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Abstract Background Pancreatic pleural effusion and ascites are defined as fluid accumulation in the thoracic and abdominal cavity, respectively, due to direct leakage of the pancreatic juice. They usually occur in patients with acute or chronic pancreatitis but are rarely associated with pancreatic neoplasm. We present here an extremely rare case of pancreatic neuroendocrine tumor with stenosis of the main pancreatic duct, leading to pancreatic pleural effusion. Case presentation A 51-year-old man complained of dyspnea. Left-sided pleural effusion was detected on the chest X-ray. Pleural puncture was performed, and the pleural fluid indicated a high amylase content (36,854 IU/L). Hence, the patient was diagnosed with pancreatic pleural effusion. Although no tumor was detected, the computed tomography (CT) scan showed a pseudocyst and dilation of the main pancreatic duct in the pancreatic tail. Magnetic resonance cholangiopancreatography showed a fistula from the pseudocyst into the left thoracic cavity. Endoscopic retrograde pancreatic drainage was attempted; however, it failed due to stenosis in the main pancreatic duct in the pancreatic body. Endoscopic ultrasound revealed a hypoechoic mass measuring 15 × 15 mm in the pancreatic body that was not enhanced in the late phase of contrast perfusion and was thus suspected to be an invasive ductal carcinoma. The patient underwent distal pancreatectomy with splenectomy and the postoperative course was uneventful. Histopathological examination confirmed a neuroendocrine tumor of the pancreas (NET G2). The main pancreatic duct was compressed by the tumor. Increased pressure on the distal pancreatic duct by the tumor might have caused formation of the pseudocyst and pleural effusion. To the best of our knowledge, this is the first case report of pancreatic pleural effusion associated with a neuroendocrine tumor. Conclusions Differential diagnosis of a pancreatic neoplasm should be considered, especially when a patient without a history of pancreatitis presents with pleural effusion.

• PA is a rare complication of alcoholic chronic pancreatitis (CP) that results in significant morbidity and mortality. • An initial morphological assessment is essential, particularly to determine the severity of the underlying pancreatitis and to obtain a precise topography of the lesion. • Conservative medical treatment seems to be ineffective and, if it fails, should be followed by a second-line endoscopic sphincterotomy ± endoprosthesis insertion. • Surgery is a last-line treatment, but should be considered earlier if endoscopic treatment is not possible and in cases of associated necrotising pancreatitis. • Surgery is most often necessary for pancreatico-pleural effusion associated with PA. Pancreatic ascites (PA) is an unusual and little studied complication of chronic alcoholic pancreatitis. Management is complex and is based mainly on empirical data. The aim of this retrospective work was to analyse the management of PA at our centre. A total of 24 patients with PA complicating chronic alcoholic pancreatitis were managed at the Lille University Hospital between 2004 and 2018. Treatment was initially medical and then, in case of failure, interventional (endoscopic, radiological and/or surgical). Data regarding epidemiology, therapeutic and follow-up data were collected retrospectively. Twenty-four patients were analysed; median follow-up was 18.5 months [6.75–34.25]. Exclusively medical treatment was effective in three of four patients, but, based on intention to treat, medical therapy alone was effective in only two out of 24 patients. Of 17 patients treated endoscopically, treatment was successful in 15 of them. Of the 15 who underwent surgery, external surgical drainage was effective in 13. Multimodal treatment, initiated after 6.5 days [4–13.5] of medical treatment, was effective in 12 out of 14 patients. In total, 21 patients were successfully treated (87%) with a morbidity rate of 79% and a mortality rate of 12.5% (n = 3). PA gives rise to significant morbidity and mortality. Conservative medical treatment has only a limited role. If medical treatment fails, endoscopic and then surgical treatment allow a favourable outcome in more than 80% of patients. [ABSTRACT FROM AUTHOR]

