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Korean J Pancreas Biliary Tract. 2026;31(3):126-132

Publication date (electronic) : 2026 July 31

doi : https://doi.org/10.15279/kpba.2026.31.3.126

Yumun Jeong¹, Tae Young Lee², Minjung Seo³, Sungjo Bang¹, Hoonsub So^,1

¹Department of Internal Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea

²Department of Radiology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea

³Department of Nuclear Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea

정유문¹, 이태영², 서민정³, 방성조¹, 소훈섭^,1

¹울산대학교 의과대학 울산대학교병원 내과

²울산대학교 의과대학 울산대학교병원 영상의학과

³울산대학교 의과대학 울산대학교병원 핵의학과

Corresponding author : Hoonsub So Department of Internal Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, 25 Daehakbyeongwon-ro, Dong-gu, Ulsan 44033, Korea Tel. +82-52-250-7029 E-mail: hoon3112@gmail.com

Received 2026 April 9; Revised 2026 April 29; Accepted 2026 May 7.

Abstract

Trans Abstract

INTRODUCTION

Chylous ascites is defined as the accumulation of lipid-rich lymphatic fluid within the peritoneal cavity and presents as turbid or milky peritoneal fluid with elevated triglyceride content. A triglyceride concentration greater than 200 mg/dL in ascitic fluid is commonly used as a diagnostic threshold. Chylous ascites is a rare clinical condition and its incidence has been reported to be approximately 1 in 20,000 hospital admissions [1]. The causes of chylous ascites are mainly malignancies, cirrhosis, and complications of abdominal surgery in most cases, whereas pancreatitis is an uncommon cause. Here, we report a rare case of chylous ascites with chylothorax associated with chronic alcoholic pancreatitis and was successfully managed with pancreatic duct stenting with other conservative treatment.

CASE

A 40-year-old male presented to the emergency department with a 7-day history of epigastric pain and progressive abdominal distension. His medical history was notable for hypertension, major depressive disorder, and a previous episode of acute pancreatitis two years earlier. The patient reported heavy alcohol consumption (1-2 bottles of soju, six times per week for 15 years, approximately 120-180 g of ethanol per day) and a 10 pack-year smoking history. The patient’s initial vital signs were as follows: blood pressure 129/99 mmHg, pulse rate 112 beats/min, respiratory rate 16/min, and body temperature 36.4°C. The body mass index was 15.25 kg/m². On physical examination, the abdomen was tender and distended. Initial laboratory findings revealed leukocytosis (white blood cell count 20,900/μL), elevated C-reactive protein level (7.69 mg/dL), and markedly elevated pancreatic enzymes (amylase 1,764 U/L; lipase 1,079 U/L). Liver function tests were not suggestive of cholestasis or hepatitis (total bilirubin 0.2 mg/dL; aspartate aminotransferase/alanine aminotransferase 28/7 IU/L). Serum albumin was 3.6 g/dL.

Portal venous phase computed tomography (CT) demonstrated a large volume of ascites with attenuation close to that of water (approximately 10-15 Hounsfield unit). The pancreas showed marked dilatation of the main pancreatic duct, suggestive of underlying chronic pancreatitis. Three-dimensional magnetic resonance cholangiopancreatography demonstrates marked dilatation of the main pancreatic duct with focal stricture at the pancreatic head and two pancreatic head pseudocysts measuring 2.4 cm and 1.8 cm, respectively (Fig. 1).

Fig. 1.

Initial imaging findings. (A) Abdominal CT image showed a large amount of ascites and marked dilatation of the main pancreatic duct. (b) Threedimensional MRCP demonstrated marked dilatation of the main pancreatic duct with focal stricture at the pancreatic head and two pancreatic head pseudocysts measuring 2.4 cm and 1.8 cm, respectively. CT, computed tomography; MRCP, magnetic resonance cholangiopancreatography.

Diagnostic paracentesis performed on admission showed yellow, slightly turbid fluid. Ascitic fluid analysis showed white blood cell count was 4,000/μL, total protein 3.4 g/dL, albumin 2.0 g/dL, triglyceride 54 mg/dL, and amylase 22,327 U/L. The serum–ascites albumin gradient was 0.2, supporting a non-portal hypertensive ascites and strongly suggesting pancreatic ascites.

Since the clinical manifestation suggested stricture of pancreatic duct with acute exacerbation of pancreatitis, endoscopic retrograde cholangiopancreatography (ERCP) with endoscopic retrograde pancreatic drainage (ERPD) was attempted to relieve the main pancreatic duct stricture. However, selective cannulation of the main pancreatic duct was unsuccessful despite two ERCP attempts, and ERPD placement failed. Two weeks after admission, a fully covered self-expandable metal stent (FC-SEMS) was successfully inserted using an endoscopic ultrasound-guided rendezvous technique (Fig. 2).

