Pancreatic ascites
CLINICAL COMPLEXITIES AND DIAGNOSTIC CHALLENGES IN PATIENTS WITH SUSPECTED PANCREATIC ASCITES
Abstract
Introduction:This paper presents 6 cases with suspected pancreatic ascites . The purpose of this paper is to study the clinical course ,various clinical complexities, diagnostic uncertainties and challenges posed during the hospital stay of each of these patients.
Methodology:Clinical analysis of case series of 6 patients with suspected pancreatic ascites.
Conclusion:Although our data is limited each case has tought us a complex feature of pancreatic ascites.The learning points and conclusions drawn from this case series are that Pancreatitis with normal serum amylase and lipase is possible ,The existence of pleuro peritoneal connections is possible which can cause pleural effusion with analysis similar to the ascitic fluid analysis.Tubercular or malignancy ascites can mimic pancreatic ascites posing a diagnostic challenge.Radiological confirmation of pancreatitis is superior to serum amylase and lipase.Integrated approach and active participation by Gastroenterologists,General physicians,Surgeons and Radiologists is required for proper diagnosis and evidence based approach to management of pancreatitis and pancreatic ascites.
Key words:Pancreatic ascites,Pancreatic fistula,Tubercular ascites,Pleuro peritoneal connections ,Pseudocyst of pancreas,Magnetic resonance cholangiopancreatography,Endoscopic retrograde cholangiopancreatography.
Introduction
Pancreatic ascites results from a pancreatic duct injury, leading to persistent leakage of pancreatic secretions into the peritoneum.It is rare and should be suspected in patients with chronic alcoholism and pancreatitis presenting with ascites.
History and physical examination :
Patients usually present with a history of pancreatitis or chronic alcoholism.They present with Increasing abdominal girth, pain abdomen,loss of appetite,Vomitings,Nausea.Patients with concurrent pleural effusion can have Chest pain,dyspnea,Cough.Physical examination reveals moderate to massive ascites with mild or no epigastric tenderness.
Evaluation:
The required tools for evaluation are high serum amylase ,serum lipase.Diagnostic abdominal paracentesis should be performed and sample should be sent for ascitic amylase levels,Albumin levels to calculate SAAG along with ascitic cell count,cytology,ascitic total protein,culture and gram stain.Ascitic analysis usually shows raised ascitic amylase, low SAAG(non portal hypertensive), exudative ascites with high total protein and ascitic cell count. 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.In cases of suspected pancreatic ascites based on clinical and diagnostic paracentesis Radiological investigations such as ultrasonography,CT abdomen and Magnetic resonance cholangiopancreatography will be required to have a look at the detailed anatomical pathologies such as pseudocyst,pancreatic necrosis and pancreatic fistulas and also to confirm pancreatitis.
Treatment:
A combination of bowel rest, nasojejunal feeding,pain management,subcutaneous octreotide, endoscopic drainage and rarely, surgery are employed in managing this difficult to treat condition.
CASE 1:
A 31 year old male patient who is alcoholic with no known comorbidities presented to the casualty with complaints of Pain abdomen,vomitings and Shortness of breath.On physical examination patient was found to have shifting dullness of abdomen.Intial evaluation was done with serum amylase,Lipase and ultrasonography .Serum amylase was 38IU/L,Serum lipase was 57IU/L.Diagnostic abdominal paracentesis revealed a cell count of 600 with 70% lymphocytes,Ascitic fluid culture showing no growth,SAAG -0.5 suggesting a non portal hypertensive ascites,Ascitic fluid total protein-4.0g/dl and ascitic fluid amylase was 78Iu/L, Ascitic fluid ADA was 9IU which lowers the probability of Kochs.USG abdomen showing features suggestive of acute pancreatitis with pancreatic tail obscured and head and body having altered echotexture,Moderate ascites.In view of diagnostic dilemma due to normal serum lipase and continuous pain abdomen Contrast enhanced CT abdomen was done which showed acute necrotising pancreatitis with 100% necrosis,Moderate ascites.Patient was kept on nothing by mouth,Pain management,antibiotics and Later as the patient developed acute kidney injury 4sessions of hemodialysis were done.Patient was symptomatically better at the time of discharge and after 6months of follow up.This patient improved with conservative treatment alone.