The review article provides up-to-date information on the complications of pancreatitis that are important for the tactics and strategy of patient management both at the inpatient and outpatient stages of observation. The purpose of the review was to emphasize the importance of complications for the course and life of patients with chronic pancreatitis. The authors draw the attention of internists to the course of such complications as pseudocysts, cysts, fistulas, thrombohemorrhagic, cholestatic syndromes, compression syndrome of adjacent organs, pancreatic encephalopathy (acute and chronic). The symptomatology of complications of chronic pancreatitis is discussed in detail, which is very important for differential diagnosis with the corresponding diseases. Such complications include the formation of erosive and ulcerative lesions, varicose veins of the esophagus and bleeding from varicose veins of the esophagus and stomach, portal hypertension syndrome with pancreatic ascites and chronic pancreatic encephalopathy, idiopathic non-cirrhotic portal hypertension, pancreatic cancer. The authors emphasize the need to analyze the corresponding symptoms, indicating the possibility of complications, negative consequences with each recurrence or exacerbation of chronic pancreatitis, since it concerns the prognosis and life of the patient. [ABSTRACT FROM AUTHOR]

Purpose: This study aims to evaluate the clinical effectiveness of continuous peritoneal lavage in moderately severe to severe acute pancreatitis (AP). Materials and Methods: We studied 58 patients with moderately severe to severe AP who were admitted from January 2015 to April 2017. Among these patients, 31 patients were treated only conventional therapy (control group). Twenty-seven patients were received continuous peritoneal lavage with conventional therapy (study group). Laboratory parameters and severity scores were compared before and 7 days after therapy between two groups. Mortality rate, the incidence of local complications and length of hospital stay were also compared between two groups. Results: There were no adverse events (bowel perforation and bleeding) associated with abdominal paracentesis for peritoneal lavage. The level of all parameters (white blood cell [WBC], C reactive protein [CRP], serum amylase, lactate dehydrogenase [LDH], blood glucose, serum creatinine, base excess, and serum calcium) and all the severity scores (systemic inflammatory response syndrome [SIRS], Marshall) were significantly improved 7 days after treatment compared before therapy in two groups (P < 0.05). We also compared the level of all laboratory parameters and severity scores between two groups 7 days after therapy. The level of serum amylase, blood glucose, and serum calcium was similar between two groups 7 days after treatment. In the study group, the level of WBC, CRP, LDH, serum creatinine, base excess, and severity scores (SIRS, Marshall) was significantly improved compared with control group 7 days after therapy (P < 0.05). Mortality rate was significantly decreased in the study group compared with control group (7.4% vs. 16.1%, P < 0.01). The incidence of local complication had also a significant difference between two groups (22.2% vs. 35.5%, P < 0.05). The length of hospital stay was significantly reduced in the study group compared with control group (33.1 ± 28.0 vs. 48.9 ± 36.2 days, P < 0.01). Conclusion: Continuous peritoneal lavage can significantly reduce mortality, complications, and length of hospital stay in moderately severe to severe AP.

Pancreatic ascites is not an uncommon condition but requires a high degree of suspicion for prompt diagnosis. Since both hepatic cirrhosis and pancreatitis are related to ethanol abuse, routine investigation of patients with cirrhotic ascites for the rise of ascitic fluid amylase levels will facilitate early diagnosis. The combination of inflammation of pancreas and portal hypertension due to hepatic cirrhosis could give a picture of 'inflammatory transudate'.

Background Acute pancreatitis is fraught with a variety of complications, which account for the mortality associated. Our case had a fulminant course, with three rare, near-fatal complications and was successfully managed conservatively. Pleural effusion due to pleuro-pancreatic fistula is uncommon, seen in only 1% cases, of which right-sided effusions are rarer still. Management modalities include conservative, endoscopic, and surgical options. Chylous ascites is an extremely rare complication of pancreatitis and is managed with high protein, low lipid diet, restricted to medium-chain triglycerides (MCTs). Extra-splanchnic venous thrombosis is uncommon in pancreatitis, and isolated renal vein thrombosis is very rare. Case Presentation A 34-year-old, chronic alcoholic male, presented to the outpatient department (OPD) in a state of shock and respiratory distress. Chest radiograph showed massive right-sided pleural effusion. The pleural fluid was hemorrhagic with markedly elevated amylase levels, and contrast-enhanced computed tomography (CECT) confirmed the presence of a right-sided pleuro-pancreatic fistula. Left renal vein thrombosis was also noted. The patient improved with chest drain, intravenous (IV) octreotide, and anticoagulants. Subsequently, he developed hemorrhagic pancreatic ascites, which later turned chylous. This was managed with dietary modifications. The patient had a prolonged recovery but was finally discharged after 45 days. Conclusion It is a challenge managing the various complications of acute severe pancreatitis. We describe this case to emphasize maintaining a high sensitivity for timely diagnosis and appropriate addressal of all the complications for better patient outcomes.

