Complication Of Pancreatitis Research Articles

A Clinical Study on Pseudocyst of Pancreas

Background: Pancreatic pseudocyst is seen in acute and chronic pancreatitis as a complication. It has a well-defined wall which is not made of epithelium. After an acute attack of pancreatitis, pancreatic pseudocyst develops after 4-8 weeks. There is a increased incidence of pancreatitis and complications of pancreatitis, despite of treatment and recent advances. So, I would like to study the clinical features, etiology, various treatment modalities and asses outcome of the patients. Methods: The study is conducted in 50 patients in S.V.R.R.G.G.H. hospital, Tirupati in the department of general surgery. Thorough history and clinical examination have been recorded. Investigations were done which are basic and definitive. The study patients were managed with different modalities like conservative, external catheter drainage, cysto-gastrostomy, cysto-jejunostomy, percutaneous drainage. Data regarding the age distribution, gender distribution, symptoms, signs, complications, treatment, post op complications, duration in the hospital, follow up were collected. The final outcome is observed in terms of most common age group, most common gender affected, most common etiological factor, symptoms, signs, associated complications and treatment, post complications in S.V.R.R.G.G.H. Tirupati, in the department of general surgery. Results: The study conducted in 50 patients shows that, the pancreatic pseudocyst is seen in the age group of 31-50 years (74%). The male patients were affected more when compared to females with 94% male and 3% female. Alcohol consumption is the common etiology. The most common presentation was pain abdomen in all study patients followed by nausea and vomiting in 84% of patients and abdominal distension in 58% of patients. Abdominal tenderness is seen in all study patients followed by mass abdomen in 60% of patients. Associated complications include infection which is seen in 12% of patients followed by ascites and ileus/obstruction in 2% of patients. USG and Computed Tomography done in all patients. Conservative treatment was effective in uncomplicated pancreatic pseudocyst. Internal drainage procedure shows good results with 42% of patients with minimal complications. The most common post operative complication include abdominal pain in 16% followed by infection of wound in 6% of patients. Conclusion: The most common complication of acute pancreatitis is pancreatic pseudocyst. Early diagnosis with USG, CT and intervention with conservative treatment for uncomplicated cyst, internal drainage for mature cyst, external drainage for complicated cyst shows good prognosis.

Serum Lactate Dehydrogenase Is a Sensitive Predictor of Systemic Complications of Acute Pancreatitis.

Acute pancreatitis (AP) is a common and potentially life-threatening inflammatory disease that can cause various complications, including systemic inflammatory response syndrome (SIRS), pleural effusion, ascitic fluid, myocardial infarction, and acute kidney injury (AKI). However, there is still a lack of rapid and effective indicators to assess the disease. The aim of this study was to investigate the associations of high serum lactate dehydrogenase (LDH) levels with AP severity and systemic complications. AP patients treated from July 2014 to December 2020 were retrospectively enrolled. They were divided into elevated (n = 93) and normal (n = 143) LDH groups. Their demographic data, clinical data, hospital duration, and hospital expenses were analyzed. Linear and binary logistic regression analyses were used to determine whether elevated LDH is a risk factor for AP severity and complications after adjusting for confounders. There were significant differences in AP severity scores (Ranson, MODS, BISAP, APACHE II, and CTSI), hospital duration, hospital expenses, and the incidences of complications (SIRS, pleural effusion, ascitic fluid, myocardial infarction, and AKI) between the elevated and normal LDH groups. After adjusting for confounders, elevated LDH was associated with AP severity scores and hospital duration and expenses (based on linear regression analyses) and was a risk factor for the occurrence of AP complications and interventions, that is, diuretic and vasoactive agent use (based on binary logistic regression analyses). Elevated LDH is associated with high AP severity scores and high incidences of complications (SIRS, pleural effusion, ascitic fluid, myocardial infarction, and AKI).

Risk factors for complications in elderly patients aged 85 years and over undergoing endoscopic biliary stone removal.

Background and aimThe number of elderly patients with biliary stones is increasing. Endoscopic retrograde cholangiography (ERCP) is considered to be an effective treatment for biliary stones. Having a sound knowledge of the risk factors can help reduce the incidence and severity of complications for ERCP. Furthermore, limited research has been published on patients aged over 85 years undergoing endoscopic biliary stone removal. This study aims to determine the risk factors that lead to complications of ERCP in patients over 85 years of age.MethodsThis was a single-center retrospective study. We analyzed 156 patients aged ≥ 85 years with biliary stones who underwent their first ERCP at Chinese PLA General Hospital from February 2002 to March 2021. Logistic regression models were employed to identify the independent risk factors for complications.ResultsA total of 13 patients (8.3%) had complications. Thereinto, pancreatitis, cholangitis, bleeding, and other complications occurred in 4 cases (2.6%), 1 cases (0.6%), 4 cases (2.6%), and 4 cases (2.6%), respectively. There was no perforation or death related to ERCP. Independent risk factors for complications were acute biliary pancreatitis (ABP) (P = 0.017) and Charlson Comorbidity Index (CCI) (P = 0.019). Significantly, reasons for incomplete stone removal at once were large stone (>10 mm) (P < 0.001) and higher acute physiology and chronic health evaluation scoring system (APACHE-II) (P = 0.005).ConclusionsERCP was recommended with caution in patients ≥ 85 years of age with ABP or higher CCI undergoing endoscopic biliary stone removal. In patients with ABP without cholangitis or biliary obstruction we recommend against urgent (within 48 h) ERCP. Patients with higher CCI who can tolerate ERCP can undergo rapid ERCP biliary stenting or nasobiliary implantation with later treatment of stones, and patients who cannot tolerate ERCP are treated promptly with PTCD and aggressive conservative treatment.