CECT abdomen report and images
CASE 2:
A 33 year old male patient who is an alcoholic with no comorbidities presented to the casualty with pain abdomen,Vomitings ,fever and shortness of breath.Physical examination revealed tachycardia,Tachypnea,Fever.mild ascites and epigastric,umbilical area tenderness.So intial evaluation was done with complete blood picture,Renal function tests,serum amylase,lipase and ultrasound abdomen.Leukocytosis(21,300cells/cumm) was present with normal Renal function tests.Serum amylase and lipase were 587 and 690 respectively suggesting pancreatitis and USG abdomen also revealed the presence of pancreatic psuedocyst.Contrast enhanced CT abdomen was done which showed features suggestive of Acute on chronic pancreatitis,Large pseudocyst compressing stomach,Multiple fluid collections.Chest x ray showed left sided moderate pleural effusion.Diagnostic pleural tap was done which showed exudative type of pleural effusion with raised pleural fluid amylase of 469.Surgical Drainage of the pseudocyst was considered as it is very large and compressing the stomach.Surgical drainage of pseudocyst was done on day 3 of admission.The pseudocyst was drained per cutaneously per abdominally under local anaesthesia with USG guidance and malecot drain placed inside and pus was drained.Also 2 other USG guided drains were placed for the Peri pancreatic collections per cutaneously per abdominally.Following a day after the placement of the drain patient had dramatically improved with reduced fever spikes and the total leukocyte count has dropped from 30.000 to 18,000 cells/cumm,but in the mean time patient had developed left sided pneumothorax,suspected iatrogenic pneumothorax after pleural procedure.Intercoastal drainage was placed.The pneumothorax slowly resolved over time.The peri pancreatic fluid and pseudocyst fluid were sent for analysis which showed a cell count of 890cells(60% neutrophils),total protein-4g/dl,SAAG -0.9 suggesting a non portal hypertensive etiology for the fluid collections,Ascitic amylase was high(448Iu),Culture showed E.Coli growth sensitive to Amoxicillin with clavulinic acid and Meropenem .Patient was intiated on Meropenem,IV fluids,Pain management,Nothing by mouth ,Total parenteral nutrition and inj Octreotide .Patient improved and was discharged after removal of ICD and drains on day 12 of admission with stable vitals and with no fever,tachycardia,tachypnea and leukocytosis.Patient reported that he is symptomatically better 5days after discharge He reported to be asymptomatic and abstinent from alcohol during a on phone follow up after 6months.
CASE 3:
A 30 year old male alcoholic, came to the casualty with chief complaints of pain abdomen since 2days following alcohol binge,Shortness of breath since 1 day.He had similar complaints previously when he was admitted and treated for pancreatitis.Physical examination revealed epigastric tenderness,reduced breath sounds (right more than left).Initial evaluation showed no leukocytosis,normal renal and liver function tests.Serum amylase was mildly elevated -179IU/L,Serum lipase was 3,732IU/L,USG abdomen showed grade 2 fatty liver, pancreas obscured due to bowel interposition,minimal perihepatic free fluid,mild ascites.Ascitic tap was tried under ultrasound guidance but the fluid was very minimal to perform a diagnostic paracentesis.So the ascitic fluid could not be evaluated.Chest x ray showed gross right sided pleural effusion.Therapeutic Pleural tap was done(1litre) and was sent for which showed pleural fluid protein-5.5,Pleura fluid LDH-1,218IU/L.According to Lights criteria the pleural fluid is exudative as Serum protein/pleural fluid ratio was 6.9/5.5=1.25 