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

## TL;DR

This paper shows that identifying the specific cause of lymphatic ascites after liver transplants allows for successful percutaneous treatment.

## Contribution

The study identifies three distinct mechanisms of post-transplant lymphatic ascites and demonstrates successful targeted interventions.

## Key findings

- Three mechanisms of post-transplant lymphatic ascites were identified and successfully treated.
- Percutaneous embolization resolved ascites in all patients within a median of 14–27 days.
- Dynamic contrast MR lymphangiography and liver lymphangiography were key diagnostic tools.

## Abstract

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.

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.

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.

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.