A rare case of severe anaemia due to pancreatic pseudoaneurysm complicated by COVID-19

Pancreatitis in children is now diagnosed more frequently with an incidence of acute pancreatitis turning to chronic being 20–25%. Pancreatic pseudoaneurysm is a rare and life-threatening complication of chronic pancreatitis. An adolescent a known case of chronic pancreatitis for 3 years, presented with a history of recurrent black-coloured stools for 1 month and haematemesis, fever and cough for 2 days. The child was pale and febrile with tachypnoea and tachycardia with severe tenderness in the epigastric and umbilical regions. Investigations showed severe anaemia (Hb-1.4 g/dL) with positive COVID-19 Reverse transcription-polymerase chain reaction. Computed tomography abdomen showed pancreatitis with a pseudocyst, pseudoaneurysm from the gastroduodenal artery and consolidation in lung COVID 19 Reporting and data system. The child was treated symptomatically along with multiple packed red blood cells transfusions. Selective catheterisation and stent grafting of the gastroduodenal artery was performed. This case report highlights an unusual complication of pancreatitis with concurrent COVID infection.

An Atypical Complication of Chronic Pancreatitis

An Atypical Complication of Chronic Pancreatitis

S1711 Cerebral Infarction as a Rare Downstream Complication of Pancreatitis

Introduction: Pancreatitis is characterized by progressive and irreversible loss of function. Long term complications of pancreatitis include refractory abdominal pain, malabsorption, and diabetes. The downstream complications may also be systemic. In the case below we suggest that the acute release of pancreatic enzymes led to a hypercoagulable state and severe inflammatory reaction contributing to an acute cerebrovascular stroke presentation. Case Description/Methods: 55-year-old right-handed woman with a past medical history significant for chronic idiopathic pancreatitis, HTN, chronic thrombocytosis, and HLD presented to the hospital with complaints of nausea and vomiting. Initial work-up was significant for a lipase of 1,178 U/L and subsequent imaging showed peritoneal thickening and nodularity extended from the pancreatic head / neck junction most likely due to ongoing pancreatitis. Patient was admitted to hospital medicine but unfortunately that night the patient became acutely aphasic and confused. She developed right-sided neglect, profound aphasia, and left gaze preference. She was immediately evaluated by neurology and a stat CT revealed acute ischemic changes but no large vessel occlusion. She received intravenous tPA and was transferred to the critical care unit. CT angiogram revealed thrombus within the aortic arch at the origins of the right brachiocephalic arteries and follow-up MRI brain revealed scattered infracts within the left MCA territory. It was suspected that her stroke was likely precipitated by artery-to-artery embolus worsened in the setting of her acute on chronic pancreatitis attack. Patient worked extensively with rehabilitation services for weeks before eventually being discharged home with residual weaknesses. Discussion: Acute on chronic pancreatitis is an inflammatory process that can produce complications through both loss of endocrine and exocrine function. Additionally, the thrombotic tendency in pancreatitis may be related to systemic hypercoagulability resulting from inflammatory cytokines, endothelial dysfunction due to release of proteases and lytic enzymes, and compression of vessels from surrounding inflammation. These factors could contribute to the development of acute cerebrovascular stroke as seen in our patient. Furthermore, this case serves to highlight the need for further study into the systemic effects of acute on chronic pancreatitis and to serve as a reminder that though rare cerebral infarction can be a rare complication of pancreatitis.

S1720 Diabetic Ketoacidosis as a Rare Complication of Alcoholic Pancreatitis in a Previously Euglycemic Patient

Introduction: Acute alcoholic pancreatitis is an acute inflammation of the pancreas secondary to alcohol intake due to autodigestion from an increase in pancreatic enzyme release. Most commonly due to gallstones, alcohol intake, and hypertriglyceridemia, pancreatitis commonly presents with severe epigastric abdominal pain, nausea and vomiting and is managed with aggressive intravenous (IV) fluid resuscitation. Some complications include acute respiratory distress syndrome and compartment syndrome. A very rare complication of acute pancreatitis is diabetic ketoacidosis (DKA), especially in patients without a history of diabetes mellitus. Case Description/Methods: A 25-year-old female with a medical history significant for alcohol abuse presented with nausea, vomiting, and abdominal pain for 2 days. The patient reported drinking one pint of liquor per day. She was tachycardic with a heart rate of 115 and other vitals were normal. Significant laboratory studies showed a lipase of 1715, aspartate transaminase of 292, alanine transaminase of 155, glucose of 540, venous pH of 7.277, bicarbonate of 9, anion gap of 21, and beta-hydroxybutyrate of 5.1. A computed tomography scan of her abdomen and pelvis without IV contrast showed edematous and inflammatory changes in the tail of the pancreas and severe hepatic steatosis (Figure). The patient was managed with aggressive IV fluids and IV insulin infusion. Her abdominal pain and anion gap resolved on day 2 of admission and she was able to tolerate a diet. Glycated hemoglobin (HbA1c) returned a value of 4.7 and C-peptide was low at < 0.10; the subsequent pancreatic antibody panel was negative. The patient was seen in the clinic 6 months later and HbA1c at that time was 4.8. Discussion: This case illustrates DKA as a rare complication of acute pancreatitis. It provides an example of why a high level of suspicion for DKA should be present in patients presenting with alcoholic pancreatitis even in the absence of any diabetic history. Though there is no definitive mechanism of action for this presentation, it is likely from a combination of pancreatic beta-cell destruction and counter-regulatory hormone effects. Pancreatic beta-cell destruction causes impaired insulin production, leading to acute hyperglycemia. Furthermore, as acute pancreatitis can lead to severe intravascular depletion, increased secretion of counter-regulatory hormones such as cortisol and glucagon, in combination with impaired insulin secretion, can precipitate DKA in such a scenario.Figure 1.: CT abdomen without contrast demonstrating edematous and inflammatory changes in the tail of the pancreas.

