Acute Interstitial Edematous Pancreatitis Research Articles

FRI657 Case Series On GLP-1 Receptor Agonist Related Acute Pancreatitis

Abstract Disclosure: A.U. Kulkarni: None. V. Mehta: None. M. Renzu: None. K. Pereira: None. M.A. Rather: None. Introduction: Acute pancreatitis (AP) has now become one of the leading causes of GI related hospital admissions in the United States. With increasing use of GLP-1 Receptor Agonists (GLP-1 RA) in T2DM and obesity, they are now being identified as one such class of drugs which can cause AP. We present this case series to discuss these adverse effects. Case 1: A 50 yo AA male with a history of T2DM and hypertension presented with acute severe epigastric pain, nausea and vomiting for 5 days. Vitals were stable. On physical exam, tenderness in the RUQ was noted. Labs revealed lipase of 313 U/l (11-82 U/l), BG of 213 mg/dL, HbA1c 11.3, normal LFT and lipid panel. Blood EtOH was negative. He denied tobacco, alcohol, and illicit drug use. CT abdomen showed acute interstitial edematous pancreatitis without cholelithiasis or choledocholithiasis. Liver ultrasound showed hepatic steatosis. He noted recent initiation of Semaglutide 6 months ago which was stopped 3 weeks prior to this visit due to abdominal discomfort. Previous Dulaglutide therapy was also discontinued due to GI intolerance. Home medication for DM otherwise included metformin and basal insulin. Case 2: A 68 yo AA woman with a history of T2DM, hypothyroidism presented after a week of severe epigastric pain, radiating to her back, with nausea and vomiting. Labs showed lipase 593 U/l (11-82 U/l), BG of 427 mg/dl, HbA1c of 10. Social history was non-contributory. CT Abdomen showed AP and no gallstones or bile duct dilatation. LFTs and lipid panel were unremarkable. Chart review noted prior admission for AP a month ago. Her home medications were basal Insulin and Dulaglutide (4 yrs). Drug induced AP from Dulaglutide was suspected. Lack of clinical improvement after 3 days of management prompted RUQ ultrasound, which was prematurely terminated due to pain during the scan. Subsequent CCK-HIDA was negative for acute cholecystitis but noted low gallbladder EF. Thus dulaglutide was identified as a potential trigger along with gallbladder dysmotility as a possible etiology for her recurrent AP. Both patients were managed with IV fluids, NPO diet and morphine. They were instructed to stop GLP-1 RA and discharged with PCP follow-up. Discussion: GLP-1 RA are now being widely used due to low risk of hypoglycemia and weight loss. Clinical trials with GLP-1 RA have shown mild, asymptomatic increase in lipase, amylase levels as well as rare incidences of AP. This has been attributed to the stimulation of pancreatic beta cells and exocrine duct cells leading to acinar cell hypertrophy, proinflammatory cytokine induction, causing pancreatic injury. Though drug-induced AP is uncommon and is a diagnosis of exclusion, detailed history taking, medication review and investigating for all other causes is of utmost importance. A good understanding of the drugs associated with AP should alert the physician to identify these agents and promptly discontinue them to prevent further complications. Presentation: Friday, June 16, 2023

Successful Treatment of Pancreatic Pseudocysto-Duodenum Fistula with Ultrasound Endoscopic Drainage: A Case Report

Pancreatic pseudocysts represent a complication of acute interstitial edematous pancreatitis with a frequency of about 10–20%, and most of these resolve spontaneously. Treatment is indicated only in patients who develop symptoms such as abdominal pain, gastric outlet obstruction, jaundice for compression of the biliary system, or in case of infection. Pancreatic pseudocysts’ complications include pseudocyst infection leading to sepsis, rupture with pancreatic ascites, bleeding or formation of pseudoaneurysm, and, rarely, fistulization to other viscera. The most common sites for fistulas are between cysts and the stomach, duodenum, and colon. Here, we present the case of a patient with severe acute pancreatitis who developed multiple infected fluid collections with a cysto-duodenum fistula that was successfully treated with endoscopic intervention.

