VOLUME 13 | ISSUE 4 | JULY 1993

Case Report Font size: Decrease font Enlarge font

Chylous Ascites: A Rare Complication of Liver Cirrhosis

Shahid Barlas, MRCP(UK); Abdullah Hussain Awad, FRCS(Ed); Khalid A. Khan, MD; Mamoon Ur Rashid Safdar, FCPS

From the Department of Medicine (Drs. Barlas and Safdar), Department of Surgery (Dr. Awad), and Department of Histopathology (Dr. Khan), King Fahd Hospital, Madinah Al Munawarah.

How to cite this article:

S Barlas, AH Awad, KA Khan, MUR Safdar, Chylous Ascites: a Rare Complication of Liver Cirrhosis. 1993; 13(4): 372-374


Chylous ascites is a rare condition. It often poses diagnostic and management dilemmas. The most common cause of chylous ascites is malignancy. Rarely has it been reported in association with cirrhosis of the liver. It is almost always refractory to medical therapy and carries a poor prognosis. A case of liver cirrhosis complicated with chylous ascites is presented herein. To the best of our knowledge, this is the first case report of this condition from the Middle East.




A 60-year-old male was admitted with a three month history of progressively increasing abdominal distention and discomfort. There was no loss of appetite and his bowel movements were regular. He denied any past history of jaundice or blood transfusion. On examination, he was mildly jaundiced, conscious, and oriented. His blood pressure was 110/70 mm/Hg, pulse 80/min and regular, and temperature 37.6°C. There was bilateral pedal edema. The abdomen was distended due to the presence of massive ascites. No abdominal viscera were palpable at this stage. There were no signs of chronic liver disease. Digital rectal examination was normal.


Laboratory workup revealed a hemoglobin of 14 g/dl, total white cell count of 6.4x109/L and a platelet count of 125xl09/L. Liver function tests were abnormal; albumin-globulin ratio was reversed advanced liver disease (Table 1). Urea, creatinine, and prothrombin time was elevated, all indicating electrolytes, fasting blood sugar, urine and stool analysis were all normal. He was negative for HBsAg and anti-HCV. Anti-HBc (type G) was positive, indicating previous infection with hepatitis B virus. Blood film was negative for microfilaria. Ultrasonography and computerized axial tomographic (CAT) scan of the abdomen revealed small, shrunken liver, splenomegaly, and massive ascites. No masses or lymph nodes were noted. CAT scan of the thorax was unremarkable. Abdominal paracentesis was performed and three liters of milky ascitic fluid were aspirated. Results of ascitic fluid analysis are shown in Table 2.


A few days later, diagnostic laparoscopic examination was performed. The liver was whitish, macronodular, and markedly shrunken. Tiny raised areas of subcapsular collection of chyle were noted. The spleen was enlarged. Peritoneum was normal, and no abnormal masses or lymph nodes were seen. Residual milky ascitic fluid was aspirated during the procedure. A Tru-Cut biopsy from the left hepatic lobe was taken and histopathological examination revealed the distortion of normal hepatic architecture. Pseudolobules were seen separated by thick fibrous bands; the fibrous capsule was thick and contained distended lymphatics.


All these features were highly suggestive of well established liver cirrhosis complicated with chylous ascites. The patient was treated with conventional measures which included bed rest, restricted salt intake, IV human albumin, Frusemide and spironolactone. His ascites remained refractory to these measures, necessitating repeated abdominal paracentesis. The possibility of liver transplantation was discussed with him and his family, to which they assented. However, after discharge from the hospital, he did not return for further follow-up.


Table 1. Laboratory Data.




Serum bilirubin

33.3 μmol/L

0.0 - 19.0


133 iu/L

0.0 - 37.0


82 iu/L

0.0 - 40.0


251 iu/L

98 - 279.0


20.70 g/L

35.0 - 55.0


39.0 g/L

25.0 - 32.0


21 seconds

13 seconds

S Triglycerides

0.86 mmol/L

0.55 - 2.3

S cholesterol

3.4 mmol/L


NV=normal values; AST=aspartate transaminase; ALK-P=alkaline phosphatase; PT=prothrombin time; S=serum.

Table 2. Ascitic fluid analysis. 




