Pancreatic ascites is a somewhat rare entity. It results from persistent leakage of pancreatic secretions in the peritoneum from pancreatic duct injury. The severity of this condition varies widely, often depending on the location and degree of ductal injury and infection in the fluid. While mild cases of pancreatic ascites resolve spontaneously, persistent pancreatic ascites and infection are associated with significant morbidity and mortality. The mainstay of treatment is diverting pancreatic fluid away from the leakage to the small bowel with a pancreatic stent, allowing the leak to heal. Adjunct treatment includes medical therapy to decrease pancreatic exocrine secretions and salvage treatment with surgery. However, due to the low incidence of this condition, comparative studies with different treatment approaches are not available.
Minor pancreatic duct injuries are common in acute severe pancreatitis resulting in peripancreatic fluid collection. This fluid collection is often contained and results in pseudocyst formation. Pancreatic necrosis can cause major pancreatic duct injury. Leakage of pancreatic fluid into the necrosis delays resorption of walled off necrosis. A persistent internal fistula into peritoneum causes pancreatic ascites. The presence of a pseudocyst or walled off necrosis increases the odds of pancreatic ascites. Pancreatic fistula could result from a pancreatic duct injury from blunt abdominal trauma, ductal lithiasis, ampullary stenosis, or an iatrogenic cause. Iatrogenic causes of duct injuries include pancreatectomy, endoscopic retrograde cholangiopancreatography (ERCP), and pancreatic biopsy or fine-needle aspiration. Many cases remain idiopathic, and at times, the site of ductal disruption is unable to be found.
The epidemiology of pancreatic ascites is not well studied and has mostly been reported by smaller retrospective studies and case series. Males make up a majority of the cases (75% to 85%). Mean age is the fifth decade of life. A history of alcohol use disorder and gallstones are common.
Pancreatic ascites is due to leakage of pancreatic secretions into the peritoneum. Most often this occurs in the setting of a pseudocyst or walled off necrosis. Pseudocysts, in the setting of chronic pancreatitis, tend to have a less robust fibrinous wall and allow pancreatic secretions to leak from the disrupted duct, into the pseudocyst, and out into the peritoneum. At other times, pancreatic duct disruption without a pseudocyst will form a fistulous tract. Depending on the route of the fistula, fluid collections will manifest differently. Fistulas from an anterior pancreatic duct disruption allow for pancreatic secretions to empty directly into the peritoneum leading to ascites. Posterior pancreatic duct ruptures allow for fistula formation through the aortic or esophageal hiatus or sometimes through the dome of the diaphragm leading to pleural effusions. In either case, the ascites is typically exudative with high amylase activity. Some have attributed this exudative quality to the pancreatic fluid causing an inflammatory process leading to increased vaso-permeability.
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.
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.
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.
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