Fig. 2.

EUS-guided rendezvous technique for pancreatic duct access. (A) A guidewire was advanced into the duodenum to facilitate pancreatic duct cannulation during ERCP. (b) Placement of an FC-SEMS (6 mm×7 cm) across a stricture in the pancreatic head. EUS, endoscopic ultrasound; ERCP, endoscopic retrograde cholangiopancreatography; FC-SEMS, fully covered self-expandable metal stent.

Given persistent symptoms and ongoing large-volume ascites, peritoneal drainage with a pigtail catheter was performed for symptomatic control. On hospital day 18, follow-up ascitic fluid showed decreased pancreatic enzymes (amylase 42 U/L; lipase 28 U/L) but increased triglyceride (230 mg/dL). However, the TG level was not initially recognized, and the pigtail catheter was removed after symptomatic improvement. The patient was discharged.

One month after discharge, the patient was readmitted for follow-up ERCP and scheduled pancreatic stent exchange. At that time (on day 54 from the first admission), CT revealed ascites and pleural effusion. Grossly, both ascitic and pleural fluids appeared milky (Fig. 3). Ascitic fluid triglyceride was 963 mg/dL (total cholesterol 97 mg/dL), and pleural fluid triglyceride was 1,056 mg/dL (total cholesterol 81 mg/dL), confirming chylous ascites and chylothorax. Serial ascitic fluid analysis results are summarized in Table 1. During ERCP, the metal stent was removed and changed to plastic pancreatic stents. The patient was managed with fasting and total parenteral nutrition, which led to a gradual decrease in ascites and pleural effusion. On hospital day 6 of the second admission, both ascites and pleural effusion had improved, and the patient was started on a low-fat, high-protein diet and discharged.

Fig. 3.

Milky appearance of ascitic and pleural fluids consistent with chylous ascites and chylothorax.

Table 1.

Serial follow-up results of ascitic fluid analysis

At outpatient follow-up approximately three weeks after discharge, both ascites and pleural effusion had resolved. Lymphoscintigraphy using Tc-99m Phytate showed no abnormal tracer activity in the abdominopelvic cavity (Fig. 4). At 5-month follow-up, CT demonstrated resolution of main pancreatic duct dilatation and disappearance of the pancreatic head pseudocyst with only minimal residual ascites.

Fig. 4.

Lymphoscintigraphy of the lower extremities using Tc-99m phytate does not showed no evidence of lymphatic leakage on 1- and 2-hour post-injection images.

DISCUSSION

Chylous ascites is a rare clinical entity characterized by the accumulation of triglyceride-rich lymphatic fluid within the peritoneal cavity. The most common etiologies include malignancy, cirrhosis with portal hypertension, and infectious diseases. Pancreatitis-associated chylous ascites is extremely rare, accounting for only approximately 4% of cases in a previous review [2].

According to our review of the literature, 13 case reports have been published during the past 10 years (2016-2025) describing chylous ascites secondary to pancreatitis (Table 2) [3-15]. Among the 13 reported cases, the median age was 59 years (range, 15-73 years), and 9 patients (69.2%) were male while four (30.8%) were female. Chylous ascites was attributed to biliary pancreatitis and idiopathic pancreatitis (each n=6, 46.2%), and alcoholic pancreatitis (n=1, 7.7%). Five cases (38.5%) were associated with necrotizing pancreatitis or pancreatic pseudocysts while five (38.5%) involved vascular thrombosis or stenosis of the portal, splenic, or superior mesenteric vein.

Table 2.

Summary of case reports (2016-2025) describing pancreatitis-associated chylous ascites

