Pancreatic Parenchymal Necrosis Research Articles

Long-term follow-up study of necrotising pancreatitis: interventions, complications and quality of life

ObjectiveTo describe the long-term consequences of necrotising pancreatitis, including complications, the need for interventions and the quality of life.DesignLong-term follow-up of a prospective multicentre cohort of 373 necrotising pancreatitis patients...

Risk factors and Nomogram Prediction for Splanchnic Venous Thrombosis in Moderate and Severe Acute Pancreatitis

BACKGROUND: Acute pancreatitis is one of the most common gastrointestinal diseases with significant morbidity and mortality, especially in the moderate to severe types. Splanchnic vein thrombosis(SVT) is related to acute pancreatitis but the pathogenesis of SVT in patients with AP is incompletely understood. AIM To investigate the risk factors of moderately severe acute pancreatitis (MSAP) and severe acute pancreatitis (SAP) complicated by splanchnic venous thrombosis. METHODS The clinical data of 290 patients with MSAP and SAP admitted to Xuanwu Hospital of Capital Medical University between December 2015 and December 2020 were retrospectively analyzed. Patients were divided into two groups: 1) with thrombosis and 2) without thrombosis. Sex, age, etiology, severity of acute pancreatitis, platelet (PLT), C-reactive protein (CRP), procalcitonin (PCT), interleukin-6 (IL-6), prothrombin time (PT), activated partial thrombin time (APTT), D-dimer (D-D) levels, type of pancreatic necrosis, proportion and location of pancreatic parenchymal necrosis (PPN), location of local complications, computed tomography severity index (CTSI) and modified CTSI(mCTSI) were recorded. Univariate, logistic multivariate regression analyses and nomogram were used to determine the risk factors for splanchnic venous thrombosis complicated by acute pancreatitis (AP). A receiver operating characteristic (ROC) curve, decision curve and calibration curve were drawn. RESULTS Among 290 patients with AP, 71 (24.5%) had SAP, and 219 (75.5%) had MSAP. The median age of all the patients was 49 years; 172 patients (59.3%) had biliary disease, 91 patients (31.4%) had hypertriglyceridemia, 13 patients (4.5%) had alcohol disease, and 14 patients (4.8%) had other diseases. Of the 290 patients, SVT was detected in 35 (12.1%). Univariate analysis showed that the severity of acute pancreatitis, PLT, CRP, PCT, IL-6, PT, D-D, proportion of pancreatic parenchyma necrosis (PPN), necrosis of body-tail, and necrosis involving perihepatic and right subphrenic space, CTSI and mCTSI in the thrombus group were all statistically significant (P < 0.05). The results of multivariate analysis showed that PLT≧422 × 109/L, necrosis of body-tail, and necrosis involving perihepatic and right subphrenic space were independent risk factors for AP complicated with splanchnic venous thrombosis. The nomogram incorporating these factors demonstrated good discrimination, calibration and clinical utility. The area under the curve was as high as 0.845. CONCLUSION PLT≧422 × 109/L, necrosis of body-tail, and necrosis involving perihepatic and right subphrenic space are independent risk factors for splanchnic vein thrombosis. A simple nomogram tool helps in the early, accurate prediction of AP. Early and relevant clinical intervention should be provided.

Nomenclature of Pancreatic Fluid Collections following Acute Pancreatitis: Need to Further Revise the Atlanta Classification System!

AbstractA better understanding of the disease pathophysiology, improved imaging modalities, and the development of minimally invasive interventions led to the revision of the Atlanta classification and new terminologies for the pancreatic fluid collections (PFCs) occurring in acute pancreatitis. Peripancreatic necrosis (PPN) or extra-pancreatic necrosis (EPN) has been reported as a distinct morphological entity with a better outcome than combined pancreatic and peripancreatic necrosis as well as pancreatic parenchymal necrosis alone and slightly worse than acute interstitial pancreatitis. In this news and views, we discuss a study that compared the morphological features and outcomes of endoscopic drainage of walled off necrotic collections developing after EPN alone with those developing after PN with or without EPN.