Pancreatic duct disruption may follow acute pancreatitis, chronic pancreatitis, pancreatic surgery, and trauma. Diagnosis in these patients is usually made by endoscopic retrograde cholangiopancreaticogram or secretin-stimulated magnetic resonance cholangiopancreaticogram. We report five cases where pancreatic duct disruption was diagnosed by contrast-enhanced computed tomography (CECT). Five patients with acute pancreatitis were studied; three were secondary to alcohol and two were posttraumatic. Three patients developed pancreatic ascites, one developed pancreatico-pleural effusion, and the other had pancreatic pseudocyst. CECT of the abdomen revealed pancreatic ductal injury in all the patients. In one patient with pancreatic ascites, multiple peripancreatic collections and dilated and disrupted pancreatic duct communicating with the peritoneal cavity were noted. The patient of traumatic pancreatitis had a fracture of the head of the pancreas, with peripancreatic collection communicating with the main pancreatic duct (MPD). In the other traumatic pancreatitis, there was a pseudocyst near the head of pancreas communicating with the MPD. CECT can provide a comprehensive assessment in acute pancreatitis including duct integrity, type and location of pancreatic ductal injury and can be an effective noninvasive alternative imaging modality in diagnosing pancreatic duct disruption.

It is reported that pancreatic ascites represents an extremely rare entity with unfavorable outcomes. It results from persistent leakage of pancreatic secretions in the peritoneum from pancreatic duct injury. Herein, we deal with a very rare case of a high-risk patient who underwent subtotal gastrectomy in emergency setting due to a 'huge' gastric perforation. The seventh post-operative day the patient presented severe pancreatic ascites due to iatrogenic disruption of the pancreatic duct during the subtotal gastrectomy and underwent emergency laparotomy. It has to be highlighted that pancreatic ascites is an extremely rare entity and treatment options depend on the etiology and on the degree of pancreatic duct injury. It has to be highlighted that the operating surgeon should always take into account the patient's overall condition in order to decide which therapeutic option is the most appropriate. [ABSTRACT FROM AUTHOR]

Acute pancreatitis is an inflammatory disease of pancreas which could lead to a number of complications including pancreatic ascites and pseudocysts. When these complications are severe, the secondary changes in colon, peritoneum or mesentery can make it difficult to distinguish from peritoneal carcinomas. Herein, we report a case of acute pancreatitis that was difficult to differentiate from peritoneal carcinoma. We performed a sequential procedure without peritoneal biopsy to exclude the possibility of peritoneal cancer, and we could diagnose pancreatic ascites and pseudocyst resulting from pancreatic injuries. [ABSTRACT FROM AUTHOR]

A 39-year-old man was referred to our hospital for the investigation of abdominal fluid collection. He was pointed out to have alcoholic chronic pancreatitis. Laboratory data showed inflammation and slightly elevated serum direct bilirubin and amylase. An abdominal computed tomography demonstrated huge fluid collection, multiple pancreatic pseudocysts and pancreatic calcification. The fluid showed a high level of amylase at 4,490 IU/l. Under the diagnosis of pancreatic ascites, endoscopic pancreatic stent insertion was attempted but was unsuccessful, so surgical treatment (Frey procedure and cystojejunostomy) was performed. During the operation, a huge amount of fluid containing bile acid (amylase at 1,474 IU/l and bilirubin at 13.5 mg/dl) was found to exist in the extraperitoneal space (over the peritoneum), but no ascites was found. His postoperative course was uneventful and he shows no recurrence of the fluid. Pancreatic ascites is thought to result from the disruption of the main pancreatic duct, the rupture of a pancreatic pseudocyst, or possibly leakage from an unknown site. In our extremely rare case, the pancreatic pseudocyst penetrated into the hepatoduodenal ligament with communication to the common bile duct, and the fluid flowed into the round ligament of the liver and next into the extraperitoneal space.