THE TROJAN HORSE: A CASE OF HEMORRHAGIC PANCREATITIS

THE TROJAN HORSE: A CASE OF HEMORRHAGIC PANCREATITIS

S109 Clinical Predictors of Ileus in Hospitalized Patients With Acute Pancreatitis: A Nationwide Analysis

Introduction: Ileus is a well-known complication of acute pancreatitis (AP). Limited data exists on incidence or factors associated with ileus in patients with AP. We aimed to investigate the incidence and clinical predictors of ileus in hospitalized patients with AP. Methods: We queried the 2016-2019 National Inpatient Sample (NIS) database using the ICD-10 codes. All adult patients with a diagnosis of AP (ICD-10 K85) were included and those with chronic pancreatitis were excluded from the analysis. We studied demographics, comorbidities, complications, and interventions in patients with AP and stratified the results by the presence of ileus. Multivariate analysis was conducted to elucidate clinical factors associated with ileus formation in patients with acute pancreatitis. We adjusted for patient demographics, hospital characteristics, elixhauser comorbidities and common complications of pancreatitis. Results: Of the 1,386,389 adult patients admitted with AP, 50,170 (3.6%) developed ileus. Female gender was associated with a 44% lower risk of ileus (aOR- 0.56, 95% CI- 0.53-0.58, p< 0.001). Hispanic patients had the lowest risk of ileus (aOR- 0.82, 95% CI- 0.76-0.88, p< 0.001) while White patients had the highest risk. Patients between the age of 18-44 had a lower risk of ileus as compared to patients in the 45-64 (aOR-1.11, 95% CI- 1.05-1.17, p< 0.001) and >65 age group (aOR-1.14, 95% CI- 1.06-1.24, p< 0.001). Other factors associated with ileus include the presence of pseudocyst (aOR- 1.52, p< 0.001), sepsis (aOR-1.72, p< 0.001), and portal vein thrombosis (aOR-1.36, p< 0.001). ERCP was not associated with ileus development, however, pancreatic drainage was associated with a higher risk of ileus (aOR-1.21, p< 0.007). The results of the multivariate analysis are depicted in Table: Patients with ileus were also noted to have a statistically significant higher mortality (a0R-1.58, 95% CI- 1.43-1.75, p< 0.001), length of stay (+4.9 days, 95% CI- 4.63-5.12, p< 0.001), total hospitalization cost (+67,855.91, p< 0.001) and charges ($16,252.6, p< 0.001). Conclusion: This study highlights age, gender, and racial disparities in the development of ileus in patients with AP. It also reveals a significant association of ileus with pseudocyst, portal vein thrombosis, and pancreatic drainage. Timing of initiation of oral feeds is essential in patients with acute pancreatitis and ileus. Physicians should be aware of this high-risk group and consider early enteral feeding to prevent disease progression. Table 1. - Predictors of ileus in patients with acute pancreatitis. In this Table, we provide the results of multivariate logistic regression with odds ratio, p-value and 95% confidence interval Ileus Odds ratio p-value 95% Confidence interval Age category 18-44 Reference 45-64 1.11 < 0.001 1.05-1.17 >65 1.14 < 0.001 1.06-1.24 Sex Male Reference Female 0.56 < 0.001 0.54-0.59 Race White Reference African American 0.95 0.149 0.89-1.02 Hispanic 0.82 < 0.001 0.76-0.88 Asian/Pacific Islander 1.01 0.846 0.89-1.15 Native American 0.72 0.01 0.56-0.93 Primary expected payer Medicare Reference Medicaid 0.83 < 0.001 0.77-0.9 Private 1.11 < 0.001 1.04-1.18 Uninsured 0.8 < 0.001 0.72-0.88 Income quartile Lowest quartile Reference Second quartile 1.04 0.227 0.98-1.1 Third quartile 1.11 < 0.001 1.04-1.17 Highest quartile 1.14 < 0.001 1.07-1.22 Bed size of Hospital Small Reference Medium 1.04 0.224 0.98-1.11 Large 1.11 < 0.001 1.04-1.17 Region of hospital Northeast Reference Midwest 1.31 < 0.001 1.21-1.42 South 1.16 < 0.001 1.08-1.25 West 1.17 < 0.001 1.08-1.26 Location of hospital Rural hospitals Reference Urban hospitals 1.03 0.502 0.94-1.13 Teaching status of hospitals Non-teaching hospitals Reference Teaching Hospitals 1.05 0.084 0.99-1.1 Etiology of pancreatitis Biliary pancreatitis Reference Alcohol pancreatits 0.98 0.583 0.89-1.17 Biliary + alcohol pancreatitis 1.81 < 0.001 1.32-2.47 Other causes 0.88 < 0.001 0.84-0.93 Number of elixhauser comorbidities 0 Reference 1 1.26 < 0.001 1.11-1.43 2 1.41 < 0.001 1.24-1.6 3 or more 1.54 < 0.001 1.35-1.76 Comorbidities Cardiac arrhythmias 0.86 < 0.001 0.8-0.93 Congestive heart failure 1.26 < 0.001 1.19-1.33 Valvular disease 0.97 0.587 0.86-1.09 Pulmonary circulation disorders 0.96 0.558 0.85-1.09 Peripheral vascular disorders 0.95 0.279 0.87-1.04 Paralysis 1.32 0.009 1.07-1.62 Other neurological disorders 1.01 0.83 0.94-1.08 Chronic pulmonary disease 1.01 0.704 0.95-1.07 Chronic kidney disease 0.83 < 0.001 0.78-0.89 Liver disease 1.01 0.637 0.96-1.07 Metastatic solid tumor 0.84 0.036 0.72-0.99 Non-metastatic solid tumor 1.05 0.407 0.93-1.19 Rheumatoid arthritis/collagen vascular disorder 0.87 0.054 0.76-1 Coagulopathy 0.98 0.647 0.92-1.05 Malnutrition 1.32 < 0.001 1.24-1.41 Fluid/electrolyte disorders 1.59 < 0.001 1.51-1.67 Blood loss anemia 1.17 0.146 0.95-1.45 Deficiency Anemia 0.93 0.152 0.84-1.03 Alcohol abuse 0.73 < 0.001 0.68-0.78 Drug use 0.88 0.003 0.81-0.96 Psychosis 0.97 0.721 0.8-1.17 Depression 0.87 < 0.001 0.81-0.92 Diabetes 0.71 < 0.001 0.68-0.75 Hypertension 0.98 0.348 0.93-1.03 Complications Pneumonia 1.63 < 0.001 1.52-1.76 Bacteremia 0.97 0.787 0.76-1.23 Acute kidney injury 1.38 < 0.001 1.31-1.46 Portal vein thrombosis 1.41 < 0.001 1.2-1.66 Pseudocyst 1.57 < 0.001 1.44-1.72 Sepsis 1.75 < 0.001 1.63-1.89 Shock 1.18 < 0.001 1.08-1.29 ICU admission 1.99 < 0.001 1.83-2.17 Interventions TPN 4.22 < 0.001 3.84-4.64 ERCP 1.05 0.203 0.97-1.13 Pancreatic drainage 1.25 0.009 1.06-1.48