Pancreatic necrosis volume for predicting readmission and reintervention in acute necrotizing pancreatitis

PurposeTo determine the correlation between the pancreatic necrosis volume (PNV) and readmission as well as reintervention. MethodThis was a retrospective cohort study that included necrotizing pancreatitis (NP) patients who were examined with contrast-enhanced computed tomography (CT) one week before discharge. The PNV was calculated manually based on the postprocessing workstation software. Multivariate logistic regression analysis was employed to determine the independent risk factors for readmission and reintervention. ResultsA total of 167 NP patients were included. Among them, 94 (56.3%) patients were readmitted after discharge, and 55 (32.9%) patients needed further invasive intervention. The median PNV of all patients was 376.6 (interquartile range (IQR), 129.3–820.5) cm3, and the PNV was significantly higher in patients needing readmission or reintervention. Multivariate analysis showed that PNV ≥ 620 cm3 (adjusted odds ratio (adjOR), 3.08; 95% confidence interval (CI), 1.47–6.43; P = 0.003) and modified computed tomography severity index (CTSI) score ≥ 7 points (adjOR, 6.36; 95% CI, 2.05–10.70; P = 0.001) were independently associated with readmission. Stent or drainage tube placement at discharge (adjOR, 2.94; 95% CI, 1.27–6.77; P = 0.011), PNV ≥ 620 cm3 (adjOR, 5.11; 95% CI, 2.19–11.95; P < 0.001), pancreatic parenchymal necrosis (adjOR, 3.37; 95% CI, 1.42–7.96; P = 0.006), and modified CTSI score ≥ 7 points (adjOR, 4.23; 95% CI, 1.46–12.27; P = 0.008) were independent risk factors for reintervention. ConclusionsThe PNV is a useful tool for quantifying pancreatic necrosis and is strongly associated with readmission and reintervention. Additional prospective studies with larger sample sizes are needed to confirm these findings.

Endoscopic transluminal drainage for infected pancreatic necrosis

To evaluate the effectiveness of intraluminal drainage of acute fluid accumulations for infected pancreatic necrosis. There were 848 patients with acute pancreatitis between January 2018 and December 2020 at the Sklifosovsky Research Institute for Emergency Care. Necrotizing pancreatitis was detected in 232 (27.4%) patients. Among necrotic forms, pancreatic parenchymal necrosis was detected in 56 (24.1%) patients, its combination with peripancreatic necrosis - in 176 (75.9%) patients. All patients underwent transabdominal ultrasound, CT of the abdomen and retroperitoneal space, esophagogastroduodenoscopy, endo-ultrasonography of pancreatobiliary zone. Dimensions and localization of acute necrotic accumulations were established using ultrasound and CT data. Endoscopic transluminal drainage was performed in 22 patients with necrotizing pancreatitis and fluid accumulations attached to the stomach or duodenum. There were 12 men (55%) and 10 women (45%) aged 48.5 [39; 56] (35; 88) years. Effectiveness of endoscopic treatment was assessed considering clinical, endoscopic data and reduction of fluid accumulations confirmed by ultrasound and CT data. Among 22 patients, connection with pancreatic ductal system was detected in 3 patients (13.6%) that required pancreaticoduodenal stenting. Early postoperative period was complicated by bleeding from the area of pancreatogenic destruction in 4 patients (18.1%). Therefore, angiography and endovascular embolization of a. gastroduodenalis were required in 2 (9.1%) cases. In 1 (4.5%) case, we performed endoscopic hemostasis using Hemoblock hemostatic solution (4 ml). Combination of both methods was used in 1 (4.5%) patient. In 11 (50%) patients, endoscopic drainage was the final method of surgical treatment of necrotizing pancreatitis. Four patients (18.1%) died. Multiple organ failure caused mortality in 3 patients (13.6%). One (4.5%) patient died from severe nosocomial pneumonia developed in 32 days after drainage. Spurs not drained into the stomach with US-confirmed suspension and sequestration were observed in 11 (50%) out of 22 patients. These accumulations required additional ultrasound-assisted percutaneous drainage. Endoscopic transluminal drainage is a perspective minimally invasive method for necrotizing pancreatitis.

Biliary Stricture After Necrotizing Pancreatitis: An Underappreciated Challenge.