and Serum LDH/Pleura fluid LDH ratio was 368/1218=0.3.As the protein ratio is more than 0.5 the pleural fluid is considered exudative.Pleural fluid amylase and lipase were found to be very high-4,720 IU/L and 3,732IU/L respectively.Contrast enhanced CT abdomen was done for a better visualisation of pancreas which showed Multiple small coarse calcifications in uncinate process of pancreas,Mild MPD dilatation with peri pancreatic stranding,Mild ascites.Small cystic fluid collections around the head and neck of pancreas with a linear tract like extension upto the right pleural cavity suggesting a pancreatico pleural fistula.Superior mesentric vein and splenic vein showed chronic thrombosis.Large pleura effusion causing compression collapse of right lung,Blood ilots within the pleural effusion,Moderate high density left pleural effusion.The pleural effusion was rapidly refilling inspite after the therapeutic drainage also.So,Placement of ICD was considered but patient has left against medical advice as they were having affordability issues and was lost to follow up
| Chest x ray showing gross right pleural effusion secondary to pancreatico pleural fistula. |
| CECT abdomen reports |
CASE 4:
A 65 year female alcoholic with no known comorbidities presented to the casualty with abdominal distension since 6days and shortness of breath since 6 days.Physical examination revealed shifting dullness of abdomen.Initial evaluation showed raised serum amylase and lipase ,548 and 289 respectively.Diagnostic abdominal paracentesis revealed a cell count of 3750(70% neutrophils),total protein-4.3g/dl,SAAG-0.7,Ascitic amylase 333,ADA-19.Contrast enhanced CT abdomen was not done due to AkI .Patient was taken to other hospital by one of our doctors for MRCP.After MRCP patient was brought back to our hospital.After returning patient had suddenly complained of shortness of breath and collapsed just over few seconds.She had sudden cardiac arrest.CPR and other resuscitative measures were done but of no use unfortunately.Post MRCP pulmonary air embolism was suspected to be the cause of death in this patient.Pancreatic ascites was suspected in this patient because of raised serum amylase,lipase,low SAAG and raised ascitic amylase but MRCP to our surprise showed normal size,contour of pancreas and normal pancreatic duct.It showed gross ascites with severe diffuse Omental thickening with caking in upper and mid abdomen suggesting Omental biopsy with suspicion of kochs
MRCP REPORT
Case 5:
66 year old male patient alcoholic and no known comorbidities presented to the OPD with chief complaints of Pain abdomen since 7days,Abdominal distension since 1 month,Decreased appetite and urine output.Physical examination showed revealed fluid thrill and no tenderness per abdomen.Initial evaluation showed high serum amylase and lipase,1098IU and 514IU respectively.Diagnostic abdominal paracentesis was done which revealed cell count of 1155(80% neutrophils),total protein-3.9g/dl,SAAG-0.5 suggesting a non portal hypertensive ascites,ADA-13IU.Ascitic amylase is as high as 4761.USG abdomen showing gross ascites and pancreas obscured by bowel .Contrast enhanced CT abdomen showed severe ascites,Pancreatic calcifications,small pancreatic cyst,Omental thickening and mesentric lymphadenopathy.Patient was adviced for MRCP suspecting a pancreatic fistula and Omental biopsy to rule out kochs ,but were not done because of affordability issues.He was kept nothing by mouth,IV fluids,Pain management and antibiotics.Patient was discharged with stable vitals after the abdominal distension has decreased to some extent.After 1 month of on call follow up we came to know that the patient has expired.
