf A. Hoteit,
  • Gregory J. Nadolski,
  • Deborah Rabinowitz,
  • Maxim Itkin

摘要

Purpose

Approximately 1–7% of patients develop persistent lymphatic ascites after liver transplantation. This study describes the diagnosis and treatment of lymphatic ascites in patients post liver transplantation, refractory to conservative therapy.

Materials and Methods

A review of the prospectively collected database was conducted to identify patients who received interventions for persistent lymphatic ascites following liver transplantation. Patient demographics, baseline characteristics, imaging findings, procedural details, and follow-up information were gathered.

Results

Four adult patients after orthotopic liver transplantation with chylous ascites (CA) and 4 pediatric patients after split liver transplantation with hepatic lymphorrhea (HL) were included in this study. CA patients were characterized by elevated triglycerides (1010 mg/dL, 442–1769), and HL patients were characterized by low serum albumin ascites gradient (SAAG < 1.1) and low triglycerides. In 3/4 patients with CA, dynamic contrast MR lymphangiography and intranodal lymphangiography demonstrated obstruction of the central lymphatic system. The mesenteric lymphatics were then embolized with either n-BCA glue or lipiodol. One-fourth patients had stenosis of the portal vein anastomosis, which was balloon dilated using a transjugular approach. All 4 patients reached resolution of ascites at a median of 27 days. In 3/4 patients presenting with HL, liver lymphangiography demonstrated extravasation of the contrast. That was embolized with either glue or lipiodol. One-fourth patient demonstrated no extravasation but significant lymphangiectasia. In all patients, there was a resolution of ascites at a median of 14 days after intervention.

Conclusion

Three mechanisms of post-transplantation lymphatic ascites were identified: portal venous hypertension due to iatrogenic obstruction; obstruction of central lymphatics resulting in congestion of the mesenteric lymphatic system and mesenteric lymphatic leak; and liver lymphorrhea. Identification of the mechanism of ascites allowed for successful percutaneous treatment in all patients.

Graphical Abstract