Pancreatic ascites is a rare complication of acute and chronic pancreatitis. The underlying cause of this complication likely is leakage from a pancreatic pseudocyst or ductal disruption. Treatment includes medical therapy and surgery. Here we described a patient with abdominal pain and ascites with a history of chronic alcoholism. The abdominal computed tomography scan revealed the presence of massive ascites and endoscopic retrograde cholangiopancreaticography showed pancreatic duct dehiscence. A pancreatic stent was inserted but the patient ultimately died as a result of septic shock with multi-organ failure. This case report highlights how difficult it is to manage patients with pancreatic ascites. [ABSTRACT FROM AUTHOR]

Introduction: our objective was to investigate the effects of the administration of pancreatic homogenates, with or without enzymatic activation, to healthy animals regarding cytokine serum levels and the development of pulmonary distress. Material and methods: 106 male Wistar rats, divided into three groups, were studied: group A, intraperitoneal administration of homogenates activated with enterokinase; group B, homogenates without enterokinase; and group C, control group with administration of physiological saline solution. Each group was divided into 4 subgroups according to the time of sacrifice: 0, 2, 6 and 24 hours. We studied the pulmonary and pancreatic histology, serum parameters of renal and hepatic function, and serum levels of IL-1ß, IL-6 and TNFa. Results: there was no mortality in any group. Pancreatic disorders in A and B groups were noted at 24 hours. These two groups had statistically significant higher transaminase serum levels than those of the control group, as well as statistically significant higher creatinine levels in group A. IL-1ß showed a statistically significant higher level at 6 h in both groups, A and B, but was higher in group A, which also exhibited significant pulmonary histologic damage with respect to controls at 6 h. Conclusions: the higher IL-1ß level in group A may result from production by peritoneal macrophages under the influence of homogenate enzymatic activation. This may be the reason for lung damage.Introducción: nuestro objetivo es investigar, en animales sanos, los efectos de la administración de homogeneizado pancreático, con y sin activación enzimática, sobre los niveles séricos de citoquinas y el desarrollo de lesiones pulmonares. Material y métodos: se estudiaron 106 ratas Wistar macho divididas en 3 grupos: A: administración intraperitoneal de homogeneizado pancreático activado con enteroquinasa; B: homogeneizado sin enteroquinasa; y C: control, con la administración de suero fisiológico. Cada grupo fue dividido en 4 subgrupos de acuerdo al tiempo de sacrificio: 0, 2, 6 y 24 horas. Estudiamos la histología pancreática y pulmonar, parámetros séricos de función renal, hepática y los niveles séricos de IL-1ß, IL-6 y TNFa. Resultados: no hubo mortalidad en ningún grupo. Se observaron alteraciones pancreáticas en los grupos A y B a las 24 horas. Estos dos grupos presentaron niveles de transaminasas significativamente más elevados que aquellos del grupo control. Los niveles séricos de creatinina estaban más elevados en el grupo A. Los valores de IL-1ß fueron significativamente más altos a las 6 horas en ambos grupos A y B, aunque mayor en el grupo A, el cual también presentó más lesiones histológicas pulmonares en relación con los controles a las 6 horas. Conclusiones: los niveles de IL-1ß más elevados en el grupo A podrían deberse a la activación enzimática del homogeneizado que podría inducir la producción de esta citoquina por los macrófagos peritoneales, lo que a su vez podría ser el promotor de las lesiones pulmonares.

