Under the guidance of Gillian Lieberman, MD March 2016 RADIOLOGICAL HALLMARKS OF NECROTIZING PANCREATITIS Siddharth Gosavi, Vydehi Institute of Medical Sciences & Research Centre, India Under the guidance of Gillian Lieberman, MD
1 AGENDA Discuss the etiology, symptomatology and signs of necrotizing pancreatitis. Review the pathogenesis of necrotizing pancreatitis. Discuss the investigations and cardinal radiologic features of necrotizing pancreatitis. Discuss the management and interventional procedures in necrotizing pancreatitis. Discuss the complications of necrotizing pancreatitis.
2 OUR PATIENT: BACKGROUND A 62 year old male presented to the ED with onset of severe abdominal pain. He has a past history of IgA nephropathy, failed left renal transplant in 1991, HTN, CKD, TIA, right hip surgery and osteoporosis. On examination, he was tachycardic and dyspneic. Abdomen was tender in the epigastrium. Labs revealed leukocytosis of 13K with left shift, normal LFTs and a lipase > 5000. He received aggressive fluid resuscitation with 6L in total crystalloid boluses. Peritoneal fluid sampling revealed a dark red color fluid. CT abdomen and pelvis with contrast was performed and showed severe necrotizing pancreatitis.
3 Definition: Necrotizing pancreatitis can be defined as an inflammation associated with pancreatic parenchymal necrosis with or without peripancreatic necrosis. CECT criteria defines necrotizing pancreatitis as lack of pancreatic parenchymal enhancement and/or presence of peripancreatic necrosis like acute necrotic collection and walled off necrosis. Classification: 1) Acute necrotic collection-<4 weeks after disease onset. 2) Walled off necrosis->4 weeks after disease onset-parenchymal necrosis or peripancreatic necrosis or combined necrosis. Source: Jeffrey Y.Shyu et al. Necrotizing Pancreatitis: Diagnosis, Imaging and Intervention. RadioGraphics 2014; 34:1218 1239.
4 PATHOPHYSIOLOGY Pancreatitis begins in acinar cells and leads to the premature, intra-acinar activation of digestive zymogens into their active forms. This leads to inflammation and parenchymal cell death through apoptosis and necrosis. The activated pancreatic enzymes cause autodigestion. Injury to the pancreatic duct or its branches lead to leakage of pancreatic enzymes into the lesser sac and the retroperitoneum. The enzyme rich fluid and necrotic collections if persistent will eventually develop fibrosis around its periphery leading to pseudocysts and WOPN. Source: Abraham Mathew, B S Anand. Pancreatic Necrosis and Pancreatic Abscess. http://emedicine.medscape.com/article/181264-overview
5 CAUSES Alcohol (>100g/day for >3 to 5 years) Gallstones Infection (Coxsackie B Virus, CMV, Mumps) Post ERCP Hypercalcemia, Hypertriglyceridemia Medications like ACE inhibitors, aspariganase, azathioprine, oral estrogens, antibiotics, furosemide, pentamidine, sulfa drugs, valproate, thiazide diuretics and corticosteroids Choledochal Cyst Post renal transplant Hereditary familial pancreatitis Peptic Ulcer Vasculitis Sphincter of Oddi stenosis Blunt or penetrating trauma Cystic Fibrosis Source: Amy Dean, Elaine Lonnemann, Dave Pariser, Scott Buxton, Wendy Walker. Pancreatitis. http://www.physio-pedia.com/pancreatitis
6 CLINICAL PICTURE Symptoms: pain abdomen radiating to the back, nausea, loss of appetite, fever and vomiting are the commonest symptoms. Signs: fever, malaise, abdominal tenderness in upper quadrants, rigidity of the upper abdominal muscles, decreased bowel sounds, tachycardia, tachypnea, hypotension, hypovolemia, jaundice, changes in mental status, Grey-Turner s sign and Cullen s sign. Vascular: shock, pericardial effusion and tamponade. Pulmonary: hypoxia, atelectasis, pneumonia, ALI, pleural effusion. GI: bleeding, abdominal compartment syndrome. Urogenital: ARF, renal artery or vein thrombosis. Metabolic: hypocalcemia, hyperglycemia, metabolic acidosis, hypomagnesia. Hematologic: vascular thrombosis, DIC.
7 MANAGEMENT INVESTIGATIONS: CBC, LFT, BUN, serum creatinine, serum amylase, serum lipase, serum calcium, serum magnesium, glucose, lipid profile, ECG, C-reactive protein, procalcitonin. Contrast enhanced tomography of the abdomen is the standard modality of imaging for identifying severe pancreatic necrosis, fluid collection or pseudocysts and the development of its complications. MRI is used if there is a contraindication to contrast enhanced CT. MRCP is a noninvasive technique that is used preoperatively to determine if patients can benefit from ERCP. It is as accurate as contrast enhanced CT in assessing pancreatic necrosis, pancreatic and peripancreatic cysts. ERCP is useful in identifying the less common causes of pancreatitis such as microlithiasis, sphincter of Oddi dysfunction, pancreatic strictures. It is performed in patients with biliary obstruction, cholangitis, elevated bilirubin, worsening jaundice. Source: Jeffrey Y.Shyu et al. Necrotizing Pancreatitis: Diagnosis, Imaging and Intervention. RadioGraphics 2014; 34:1218 1239.
