The abnormal intraperitoneal accumulation of lymph resulting from extravasation into the abdominal cavity is defined as “chylous ascites” (CA) or “chyloperitoneum”.1 It is produced after the disruption or obstruction of thoracic or abdominal lymphatic circulation. Considered a rare entity, it has an incidence of approximately one case per 20,000 patients and is related to malignant (lymphomas), congenital, and inflammatory (acute pancreatitis) diseases.

A 61-year-old man had presented with severe acute pancreatitis complicated with a pancreatic pseudocyst one year earlier. He sought medical attention due to nausea and vomiting 5-6 times per day, increase in abdominal perimeter, and weight loss of 12 kg, of 4-month progression. He stated he had no dyspnea, orthopnea, or previous surgeries. Physical examination revealed poor general status; the patient was wasting (weight: 50 kg, height: 1.65 m, BMI: 18.3), dehydrated, with mild pallor, a nonpainful distended abdomen, a positive fluid wave, and no hepatic stigmata.

Laboratory tests showed mild anemia, hypoalbuminemia, and no alterations in blood chemistry, electrolytes, or liver function tests. In addition, fecal elastase was measured and found to be low (130 µg/g), and so treatment with pancreatic enzymes and a proton pump inhibitor was started in the context of a patient with exocrine pancreatic insufficiency.

Paracentesis revealed a whitish, milky fluid (Fig. 1) and its analysis (Table 1) showed a hyperintense serum ascites albumin gradient, with elevated proteins and triglycerides of more than 200 mg/dL, confirming the diagnosis of chylous ascites. Elastography was not carried out due to the presence of ascites, and the echocardiogram showed no alterations.

Figure 1.

Milky-appearing ascitic fluid.

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Magnetic resonance imaging of the abdomen identified a 95 x 110 x 95 mm collection (volume: 496 mL), dependent on the body and tail of the pancreas, and abundant free fluid. The liver and portal venous system appeared normal, and there was no adenomegaly (Fig. 2).

Figure 2.

A–B: Capsular hyperintense image, with partial septa in the body and tail of the pancreas, associated with abundant free fluid.

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Parenteral nutrition was started with a special regimen and enteral tube feeding with a low-fat diet and medium-chain triglyceride supplementation. Octreotide 100 mcg was administered subcutaneously every 8 h, and the milky peritoneal fluid became clearer, turning to citrine yellow.

The patient underwent percutaneous drainage of the pancreatic pseudocyst due to the lack of access to endoscopic ultrasound (EUS) at our hospital. A total of 500 mL of the pancreatic collection was extracted, leaving catheters in the pancreatic bed and peritoneal cavity, with progressively descending flows. The patient did not undergo surgery. His evolution was favorable, with improvement in tolerating oral intake and weight gain (a current IBM of 22), as well as tomographic evidence of reduced volume of the pancreatic collection and free fluid (Fig. 3).

Figure 3.

Multi-slice spiral computed tomography of the abdomen, with contrast. A) Pancreatic collection showing less volume than in previous images. B) Gastric chamber with adequate distension.

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The diagnosis of CA was made by consensus, with a concentration of triglycerides > 200 mg/dL in the ascitic fluid.2 Its origin is more frequently associated with portal hypertension, endothelial involvement, and rupture of dilated lymph channels. In causes not associated with portal hypertension (congenital, inflammatory, infectious, neoplastic, postoperative, and traumatic), lymphatic fluid is released by the dilated retroperitoneal vessels into the abdominal cavity through a fistula with the peritoneum.2,3

Inflammatory causes are reported to be associated with acute and chronic pancreatitis. Two mechanisms are reported in both: filtration through the lymph vessels damaged by pancreatic enzymes or lymph exudation due to flow obstruction secondary to inflammatory changes in the retroperitoneum adjacent to the pancreas. This usually occurs after days or weeks of presenting with pancreatitis.4,5

CA management depends on the etiology. Dietary measures include a high-protein low-fat (triglycerides) diet to prevent conversion into monoglycerides and free fatty acids, reducing lymph flow.2,6 For nonresponders, bowel rest is suggested to reduce the lymph flow and establish total parenteral nutrition.7

Concerning drugs, orlistat prevents the conversion of triglycerides into fatty acids in the intestinal lumen, whereas somatostatin and octreotide aid in inhibiting lymph fluid excretion.3,8

The invasive procedures include large-volume paracentesis, transjugular intrahepatic portosystemic shunt (TIPS) placement, and peritoneovenous shunt (PVS) placement. Paracentesis is carried out using pharmacologic and drug measures in patients with symptomatic ascites. PVS is an option for cases that are refractory to medical treatment, in which surgery is not indicated, albeit it has potential complications.9,10

In the case reported herein, multiple large-volume paracenteses were carried out, with partial symptom alleviation. Due to the recurrence of the ascites, percutaneous drainage of the pancreatic pseudocyst was performed. After this, and in addition to octreotide use and the dietary measures put in place, the patient progressed favorably, with significant improvement in oral intake, abdominal perimeter reduction, ascites clarification, and weight gain.

Identifying CA is important for providing specific and definitive treatment, including dietary, nutritional, and pharmacologic management, and correcting the underlying cause.