Biliary stricture in necrotizing pancreatitis (NP) has not been systematically categorized; therefore, we sought to define the incidence and natural history of biliary stricture caused by NP. Benign biliary stricture occurs secondary to bile duct injury, anastomotic narrowing, or chronic inflammation and fibrosis. The profound locoregional inflammatory response of NP creates challenging biliary strictures. NP patients treated between 2005 and 2019 were reviewed. Biliary stricture was identified on cholangiography as narrowing of the extrahepatic biliary tree to <75% of the diameter of the unaffected duct. Biliary stricture risk factors and outcomes were evaluated. Among 743 NP patients, 64 died, 13 were lost to follow-up; therefore, a total of 666 patients were included in the final cohort. Biliary stricture developed in 108 (16%) patients. Mean follow up was 3.5 ± 3.3 years. Median time from NP onset to biliary stricture diagnosis was 4.2 months (interquartile range, 1.8 to 10.9). Presentation was commonly clinical or biochemical jaundice, n = 30 (28%) each. Risk factors for stricture development were splanchnic vein thrombosis and pancreatic head parenchymal necrosis. Median time to stricture resolution was 6.0 months after onset (2.8 to 9.8). A mean of 3.3 ± 2.3 procedures were performed. Surgical intervention was required in 22 (20%) patients. Endoscopic treatment failed in 17% (17/99) of patients and was not associated with stricture length. Operative treatment of biliary stricture was more likely in patients with infected necrosis or NP disease duration ≥6 months. Biliary stricture occurs frequently after NP and is associated with splanchnic vein thrombosis and pancreatic head necrosis. Surgical correction was performed in 20%.

New Risk Factors for Infected Pancreatic Necrosis Secondary to Severe Acute Pancreatitis: The Role of Initial Contrast-Enhanced Computed Tomography.

Pancreatic necrosis is a risk factor for poor prognosis of acute pancreatitis (AP). However, the associations between the findings on initial contrast-enhanced computed tomography (CT) of the pancreas and infected pancreatic necrosis (IPN) are unclear. This was a retrospective cohort study. Patients with severe AP (SAP) from January 2014 to December 2016 at the First Affiliated Hospital of Nanchang University were enrolled and assigned to an IPN group and a non-IPN group. Univariate and multivariate logistic regression analyses were sequentially performed to assess the associations between the variables and IPN development. A receiver operating characteristic (ROC) curve was generated for the qualified independent risk factor. Forty-two patients with IPN were compared with 100 patients without IPN. Contrast-enhanced CT was performed 7 (range 3-10) days after AP onset. Multivariate stepwise logistic regression analyses showed that the number of acute peripancreatic fluid collections (APFCs) (OR 1.328, P = 0.006), presence of peripancreatic and pancreatic parenchymal necrosis (OR 4.001, P = 0.001), and gastrointestinal wall thickening (OR 3.353, P = 0.006) were independent risk factors for IPN secondary to SAP. The area under an ROC curve for the number of APFCs was 0.714, the sensitivity was 78.60%, and the specificity was 57.30% at a cutoff value of 4.5. The number of APFCs, presence of peripancreatic and pancreatic parenchymal necrosis, and gastrointestinal wall thickening were independent risk factors associated with IPN. As initial contrast-enhanced CT (about 7days from AP onset) plays an important role in predicting IPN, it is important for clinicians to consider initial imaging of the pancreas.

Impact of the site of necrosis on outcome of acute pancreatitis.

ObjecivesTo compare the clinical outcome of patients with extrapancreatic necrosis (EXPN) alone with that of acute interstitial pancreatitis (AIP), pancreatic parenchymal necrosis (PPN) alone, and combined PPN and EXPN.BackgroundThere are only a few studies in the literature in which EXPN has been recently recognized as a subtype of acute necrotizing pancreatitis (ANP), with a better prognosis.MethodsWe analyzed clinical data and outcome variables of 411 consecutive acute pancreatitis (AP) patients between January 2012 and December 2014. Contrast‐enhanced computed tomography (CECT) images of each patient were reviewed and characterized as AIP or ANP. Patients with ANP were divided into EXPN alone, PPN alone, and combined PPN and EXPN. Outcome variables were then compared between these groups.ResultsOf the 411 patients, 74 (18%) had AIP, and 337 (82%) had ANP. Patients with EXPN alone (n = 40; 11.8%) had similar outcomes as patients with PPN alone (n = 12; 3.5%); however, their outcome was worse than that of patients with AIP, with a higher frequency of persistent organ failure (POF), need for percutaneous catheter drainage (PCD), and longer length of hospitalization (LOH). Patients with combined PPN and EXPN (n = 285; 84.7%) had the worst clinical course, with higher frequency of POF, infected necrosis, intervention requirement, and longer LOH.ConclusionPatients with combined PPN and EXPN have a severe disease course with the worst clinical outcomes; patients with AIP patients have the most benign course, while patients with EXPN alone stand between the two extremes of disease course with an intermediate grade of severity.