S2659 Splenic Artery Pseudoaneurysm as a Rare Cause of Upper Gastrointestinal Bleeding

Introduction: Upper gastrointestinal bleeding (UGIB) is one of the most common causes for hospital admission in the US. Common etiologies for UGIB include peptic ulcer disease, erosive esophagitis, varices, and less commonly malignancies. Splenic artery pseudoaneurysm (PSA) is a known complication of pancreatitis. It may be asymptomatic or present with left upper quadrant or epigastric pain, and rarely as hemorrhagic shock. Splenic artery PSA presenting with UGIB is extremely unusual. Case Description/Methods: We present the case of a 57-year-old male with alcohol use disorder complicated by a prior episode of alcoholic pancreatitis, who presented with 3 days of hematemesis, melena, and recurrent syncopal episodes. In the ED his vitals and physical exam were notable for tachycardia, hypotension, and melena. Labs revealed a hemoglobin of 4.2. Non-contrast CT of the abdomen and pelvis showed evidence of blood in the antrum and a 2.0 x 1.6 cm out-pouching from the greater curvature of the stomach which was postulated to be a gastric diverticulum (image 1). Upper endoscopy revealed fresh blood in the antrum and duodenum, as well as a massive adherent clot in the fundus. Since no single site of active bleeding was identified, the patient was started on IV PPI with continued close monitoring in the ICU. He continued to have melena, and increased PRBC requirements. Repeat EGD was performed but was unchanged from prior. A CT angiogram of the abdomen and pelvis demonstrated a 1.5 cm actively bleeding PSA arising from a first divisional branch of the splenic artery communicating with the fundus of the stomach (images 2 & 3). The patient underwent successful coil embolization (image 4). Hemoglobin remained stable throughout the remainder of his admission with no further evidence of bleeding. Discussion: This case demonstrates PSA as a rare cause of UGIB. Lesions are most commonly caused by chronic pancreatitis, pancreaticobiliary surgery, and trauma. This patient’s PSA was likely secondary to his prior episode of alcoholic pancreatitis. Prompt diagnosis of PSA is essential given the high mortality rate associated with rupture. Clinicians should maintain a high index of suspicion for gastrointestinal PSA in patients with a history of pancreatitis who present with UGIB for whom no obvious source of bleeding can be identified on endoscopy.Figure 1.: CT Thx/Abd/Pel demonstrating a 2.0 x 1.6 cm out-pouching from the greater curvature of the stomach (arrow), postulated to be a gastric diverticulum, 2. CT Angiogram Abd/Pel demonstrating the splenic artery PSA (arrow), 3. Fluoroscopic imaging re-demonstrating the splenic artery PSA with extravasation of contrast into the gastric lumen, 4. Splenic Artery PSA after successful coil embolization.

S1922 A Twisted Plot: Pancreas Divisum With Right-Sided Pancreaticopleural Fistula

Introduction: We report on a 53-year-old male with a past medical history significant for chronic pancreatitis who presented with a right-sided pleural effusion secondary to pancreaticopleural fistula with pancreatic divisum. Pleural effusion secondary to pancreaticopleural fistula (PPF) is a rare complication of acute or chronic pancreatitis and usually presents with a left-sided pleural effusion. This case also highlights the difficulty and significant delay in diagnosing pancreas divisum on cross-sectional imaging. Case Description/Methods: A 53-year-old male with a medical history significant for chronic pancreatitis complicated by pancreatic ascites, walled-off necrosis, splenic and portal vein thrombosis, alcoholic gastritis, and polysubstance use presented with five days of dyspnea with new and worsening oxygen requirements. Chest x-ray showed a new moderate right-sided pleural effusion. Pleural fluid analysis revealed elevated lipase of >3,000 U/L and amylase of 21,008 U/L concerning for a pancreaticopleural fistula. MRI of pancreas showed a disconnected duct at the tail of the pancreas with a fistula extending into the mediastinum and peritoneum. During ERCP a bulging minor papilla was noted. After failed initial attempts at cannulating ventral duct, minor papilla was approached and dorsal duct was cannulated. Pancreatogram revealed a complete pancreatic divisum with a leak in the tail of the pancreas. A temporary plastic stent was placed in the dorsal duct after minor papilla sphincterotomy. The patient's symptoms resolved and he was discharged home with outpatient follow-up (Figure). Discussion: PPF is a rare complication of pancreatitis that typically presents as large, recurrent, left-sided pleural effusion often refractory to thoracentesis management. Transpapillary stent placement in the pancreatic duct is widely used in the management of PPF. Our case shows a rare right-sided presentation of PPF in the setting of a newly diagnosed pancreas divisum missed on numerous previous cross-sectional imaging. High clinical suspicion of underlying divisum raised by endoscopic and imaging findings led to successful endoscopic management of this complex case.Figure 1.: MRCP Pancreas showing pancreas divisum and disconnected duct.