| CECT abdomen report of 66 year old male |
Case 6:
50 year old male patient alcoholic and with no known comorbidities came to the OPD with chief complaints of abdominal distension,loss of appetite,shortness of breath and pedal oedema.Physical examination showed pallor,Pedal oedema,dilated abdominal veins with flow of blood away from the umbilicus and shifting dullness on per abdomen examination.Provisional diagnosis considered was
1.Ascites secondary to Chronic liver disease looking at the dilated abdominal veins with flow away from the umbilicus
2.Pancreatic ascites with pancreatitis secondary to alcohol.Initial evaluation revealed mild Leukocytosis -14000cells/cumm,normal Renal function tests,hypoalbuminemia of 2.0gm/dl,normal Total bilirubin and liver enzymes,Mild deranged PT,INR(16seconds,1.7 respectively) suggesting a chronic liver disease.USG abdomen showed altered echotexture with surface irregularity in liver suggesting a chronic liver disease,Pancreas obscured by bowel,Moderate ascites.Diagnostic paracentesis was done which showed 50cells,total protein-2.2g/dl,SAAG-0.95,low SAAG contrary to the provisional diagnosis made,that is non portal hypertensive ascites.Ascitic fluid amylase was very high -9,614 IU/L,ADA was normal-23 IU/L.As Ascitic amylase was very high pancreatic ascites was suspected and serum amylase and lipase levels were sent ,which showed high serum amylase and lipase 1184 IU/L and 364 IU/L respectively.Pancreatic ascites with underlying Chronic liver disease was considered and contrast enhanced CT abdomen was done.CT abdomen showed gross ascites with diffuse omental haziness,Unicinate process of pancreas showing mild heterogeneous enhancement with peri pancreatic fat stranding and few parenchymal calcifications suggesting acute on chronic pancreatitis,Mild quadrate lobe hypertrophy with mild irregular margins which were features suggestive of early chronic liver parenchymal disease.Patient was kept nil by mouth,pain management was started.As his ascitic amylase is very high suspecting pancreatic fistula patient was referred to higher centre.Due to affordability issues patient did not get a ERCP done .At an outside hospital patient was placed on naso jejunal tube and followed by confirmation of the position as beyond second part of duodenum.Upper GI endoscopy showed no varices.He was kept on Naso jejunal feeds and therapeutic paracentesis of 1.5litres was done.He was discharged as his abdominal circumference has come down.2 days after discharge patient started to have altered sensorium and was taken to the same hospital where he was initiated on continuous Renal replacement therapy in view of Acute kidney injury.The next day patient had sudden cardiac arrest and was revived after CPR ,was kept on mechanical ventilator for few hours after which patient had expired.
| CECT abdomen images |
Dilated abdominal veins over abdomen
DISCUSSION :
This limited study with 6 cases was done in our hospital which is a low resource setting with an existing framework of CBBLE .Pancreatic ascites occurs due to varied pathophysiologies which includes
1.Minor pancreatic duct injury
2.Association with Pseudocyst
3.Necrotising pancreatitis with major pancreatic duct injury
4.Pancreatic fistula which communicates with the peritoneum
A detailed analysis of the patients events and investigations provided us with new insights and learning points about pancreatic ascites
Case discussion:
Case 1:
31 year male with acute necrotising pancreatitis with 100% necrosis and moderate ascites who had normal serum amylase, lipase and ascitic amylase.
The cause of pancreatitis is alcohol and the cause of pancreatic ascites in this patient is the pancreatic necrosis
Here are the 2 cases which were previously reported as pancreatitis with Normal serum amylase and lipase which is usually a rare entity.A 49 year old male who was initially treated only for gastritis because of Normal serum amylase and lipase inspite of severe pain and epigastric tenderness which later was evaluated with CT abdomen which showed acute inflammation of the pancreas and peri pancreatic fat without necrosis or free fluid.A 43 year old male admitted with pain abdomen and has hypertriglyceridemia.Patient had Normal serum amylase and lipase but CT revealed acute inflammation of the pancreatic tail and peri pancreatic fat and was diagnosed with acute pancreatitis secondary to hypertriglyceridemia.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4882216/
Case 2:
33 year male with Acute on chronic pancreatitis, Large pseudocyst which was drained and left exudative pleural effusion. The pancreatic ascites in this patient is contained to form pancreatic pseudocyst and the cause of his pleural effusion could be due to pleuro peritoneal connections.
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
Pancreatic pseudocyst are localised fluid collections as a result of acute or chronic pancreatitis.These structures are surrounded by fibrous and granulation tissue and contain fluid rich in amylase and other pancreatic enzymes. The pseudocysts appear to arise from an insult to the pancreatic duct leading to extravasation of pancreatic secretions. Pseudocysts occur in 25% of patients with chronic pancreatitis and has been observed more commonly in alcohol aetiology. Large pseudocysts can cause compression of adjacent structures leading to various complications and will warrant aggressive management.
https://casereports.bmj.com/content/2018/bcr-2018-226296#ref-1
In a longitudinal study by Mehta et al, cyst >7.5 cm or >250 mL needs either surgical or endoscopic intervention.Spontaneous rupture of pancreatic pseudocysts has been reported in <5% of cases.