Pancreatic Pseudocysts and Parenchymal Necrosis in Patients With Autoimmune Pancreatitis: A Systematic Review.

To investigate the prevalence and natural history of pancreatic pseudocysts (PCs) and parenchymal necrosis in autoimmune pancreatitis (AIP). A search using PubMed, Embase, Scopus, and Cochrane was performed. Search terms were AIP, PC, acute fluid collection, and pancreatic necrosis. Fifteen studies with 17 patients were included. In 8 of 17 patients, PC was noted concurrently with the AIP diagnosis, whereas in the other half, PC appeared months or years after. In 10 of 17 cases, PC appeared as solitary. The location was variable. Pseudocysts were small (<3 cm) in 4 cases and large (>3 cm) in 13 cases. A normal pancreatic duct was observed in 6 of 17 cases, whereas 9 of 17 had pancreatic duct stenosis. Steroids were given to 4 of 4 small and 10 of 13 large PC. All small PC resolved with steroids, whereas only 4 of 10 large PC treated had some response. Most (9/13) of large PC underwent endoscopic or surgical procedures. None of the 17 cases developed necrosis. Pseudocysts in AIP are rare. Pancreatic pseudocyst can present in variable number, size, and location. Small PC resolved with steroids. Large PC had poor response to steroids requiring invasive interventions. Necrosis in AIP has not been reported.

Short- and long-term results of endoscopic ultrasound-guided transmural drainage for pancreatic pseudocysts and walled-off necrosis.

AIMTo evaluate the short- and long-term results of endoscopic ultrasound-guided transmural drainage (EUS-GTD) for pancreatic fluid collection (PFC) and identify the predictive factors of treatment outcome for walled-off necrosis (WON) managed by EUS-GTD alone.METHODSWe investigated 103 consecutive patients with PFC who underwent EUS-GTD between September 1999 and August 2015. Patients were divided into four groups as follows: WON (n = 40), pancreatic pseudocyst (PPC; n = 11), chronic pseudocyst (n = 33), and others (n = 19). We evaluated the short- and long-term outcomes of the treatment. In cases of WON, multiple logistic regression analyses were performed to identify the predictor variables associated with the treatment success. In addition, PFC recurrence was examined in patients followed up for more than 6 mo and internal stent removal after successful EUS-GTD was confirmed.RESULTSIn this study, the total technical success rate was 96.1%. The treatment success rate of WON, PPC, chronic pseudocyst, and others was 57.5%, 90.9%, 91.0%, and 89.5%, respectively. Contrast-enhanced computed tomography using the multivariate logistic regression analysis revealed that the treatment success rate of WON was significantly lower in patients with more than 50% pancreatic parenchymal necrosis (OR = 17.0; 95%CI: 1.9-150.7; P = 0.011) and in patients with more than 150 mm of PFC (OR = 27.9; 95%CI: 3.4-227.7; P = 0.002).The recurrence of PFC in the long term was 13.3% (median observation time, 38.8 mo). Mean amylase level in the cavity was significantly higher in the recurrence group than in the no recurrence group (P = 0.02).CONCLUSIONThe reduction of WON by EUS-GTD alone was associated with the proportion of necrotic tissue and extent of the cavity. The amylase level in the cavity may be a predictive factor for recurrence of PFC.

Pancreatic Pseudocysts and Parenchymal Necrosis in Patients With Autoimmune Pancreatitis: A Systematic Review