S2694 An Uncommon Cause of Upper Gastrointestinal Bleeding

Introduction: We present a case of GI bleeding due to a direct communication between a pancreatic fistula and the splenic vein. Case Description/Methods: A 55 year-old female with a history of endometrial cancer, superficial lower extremity thrombus, and alcohol use presented with abdominal pain and dark red blood in her stools requiring blood transfusion. She reported recent ibuprofen use. An upper endoscopy showed small esophageal varices without red wales or stigmata of recent hemorrhage. A CT demonstrated extensive subacute thrombosis of the right and left portal veins, main portal vein (PV), proximal superior mesenteric vein (SMV) and splenic vein (SV). The pancreas appeared atrophic and contained small cysts. There was small ascites. Liver biopsy demonstrated mild steatohepatitis without fibrosis. She underwent placement of a transjugular intrahepatic portosystemic shunt (TIPS) with thrombectomy from the PV, SMV, and SV and was started on anticoagulation. Due to bleeding recurrence, she underwent TIPS revision with tPA injection and additional mechanical thrombectomy. Subsequently on an ultrasound, TIPS thrombosis was again noted and during TIPS revision, a communication was noted between the pancreatic duct and splenic vein, finally identifying the likely source of bleeding. A splenic vein stent was placed. Discussion: This case highlights an uncommon cause of upper GI bleeding and reinforces the importance of keeping a broad differential diagnosis for a patient with portal hypertension. Our patient had a complicated course with 2 TIPS revisions and esophageal varices, but the source of her bleeding was neither variceal nor mucosal. (Figure) Splenic vein thrombus can result as a complication of pancreatitis and subsequently lead to “sinestrial” (left-sided) portal hypertension and the formation of gastric varices which can also present with gastrointestinal bleed (GIB). Our patient did not have the classic finding of sinestral portal hypertension associated with SV thrombosis: gastric varices. Furthermore, during her initial TIPS placement and even her initial thrombectomy, no pancreatic fistula was observed. Although not always visualized due to the intermittent nature of bleeding, hemosuccus pancreaticus in the setting of chronic alcoholic pancreatitis most commonly involves the splenic artery (60-65%) and less commonly involves the gastroduodenal artery. Our patient’s case is unusual because angiogram demonstrated direct communication between a pancreatic fistula and the splenic vein, not the splenic artery.Figure 1.: Large clot burden at superior mesenteric vein.

Management of Splanchnic Vein Thrombosis in Patients With Acute Pancreatitis: An International Survey of Current Practice.

Splanchnic venous thrombosis (SpVT) is a complication of acute pancreatitis (AP). There is scarce literature on the prevalence and treatment of SpVT in AP. The aim of this international survey was to document current approaches to the management of SpVT in patients with AP. An online survey was designed by a group of international experts in the management of AP. Twenty-eight questions covered the level of experience of the respondents, disease demographics, and management of SpVT. There were 224 respondents from 25 countries. Most respondents (92.4%, n = 207) were from tertiary hospitals and predominantly consultants (attendings, 86.6%, n = 194). More than half of the respondents (57.2%, n = 106) "routinely" prescribed prophylactic anticoagulation for AP. Less than half of the respondents (44.3%, n = 82) "routinely" prescribed therapeutic anticoagulation for SpVT. A clinical trial was considered justified by most respondents (85.4%, n = 157) and 73.2% (n = 134) would be willing to enroll their patients. The approach to anticoagulation in the treatment of patients with SpVT complicating AP was highly variable. Respondents indicate that a position of equipoise exists to justify randomized evaluation.

S1838 Spontaneous Gastro-pancreatic Fistula: A Rare Complication of Acute Pancreatitis

Introduction: Although Gastrointestinal fistula is a well-recognized complication of acute pancreatitis, it has been rarely reported. Here we present a rare case of spontaneous gastro-pancreatic fistula following acute pancreatitis. Case Description/Methods: 42 y/o female with PMH of SLE with a recent prolonged hospitalization for acute drug-induced pancreatitis with pseudocyst came to ED with fever, abdominal pain, nausea, and vomiting. She was tachycardic, had leukocytosis, and was positive for COVID-19. CT Scan A/P showed multiple infected peripancreatic collections with communication of the left upper quadrant collection with the gastric lumen (Figure). The patient was hospitalized, Kept NPO, and started on fluids and antibiotics. IR evaluated and put 2 pigtail catheters for drainage of peripancreatic collections. The tip of the pigtail catheter in the left peripancreatic/retroperitoneal collection was in the gastric lumen. The surgery team recommended continuing with conservative treatment with parenteral nutrition, and IV antibiotics as the patient were nontoxic with no signs of free perforation, and pancreatitis would more likely erode a staple or suture line and would put the patient at further risk of free perforation if repair attempted. IR was successful in pulling the drain out of the gastric lumen on the second attempt to allow gastric perforation to heal. Antibiotics were upgraded as per the culture and sensitivity results of the drain fluid. Repeated multiple bedside leak tests and CT scans with oral contrast continue to be positive for patent gastro-pancreatic fistula. Pigtails catheter continues to drain significant necrotic collection. The patient continues to be hospitalized and is being managed conservatively with Parenteral nutrition, and IV antibiotics. Discussion: Fistula of the GI tract following acute pancreatitis can be caused by multiple reasons. Necrosis of the bowel may occur concomitantly with the pancreatic or peripancreatic tissue. Furthermore, enzyme-rich fluid and necrosis can lead to vascular thrombosis, which compromises the blood supply of the segmental GI tract, eventually leading to bowel necrosis. GI fistulas are more common in patients with necrotizing pancreatitis with infected pancreatic necrosis. Despite pharmacologic suppression of pancreatic exocrine secretion and advances in endoscopic and percutaneous therapeutic techniques, pancreatic fistula continues to be a source of morbidity and mortality following pancreatitis and requires multidisciplinary treatment.Figure 1.: Peripherally enhancing fluid collection in the left upper quadrant/gastric wall. There is a communication between this collection with the gastric lumen.

