Patients often will not present with symptoms suggestive of a chronic inflammatory process. Many patients will not have had previous episodes of acute pancreatitis or had previous episodes which occurred months to years before. Symptoms are usually increasing abdominal girth with mild abdominal discomfort. Weight loss may also occur due to loss of appetite despite fluid retention in the abdomen. Patients with concurrent pancreatic effusion will complain of a cough, chest pain, and increased dyspnea on exertion. A physical exam will often reveal a large volume of ascites with little to no abdominal tenderness. In some patients, erythematous lesions may exist on the extremities as a result of metastatic fat necrosis.

Diagnostic paracentesis should be performed, and fluid amylase and protein measurements should be measured along with cell count, culture, gram stain, and cytology. Pancreatic ascites is characterized by an amylase level over 1000 IU/L and protein level greater than 3 g/dL. The calculated serum-ascites albumin gradient (SAAG) is normally less than 1.1 g/dL. This distinguishes from ascites secondary to portal hypertension where amylase levels of ascitic fluid are not elevated, and fluid albumin levels are normally below 1.5 g/dL with a SAAG greater than 1.1 g/dL.

In patients where pancreatic ascites is suspected based on clinical features and peritoneal fluid assessment discussed above, further diagnostic workup includes endoscopic retrograde cholangiopancreatography (ERCP) and secretin augmented magnetic resonance cholangiopancreatography to determine the presence and site of the pancreatic duct leak. Use of ERCP for diagnosis also allows for intervention at the time of diagnosis as described below.[10][11][12]

Management of pancreatic ascites has three approaches: medical, endoscopic, and surgical intervention. A combination of these approaches is often used and clear superiority of one over another is not established.

Medical management consists of keeping the patient nothing by mouth and providing nutrition via total parenteral or nasojejunal route. Electrolyte imbalances often associated with active fistulous losses must be carefully managed. Somatostatin or octreotide are used to decrease the exocrine function of the pancreas and allow for healing of the disrupted duct, though their efficacy is questionable. For patients symptomatic from their ascites, repeated therapeutic paracentesis can be considered. A course of medical treatment for less severe cases is proposed since resolution without intervention can occur in approximately 30% to 50% of patients. The mainstay of management remains endoscopic therapy. A transpapillary stent at the pancreatic duct sphincter decreases intraductal pressure and diverts pancreatic secretion to the small bowel, thereby enhancing healing of the ductal disruption. Ideally, the ductal disruption should be bridged by the stent to maximize the outcome. In cases with large pancreatic necrosis, stenting through the disruption is challenging. In these cases, transpapillary stenting has shown a 48% to 100% success in controlling pancreatic ascites and distal pancreatic segment atrophies over time. Other endoscopic interventions include the use of injectable endoscopic glues or fibrinogen injections into the fistula to block further leakage of fluid into the peritoneum, though strong evidence is lacking for recommending their use. Overall, the endoscopic approach has shown promising results without the higher mortality and morbidity associated with a surgical approach.

The surgical approach to pancreatic ascites was formerly the standard of care in those failing medical therapy; however, now it is mostly reserved for failure of endoscopic intervention or for cases where there has been complete disruption of the pancreatic duct with no opacity proximal to the duct disruption on cholangiography. Surgical intervention must carefully weigh the risks and benefits for the individual patient. Specific surgical interventions depend upon the location of ductal disruption with distal lesions often being amenable to partial pancreatectomy if the remaining pancreatic volume is deemed likely able to carry out sufficient endocrine and exocrine function. More proximal lesions of the main pancreatic duct are often treated via pancreaticojejunostomy.

When considering the differential for ascites, it can often be helpful to determine the SAAG that can further guide the differential along with history, physical, and further testing. Pancreatic ascites occurs most often in those with chronic pancreatitis, and therefore, often coincides with a history of excessive alcohol use. In such cases, ascites secondary to increased portal pressure from cirrhosis must be considered. Other etiologies of cirrhosis as a cause of ascites in the absence of alcohol use should also be considered. While ascites from cirrhosis usually have a SAAG greater than 1.1, the presence of an infectious process can affect this ratio. Other processes with ascites and SAAG greater than 1.1 are hepatic vein occlusion (Budd Chiari), portal vein thrombosis, and right heart failure.