Citation: Mehta R, Suvarna D, Sadasivan S, et al.Natural course of asymptomatic pancreatic pseudocyst: a prospective study. Indian J Gastroenterol 2004;23:140–2
Pleural effusion secondary to congenital pleuro peritoneal connections or pancreatico pleural fistula was considered because of the exudative nature and high pleural fluid amylase similar to ascitic fluid without any heart failure.ERCP or MRCP can establish this connection but was not done for this patient.
Pleuro peritoneal communication is caused by congenital or acquired diaphragmatic defects because of an elevated intra‐abdominal pressure. Recently, technetium‐99m peritoneal scintigraphy has been utilized for the definitive diagnosis of pleuroperitoneal communication
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5675148/
Pancreatico pleural fistula and pancreatic ascites have been termed as internal pancreatic fistulae which share common pathogenesis which includes the disruption of main pancreatic duct, resulting in leakage of pancreatic fluid. It is characterized by massive pleural fluid and has a tendency to recur following treatment. While conservative management with pancreatic duct stenting and inhibition of pancreatic secretion with octreotide may achieve closure of fistula in 31 to 45% of cases, surgery leads to healing in 80 to 90% of cases but carries a mortality up to 10%
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3290893/
As the patient recovered well and there was no recurrence of pleura effusion ,pleuro peritoneal connections was more likely rather than a pancreatic fistula but even fistula is a considered possibility.There was no evidence of pancreatico pleural fistula on CT abdomen.
Case 3:
30 year old male with acute pancreatitis and pancreatico pleural fistula.
Pancreaticopleural fistula is an infrequent complication that may be secondary to acute or chronic pancreatitis, as well as to external or iatrogenic pancreatic trauma. However, this complication is related to chronic pancreatitis of alcoholic origin in 99% of cases. The pathophysiology of the pancreaticopleural fistula consists of the formation of a posterior pathway of the pancreatic duct to the pleura or, more frequently, after the formation of a pseudocyst and subsequent communication with the pleural cavity. In both cases, the fluid flows through the retroperitoneum through the plane of least resistance into the pleural cavity, usually through the esophageal hiatus. Communications with the pericardium, bronchial tree and esophagus have also been described. Transdiaphragmatic communication is the less common situation. Many patients undergo extensive lung investigation before the pancreas is identified as the primary site of the disease. Diagnosis is usually performed by thoracocentesis after chest radiography, with laboratory findings of elevated levels of amylase and lipase in the pleural fluid.
The diagnosis can be confirmed by endoscopic retrograde cholangiopancreatography in 80% of the cases, showing the fistulous pathway in 59%. In 70% of cases, computed tomography associated with it identifies the fistulous path. Magnetic resonance cholangiopancreatography may demonstrate pancreatic involvement and fistula, without the need for contrast, constituting a non-invasive alternative
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5630219/#!po=19.6429
Case 4::
65 year old female with suspected pancreatic ascites who turned out to be suspected Tubercular ascites.
Review of literature failed to show a association between tubercular ascites and raised serum amylase ,lipase and raised ascitic amylase.So,This patient is still posing a diagnostic uncertainty.
Tuberculosis of the pancreas is extremely rare and in most of the cases mimics pancreatic carcinoma. It is difficult to diagnose tuberculosis of pancreas on imaging studies as they may present with masses, cystic lesions or abscesses and mass lesions in most of the cases mimic pancreatic carcinoma. As it is a rare entity, it cannot be recommended but suggested that pancreatic tuberculosis should be considered in cases with a large space occupying lesions associated with necrotic peripancreatic lymph nodes and constitutional symptoms.As our patient had absolutely normal pancreas on MRCP ,Tubercular pancreatitis was not considered.
The sensitivity and specificity of serum lipase for pancreatitis at a cut-off of three times the ULN range from 64% to 100% and from 99% to 100%, respectively. In comparison, at the same cut-off, the sensitivity and specificity of amylase range from 50% to 78.6% and from 99% to 100%
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299384/#!po=14.1892
Inspite of the high specificity of lipase ,it was high in our patient with radiologically proven normal pancreas.In view of severe omental thickening and caking tubercular ascites or malignancy was considered as a possibility.This proves that ultimately radiological confirmation is needed in cases suspected to have pancreatitis.If the patient was alive omental biopsy would be good diagnostic tool to resolve the uncertainty.