Introduction: Autoimmune Pancreatitis (AIP) is being increasingly recognized as a cause of acute pancreatitis (AP). The resulting potential complications of AP such as pancreatic pseudocysts (PC) and parenchymal necrosis and their natural history and management are unknown in patients with AIP. The aim of this systematic review was to examine the prevalence of the AP complications of PC and pancreatic necrosis in patients with AIP as well as their characteristics, management and outcomes. Methods: A systematic search using PubMed/Medline, Embase, Scopus, and Cochrane was performed without language or year limitations to October 1, 2016 with a medical reference librarian. Search terms were “Autoimmune pancreatitis”, “pancreatic pseudocyst”, “acute fluid collection” and “pancreatic necrosis” with all permutations. AIP was defined according to international guidelines. The search yielded 271 results. 17 case reports dating from 2004 to 2015 were included in this systematic review. Results: 12/17 (70.6%) patients were men, with a mean age of 54.82 ± 10.97 years (Range 26-75 years). In 8/17 cases, the PC were noted concurrently with the AIP diagnosis, while in the other half, the PC appeared several months or even years after the initial AIP diagnosis. In 10/17 cases, the PC appeared on imaging as solitary, while in the remaining 7 there were multiple PC. The location of the PC was variable, being present in any segment of the pancreas. PC ranged in size from small (3cm) in 13 cases. 9cm was the maximal diameter reported. 6/17 (35%) cases had a normal pancreatic duct on imaging, while 9/17 (53%) had a narrowed/stenotic pancreatic duct. 14/17 cases received steroid therapy (4/4 small, and 10/13 large PC). All 4 small PC responded completely to steroid therapy, while only 4 of 10 (40%) with large PC treated with steroids had response. 9 of the 13 cases of large PC eventually went on to undergo endoscopic or surgical interventions. None of the 17 cases had pancreatic necrosis. Conclusion: The development of PC in AIP is a rare phenomenon with only 17 cases reported. PC can be single or multiple with variable size and location. Small PC all responded to steroid therapy. Conversely, large PC had poor response to steroid therapy, and required endoscopic or surgical drainage. AIP has not been reported to be associated with development of pancreatic necrosis.

Drug-Induced Necrotizing Pancreatitis with a Focus on Canagliflozin

Introduction: Acute necrotizing pancreatitis is an inflammatory condition of the pancreas characterized by inflammation associated with pancreatic parenchymal necrosis most commonly attributed to gallstones, alcohol abuse and metabolic disorders such as hyperlipidemia and hypercalcemia. Although several drugs have been implicated in acute pancreatitis they are often overlooked. Here we present a case of necrotizing pancreatitis likely associated to canagliflozin; a new drug in the class of subtype 2 sodium-glucose transport protein inhibitors used for the treatment of type 2 diabetes mellitus (DM T2). Case: A 71 year old female with a history of DM T2 on sitagliptin-metformin 50-1000mg twice daily and canagliflozin 100mg daily (started 84days prior to presentation) presented with complaint of sharp right upper quadrant abdominal pain, radiating to her spine and right flank with severity of 9/10. She denied recent fever/chills, nausea/vomiting or night sweats. She did report a poor appetite with 20lbs weight loss over the preceding several weeks along with daily soft stools, but no melena or hematochezia. MRI abdomen revealed a 13.0cm x 5.0cm x 5.8cm air containing mass like lesion partially encasing the pancreas. The lesion was noted to be displacing the duodenum and encasing the superior mesenteric vein. These findings were most concerning for necrotizing pancreatitis although hemorrhage or neoplasm could not be excluded by the imaging. A hepatobiliary scan was also performed showing no evidence for common bile duct or cystic duct obstruction. The results of an ultrasound guided endoscopic FNA of the pancreatic lesion showed an acute inflammatory process without nuclear atypia. The patient was treated for necrotizing pancreatitis with ertapenem and subsequent repeat CT imaging of the abdomen showed interval decrease in the size of fluid collection in the pancreatic bed. Discussion: As the prevalence of DM T2 in the United States increases, the medications used to combat the disease will increase. Our case highlights canagliflozin in the treatment of DM T2 and its potential side effects. The case identifies the importance of drug-induced pancreatitis, as it is commonly neglected in patients with multiple medical comorbidities who are on numerous medications. Current literature review revealed 3 other cases of reported canagliflozin induced pancreatitis. Prompt identification can decrease morbidity and mortality in these individuals.

Severe Acute Pancreatitis Presenting As Appendicular PerforationAn Unusual presentation

Pancreatic & Peripancreatic fluid collection is a common complication of severe Acute Pancreatitis. But rarely it can lead to collections at remote sites in peritoneal, retroperitoneal, mediastinal or inguinoscrotal region and manifesting rare presentations. Here is a case of a non alcoholic, non diabetic male, presented with abdominal pain, localized at right iliac fossa with rebound tenderness & features of peritonism. Ultrasonography of abdomen & pelvis shows moderate pelvic collection with internal echos & probe tenderness at right iliac fossa. Patient was diagnosed as a case of Appendicular perforation. On Laparotomy the case was diagnosed as severe acute pancreatitis with secondary/ reactionary appendicitis with pancreatic ascitis, peri pancreatic & pancreatic parenchymal necrosis & pelvic retroperitoneal collection in right iliac fossa extending to the base of appendix. The patient was managed with appendicectomy, draining of pelvic & retroperitoneal pelvic collection, debridement of necrotic fissure in pelvis in right iliac fossa towards right psoas muscle, debridement of patchy necrotic tissue over small bowel mesentery. Thorough irrigation, lavage & suctioning of necrotic & slaughed area on pancreas & peripancreatic tissue had also been done.