3.29 mmol/L

Total proteins

9 g/L



(98 % lymphocytes)

Gram stain






Cytology for

malignant cells


WCC=white cell count; AFB=acid fast bacilli.

Table 3. Important causes of chylous ascites.






Postoperative complication








Liver cirrhosis


Chronic lymphatic leukemia






Acute chylous peritonitis


Infantile chylous ascites



Chylous ascites is a rare condition and often poses diagnostic and management dilemmas. It occurs due to accumulation of lipid-rich lymph in the peritoneal cavity and is usually secondary to lymphatic obstruction or leakage. The diagnosis of chylous ascites is made on (1) a milky or creamy ascites; (2) an ascitic fluid triglyceride concentration higher than that of serum and/or higher than 1.5 mmol/1 [1]. Our patient had milky ascites with markedly elevated ascitic fluid triglycerides (3.29 mmol/1), fulfilling the diagnostic criteria.


Malignancy is the most common cause of chylous ascites [1,2]. Other reported causes are inflammation, trauma, congenital, liver cirrhosis, and idiopathic (Table 3). In cases of malignancy, the tumor is usually extensive. The most commonly encountered tumors are lymphomas and carcinoma of the pancreas and the stomach.


The inflammatory causes include pancreatitis, tuberculosis, mesenteric adenitis, and radiation. Post-traumatic chylous ascites is usually surgical in origin. It is an infrequent but alarming complication of abdominal surgery. It is occasionally encountered following operations on the abdominal aorta, mesocaval shunts, colectomy and vagotomy [3-6]. Chylous ascites may also be seen rarely (0.5%-1.0%) in uncomplicated cirrhosis [7,8]. In our patient, all clinical and laboratory data along with liver biopsy conclusively demonstrated the presence of liver cirrhosis. The possibility of underlying malignancy was ruled out by laparoscopy and CAT scanning of the thorax and abdomen. In cirrhosis of the liver, chyle accumulates in the peritoneum from the rupture of distended subserosal lymphatic channels and hepatic subcapsular lymphatics. Chylous ascites, when secondary to liver cirrhosis, is invariably refractory to medical therapy [8]. Diuretics and salt restriction are not of much value. Our patient did not respond to any of these measures and required frequent abdominal paracentesis to relieve abdominal discomfort resulting from rapid accumulation of chyle. Treatment with a low fat diet and medium chain triglycerides has been tried with response in some patients [8]. Peritoneovenous shunts have been used but were complicated by occlusion and infection [9].


Chylous ascites, when complicating cirrhosis, carries a poor prognosis and the one year mortality rate is 69% [1]. Hepatic transplantation should be considered in appropriately selected patients.



1. Sultan S, Pauwels A, Poupan R, Levy VG. Chylous ascites in adults: etiological, therapeutic, and prognostic aspects. Apropos of 35 cases. Ann Gastroent Hepatol Paris, 1990 Oct;26(5):187-91.

2. Kollerup GB, Mogensen S. Chylous ascites in adults: a review of etiology, physiopathology, diagnostic methods, and therapeutic possibilities. Ugeskr Laeger 1991;153(13):919-21.

3. Ablan CJ, Litooy FN, Freeark RJ. Postoperative chylous ascites: Diagnosis and treatment: a series report and literature review. Arch Surg 1990;125(2):270-3.

4. Williams RA, Vetto J, Quinones-Baldrich W, et al. Chylous ascites following abdominal aortic surgery. Ann Vasc Surg 1991;5(3):247-52.A

5. Al Mousaw M, Abu Nema T. Chylous ascites: a rare complication of vagotomy. Eur J Surg 1991; 157(2): 149-50.

6. Ohri SK, Patel T, Desa LA, Spencer J. The management of postoperative ascites, a case report and literature review. J Clin Gastroent 1990;12(6):693-7.

7. Rector WG Jr. Spontaneous chylous peritonitis of cirrhosis. J Clin Gastroent 1984;6:369.

8. Sultan S, Pauwels A, Poupon R, Levy VJ. Chylous ascites in cirrhosis: retrospective study of 20 cases. Gastroent Clin Biol 1990;14(11):842-7.

9. Kerr SC, Powis SJA, Ross JR, et al. Peritoneovenous shunt in the management of pediatric chylous ascites. Br J Surg 1985;72:443.


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