Chylous Ascites From Cirrhosis-Related Portal Hypertension Treated With Medium-Chain Triglycerides, Octreotide, and Paracentesis.

INTRODUCTION
Chylous ascites, the accumulation of lymphatic fluid within the peritoneal cavity, is a rare and challenging clinical entity. It accounts for less than 1% of all ascitic presentations and is often secondary to traumatic, malignant, or infectious etiologies.1 However, its association with portal hypertension in the context of liver cirrhosis is particularly rare, with limited reported cases in the literature.2 The pathophysiology of chylous ascites in cirrhosis is multifaceted. Portal hypertension leads to increased pressure within the lymphatic system, disrupting lymphatic flow and causing leakage into the peritoneal cavity.3 This complex interplay of mechanisms demands a multidisciplinary approach to management. Traditional treatment modalities, including dietary modifications and therapeutic paracentesis, have been met with variable success.4 Emerging evidence highlights the role of medium-chain fatty acids, which bypass the lymphatic system, in mitigating chyle production.5 Similarly, octreotide, a somatostatin analog, has shown promise in reducing lymphatic output by inhibiting splanchnic blood flow and lymphatic secretion.6 When combined with large-volume paracentesis, these interventions provide a novel, synergistic approach to management, as seen in this case.2 This report contributes to the growing body of evidence on the effective treatment of chylous ascites and underscores the importance of individualized care. By highlighting a rare manifestation of portal hypertension and its resolution through a multimodal therapeutic strategy, we aim to bridge the gap between clinical challenges and innovative management.1

CASE REPORT
The patient is a 76-year-old woman who presented with abdominal enlargement and bloating. She experienced shortness of breath while lying down, accompanied by generalized weakness, prompting admission to the emergency department. She was diagnosed with moderate-risk community-acquired pneumonia. The patient is a known case of type 2 diabetes and liver cirrhosis for 6 years with Child-Pugh B score 8 with a model for end-stage liver disease–sodium score of 11, likely secondary to metabolic dysfunction–associated liver disease. Previous workup of liver cirrhosis that is, liver fibroscan done 6 years ago showed liver stiffness value of 25.8 (F > 4). Positron emission tomography–computed tomography scan showed nodular hepatic contour, which is suggestive and compatible with her history of liver cirrhosis. The viral hepatitis panel for A, B, and C showed negative results. Significant hypoalbuminemia was attributed to multifactorial causes, including liver disease, inadequate protein intake, potential renal loss (suspected nephrotic syndrome), and infection (pneumonia).
Abdominal ultrasound identified approximately 3 L of ascites. Therapeutic and diagnostic paracentesis yielded a pinkish milky chylous fluid, and ascitic triglyceride levels of 269 mg/dL, which is above triglyceride content >200 mg/dL, and serum–ascites albumin gradient ratio 1.6 g/dL supporting the diagnosis of chylous ascites secondary to portal hypertension and possible malignancy. Given the patient's history of breast cancer postmastectomy and rapid reaccumulation of fluid, malignancy was suspected. Positron emission tomography–computed tomography scan showed new pulmonary nodules and one of which was hypermetabolic, considering pulmonary metastases. Malignancy was considered due to aforementioned lesions on positron emission tomography scan, but cytology and cell block analysis of the ascitic fluid was negative, and the family chose to defer further metastatic workup.
Patient was managed conservatively, which included dietary modification (high protein: 1–1.5 g/kg/d; low fat: <25 g/d, emphasizing medium-chain triglycerides), fat-soluble vitamin supplementation (A, D, E, K), diuretics with albumin for high-gradient ascites, and measures to limit fat absorption (orlistat and subcutaneous octreotide 200 μg/d in 2 divided doses). Over time, the patient's ascitic triglyceride levels improved from 269 to 165.5 mg/dL. Clinical condition stabilized, drainage requirements via pigtail catheter decreased, and she transitioned successfully to diuretics. Transjugular intrahepatic portosystemic shunt was suggested; however, family was not amenable and preferred palliative care. The patient was discharged in a stable condition. On the succeeding admissions, the patient had volumes of ascitic fluid ranging from 20 to 1,152 mL estimated free fluid. The patient was continued on previous medical interventions and no subsequent paracentesis was warranted.

DISCUSSION
Chylous ascites results from disruption or obstruction of lymphatic flow, leading to the accumulation of triglyceride-rich lymph in the peritoneal cavity. Diagnosis is established by paracentesis showing milky fluid with elevated triglyceride levels (>200 mg/dL), lymphocyte predominance, and exclusion of other causes by cytology and imaging.7 Initial evaluation includes cell count with differential, total protein and albumin for serum–ascites albumin gradient calculation, triglyceride level, cytology, microbiology, and cross-sectional imaging (computed tomography or magnetic resonance imaging) or lymphangiography to localize leaks or obstruction.7,8
The differential diagnosis includes postoperative lymphatic injury, malignancy (particularly lymphoma), congenital malformations, infections such as tuberculosis or filariasis, traumatic disruption, and portal hypertensive mechanisms in cirrhosis.7 In cirrhosis, portal hypertension elevates lymph production and pressure, predisposing to lymphatic leakage. Malignancy should always be excluded due to its frequency in nonportal causes.7,9
On management, the portal-hypertension and ascites recommendations are routinely applied to cirrhosis-related chylous ascites; however, there are reviews that specifically address chylous ascites or lymphatic interventions. These include therapeutic paracentesis for symptomatic relief and dietary modification with a high-protein, low-fat diet enriched with medium-chain triglycerides, which are absorbed directly into the portal system and reduce lymph flow.10,11 Fat-soluble vitamin supplementation and orlistat may further limit chyle production. For patients who fail dietary measures or exhibit high-output ascites, total parenteral nutrition and bowel rest can help reduce lymphatic flow.7,10
Pharmacologic therapy with somatostatin analogs such as octreotide has demonstrated efficacy in decreasing lymph production and promoting resolution. Subcutaneous or intravenous administration at 100–200 µg/d, as adjunctive therapy, has been effective in several reports, even serving as a bridge to liver transplantation in advanced cases.1,11
In refractory or high-output chylous ascites unresponsive to medical therapy, interventional and surgical options should be considered. Transjugular intrahepatic portosystemic shunt effectively reduces portal and lymphatic pressures and has been associated with resolution of chylous ascites in cirrhotic patients.2,12 Liver transplantation offers definitive treatment in cases of cirrhosis-related chylous ascites refractory to medical and procedural interventions. Most post-transplant chylous leaks are self-limited and resolve with conservative management.8,13 This report contributes to the growing body of evidence on the effective treatment of chylous ascites and underscores the importance of individualized care. By highlighting a rare manifestation of portal hypertension and its resolution through a multimodal therapeutic strategy, we aim to bridge the gap between clinical challenges and innovative management.1

DISCLOSURES
Author contributions: JDC Clutario wrote the first draft of the original manuscript. MED Labio, JDC Clutario, and CP Velasquez conceptualized the study. JDC Clutario and SNL Chan contributed to manuscript editing. AJD Cruz critically appraised and approved the final manuscript before submission. JDC Clutario is the article guarantor.
Financial disclosure: None to report.
Previous presentation: Presented as oral presentation at Asian Pacific Association for the Study of the Liver (APASL); March 29, 2025; Beijing, China.
Informed consent was obtained for this case report.