PSUN272 Opportunity for Inpatient Use of Continuous Glucose Monitoring: A Case Report of Acute Pancreatitis Secondary to Hypertriglyceridemia

Abstract Background Continuous glucose monitoring (CGM) is a convenient method of estimating blood glucose (BG) levels through a minimally invasive subcutaneous electrode that senses interstitial fluid glucose readings. With recent advancements, this technology has the potential to transmit interstitial fluid glucose readings to electronic health records (EHR) in real-time. While some benefits of CGM have been studied in outpatient settings, current CGM research is beginning to explore the use and benefits of CGM in inpatient settings. The following case of acute pancreatitis (AP) secondary to hypertriglyceridemia (HTG) presents a novel opportunity for inpatient use of CGM. Clinical Case A 33-year-old-man with anxiety, alcohol use disorder, and without insulin resistance, presents as a transfer to a tertiary-care-center for consideration of plasmapheresis in the setting of AP secondary to HTG. He initially presented to outside hospital with acute onset diffuse abdominal pain. Family history of father with controlled HTG and hyperlipidemia on statins. Hemodynamically stable. Examination revealed diffuse abdominal tenderness. Labs revealed triglyceride (TG) level 3550 mg/dL (n<150 mg/dL), lipase 1423 U/L (n 0-160 U/L), TSH normal, A1c 5.2% (n<5.7%). CT abdomen pelvis with contrast revealed moderate acute interstitial edematous pancreatitis without necrosis, pseudocyst, or mass. He was volume resuscitated with intravenous (IV) fluids, then started on a non-titratable regular insulin infusion (N-TII) at 2 U/hr and continuous IV fluids with dextrose. Upon arrival, his BG was 101 mg/dL. The N-TII rate was decreased to 1 U/hr and managed with hourly finger-stick BG checks and continuous IV fluids with dextrose plus KCl. Arrival TG was 954 mg/dL. The case was discussed with Transfusion Medicine—given the down-trending TG level, plasmapheresis was not initiated. The next morning, repeat TG level was <500 mg/dL, thus, the N-TII was discontinued. During admission, BG ranged from 86-179 mg/dL and IV fluids with dextrose required titration of rate and concentration to avoid hypoglycemia while severe HTG resolved. Conclusion This case presents a novel scenario in which there is an opportunity for inpatient use of CGM. In addition to point-of-care finger-stick BG checks, the implementation of inpatient CGM may be beneficial in tracking glucose trends when N-TII are required for management of severe HTG, but risk iatrogenic hypoglycemia. Not only does this highlight an area in need of further research and technological developments that link CGM data to EHR in real-time, but also, by continuing to identify new opportunities for inpatient CGM use, we can better understand its nuances and implications, thus, thoughtfully advocate for policies and protocols that optimize benefits and justify cost of inpatient CGM. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

Acute pancreatitis in pregnancy following COVID-19 vaccine: a case report

BackgroundSince the approval of the Pfizer–BioNTech (BNT162b2) mRNA vaccine for COVID-19 infection, a few adverse effects have been reported. Acute pancreatitis has been reported in a few patients. However, there is currently no research showing a direct relationship between the vaccine and acute pancreatitis. Here, we report a case of acute pancreatitis following Pfizer vaccination in a young healthy pregnant woman without any known risk factors. To our knowledge, this is the first case report of possible vaccine-induced pancreatitis in a pregnant woman.Case presentationThe patient, a 24-year-old South-Asian female, at 31 weeks of gestation, presented with severe epigastric pain radiating to the back and worsening on lying supine, associated with nausea and vomiting. She was diagnosed with acute pancreatitis with a serum lipase level of 4376 U/L and an ultrasound showing features of pancreatitis. The patient received her first dose of the Pfizer vaccine 1 week prior to these symptoms. Detailed evaluation did not show any etiological cause of pancreatitis. The patient had a spontaneous vaginal delivery and the baby was shifted to the neonatal intensive care unit in a stable condition. A computed tomography scan postpartum (day 2) demonstrated acute interstitial edematous pancreatitis. The patient was managed conservatively in the intensive care unit and discharged home in a stable condition.ConclusionThis report highlights the importance of a detailed history and evaluation, and the close monitoring of any patient presenting with abdominal pain after vaccination. Acute pancreatitis can be fatal if not picked up early.