S2848 Massive Pseudo-Pneumoperitoneum After Endoscopic Necrosectomy

Introduction: Encapsulated peripancreatic fluid collection and walled-off necrosis are some of the complications of acute pancreatitis. Most resolve spontaneously but symptomatic pseudocysts or walled-off necrosis require drainage. The preferred therapeutic management is endoscopic ultrasound (EUS) guided drainage with stent placement. Known iatrogenic complications of the procedure include bleeding and perforation. Case Description/Methods: A 39-year-old woman with history of ulcerative colitis, in remission on certrolizumab presented with symptomatic walled-off necrosis after idiopathic necrotizing pancreatitis. EUS-guided drainage and stent placement was successfully performed. On subsequent upper endoscopy for necrosectomy, post-procedure large pneumoperitoneum was noted on imaging leading to emergent surgical evaluation with laparoscopy. However, no perforation or pancreatic fluid contamination was seen. On post-operative day 1, patient was asymptomatic and tolerating diet. She was discharged on post-operative day 2. At 3-month follow-up, patient remained asymptomatic and plastic stents were removed. Discussion: Pneumoperitoneum is an uncommon but dreaded complication of EUS guided cystogastrostomy. This occurs when there is separation of the gastric wall and the wall of the pancreatic cyst or walled-off necrosis. If perforation is detected during cystgastrostomy, it may be possible to use a LAMS to close the defect by bridging the walls or close the gastric defect endoscopically with clips or sutures. Immediate surgery (such as cyst-enterotomy with closure of the wall defect) should be performed if there is generalized contamination of the peritoneum with cyst fluid content and subsequent signs of peritonitis. (Figure) Our case, to our knowledge, is the only one that describes pneumoperitoneum after endoscopic necrosectomy, two weeks after placement of LAMS. Our hypothesis is that the walled-off necrosis moved away from the gastric wall after removal of LAMS, which had aided apposition of the gastric wall and cyst wall due to its flanges and short saddle length. Pneumoperitoneum, in the absence of peritoneal findings, is referred to as benign peritoneum. Our case describes massive benign pneumoperitoneum after endoscopic necrosectomy without perforation. There is a paucity of literature on non-surgical management of post-endoscopic pneumoperitoneum and we hope that our case, will help endoscopists carefully select patients who will benefit from surgical management of pneumoperitoneum.Figure 1.: Figure A. CT abdomen showing pancreatic walled off necrosis containing turbid fluid and debris. Figure B. Massive pneumoperitoneum seen on CT abdomen after EUS-guided drainage and double pig-tailed stent placement for continued drainage.

S1798 Pancreatic Duct Injury Secondary to Pancreatic Trauma Successfully Treated With Transgastric Pancreatic Drainage

Introduction: Disconnected pancreatic duct syndrome (DPDS) is an underrecognized complication of pancreatic trauma and acute pancreatitis. DPDS is characterized by a disruption of the main pancreatic duct. Its diagnosis is confirmed by either MR cholangiopancreatography (MRCP) or retrograde cholangiopancreatography (ERCP). In this case, we present a patient who developed DPDS secondary to blunt abdominal trauma, successfully treated with a transgastric pancreatic drainage. Case Description/Methods: A 36-year-old female with a medical history of renal dysplasia and chronic kidney disease stage V arrived at our institution after presenting with epigastric abdominal pain, nausea, and early satiety of a week of evolution. The patient was recently discharged from a trauma center after being admitted for 2 weeks after a domestic violence incident involving blunt abdominal trauma. Upon initial evaluation, the abdominal exam was remarkable for tenderness in the epigastric area upon deep palpation. Laboratory were remarkable for elevated renal parameters and severely elevated pancreatic enzymes. Initial Abdominopelvic CT showed pancreatic transection across the head and neck pancreatic junction, with an associated fluid collection consistent pancreatic fluid extravasation. MRCP was performed, which confirmed the pancreatic transection with an associated pseudocyst at the pancreatic genu consistent with disconnect pancreatic duct syndrome. After interdisciplinary evaluation, an endoscopic ultrasound-guided cystgastrostomy stent was placed. After the procedure, the patient significantly improved symptoms and was discharged 2 days later. The patient was re-evaluated 2 weeks later with a CT scan, which showed transgastric pancreatic drainage with complete resolution of peripancreatic fluid collection. Transgastric pancreatic drainage was removed 2 months later. Follow up Ct scan done 2 months after stent removal showed normal anatomy of the pancreas with no distinct inflammatory tissue reaction and no evidence of peripancreatic collection. Discussion: Pancreatic ductal injury after trauma is mainly managed surgically but may result in high morbidity and mortality. Advances in endoscopy have allowed minimally invasive interventions as an alternative that can be performed in dstan effective and safe manner.