Mo1406 Does Outcome of Isolated Extrapancreatic Necrosis (EPN) in Patients With Acute Pancreatitis Differs From Both Pancreatic Parenchymal Necrosis (PPN) and EPN? Single Center Experience

Mo1406 Does Outcome of Isolated Extrapancreatic Necrosis (EPN) in Patients With Acute Pancreatitis Differs From Both Pancreatic Parenchymal Necrosis (PPN) and EPN? Single Center Experience

Clinical significance of presence and extent of extrapancreatic necrosis in acute pancreatitis.

Extrapancreatic necrosis (EPN) alone represents a subgroup of pancreatitis with better outcome than patients with pancreatic parenchymal necrosis (PN). However, data on clinical significance of EPN is limited, and significance of the extent of EPN is not known. Two hundred thirteen patients (136 [63.8%] males; mean age: 39.8 ± 13.2 years) with acute pancreatitis were prospectively enrolled and followed up till recovery or death. Contrast-enhanced computed tomography of each patient was retrospectively evaluated for presence of PN and EPN, pleural effusion and ascites. EPN was termed extensive if it extended to paracolic gutters or pelvis. Twenty-one (9.9%) patients had interstitial pancreatitis, seven (3.3%) patients had PN alone, 48 (22.5%) patients had EPN alone, and 137 (64.3%) patients had combined PN and EPN. Patients with EPN alone had significantly higher frequency of organ failure than patients with interstitial pancreatitis. Compared with patients with EPN alone, the patients with combined necrosis had significantly higher frequency of pleural effusion (88.2% vs. 75%), ascites (41% vs. 20.8%), and need for intervention (32.6% vs. 14.6%). Patients with extensive EPN (n = 57) had significantly higher frequency of pleural effusion, ascites, and multi-organ failure than those with limited EPN. EPN alone should be considered as a separate category of acute pancreatitis as it has less severe course than PN but has more severe course than interstitial pancreatitis. Patients with extensive EPN in spite of having increased frequency of ascites, pleural effusion, and multi-organ failure had similar outcome as compared to patients with limited EPN.

Multidrug Resistant Acinetobacter buamanii-Infected Pseudocyst of the Pancreas in an Immunocompetent Patient

Introduction:Acinetobacter buamanii is a pleomorphic, nonmotile gram-negative aerobic bacillus that is being increasingly reported as a causative organism of various nosocomial infections. A. buamanii is an opportunistic pathogen having a high incidence among immunocompromised individuals. We present a case of infected pseudocyt of pancreas with A. buamanii in an immunocompetent patient. Only 1 such case has been reported so far in literature. Case Report: A 50-year-old male with history of hypertension and chronic alcoholism who was recently discharged from another hospital about 1 month ago for an admission for acute severe pancreatitis, presented with complaints of abdominal pain and distention for 3 days. Patient was febrile with temperature of 38.3 C, heart rate of 104 bpm. Physical exam was significant for mildly distended abdomen, tenderness in the left lower quadrant and epigastric region, and decreased bowel sounds in all quadrants. CT abdomen showed loculated complex fluid collection surrounding the pancreas with fat necrosis and no pancreatic parenchymal necrosis, suggestive of pancreatic pseudocyst. He was started on intravenous zosyn and vancomycin. After the current management, patient did not show clinical improvement. Repeat CT abdomen showed enlarged anterior abdominal fluid collection replacing the pancreas most consistent with pancreatic necrosis, which prompted switching vancomycin and zosyn to meropenem and tobramycin, pending cultures per infectious disease recommendations. Subsequently, CT-guided pancreatic percutaneous drainage followed by surgery was done due to persistent symptoms. Exudate culture was sent, which grew multidrug resistant A. buamanii. Patient’s condition declined despite aggressive treatment and the patient unfortunately died. Conclusion: We propose that the prolonged hospital stay and history of alcoholism made the patient susceptible to infection with A. buamanii. A. buamanii should therefore be considered as a differential for infected pseudocysts in high-risk patients.Figure 1: CT abdomen showing fluid collection in the pancreas.