Hypertriglyceridemia-Induced Acute Pancreatitis During Pregnancy: A Case Report

Hypertriglyceridemia-induced acute pancreatitis is a rare and serious condition that places both the mother and the fetus at severe risk for morbidity and mortality. The goal of this case report is to describe the management of a pregnant patient with severely elevated triglycerides in the setting of acute pancreatitis. A 28-year-old female G2P1001 at 29 weeks of gestational age presented with epigastric abdominal pain. A computed tomography scan of the abdomen and pelvis with contrast demonstrated acute interstitial edematous pancreatitis. A lipid panel was performed, revealing a serum triglyceride level of 3,949 mg/dL. Insulin and maternal bowel rest reduced her serum triglyceride levels; however, additional medical therapy including fibrate and statin drugs were initiated to achieve goal levels of triglycerides and improve patient symptoms. The patient ultimately recovered and remained on treatment until delivery. Initial management addresses acute pancreatitis and involves fluid resuscitation, pain control, and bowel rest. Triglyceride-lowering drug therapies are rarely used during pregnancy due to the potential for fetal teratogenicity; however, given the severity of hypertriglyceridemia fenofibrate and atorvastatin were prescribed. Additional medical treatment included insulin, omega-3, and ethyl eicosapentaenoic acid.

Beyond acute cholecystitis—gallstone-related complications and what the emergency radiologist should know

The purpose of this study is to emphasize the imaging features of complications of gallstones beyond the cystic duct on ultrasound (US), enhanced and nonenhanced computed tomography (CECT and NECT), magnetic resonance imaging (MRI), magnetic resonance cholangiopancreatography (MRCP), and endoscopic retrograde cholangiopancreatography (ERCP). This article includes a brief overview of gallstone imaging and emerging trends in the detection of gallstones. This review article will highlight complications of gallstones, including choledocholithiasis, gallstone pancreatitis, acute cholangitis, Mirizzi syndrome, cholecystobiliary and cholecystoenteric fistulas, and gallstone ileus. Imaging findings and limitations of US, CT, MRI, and ERCP will be discussed. The review article will also briefly discuss the management of each disease. The presence of gallstones beyond the level of the cystic duct can lead to a spectrum of diseases, and emergency radiologists play a critical role in disease management by providing a timely diagnosis. Documenting the location of a gallstone within the common bile duct (CBD) in symptomatic cholelithiasis and the presence of acute interstitial edematous pancreatitis and/or ascending cholangitis plays a pivotal role in disease management. Establishing the presence of ectopic gallstones and biliary-enteric fistulae has a significant role in directing patient management.

Role of Computed Tomography in Predicting Severity of Acute Pancreatitis

The current study was based on Computed Tomography (CT) findings and results. We found 63% of patients with acute interstitial edematous pancreatitis, and we found 37% of patients with acute necrotic pancreatitis in 46 cases. Based on our findings, we observed bulky pancreas among 26 cases (56.52%), 17 cases (36.95%) of pancreatic necrosis, 9 cases of pancreatic atrophy, 11 cases of pseudocyst, and 9 cases of peri-pancreatic fluid. When we evaluated the Modified CT Severity index among the study cases, we observed that 19.56% cases have mild index, the majority (56.52% cases) have moderate index while 23.91% have severe index. We also found that majority of the cases were clinically cured and discharged, i.e., 47.82%. 19.56% of the total study subjects reported recurrence of episodes of pancreatitis, while 30.43% of the total patients turned into chronic pancreatitis. This study presents a cross-sectional hospital-based analytical study carried out among 46 cases of AP referred to under the radiology department for further diagnostic evaluation, in a tertiary healthcare facility in Maharashtra. The present study Data Source included all the AP patients referred to the radiological department in a tertiary health research center. They met the standards for inclusiveness, which assented to the analysis. Type of study is Hospital analytical based study. The study duration is 18 months. Data collection was done through semi-structured, pre-designed, and pre-validated proformas in patients meeting inclusion requirements that included disease history, clinical outcomes, investigative records, and descriptions of surgical interventions.