S1140 Gender and ERCP Complications: A Nationwide Inpatient Sample Database Analysis

Introduction: Endoscopic retrograde cholangiopancreatography (ERCP) can involve a variety of complications including pancreatitis, hemorrhage, and cholangitis. Some studies have identified female gender as a risk factor for post-ERCP pancreatitis, cholangitis, and overall complications, however other studies have shown contradictory results. Given these discrepancies, we evaluated gender as a risk factor for post-ERCP complications using the National Inpatient Sample database. Methods: The National Inpatient Sample (NIS) database was used to identify hospitalized patients over 18 years old who had an ERCP procedure between 2007 - 2017 using ICD-9 and ICD-10 codes. Patients were divided into two groups: males (726,352 [40.1%]) or females (1,084,048 [59.9%]), as defined by NIS as “indicator of sex”. Patients were matched by age, race, and by Elixhauser comorbidity index. Primary outcomes were rates of post-ERCP pancreatitis, cholangitis, cholecystitis, infection, hemorrhage, and perforation. Chi-squared tests were used to compare categorical data and multivariate analyses were performed to assess primary outcomes. Results: There were 1,810,400 patients hospitalized from 2007-2017 who underwent an ERCP procedure, of which 1,084,048 (59.9%) were female and 726,352 (40.1%) were male. Primary outcomes were significant for increased odds ratio of post-ERCP pancreatitis (OR 1.2, p< 0.001) and decreased odds ratio of post-ERCP cholangitis (OR 0.7, p< 0.001), cholecystitis (OR 0.4, p< 0.001), infection (OR 0.7, p< 0.001), and hemorrhage (OR 0.6, p< 0.001) in females compared to males. No significant difference was found between men and women for post-ERCP perforation. Conclusion: Although there are differences in the effects of gender on post-ERCP complications in the literature, the mechanisms causing these effects are not known. Women are known to have higher risks for biliary stones and sphincter of Oddi dysfunction which can further increase the odds of post-ERCP pancreatitis. We postulate that the decreased rates of cholangitis, cholecystitis, infection, and hemorrhage in women compared to men could be from an anatomical variation in the biliary tree that is gender specific. Therefore, endoscopists should further explore and consider this possibility when performing ERCPs. Table 1. - Clinical Outcomes in Females and Males who underwent ERCP p value Odds Ratio Confidence Interval Post-ERCP Pancreatitis < 0.001 1.2 1.1-1.3 Post-ERCP Cholangitis < 0.001 0.7 0.7-0.8 Post-ERCP Cholecystitis < 0.001 0.4 0.4-0.5 Post-ERCP Infection < 0.001 0.7 0.7-0.7 Post-ERCP Hemorrhage < 0.001 0.6 0.5-0.7 Post-ERCP Perforation 0.304 1.1 1.0-1.2

S1889 A Case of Ruptured Gastroduodenal Artery Pseudoaneurysms in a Patient With Chronic Pancreatitis

Introduction: Pancreatic pseudoaneurysm is a rare vascular complication of pancreatitis, with an estimated prevalence of 10%. Pseudoaneurysm can result from trauma, inflammation, infection, and iatrogenic causes. Due to its weak structural support, the risk of rupture is higher for pseudoaneurysm than that of a true aneurysm of similar size. Pancreatic pseudoaneurysms can lead to life-threatening complications such as rupture and bleeding, with increased morbidity and mortality up to 90% in untreated patients and 12.5% despite treatment. Due to its high mortality rate with rupture, pseudoaneurysms should be treated immediately once it is identified, regardless of their size or whether it is symptomatic or not Case Description/Methods: We present a case of a 68-year-old male patient with a past medical history significant for chronic pancreatitis who presented with altered mental status and hypovolemic shock secondary to unexplained gastrointestinal and retroperitoneal hemorrhage (Table). Computed tomography (CT) Angiography was done which showed an enlarging retroperitoneal and right-sided intraperitoneal hematoma with suspicion for active arterial extravasation or punctate pseudoaneurysms in the pancreatic head (Figure). Celiac angiogram was done under fluoroscopic guidance, which showed gastroduodenal and superior pancreaticoduodenal artery pseudoaneurysms. He underwent successful endovascular coil embolization of the gastroduodenal artery. Post procedure he was monitored in intensive care unit. His clinical condition continued to improve and was discharged to a skilled nursing facility in stable condition. Discussion: Physicians should be aware of pancreatic pseudoaneurysms as rare vascular complication associated with chronic pancreatitis that may lead to fatal gastrointestinal or retroperitoneal bleeding with a high mortality rate. Our case highlights the importance of early diagnosis and prompt treatment in these patients.Figure 1.: A: CT abdomen and pelvis without intravenous contrast showing peripancreatic inflammation surrounding the pancreatic body and head along with retroperitoneal bleed (red arrow). Pancreatic calcifications present (yellow arrow) signifying radiologic evidence of chronic pancreatitis B: CT Angiography showing retroperitoneal and right-sided intraperitoneal hematoma with active arterial extravasation or punctate pseudoaneurysms in the pancreatic head. Table 1. - Laboratory Investigation Investigation Day 1 of Hospitalization Day 5 At Time of Discharge Reference Range White Blood Cell count 24.3 14.3 k/uL 7 k/uL 4.8-10.8 k/uL Red Blood Cell Count 4.77 2.69 MIL/uL 3.19 MIL/uL 4.50-5.90 MIL/uL Hemoglobin 15.8 8.5 mg/dl 10.2 mg/dl 12.0-16.0 g/dL Hematocrit 47.6 25.7 % 30.5% 42-51 % Platelet count 171 155 k/uL 215 k/uL 150-400 k/uL Sodium, Serum 132 139 mEq/L 140 mEq/L 135-145 mEq/L Potassium, Serum 3.0 3.2 mEq/L 3.9 mEq/L 3.5-5.0 mEq/L Blood Urea Nitrogen, Serum 41 17 mg/ml 10 mg/ml 8-26 mg/dL Creatinine, Serum 1.2 0.5 mg/dl 0.6 mg/dl 0.5-1.5 mg/dL Bilirubin, Serum total 0.5 0.7 mg/dl 0.3 mg/dl 0.2-1.1 mg/dL Serum Direct Bilirubin 0.3 0.3 mg/dl < 0.2 mg/dl 0.0-0.3 mg/dL Alkaline Phosphatase 51 48 units/L 73 units/L 56-155 unit/L Aspartate Transaminase 125 21 units/L 18 units/L 9-48 unit/L Alanine Aminotransferase 81 30 units /L 12 units /L 5-40 unit/L Lactic acid Level 8.2 0.8 mmoles/L 1.1 mmoles/L 0.5-1.6 mmoles/L Prothrombin Time 15.2 13.9 sec 10.5 sec 9.9-13.3 seconds International Normalized Ratio 1.31 1.20 0.92 0.85-1.14 Serum Calcium 6.6mg/dl 7.6 mg/dl 9.2 3 mg/dl 8.5-10.5 mg/dl Serum Lipase 24 U/L < =61U/L Serum Triglyceride 163mg/gl 55-150 mg/dl Serum Ethanol < 10 < = 10mg/dl Urine Toxicology Cocaine and methadone Negative