Walled-off pancreatic necrosis and other current concepts in the radiological assessment of acute pancreatitis.

Acute pancreatitis is an inflammatory condition caused by intracellular activation and extravasation of inappropriate proteolytic enzymes determining destruction of pancreatic parenchyma and peripancreatic tissues. This is a fairly common clinical condition with two main presentations, namely, endematous pancreatitis - a less severe presentation -, and necrotizing pancreatitis - the most severe presentation that affects a significant part of patients. The radiological evaluation, particularly by computed tomography, plays a fundamental role in the definition of the management of severe cases, especially regarding the characterization of local complications with implications in the prognosis and in the definition of the therapeutic approach. New concepts include the subdivision of necrotizing pancreatitis into the following presentations: pancreatic parenchymal necrosis with concomitant peripancreatic tissue necrosis, and necrosis restricted to peripancreatic tissues. Moreover, there was a systematization of the terms acute peripancreatic fluid collection, pseudocyst, post-necrotic pancreatic/peripancreatic fluid collections and walled-off pancreatic necrosis. The knowledge about such terms is extremely relevant to standardize the terminology utilized by specialists involved in the diagnosis and treatment of these patients.

Pancreatitis In Patients Treated With Brentuximab Vedotin: A Previously Unrecognized Serious Adverse Event

BackgroundBrentuximab vedotin (BV) is a novel antibody drug conjugate consisting of an anti- CD30 IgG1 antibody, cAC10, linked to monomethylauristatin E, a potent inhibitor of microtubule polymerization. It is approved for treatment of relapsed classical Hodgkin lymphoma (cHL) and anaplastic large cell lymphoma (ALCL) in the US (FDA; 8/2011) and Europe (EMA; 10/2012). Peripheral neuropathy was the most frequent treatment-related adverse event (AE) in phase II trials, and the most common Grade 3 or higher toxicity apart from cytopenias. Although abdominal pain has been observed in up to 25% of all patients, pancreatitis is a previously unrecognized AE. We now report 8 cases of BV-associated pancreatitis, 2 of them fatal. MethodsFollowing a grade 5 AE from pancreatitis in a patient receiving single-agent BV on an ongoing clinical trial (NCT01476410), collaborating investigators examined their collective cases of pancreatitis associated with BV. Lymphoma specialists at other centers were solicited for additional events. IRB or Ethics Committee approval as required was obtained in all cases. AE's reported to the FDA Adverse Event Report Systems (FAERS) from 6/2011-7/2013 were also examined. Data was collected and analyzed through the Research on Adverse Drug Events and Reports Project. Immunohistochemical staining with the anti-CD30 antibody BER-H2 (DAKO) was performed on residual normal pancreas from one of the fatal cases and normal control pancreas. ResultsEight cases of BV-associated pancreatitis were identified by collaborators, and one additional report with limited information was listed in FAERS. Demographic, treatment and AE information for the eight complete cases is detailed in Table 1. In all cases, BV was administered as a single agent. In seven cases, the dosing was 1.8 mg/kg every 21 days with a maximum of 180 mg; in one case, BV was administered weekly at 1.2 mg/kg (days 1,8,15, q 28). Two patients were retreated with BV after resolution of pancreatitis; one had no further evidence of pancreatitis and proceeded to a stem cell transplant, whereas the other patient, having recovered from Grade 4 pancreatitis, experienced a second episode (Grade 3). All patients demonstrated clinical evidence of pancreatitis as manifested by severe abdominal pain and nausea. In addition, all patients had biochemical and radiologic evidence of pancreatitis. Notably, no patient had an antecedent history of excess alcohol use or radiologic evidence of biliary pathology. Two patients developed progressive and fatal multiorgan dysfunction as a consequence of acute pancreatitis. An autopsy performed on one of the two fatalities showed evidence of acute necrotizing pancreatitis as the cause of death; diffuse pancreatic parenchymal necrosis and fat necrosis were seen but no cholelithiasis. Although the anti-CD30 antibody BER-H2 was previously reported to stain normal pancreas (BLOOD 1989 74:1678), routine immunohistochemical staining for CD30 on both the patient pancreas and normal pancreas controls were negative. ConclusionThis is the first series describing pancreatitis as a rare, but serious and potentially fatal toxicity related to BV. Pancreatitis has been previously reported with other microtubule inhibitors such as taxanes and vinca alkaloids, but the mechanism, as with BV, remains unclear. Genetic factors that predispose to both acute and chronic pancreatitis have been reported and may underlie a susceptibility to this uncommon complication of treatment with BV. Clinicians prescribing BV should evaluate patients who present with abdominal pain for pancreatitis, and should consider pre-treatment biochemical assessments with serum lipase and/or amylase. Disclosures:Off Label Use: Brentuximab Vedotin is approved for relapsed, refractory Hodgkin Lymphoma in patients who have already had a transplant or are ineligible for one, or for patients with relapsed, refractory anaplastic large cell lymphoma. Patients treated on clinical trials or off label will be included in this presentation. Evens:Seattle Genetics : Consultancy, Honoraria. Fenske:Seattle Genetics: Consultancy. Hamlin:Seattle Genetics : Consultancy, Honoraria. Coiffier:Millennium Pharmaceuticals : Consultancy. Engert:Millennium Pharmaceuticals : Consultancy. Moskowitz:Seattle Genetics : Research Funding. Ghosh:Millennium Pharmaceuticals : Membership on an entity's Board of Directors or advisory committees. Petrich:Seattle Genetics : Consultancy, Honoraria, Research Funding. Gordon:Seattle Genetics : Research Funding. Winter:Seattle Genetics : Research Funding.