Pancreatic duct leaks can occur as a result of both acute and chronic pancreatitis or in the setting of pancreatic trauma. Manifestations of leaks include pseudocysts, pancreatic ascites, high amylase pleural effusions, disconnected duct syndrome, and internal and external pancreatic fistulas. Patient presentations are highly variable and range from asymptomatic pancreatic cysts to patients with severe abdominal pain and sepsis from infected fluid collections. The diagnosis can often be made by high-quality cross-sectional imaging or during endoscopic retrograde cholangiopancreatography ( ERCP). Because of their complexity, pancreatic leak patients are best managed by a multidisciplinary team comprised of therapeutic endoscopists, interventional radiologists, and surgeons in the field of pancreatic interventions. Minor leaks will often resolve with conservative management while severe leaks will frequently require interventions. Endoscopic treatments for pancreatic duct leaks have replaced surgical interventions in many situations. Interventional radiologists also have the ability to offer therapeutic interventions for many leak patients. The mainstay of endotherapy for pancreatic leaks is transpapillary pancreatic duct stenting with a stent that bridges the leak if possible, but varies based on the manifestation and clinical presentation. Fluid collections that result from leaks, such as pseudocysts, can often be treated by endoscopic transluminal drainage with or without endoscopic ultrasound or by percutaneous drainage. Endoscopic interventions have been shown to be effective and have an acceptable complication rate. [ABSTRACT FROM AUTHOR]

Background Internal pancreatic fistula (IPF) is a complex disease with different etiologies, varied clinical presentations, and multiple management options. Unlike postoperative pancreatic fistula, IPF lacks guidelines for classification and management. The rarity of the disease makes randomized control studies unlikely and difficult to formulate guidelines. This has resulted in different approaches to managing IPF. IPF associated with both acute and chronic pancreatitis is treated with a step-up approach. Chronic pancreatitis-associated IPF treated with the traditional step-up approach is associated with increased morbidity. Prolonged fasting, drainage of protein-rich pancreatic fluid, and extended hospital stay add to the morbidity. Early surgical intervention in patients with IPF associated with chronic pancreatitis can treat both the fistula and underlying disease processes simultaneously. This may contribute to reduced morbidity and hospital stay. Methodology A retrospective observational study was conducted between June 2018 and May 2019. IPF patients with fluid amylase >1,000 IU/L and fluid albumin >3 g/dL were included in the study. Results In total, 32 patients were included in the study. A total of 13 patients had acute pancreatitis and 19 were associated with chronic pancreatitis. Pseudocyst and walled-off pancreatic necrosis were present in 18 patients. The duration of treatment for the traditional group was 8-14 weeks, and for the early surgery group, it was 8-10 days. Patients were followed up for two years, and none of the patients in the early surgery group had a recurrence. Conclusions The overall mortality of IPF is low but it has high morbidity. The delay in treatment may contribute to high morbidity; hence, early surgical intervention may change the clinical course. The primary pathology of the pancreas can be addressed simultaneously as well. In our study, early surgical intervention was associated with lesser morbidity and decreased duration of hospital stay while recurrence rates and mortality were comparable to the traditional management protocol., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2022, Siva Sankar et al.)

Background: Ascites and pleural effusion are well recognized complications of pancreatic diseases. Drug therapy of these is limited by high cost, prolonged hospitalization and failure rates; surgery is invasive and is associated with considerable morbidity and mortality. Objective: To analyze the data on patients with pancreatic ascites and/or pleural effusion treated endoscopically over a ten-year period. Methods: Patients with symptomatic ascites/pleural effusion for at least 3 weeks with a fluid amylase level of > 1000 S units/dl and underlying pancreatic disease were included. The interventions were a 5 mm sized pancreatic sphincterotomy and placement of a 7 Fr pancreatic stent. Somatostatin/octreotide and parenteral nutrition were not used after endoscopic therapy. Results: Of the 28 patients included (22 men), 17 (60.7%) had chronic pancreatitis. The causes were tropical pancreatitis (13, 46.4%), alcohol abuse (10, 35.7%), idiopathic acute pancreatitis (4, 14.3%) and resective surgery for gastric cancer (1, 3.6%). Ascites alone was seen in 15, pleural effusion alone in 6 and both in 7 patients. Ten patients (35.7%) had 14 pseudocysts. Endotherapy was successful in 27 (96.4%). Twenty-six (92.8%) patients had complete resolution of ascites/effusion over a median 5 weeks. The stents were removed 3–6 weeks later without any recurrence over the next 6–36 (median = 17) months. Complications (7, 25%) included severe pain in 2 (7.1%) and fever in 5 (17.8%) of which 3 (10.7%) had infection of residual fluid collections. No patient died. Conclusion: Endoscopic therapy offers an excellent therapeutic alternative in patients with pancreatic ascites and pleural effusion. [ABSTRACT FROM AUTHOR]