S1949 An Unusual Case of Chronic Pancreatitis Presenting With Recurrent Obscure Gastrointestinal Bleeding

Introduction: Chronic pancreatitis (CP) is a sequela of repeated pancreatic injury resulting in loss of exocrine and endocrine function of the pancreas. In most cases, CP presents with chronic abdominal pain and patients usually have either clinical and radiological features of CP, with gastrointestinal bleeding (GIB) as a very rare occurrence. Herein is a presentation of recurrent obscure GIB caused by chronic pancreatitis. Case Description/Methods: A 48-year-old male with a prior history of PUD and recurrent GIB episodes for several years presents with dark red bleeding per rectum for two days. Of note, the patient had undergone several endoscopies and the most recent endoscopies done six months prior were all unremarkable. He denied hematemesis, NSAIDs, or anticoagulant use. Denied liver or pancreatic disease but endorsed a prior history of moderate alcohol intake. Physical examination was unremarkable except for tachycardia and epigastric tenderness. He was mildly anemic with leukocytosis. The abdominal and pelvic CT scan was unremarkable. EGD revealed a small gastric oozing site (Figure) suspected to be an AVM or dieulafoy's lesion and clipped. He continued to have a frank bloody stool and developed hemorrhagic shock requiring multiple transfusions and vasopressors. Findings on two additional EGDs were unremarkable. He had mesenteric angiography performed with ligation of the gastroduodenal artery empirically. Despite the intervention, he continued to bleed. Abdominal CTA (Figure) noted active extravasation in the 2nd segment of the duodenum. Explorative laparotomy revealed an edematous head and uncinate portion of the pancreas with venous engorgement. There was erosion into the duodenum with acute hemorrhage (Figure). A duodenotomy and Roux-en-y (duodenojejunostomy and jejunojejunostomy) were performed. On account of the above findings, a tissue biopsy was not obtained. Following surgery, he remained hemodynamically stable and got discharged. Discussion: Massive obscure GIB due to complications of pancreatitis rarely does occur. A few cases reported are due to complications resulting from hemosuccus pancreaticus, pseudoaneurysm from a vascular supply, or erosion into adjacent viscus in the setting of known pancreatitis. Our patient represents an unusual presentation in which his recurrent obscure massive GI bleeding was the initial presentation of CP. We present this case to broaden our knowledge that obscure GI bleeding can be a complication of CP and the only manifestation of the disease.Figure 1.: The image on the left shows an EGD with the gastric oozing site with clips, and the middle image shows CTA with extravasation in the second segment of the duodenum. The image on the right shows the posterior aspect of the head of the pancreas, the uncinate, and venous engorgement.

S2825 Endoscopic Management of an Obstructing Duodenal Wall Hematoma in the Setting of Acute Pancreatitis

Introduction: Spontaneous duodenal wall hematoma is a rare condition which can be associated with acute and chronic pancreatitis. It is often complicated by small bowel obstruction. When conservative management fails, options are limited. Here we describe a case of small bowel obstruction secondary to pancreatitis-associated duodenal wall hematoma which was successfully managed endoscopically through cystduodenostomy. Case Description/Methods: A 69-year-old male with HIV and normal CD4 count presented with acute abdominal pain and non-bloody emesis with elevated lipase of 374 U/L (ULN 82). Computed tomography revealed a 5.8 cm multilobulated pancreatic pseudocyst with associated inflammation and coarse calcifications and a 10 cm circumferential submucosal mass within the duodenum with significant luminal narrowing and compression of the adjacent inferior vena cava (a). Endoscopic ultrasound confirmed a homogenous, hypoechoic subepithelial lesion obstructing the second portion of the duodenum consistent with a hematoma (b). A nasogastric-jejunal tube was placed for feeding and decompression. Due to persistent obstruction and IVC compression, on hospital day 10 endoscopic drainage of the duodenal hematoma was performed via cystduodenostomy with a 15x10 mm electrocautery-enhanced lumen-apposing metal stent (LAMS) (AXIOS, Boston Scientific, Marlborough, MA, USA) (c). The LAMS was immediately removed after near-complete evacuation of the hematoma cavity to minimize the risk of bleeding complications. A plastic double-pigtail stent was left in place to facilitate complete drainage. The duodenum was then dilated with a 12-13.5-15mm hydrostatic balloon dilator. The pigtail stent was removed 3 days later with clinical, radiographic, and endoscopic resolution of the duodenal obstruction (d). Discussion: Duodenal hematoma is a previously described rare complication of pancreatitis. Endoscopic evacuation was a safe and effective means of relieving the duodenal obstruction in this patient. This minimally invasive option resulted in immediate resolution and can be considered when conservative management fails.Figure 1.: 10 cm duodenal wall hematoma on CT scan (a) and endoscopy (b). Endoscopic drainage via cystduodenostomy with a lumen-apposing metal stent (c). Resolution of the duodenal wall hematoma (d).