Extrahepatic Portal Venous System Thrombosis in Recurrent Acute and Chronic Alcoholic Pancreatitis Is Caused by Local Inflammation and Not Thrombophilia

Extrahepatic portal venous system thrombosis (EPVST) occurs in 13% of patients with either recurrent acute (AP) or chronic (CP) alcoholic pancreatitis. The role of thrombophilia has never been assessed in this entity. All consecutive patients with alcoholic AP or CP were included in a prospective study. All patients underwent a computerized tomography (CT) scan of the pancreas to evaluate EPVST as well as thorough testing for thrombophilia (protein C, S, and antithrombin deficiency, factor II, factor V, and JAK2 gene mutations, homocystein, biological antiphospholipid syndrome). A total of 119 patients (male, n=100 (84%); smokers, n=110 (92%)) were included. EPVST was found in 41 patients (35%). The portal, superior mesenteric, or splenic veins were involved in 34%, 24%, and 93% of patients, respectively. Thrombophilia was identified in 18% (n=22), including the biological antiphospholipid syndrome, factor V Leiden mutation, and factor II G20210A gene mutation in 21 (17.6%), 2 (1.6%), and 1 patient (0.8%), respectively. On univariate analysis, the factors associated with EPVST were smoking (RR=1.6 (1.38-1.85), P=0.03), pseudocysts (RR=2.91 (1.29-6.56), P=0.008), a pseudocyst in the pancreatic tail (P=0.03), a high CT severity index for AP (P=0.007), and pancreatic parenchymal necrosis (P=0.02). The presence of hemostatic risk factors was not associated with an increased risk of EPVST. On multivariate analysis, only pseudocysts were associated with EPVST (hazard ratio: 6.402; 95% confidence interval (1.59-26.54), P=0.009). EPVST is found in 35% of patients with acute/chronic alcoholic pancreatitis. Local inflammation appears to be the major predisposing condition. The presence of some form of thrombophilia does not increase the risk of EPVST and should not be systematically searched for in case of EPVST.

Correlates of Morbidity and Mortality in Severe Necrotizing Pancreatitis

Acute severe pancreatitis is associated with a high morbidity and mortality and frequently is accompanied by underlying pancreatic parenchymal necrosis. Patients with pancreatic necrosis must be identified, because the morbidity and mortality rate in this subgroup is much higher. Our objective was to compare the clinical outcomes of these patients based on the degree of pancreatic necrosis. A total of 35 patients were noted to have pancreatic necrosis. These were divided into 2 groups based on extent of necrosis: group A had less than 50% necrosis and group B had more than 50% necrosis. The rate of mortality (5% versus 40%) was significantly higher in group B. The rate of organ dysfunction also rose along with the rates of other morbidities and variables that were related to a patient's hospital stay. Only APACHE II significantly correlated with the degree of necrosis, wherein the chances of substantial necrosis rose by 20% with each unit increase of APACHE II score. APACHE II Score could be employed and studied further prospectively to help identify patients with pancreatic necrosis.