Pancreatitis due to Clomiphene Citrate-Induced Hypertriglyceridemia: A Case Report and Literature Review

Objective: Clomiphene citrate-induced hypertriglyceridemia causing acute pancreatitis is rare. The aim of this case report is to alert physicians to the possibility of clomiphene citrate-induced hypertriglyceridemia that can lead to acute, and even chronic, pancreatitis. Methods: We describe a patient with known mild hypertriglyceridemia who presented with acute pancreatitis and severe hypertriglyceridemia after initiation of clomiphene citrate. Results: The patient had mid-epigastric tenderness with radiation around her bilateral flanks in a band-like distribution. Lab studies showed a triglyceride level greater than 4,425 mg/dL, a lipase level greater than 3,000 U/L, and computed tomography of the abdomen showed acute interstitial edematous pancreatitis. The patient's Naranjo Adverse Drug Reaction score was calculated to be a 7, and was therefore probable as clomiphene being the causative agent. The patient's triglyceride levels improved after initiation of fibrate therapy and discontinuation of clomiph...

New predictor of acute necrotizing pancreatitis: Red cell distribution width.

Acute pancreatitis (AP) is inflammation of the pancreas of various severity ranging from mild abdominal pain to mortality. AP may be classified as acute interstitial edematous pancreatitis (AEP) or acute necrotizing pancreatitis (ANP), according to the revised Atlanta criteria. Most of the patients with AP are AEP (75-85% of patients), while 15-25% of patients have ANP. The mortality rate is 3% in AEP and 15% in ANP. Thus, it is important to predict the severity of AP to decrease the morbidity and mortality. The aim of the study was to evaluate the relationship between red cell distribution width (RDW) and the severity of AP on admission to hospital. Patients admitted to Adana Numune Research and Educational Hospital with a diagnosis of AP through the time frame of January 2014-May 2016 were included in our study. Diagnosis of AP was made according to the revised Atlanta classification. Patients' age, sex, etiology of AP, and RDW values were recorded on admission to the hospital. A total of 180 patients were included in the study. Eighty patients (44%) were male and 100 patients were female. Mean age was 56.25 ±18.3 years (52.66 ±14.4 in males; 59.84 ±20.2 in females). There was no statistically significant difference between patients' age. The most frequently observed etiologic factor was gallstone disease followed by alcohol intake and the use of pharmaceuticals. Drug-related AP was associated with azathioprine, furosemide, and thiazide diuretics. One hundred forty-four (80%) patients had AEP and 36 (20%) patients had ANP. RDW values showed a statistically significant difference between patients with AEP and ANP (p = 0.011). The cut-off value of RDW was 16.4 and the area under curve (AUC) value was 0.591 (p = 0.0227) with a sensitivity of 29.2% and specificity of 89.83%. Red cell distribution width could be used to evaluate the prognosis of acute pancreatitis.

Outcome of Acute Pancreatic and Peripancreatic Collections Occurring in Patients With Acute Pancreatitis.