8 OUR PATIENT: CT IMAGING OF PANCREATIC NECROSIS CTA Abdomen 5cc/sec CTA Abdomen 5cc/sec The majority of the pancreas with the exception of the distal most tail is nonenhancing. Pancreas is enlarged and edematous. Prominent surrounding stranding. Images: PACS, BIDMC Harvard
9 OUR PATIENT: CT IMAGING OF PANCREATIC NECROSIS CTA Abdomen 5cc/sec Images: PACS, BIDMC Harvard
10 OUR PATIENT: CT IMAGING OF PANCREATIC FLUID COLLECTION CT Abdomen and Pelvis with contrast: Lym/Gen A/P A/P Multiple fluid collections in the pancreatic bed and uncinate process. Cystic lesions seen in the pancreatic tail. Cyst replacement of the pancreatic parenchyma. Increased peripancreatic stranding. CT Abdomen and Pelvis with contrast: Lym/Gen Images: PACS, BIDMC Harvard
11 OUR PATIENT: MR IMAGING OF PANCREATIC FLUID COLLECTION MRI Abdomen and Pelvis: Ax SSFSE Multiple high T2 signal fluid collections in the head and body of the pancreas. The pancreatic duct is irregular, but not dilated. Several smaller fluid collections in communication with the duct. Images: PACS, BIDMC Harvard
12 Siddharth Gosavi, Final Year MBBS OUR PATIENT: CT IMAGING OF PANCREATIC PSEUDOCYST CT Abdomen and Pelvis with contrast: Lym Gen Pancreatic pseudocyst without necrosis Pseudocysts located in pancreatic body and tail. Main pancreatic duct is not dilated. Pancreatic parenchyma enhancement is preserved. CT Abdomen and Pelvis with contrast: Lym Gen Pancreatic pseudocyst Increase in the size of the pseudocyst. Images: PACS, BIDMC Harvard
13 Siddharth Gosavi, Final Year MBBS COMPANION PATIENT 1: CT IMAGING OF ACUTE AND CHRONIC PANCREATITIS CT Abdomen and Pelvis: Lym/Gen A/P Acute pancreatitis Pancreas enhances homogeneously. Peripancreatic stranding and stranding. surrounding fluid collections. Pancreatic duct stent in place. CT Multiphase pancreas: Chronic pancreatitis Extensive calcifications in the head,body and tail of the pancreas. Main pancreatic duct dilated. Pancreatic parenchyma is diffusely hypo enhancing. Images: PACS, BIDMC Harvard
14 INTERVENTION Tenner S, Baillie J, Dewitt J, Vege SS. American College of Gastroenterology guideline: Management of acute pancreatitis. Am J Gastroenterol 2013; 108:1400.
15 CT guided FNA INTERVENTION Percutaneous catheter drainage Percutaneous necrosectomy Endoscopic and lapraroscopic necrosectomy Video-assisted debridement Hybrid techniques-combination of PCD and endoscopic necrosectomy Open surgical necrosectomy Source: Jeffrey Y.Shyu et al. Necrotizing Pancreatitis: Diagnosis, Imaging and Intervention. RadioGraphics 2014; 34:1218 1239.
16 Infection COMPLICATIONS Inflammation and mass effect on adjacent organs Biliary obstruction Disconnected pancreatic duct syndrome Pancreatic duct stricture Pseudoaneurysm Haemorrhage Venous thrombosis Source: Jeffrey Y.Shyu et al. Necrotizing Pancreatitis: Diagnosis, Imaging and Intervention. RadioGraphics 2014; 34:1218 1239.
17 PROGNOSIS In our patient, gallstones were identified as a major cause of necrotizing pancreatitis. The patient underwent ERCP stone removal and sphincterotomy. This was followed by laparoscopic cholecystectomy. Peritoneal dialysis was avoided in this patient and as an alternative, a tunneling right internal jugular haemodialysis catheter was placed for the patient to undergo haemodialysis. The patient is also being considered for another kidney transplantation by the transplant team.
18 TAKE-AWAY Urgent fluid and electrolyte replacement. Monitor vital signs. Do not use prophylactic antibiotics initially. Early enteric feeds. Supportive care in case of sterile necrosis. Consider urgent ERCP in case of biliary obstruction. Consider urgent surgical debridement in case of infected necrosis. Minimally invasive procedures have been found to have better outcomes.
19 REFERENCES 1) Jeffrey Y.Shyu et al. Necrotizing Pancreatitis: Diagnosis, Imaging and Intervention. RadioGraphics 2014; 34:1218 1239. 2) Tenner S, Baillie J, Dewitt J, Vege SS. American College of Gastroenterology guideline: Management of acute pancreatitis. Am J Gastroenterol 2013; 108:1400. 3) Amy Dean, Elaine Lonnemann, Dave Pariser, Scott Buxton, Wendy Walker. Pancreatitis. http://www.physio-pedia.com/pancreatitis 4) Abraham Mathew, B S Anand. Pancreatic Necrosis and Pancreatic Abscess. http://emedicine.medscape.com/article/181264-overview 5) Images: PACS BIDMC Harvard.
20 ACKNOWLEDGEMENT I would like to thank Dr. Gillian Lieberman for all her guidance and teaching. I would like to thank Dr. Matthew Miller and Dr. Almamoon Justanaiah for helping me with the selection of the case and guidance on the selection of the appropriate images for the presentation. I would like to thank Katherine Armstrong for help in organization of the presentation.