In new onset ascites with a SAAG less than 1.1, malignancy must be considered, keeping in mind that abnormal cytology of ascitic fluid in pancreatic ascites is sometimes due to a metaplastic response to the pancreatic fluid as opposed to a malignant process. Other differentials for abdominal ascites with SAAG less than 1.1 include peritoneal tuberculosis and nephrotic syndrome.

Overall prognosis in patients with pancreatic ascites has improved with the availability of endoscopic interventions. A course of conservative medical management leads to recovery in approximately 30% to 50% of patients. Endoscopic placement of a transpapillary stent appears to have a success rate of 82% to 100%. For those in whom medical and endoscopic management fail, a surgical approach is often taken with reported mortality ranging from 15% to 25%. Recent studies suggest that endoscopic management has reduced mortality, hospital length of stay, recurrence, and cost more than medical and surgical interventions alone.

Overall, pancreatic ascites usually can be managed effectively with the endoscopic placement of a transpapillary pancreatic duct stent, particularly when pancreatic duct rupture is evident. ERCP and placement of the stent carry an increased risk for acute post-procedural pancreatitis and guidewire complications during the procedure, leading to perforation. ERCP also carries with it an increased risk for cholangitis or an infected pseudocyst due to inoculation via instrumentation. Placement of a pancreatic duct stent can be challenging and is not always successful. Therefore the chance exists of exposure of the patient to ERCP without the benefit of stent placement. The stent itself can become blocked or infected and can migrate to distal portions of the pancreatic duct making it difficult to retrieve. Prolonged stent placement can lead to pancreatic changes similar to chronic pancreatitis, and it is suggested that the patient return for stent retrieval usually within 4 to 6 weeks. While recurrence of pancreatic ascites is thought to decrease with endoscopic intervention over that of medical intervention, there is a general lack of high-quality data in this area.

Acute severe pancreatitis can result in peripancreatic fluid collection leading to a pseudocyst. If the cyst becomes necrosed it might cause pancreatic duct injury subsequently leading to fluid that might leak through a fistula and cause ascites. Keeping in mind that the most common causes of pancreatitis are modifiable causes: Alcohol use disorder and gallstones. Limiting alcohol intake and leading a healthy lifestyle might prevent the development of pancreatitis and its complications. 

Eating a healthy diet, exercising might prevent the development of gallstones and limiting the intake/abstaining of alcohol can limit the development of pancreatitis and its complications.

• Pancreatic ascites occurs when pancreatic secretions collect in the peritoneum as a result of a pancreatic duct injury. It most often follows necrotizing pancreatitis with major pancreatic duct injury or via fistula formation which communicates with the peritoneum.
• Chronic pancreatitis is the most significant risk factor for the development of pancreatic ascites.
• Diagnostic workup includes paracentesis which characteristically shows amylase levels greater than 1000 U/L and a SAAG greater than 1.1, consistent with an exudative process. Gold-standard of diagnosis is ERCP with cholangiography showing pancreatic duct disruption.
• Management of mild disease without visible pancreatic duct disruption on pancreaticogram often can be treated with a trial of medical management consisting of nil-per-os, total parenteral or nasojejunal feeding, and octreotide or somatostatin. More severe disease with visible pancreatic duct disruption often requires ERCP with transpapillary stent placement which should bridge the ductal disruption. Salvage therapy with surgical pancreatectomy is rarely needed.
• While high-quality evidence is lacking, endoscopic intervention seems to decrease hospital length of stay and improve mortality and morbidity when compared to medical or surgical management.

Once pancreatic ascites is suspected based on history and physical as well as diagnostic paracentesis results and CT of the abdomen, consultation with a gastroenterologist will be required. At that time, the specialist may determine interventional versus medical management. An interventional gastroenterologist consultation will be required in the case that ERCP with cholangiography is needed to make the diagnosis of pancreatic duct disruption or if pancreatic duct stenting is required either for drainage of a pseudocyst or for bridging the pancreatic duct leak. Guidance of an interventional gastroenterologist will also be required in cases of complete pancreatic duct disruption to conduct ERCP with cholangiography for planning the surgical intervention. These patients often need prolonged follow up by the primary care provider and nurse practitioner who also try and maintain adequate nutrition.

The overall prognosis for patients with pancreatic ascites depends on the cause. While endoscopic intervention has helped improve the quality of life in some patients, the success rates do vary. Recent studies suggest that endoscopic management has reduced mortality, hospital length of stay, recurrence, and cost more than medical and surgical interventions alone.[1][13]