Download Radiological Hallmarks Of Necrotizing Pancreatitis

Siddharth Gosavi, Final Year MBBS
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
Siddharth Gosavi, Final Year MBBS
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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.
Siddharth Gosavi, Final Year MBBS
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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.
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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.
Siddharth Gosavi, Final Year MBBS
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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
Siddharth Gosavi, Final Year MBBS
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CAUSES
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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
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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.
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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.
Siddharth Gosavi, Final Year MBBS
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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
Siddharth Gosavi, Final Year MBBS
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OUR PATIENT: CT IMAGING OF PANCREATIC NECROSIS
CTA Abdomen 5cc/sec
Images: PACS, BIDMC Harvard
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OUR PATIENT: CT IMAGING OF PANCREATIC FLUID
COLLECTION
CT Abdomen and Pelvis with contrast: Lym/Gen
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.
Images: PACS,
• Increased peripancreatic stranding.
BIDMC Harvard
Siddharth Gosavi, Final Year MBBS
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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.
Images: PACS,
• Several smaller fluid collections in communication with the duct.
BIDMC Harvard
Siddharth Gosavi, Final Year MBBS
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OUR PATIENT: CT IMAGING OF PANCREATIC
PSEUDOCYST
CT Abdomen and Pelvis with contrast: Lym Gen
Pancreatic pseudocyst without necrosis
CT Abdomen and Pelvis with contrast: Lym
Gen Pancreatic pseudocyst
• Pseudocysts located in pancreatic body and
tail.
• Main pancreatic duct is not dilated.
• Pancreatic parenchyma enhancement is
preserved.
Increase in the size of the pseudocyst.
Images: PACS, BIDMC
Harvard
Siddharth Gosavi, Final Year MBBS
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COMPANION PATIENT 1: CT IMAGING OF ACUTE AND
CHRONIC PANCREATITIS
CT Abdomen and Pelvis: Lym/Gen A/P
Acute pancreatitis
CT Multiphase pancreas: Chronic pancreatitis
• Pancreas enhances homogeneously.
• Peripancreatic stranding and stranding.
surrounding fluid collections.
• Pancreatic duct stent in place.
• 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
Siddharth Gosavi, Final Year MBBS
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INTERVENTION
Tenner S, Baillie J, Dewitt J, Vege SS. American College of Gastroenterology guideline:
Management of acute pancreatitis. Am J Gastroenterol 2013; 108:1400.
Siddharth Gosavi, Final Year MBBS
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INTERVENTION
• CT guided FNA
• 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.
Siddharth Gosavi, Final Year MBBS
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COMPLICATIONS
• Infection
• 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.
Siddharth Gosavi, Final Year MBBS
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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.
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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.
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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.
Siddharth Gosavi, Final Year MBBS
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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.