To study the outcome of acute collections occurring in patients with acute pancreatitis BACKGROUND:: There are limited data on natural history of acute collections arising after acute pancreatitis (AP). Consecutive patients of AP admitted between July 2011 and December 2012 were evaluated by imaging for development of acute collections as defined by revised Atlanta classification. Imaging was repeated at 1 and 3 months. Spontaneous resolution, evolution, and need for intervention were assessed. Of the 189 patients, 151 patients (79.9%) had acute collections with severe disease and delayed hospitalization being predictors of acute collections. Thirty-six patients had acute interstitial edematous pancreatitis, 8 of whom developed acute peripancreatic fluid collections, of which 1 evolved into pseudocyst. Among the 153 patients with acute necrotizing pancreatitis, 143 (93.4%) developed acute necrotic collection (ANC). Twenty-three of 143 ANC patients died, 21 had resolved collections, whereas 84 developed walled-off necrosis (WON), with necrosis >30% (P = 0.010) and Computed Tomographic Severity Index score ≥7 (P = 0.048) predicting development of WON. Of the 84 patients with WON, 8 expired, 53 patients required an intervention, and 23 were managed conservatively. Independent predictors of any intervention among all patients were Computed Tomographic Severity Index score ≥7 (P < 0.001) and interval between onset of pain to hospitalization >7 days (P = 0.04). Patients with severe AP and delayed hospitalization more often develop acute collections. Pancreatic pseudocysts are a rarity in acute interstitial pancreatitis. A majority of patients with necrotising pancreatitis will develop ANC, more than half of whom will develop WON. Delay in hospitalization and higher baseline necrosis score predict need for intervention.

Necrotizing pancreatitis: diagnosis, imaging, and intervention.

Acute necrotizing pancreatitis is a severe form of acute pancreatitis characterized by necrosis in and around the pancreas and is associated with high rates of morbidity and mortality. Although acute interstitial edematous pancreatitis is diagnosed primarily on the basis of signs, symptoms, and laboratory test findings, the diagnosis and severity assessment of acute necrotizing pancreatitis are based in large part on imaging findings. On the basis of the revised Atlanta classification system of 2012, necrotizing pancreatitis is subdivided anatomically into parenchymal, peripancreatic, and combined subtypes, and temporally into clinical early (within 1 week of onset) and late (>1 week after onset) phases. Associated collections are categorized as "acute necrotic" or "walled off" and can be sterile or infected. Imaging, primarily computed tomography and magnetic resonance imaging, plays an essential role in the diagnosis of necrotizing pancreatitis and the identification of complications, including infection, bowel and biliary obstruction, hemorrhage, pseudoaneurysm formation, and venous thrombosis. Imaging is also used to help triage patients and guide both temporizing and definitive management. A "step-up" method for the management of necrotizing pancreatitis that makes use of imaging-guided percutaneous catheter drainage of fluid collections prior to endoscopic or surgical necrosectomy has been shown to improve clinical outcomes. The authors present an algorithmic approach to the care of patients with necrotizing pancreatitis and review the use of imaging and interventional techniques in the diagnosis and management of this pathologic condition.

Acute interstitial edematous pancreatitis: Findings on non-enhanced MR imaging

To study the appearances of acute interstitial edematous pancreatitis (IEP) on non-enhanced MR imaging. A total of 53 patients with IEP diagnosed by clinical features and laboratory findings were underwent MR imaging. MR imaging sequences included fast spoiled gradient echo (FSPGR) fat saturation axial T1-weighted imaging, gradient echo T1-weighted (in phase), single shot fast spin echo (SSFSE) T2-weighted, respiratory triggered (R-T) T2-weighted with fat saturation, and MR cholangiopancreatography. Using the MR severity score index, pancreatitis was graded as mild (0-2 points), moderate (3-6 points) and severe (7-10 points). Among the 53 patients, IEP was graded as mild in 37 patients and as moderate in 16 patients. Forty-seven of 53 (89%) patients had at least one abnormality on MR images. Pancreas was hypointense relative to liver on FSPGR T1-weighted images in 18.9% of patients, and hyperintense in 25% and 30% on SSFSE T2-weighted and R-T T2-weighted images, respectively. The prevalences of the findings of IEP on R-T T2-weighted images were, respectively, 85% for pancreatic fascial plane, 77% for left renal fascial plane, 55% for peripancreatic fat stranding, 42% for right renal fascial plane, 45% for perivascular fluid, 40% for thickened pancreatic lobular septum and 25% for peripancreatic fluid, which were markedly higher than those on in-phase or SSFSE T2-weighted images (P<0.001). IEP primarily manifests on non-enhanced MR images as thickened pancreatic fascial plane, left renal fascial plane, peripancreatic fat stranding, and peripancreatic fluid. R-T T2-weighted imaging is more sensitive than in-phase and SSFSE T2-weighted imaging for depicting IEP.