Pancreatic injury has a high morbidity and mortality. The integrity of the main pancreatic duct is the most important determinant of prognosis. Serum amylase, peritoneal lavage and computed tomography of the abdomen can assist with diagnosis but endoscopic retrograde pancreatography (ERP) is the most accurate investigation for diagnosing the site and extent of ductal disruption. However, it is invasive and can be associated with significant complications. Magnetic resonance cholangiopancreatography (MRCP) and secretin-enhanced MRCP probably parallel ERP in delineating pancreatic ductal injuries. They can also delineate the duct upstream to complete disruption, an area not visualized on ERP. In relation to therapy, endoscopic transpapillary drainage has been successfully used to heal duct disruptions in the early phase of pancreatic trauma and, in the delayed phase, to treat the complications of pancreatic duct injuries such as pseudocysts and pancreatic fistulae. Transpapillary drainage is especially effective in patients who have partial pancreatic duct disruption that can be bridged. Endoscopic transmural drainage has also been successfully used to treat post-traumatic pancreatic pseudocysts. Further large, prospective and randomized studies are required to adjudge the efficacy and long-term safety of pancreatic duct drainage in the treatment of post-traumatic pancreatic duct injuries. [ABSTRACT FROM AUTHOR]

The leaking pancreatic duct in childhood chronic pancreatitis presents with ascites and pleural effusion and is a potentially lethal condition. Seven children with this condition were seen in the period 2003-2006. The correct diagnosis was not entertained till a raised serum amylase was discovered. The diagnosis was confirmed by very high levels of amylase in the aspirated abdominal or pleural fluid. Computerized tomogram was the most useful imaging study and demonstrated a dilated pancreatic duct. All children were operated within 6 days of diagnosis by a Puestow's procedure in six and peripancreatic drainage in one. Six children made a prompt and lasting recovery after a Puestow's procedure while one child, also suffering from metastatic neuroblastoma, died in the immediate post operative period after peripancreatic drainage. We recommend prompt and definitive surgical management of this potentially lethal condition. [ABSTRACT FROM AUTHOR]

We have demonstrated that pancreatitis-associated ascitic fluid contributes to hepatocyte injury during acute pancreatitis; a phenomenon independent of ascites'' enzymatic content and Kupffer cell-derived cytokines. Our aim is to characterize the mechanisms of pancreatitis-associated ascitic fluid induced hepatocyte death. NIH mice were injected intraperitoneally with pathogen-free pancreatitis-associated ascitic fluid. Twenty-four hours later, serum AST, ALT, LDH, and hepatocyte apoptosis (TUNEL) were measured. Human hepatocytes (CCL-13) were treated with pancreatitis-associated ascitic fluid ±SB203580 or caspase-3 inhibitor-II. Mitochondrial membrane integrity was determined by DiOC6 staining. Apoptosis was measured by TUNEL staining and flow cytometry after dual labeling with Annexin-V/7-AAD. Data are mean ± SEM of triplicates. Pancreatitis-associated ascitic fluid increased serum AST, ALT, LDH, and apoptotic cells in the mouse liver (all P < 0.03 vs. sham). In CCL-13 cells, pancreatitis-associated ascitic fluid induced a time and dose-dependent increase in apoptosis, in addition to p38-MAPK phosphorylation (P = 0.02 vs. control), caspase-3 cleavage (P < 0.03 vs. control) and decreased DiOC6 mitochondrial staining (P < 0.01 vs. control). Both caspase-3 inhibitor-II and SB203580 decreased apoptosis, but the former had no effect on DiOC6 staining. Pancreatitis-associated ascitic fluid induces liver injury and hepatocyte apoptosis by activating p38-MAPK and caspase-3 dependent pro-apoptotic pathways. ( J Gastrointest Surg 2003;7:200–208.) [Copyright &y& Elsevier]