Peritoneal TB occurs in three types: (i) the wet type with ascites, (ii) the encysted type with abdominal swelling, and (iii) the fibrotic type with abdominal masses composed of mesenteric and omental thickening. A combination of these types may also occur.
Case 5:
61 year male patient with severe ascites and pancreatic calcifications whose ascitic amylase was 3 times higher than serum amylase,Pancreatic fistula can be suspected to be the cause of ascites.
Pancreatic fistula is an abnormal connection between the pancreatic ductal epithelium and another epithelium surface. This is due to a disruption of the pancreatic duct leading to the pancreatic fluid to leak, producing erosion, and forming different pathways resulting in internal and external pancreatic fistulas.Causes of pancreatic fistulas are iatrogenic or non-iatrogenic. Iatrogenic causes include operative trauma or during biopsy of a pancreatic mass, pancreatic resection, complications from endoscopic interventions, and percutaneous drainage of a pancreatic fluid collection such as in a pancreatic pseudocyst. It should be noted that most external pancreatic fistulas are a result of iatrogenic entities. Non-iatrogenic causes include abdominal trauma, acute pancreatitis, and chronic pancreatitis. CT would not be able to visualize and evaluate the pancreatic fistula properly. Magnetic resonance cholangiopancreatography (MRCP), endoscopic retrograde cholangiopancreatography (ERCP), or fistulography will be needed to demonstrate the fistula. The pleural and ascitic fluid amylase levels will be very elevated, usually more than 1000 U/dL
With MRCP, it provides a more precise picture of the pancreatic duct. ERCP will yield better pancreatic duct anatomy and identify any site of disruption. Also, ERCP can be used for therapeutic interventions when needed. With fistulography, the location of the fistula site and the surrounding anatomic structures are visible.
Citation: Barkin JS, Ferstenberg RM, Panullo W, Manten HD, Davis RC. Endoscopic retrograde cholangiopancreatography in pancreatic trauma. Gastrointest Endosc. 1988 Mar-Apr;34(2):102-5.
In one study the authors assessed amylase concentration in the drainage fluid collected from the left subphrenic cavity on POD1 and POD3 in 53 patients who had undergone curative gastrectomy for cancer and concluded that amylase drainage content >3 times the serum amylase was a useful predictive risk factor for pancreatic fistula
https://wjso.biomedcentral.com/articles/10.1186/s12957-014-0428-y
As this patient also had ascitic amylase more than 3 times the serum amylase pancreatic fistula can be considered a possibility.
Case 6:
50Year male patient diagnosed with Acute on chronic pancreatitis and underlying chronic liver disease with low SAAG ascites secondary to pancreatitis.This patient had the highest serum amylase of 1184 IU/L and highest ascitic amylase of 9,614 IU/L which made us suspect a pancreatic fistula as a cause of his ascites but due to a low resource setting the presence of fistula could not be objectively proven.The 2 cases with suspected pancreatic fistula had bad prognosis compared to pancreatic ascites due to other causes such as pancreatic necrosis and pancreatic duct disruption followed by pseudocyst formation.Endoscopic interventions could not be done due to low resource setting and affordability issues made the prognosis poorer in patients with suspected pancreatic fistula.
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.
https://www.ncbi.nlm.nih.gov/books/NBK507851/
CONCLUSION:
A rural medical college has received 6 cases of pancreatic ascites over the span of 2 years.The diagnostic and therapeutic challenges identified in this study need to be addressed towards the improvement of diagnostic and therapeutic outcomes of patients presenting with pancreatic ascites and various other related complications.An integrated approach and active participation of Gastroenterologists,General physician,Surgeons and Radiologists is the key to resolve these uncertainties and optimize the diagnosis and evidence based decision making on the line of management is important.Active participation of surgeons is needed also in performing omental biopsy whenever there is a diagnostic dilemma and a possibility of koch’s.The above case series has left many questions unanswered due to a low resource setting and affordability issues of the patients coming from rural areas but has also given us many new insights and learning points on in depth pathophysiologies of formation of pancreatic ascites and various associated complications.
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