The role of oxygen-derived free radicals in two models of experimental acute pancreatitis: Effects of catalase, superoxide dismutase, dimethylsulfoxide, and allopurinol

The role of oxygen-derived free radicals was evaluated in two models of experimental acute pancreatitis by testing the effects of agents which either reduce oxygen-derived free radical generation or scavenge those free radicals. Those agents (catalase, superoxide dismutase, polyethylene glycol-superoxide dismutase, dimethylsulfoxide, and allopurinol) were evaluated using the choline-deficient ethionine-supplemented diet-induced model of acute hemorrhagic pancreatic necrosis and the supramaximal caerulein stimulation model of acute interstitial edematous pancreatitis. In both models, the only effect associated with administration of the test agents was a reduction in the degree of pancreatic edema. These results suggest that oxygen-derived free radicals may play an important role in the development of pancreatic edema during pancreatitis but that those free radicals do not play an important role in the development of acinar cell injury.

Penetration of lanthanum through the main pancreatic duct epithelium in cats following exposure to infected human bile

The main pancreatic duct epithelium acts as a barrier to the diffusion of molecules from the duct lumen into pancreatic acinar and interstitial tissue. We studied sequential ultrastructural characteristics of the loss of epithelial barrier function in the cat using lanthanum, an electron-opaque tracer, following perfusion of the duct from the tail to the duodenum with infected human bile. Tight junctions between duct epithelial cells were found to become permeable to the tracer as early as after 15 min of exposure. Later, there was progressive disintegration of intercellular junctions and epithelial loss. Lanthanum penetrated the duct epithelium exclusively on an intercellular path. Loss of barrier function of the pancreatic duct epithelium was consistently associated with subsequent development of acute interstitial edematous pancreatitis. There was no association between the degree of duct epithelial damage and the severity of acute pancreatitis. Both bile and a suspension of bacteria alone were not harmful to the pancreas. Sequential perfusion produced acute pancreatitis only when at first bile and then the bacterial suspension was perfused. A reversed succession of perfusates produced no morphologic alterations. We conclude: (1) Increased tight junction permeability is an early lesion in acute bile-induced pancreatitis: (2) loss of duct epithelial barrier function is important for the initiation but not for the severity of the inflammation; and (3) bile renders duct epithelial intercellular junctions vulnerable to Escherichia coli bacteria.

Role of phospholipase A2 in human acute pancreatitis

In a prospective clinical trial, 85 patients with acute pancreatitis, including 50 with acute interstitial-edematous pancreatitis and 35 with necrotizing pancreatitis, were recruited. Serum pancreatic immunoreactive phospholipase A2 (IR-PLA2), serum phospholipase A catalytic activity (CA-PLA), and serum phospholipase A2 catalytic activity (CA-PLA2) were determined daily between day 1 and day 10 after the onset of the disease. The serum course of IR-PLA2 values for patients with acute interstitial-edematous pancreatitis was comparable to that for patients with necrotizing pancreatitis. In contrast, the determination of CA-PLA and of CA-PLA2 specific activity in the serum revealed a high differentiation between patients with interstitial edematous and those with necrotizing pancreatitis. The overall accuracy for differentiating patients with necrotizing pancreatitis from those with the interstitial-edematous type was 79% for CA-PLA and 77% for CA-PLA2 (cut-off level: CA-PLA, 15 U/L, day 1–5; CA-PLA2, 3.5 U/L, day 1–5). Patients with pancreatitis-associated pulmonary complications showed significantly higher CA-PLA and CA-PLA2 values in the serum. This study demonstrates the role of serum catalytic phospholipase A2 in human acute pancreatitis where the development of pancreatic necrosis and pulmonary failure is concerned.