Introduction. Kupffer-cell-derived cytokines mediate liver injury, yet macrophage pacification does not abolish hepatocyte injury. We undertook this study to examine the role of pancreatitis-associated ascitic fluid (PAAF) in liver injury.Methods. Pathogen-free PAAF was perfused into healthy rat livers in situ for 60 min (n = 5, sham = 5, LPS = 5). AST, ALT, LDH, and TNF were measured in the effluent. Primary cultures of rat Kupffer cells or hepatocytes were treated with PAAF; AST, ALT, LDH, and TNF were measured and cell proliferation was determined by MTT assay. A hepatocyte human cell line (CCL-13) was treated with PAAF and apoptosis was measured by flow cytometry.Results. Liver perfusion with PAAF induced a >15-fold increase in AST/ALT/LDH (P < 0.001 PAAF vs sham), but not in TNF. In vitro, Kupffer cell viability was sharply reduced by PAAF in a dose-dependent manner; however, 5% PAAF (50% viability) did not induce TNF production from Kupffer cells. PAAF induced a multifold increase in AST/ALT/LDH from fresh hepatocytes (P < 0.001 vs control), which was not attenuated by a protease inhibitor. The CCL-13 cell population was reduced to 15 ± 2% of baseline by PAAF (P < 0.001 vs control), whereas elastase, trypsin, or TNF had no effect. PAAF increased the percentage of nonviable CCL-13 cells (78 ± 4% vs 28 ± 1%, P < 0.001 vs control). Neither protease inhibitor nor heat inactivation of PAAF altered this pattern of hepatocyte death.Conclusion. PAAF induces direct hepatocyte injury and death by heat-stable factors other than pancreatic enzymes but not via local production of Kupffer-cell-derived cytokines. [Copyright &y& Elsevier]

Background: An internal pancreatic fistula involves an abnormality in the way that the pancreas communicates with organs and spaces within the body. This is usually due to a disrupted pancreatic duct or psuedocyst leakage (Ascitic or pleural fluid amylase level >1000 S units/dl and fluid protein level >3 g/dl). The study aims to report our experience with surgery for chronic pancreatitis-related pancreatic ascites and pancreatic pleural effusions., Methods: All the patients, who underwent surgical intervention for pancreatic ascites and pancreatic pleural effusion between August 2007 and December 2020 in the Department of Surgical gastroenterology, Institute of Postgraduate Medical Education and Research, Kolkata, India were retrospectively reviewed., Results: Of the total 14 patients, 10 (71.4%) were men with a median age of 40 (4-49) years. The median interval between onset of symptoms of CP and diagnosis of IPF was 27 (3-60) months. All patients had a history of chronic abdominal pain and 5 (35.7%) had a prior history of hospitalization for pain. Eleven patients (78.5%) presented with abdominal distension and 3 (21.4%) patients had respiratory distress. Six (42.8%) patients had undergone endotherapy before surgery. Contrast-enhanced computed tomography detected pancreatic pseudocyst in 10 (71.42%) patients. The most commonly performed operation was lateral pancreaticojejunostomy (n = 11, 78.5%). Seven postoperative complications developed in 4 (28.5%) patients. After a median follow-up of 60 (6-86) months, no patient developed recurrence of pancreatic ascites or pleural effusion., Conclusion: In the experienced hand, surgery can be performed with acceptable perioperative morbidity and mortality and long-term satisfactory outcomes., Competing Interests: None declared., (© 2022 The Author(s).)

Acute pancreatitis may follow a mild or a severe course. Whereas mild or edematous pancreatitis is a self-limiting disease with a low complication rate and low death rate, morbidity and mortality in severe or necrotizing pancreatitis are still unacceptably high. The major problem is the lack of a specific drug, especially in the early phase of the disease, to interfere with the systemic inflammatory response syndrome and to limit or prevent complications of the disease. Although the initiating pathophysiological process is not known, the destruction of the gland (‘autodigestion’) by digestive enzymes may be responsible for disease progression. Inhibition of pancreatic activity, which reduces exocrine secretion and further prevents the release and activation of enzymes, was therefore suggested as a specific treatment concept. The results of clinical investigations using somatostatin or its analogue are controversial, since all these trials had low statistical power. In a recent multicenter randomized controlled study with a large number of patients (n = 302) (and an adequate level of disease severity), no benefit of octreotide on progression or outcome was found. Chronic pancreatitis is characterized by an irreversible destruction of the exocrine and endocrine pancreatic parenchyma leading to maldigestion and diabetes. Pain, which may be caused by increased ductal pressure, is one of the most dominant symptoms in chronic pancreatitis. However, no beneficial effects on pain with pancreatic exocrine secretion-inhibiting drugs have been demonstrated. Treatment of other complications of the disease (pseudocyst formation, fistula and pancreatic ascites), with somatostatin or octreotide has given conflicting results. However, in a prophylactic clinical setting (e.g. elective pancreatic surgery) the inhibition of exocrine pancreatic secretion reduces complications. [ABSTRACT FROM AUTHOR]

