Milky ascitic fluid

CASE

A 71-year-old woman with a history of cirrhosis secondary to nonalcoholic steatohepatitis diagnosed 4 years ago, esophageal varices, hypertension, morbid obesity, and depression was transferred from an outside hospital due to shortness of breath, hematemesis, and hypotension. She reported having abdominal discomfort and abdominal distension but denied fever, melena, and hematochezia. Her initial vital signs showed blood pressure 108/72 mmHg, heart rate 104 beats per minute, respiratory rate 22 breaths per minute, and an oxygen saturation 95% on room air. She had a distended abdomen with a fluid wave and bilateral lower extremity edema. Laboratory tests included hemoglobin 9.0 g/dL (ref 11.2–15.7 g/dL), white blood cell count 7.51 k/µl (ref 3.98–10.04 k/µl), BUN 35 mg/dL (ref 6–20 mg/dL), creatinine 1.2 mg/dL (ref 0.5–1.2 mg/dL), and serum albumin 2.8 g/dL (ref 3.5–5.2 g/dL). Liver enzymes showed alkaline phos-phatase 146 IU/L (ref 35–129 IU/L), aspartate trans-aminase 36 IU/L (ref 5–37 IU/L), alanine transaminase 19 IU/L (ref 5–41 IU/L), total bilirubin 1.6 mg/dL (ref 0–1 mg/dL), and prothrombin time of 20.7 sec (ref 10.1–12.5 sec). Lipid profile showed serum triglyceride was 37 mg/dL (ref 50–200 mg/dL).

An abdominal paracentesis removed of 5 L of milky fluid (Figure 1). Ascitic fluid analysis revealed a yellow turbid fluid with a red cell count of 1,000/mm³, white blood cell count of 34/mm³ (neutrophil 10%, lymphocyte 70%, macrophages 20%), albumin 0.4 g/dL, amylase 10 U/L, glucose 164 mg/dL, protein 0.8 g/dL, and triglyceride 827 mg/dL. The serum-ascites albumin gradient (SAAG) was 2.4 g/dL. The Gram stain showed no white cells and no organisms, and the culture showed no growth after 5 days. After the paracentesis, her abdominal pain and her breathing improved. Esophagogastroduodenoscopy showed circumferential ulceration in the distal esophagus likely from post-variceal ligation ulceration and moderate portal hypertensive gastropathy in the entire stomach. Computed tomography (CT) of the chest, abdomen, and pelvis showed a hiatal hernia and hepatic cirrhosis with ascites. A CT of the neck with and without contrast showed no pathologic enlarged lymph nodes. A Doppler ultrasound of the abdomen showed portal hypertension with splenomegaly and ascites. She was treated with octreotide IV 100 µg daily for 9 days and discharged home. At 2 weeks follow-up, she was doing well and had no abdominal distension.

Figure 1. Abdominal paracentesis aspirated yellow-milky ascitic fluid.

DISCUSSION

Our patient had chylous ascites and SAAG 2.4 g/dL and ascitic protein 0.8 g/dL (<2.5) consistent with cirrhosis. Chylous ascites occurs when there is a disruption of the lymphatic channels from trauma or obstruction from malignancy. The etiology includes abdominal malignancy, lymphatic abnormalities, cirrhosis, and infectious etiologies (i.e., tuberculosis and filariasis). The nontraumatic causes of chylous ascites include lymphatic anomalies (32 percent), malignancy (17 percent), cirrhosis (11 percent), and miscellaneous causes.¹ About 0.5–1% of cirrhosis patients develop chylous ascites.² The pathophysiology of chylous ascites in these cases includes increased lymphatic pressure secondary to portal venous hypertension that leads to lymph stasis, lymphatic leakage, and lymphatic dysfunction (dilated subserosal intestinal lymphatics).² Chylous ascites may also develop after shunt surgery, thoracic duct injury, or hepatocellular carcinoma. Imaging studies include a CT of the abdomen, magnetic resonance lymphography, or lymphangiography to evaluate lymphatic obstruction or abnormalities and intra-abdominal lymph nodes or masses.

There is no definite treatment guideline for chylous ascites. Treatment includes conservative measures, such as a median chain triglyceride based diet, total parenteral nutrition, medical therapy such as somatostatin, and surgery in failed conservative treatment cases.^3,4 The mechanism of somatostatin is still not fully understood, but a previous study showed that somatostatin decreases intestinal absorption of fat and lowers triglyceride concentration in lymphatic system. In addition, it slows overall intestinal absorption and decreases splanchnic blood flow, which may decrease lymph production.⁴

Keywords: cirrhosis, chylous ascites, portal vein hypertension, triglycerides

REFERENCES

1. Steinemann DC, Dindo D, Clavien PA, et al. Atraumatic chylous ascites: systematic review on symptoms and causes. J Am Coll Surg 2011;212(5):899–905.e1–4. DOI: 10.1016/j.jamcollsurg.2011.01.010.
2. Kumar R, Anand U, Priyadarshi RN. Lymphatic dysfunction in advanced cirrhosis: Contextual perspective and clinical implications. World J Hepatol 2021;13(3):300–314. DOI: 10.4254/wjh.v13.i3.300.
3. Bhardwaj R, Vaziri H, Gautam A, et al. Chylous ascites: a review of pathogenesis, diagnosis and treatment. J Clin Transl Hepatol 2018;6(1):105–113. DOI: 10.14218/jcth.2017.00035.
4. Huang Q, Jiang ZW, Jiang J, et al. Chylous ascites: treated with total parenteral nutrition and somatostatin. World J Gastroenterol 2004;10(17):2588–91. DOI: 10.3748/wjg.v10.i17.2588.

Article citation: Songtanin B. Milky ascitic fluid. The Southwest Respiratory and Critical Care Chronicles 2023;11(49):59–60
From: Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, Texas
Submitted: 8/23/2023
Accepted: 9/13/2023
Conflicts of interest: none
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