Several mechanisms have been proposed to explain the development of chylous ascites in patients with pancreatitis. First, direct injury to the lymphatic system may occur due to pancreatic enzyme–mediated inflammation or necrosis. In severe or necrotizing pancreatitis, extensive retroperitoneal inflammation can disrupt lymphatic channels, resulting in leakage of chyle into the peritoneal cavity [3]. Second, inflammatory masses such as pancreatic pseudocysts or walled-off necrosis may mechanically compress adjacent lymphatics, leading to obstruction and subsequent chyle leakage. This mechanism has been described particularly in cases of severe necrotizing pancreatitis accompanied by large fluid collections [4,5]. Third, pancreatitis-related vascular complications may contribute to the development of chylous ascites through the induction of portal hypertension. Vascular thrombosis and non-cirrhotic portal hypertension are well-recognized complications of pancreatitis. Stenosis or thrombosis of the spleno-mesenterico-portal axis can increase lymphatic pressure, promoting lymphatic leakage into the peritoneal cavity [6-8]. In the present case, the initial ascitic fluid analysis showed a low serum-ascites albumin gradient (0.2) and markedly elevated amylase levels (22,327 U/L), which were diagnostic of pancreatic ascites resulting from pancreatic ductal disruption. However, the subsequent development of chylous ascites—characterized by an increase in triglyceride levels despite the resolution of amylase— suggests a multifactorial mechanism. This temporal shift indicates that the clinical presentation evolved from a pure ductal leak to a complex state of lymphatic transudation.

The diagnosis of chylous ascites is made based on the paracentesis. Turbid ascites with a triglyceride level of >200 mg/dL is considered diagnostic of chylous ascites. Lymphoscintigraphy may also be used to detect lymphatic leakage, such as chylous ascites, chylothorax, and post-surgical leaks, especially when other imaging fails [16]. Particle materials, such as Tc-99m phytate or sulfur colloid, are injected in the interstitial space and are preferentially taken up by the lymphatic system. Subsequent gamma camera imaging allows for the non-invasive visualization of lymphatic flow and studies have reported a detection rate of 64-86% for leakage sites in chylous ascites, which may be higher in patients with a higher flux of chyle leak. Although lymphoscintigraphy is a simple non-invasive modality that can confirm the presence of chylothorax and chylous ascites, ascertaining the exact site of leak is difficult on routine planar lymphoscintigraphy images. The combination of single-photon emission computerized tomography (SPECT) and CT overcomes this limitation and allows more precise anatomical localization of the leakage site [17]. In our case, lymphoscintigraphy obtained 3 weeks after diagnosis of chylous ascites, and did not show any evidence of active lymphatic leakage, reflecting clinical improvement and suggesting resolution of lymphatic leakage at the time of scanning. SPECT/CT images had not been obtained, which may have provided a more sensitive detection.

In general, chylous ascites is often successfully managed with conservative therapy. This typically includes a low-fat, high-protein diet supplemented with medium-chain triglycerides, which reduce lymphatic flow from intestinal fat absorption. Total parenteral nutrition or pharmacologic therapy such as somatostatin analogues may also be used to decrease chyle production and facilitate healing of lymphatic leaks. Although the exact mechanism of somatostatin analogues is not fully understood, somatostatin reduces portal pressure and lymphatic flow by inhibiting splanchnic vasodilation, intestinal peristalsis and intestinal fat absorption [18]. However, the optimal management of chylous ascites requires addressing the underlying cause. In our review, among the five cases with spleno-mesenterico-portal axis thrombosis or stenosis, three showed resolution of chylous ascites following venoplasty [6-8]. In another case with a large pancreatic pseudocyst, chylous ascites did not improve despite treatment with a low-fat diet and octreotide, but resolved after drainage of the pseudocyst [5]. Therefore, when an underlying condition such as a large pseudocyst, complicated necrotizing pancreatitis, or pancreatitis-associated venous insufficiency is present, conservative therapy alone may be insufficient. In such situations, additional interventions targeting the underlying cause may facilitate resolution of chylous ascites.

Chronic pancreatitis with pancreatic duct disruption appears to be a relatively uncommon cause of chylous ascites, and its occurrence remains uncertain. In a case reported in 2018, a 15-year-old patient with idiopathic chronic pancreatitis developed chylous ascites that was refractory to conservative treatment but resolved after ERCP with main pancreatic duct stent insertion [9]. In our case, the patient also had underlying chronic alcoholic pancreatitis prior to the development of chylous ascites. In addition to conservative measures such as low-fat diet and total parenteral nutrition, ERCP with pancreatic duct stent insertion was performed, which appeared to contribute to the resolution of ascites. These findings suggest that, in selected cases, pancreatic duct decompression may contribute to the resolution of chylous ascites by improving pancreatic inflammation and reducing lymphatic leakage. Accordingly, in patients with pancreatitis-related chylous ascites, ERCP may be considered as a therapeutic option when pancreatic duct obstruction is suspected.

In conclusion, we report a case of chronic alcoholic pancreatitis complicated by chylous ascites that was successfully treated with pancreatic duct stenting to bridge the ductal disruption in combination with conservative management. These findings suggest that addressing the underlying cause, in addition to conservative therapy, may facilitate resolution of chylous ascites.

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