Background: Haemosuccus pancreaticus is a rare complication of pancreatitis. It is a diagnostic problem for even the most astute clinician and a challenge for the expert endoscopist. We report a 25-year-old male patient who had all the features usually seen in haemosuccus pancreaticus patients: recurrent obscure upper gastrointestinal bleeding, pancreatitis, pseudocyst formation, ductal disruption, fistula and pancreatic ascites. The patient was treated by subtotal pancreatectomy, splenectomy and drainage of the pseudocyst. Although pancreatic duct communication with the surrounding vasculature could not be ascertained, we strongly believe the patient had haemosuccus pancreaticus because, over a follow-up period of 3 years, the patient was not only ascites free, but did not experience any further upper gastrointestinal bleeding. We believe that in evaluating patients with recurrent obscure gastrointestinal bleeding, one should always remember that the pancreas is a part of the gastrointestinal tract and, like other organs, is prone to blood loss. [ABSTRACT FROM AUTHOR]

Pancreatic ascites can occur in association with the rupture of a pseudocyst or the disruption of a pancreatic duct during the natural course of chronic pancreatitis. We report herein the successful treatment of three patients with pancreatic ascites by performing a surgical procedure after 4–6 weeks of total parenteral nutrition (TPN) proved ineffective. The principles of our surgical procedure for pancreatic ascites are as follows: (1) minimum pancreatic tissue is resected; (2) surgical intervention to repair leaking sites is not necessary; (3) pancreatic duct drainage is facilitated by an intestinal Rouxen-Y loop; (4) An external drainage tube is inserted through the Roux-en-Y loop into the main pancreatic duct. All three patients who underwent our surgical procedure had a good outcome. Although the mean follow-up time is still only 18.3 months, their condition has improved, with no evidence of recurrent ascites. Thus, our surgical procedure should be considered as an appropriate treatment for pancreatic ascites because it can be applied for all types of leakage, including leakage from the posterior wall of pancreas; it preserves pancreatif function, especially endocrine function; and it enables preservation of the spleen. [ABSTRACT FROM AUTHOR]

We describe a young patient with a family history of hereditary pancreatitis who developed extensive pancreatic necrosis complicated by pancreatic ascites. Because of failure of medical management, he was successfully treated with operative necrosectomy and primary wound closure over peripancreatic drains. A postoperative low-output pancreaticocutaneous fistula resolved with time. Pancreatic ascites, as a result of pancreatic duct disruption, is more common in chronic rather than acute pancreatitis and is exceedingly uncommon in the context of necrotizing pancreatitis. When it complicates the latter, treatment should be guided by the principles of management of necrotizing pancreatitis. However, when true pancreatic ascites persists, the pancreatic duct anatomy and site of leak should be defined with endoscopic retrograde pancreatography (ERP). Treatment options include endoscopic duct dilatation and stent placement (if a stricture exists proximal to the leak), onlay pancreaticojejunostomy, or distal pancreatectomy (especially if the leak is located in the distal pancreas or in an enterically isolated distal pancreas). [ABSTRACT FROM AUTHOR]

The treatment of pancreatic ascites remains a clinical challenge. Both medical and surgical management have high rates of mortality and recurrence. New methods in the treatment of pancreatic ascites are actively sought. We describe the successful use of a continuous infusion of octreotide acetate in the treatment of refractory alcoholic pancreatic ascites. [ABSTRACT FROM AUTHOR]