Multi modality Imaging in Acute Pancreatitis. Marsha Lynch, HMS III Gillian Lieberman, MD BIDMC Core Clerkship in Radiology March 2009

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Transcription:

Multi modality Imaging in Acute Pancreatitis Marsha Lynch, HMS III Gillian Lieberman, MD BIDMC Core Clerkship in Radiology March 2009

Our Patient R: Introduction 52M with 10d history of nausea, vomiting and abdominal pain.

Patient R: Initial Presentation PRESENTATION WBC 19.1 ARF: Cr 3.2 (baseline 1.2) BG: 235 Lipase: 2211(0 60) Amylase: 804 (0 100) ALT:10 AST:9 AP:79 Ca: 7.9 (8.4 10.2) TGs: 511 (0 149) PMH HTN Hyperlipidemia Congenital deafness Gout Obesity

Patient R demonstrates a typical presentation of acute pancreatitis

Acute Pancreatitis: Pathophysiology INFLAMMATION OF THE PANCREAS Inappropriate activation of pancreatic enzymes Intraparenchymal and extraparenchymal extravasation of enzymes cause autodigestion of pancreatic parenchyma and damage to peripancreatic tissues and vascular network Inflammatory response to this injury out of proportion to that of other organs to a similar insult Inflammatory response causes further damage Fluid sequestration, fat necrosis, vasculitis leading to occlusions and thrombosis, hemorrhage Whitcomb, D C, Acute Pancreatitis. N Engl J Med 2006 Balthazar, E J, Acute Pancreatitis: Assessment of Severity with Clinical and CT Evaluation. Radiology 2002

Acute Pancreatitis: Etiologies Etiologies of Acute Pancreatitis Mechanical Toxic Metabolic Trauma Infection Vascular Congenital Genetic Miscellaneous Gallstones (>45%), sludge, pancreatic mass, ampullary stenosis or mass,duodenal stricture or obstruction Alcohol (>35%), methanol, steroids/ drugs, scorpion venom Hyperlipidemia, hypertriglyceridemia, hypercalcemia Blunt or penetrating, ERCP, s/p abdominal surgery Viral (mumps), parasitic, bacterial Ischemia, embolism, vasculitis Pancreas divisum CFTR mutation Autoimmune, renal transplant, alpha 1 anti trypsin deficiency Adapted from etiology of acute pancreatitis ; Up-To-Date

Acute Pancreatitis: Epidemiology >200,000 US hospital admission yearly 20% have a severe course Associated with systemic and local complications and increased mortality (10 30%) Severe Course SYSTEMIC COMPLICATIONS Shock DIC Pulm. Insufficiency/ARDS LOCAL COMPLICATIONS Necrosis Abscess Pseudocyst Pseudoaneurysm Splenic vein thrombosis

Acute Pancreatitis: Severity Assessment Severity of acute pancreatitis is commonly assessed using : 1. Ranson s Criteria 5 clinical signs at presentation and 6 at 48hrs 3 associated with severe course (systemic complications and/or pancreatic necrosis) 2. APACHE II 12 routine physiologic measurement, age and previous health status 8 associated with severe course 3. CT Severity Index (CTSI) Based on extent of inflammation and presence of complications on CT scan.

Let s briefly review the anatomy of the pancreas

Pancreas Anatomy http://www.fairview.org/healthlibrary/content/pancreas.gif Retroperitoneal organ stretching from the curvature of the duodenum to the spleen. Rich arterial supply from vessels off the celiac artery superiorly and the SMA inferiorly. Glandular tissue with both endocrine and exocrine function.

Pancreas Anatomy: Axial CT View pancreas pancreas Companion Patient 1: Delayed Phase Axial CT Image from: PACS, BIDMC

Acute Pancreatitis CLINICAL DIAGNOSIS Abdominal pain Nausea/Vomiting Elevated Pancreatic Enzymes MANAGEMENT Bowel Rest/NPO IVF Analgesics http://www.fairview.org/healthlibrary/content/pancreas.gif

The diagnosis of pancreatitis is largely a clinical one based on physical signs and symptoms as well as serum levels of pancreatic enzymes. What then is the role of Radiology in its management?

Role of Radiology in Acute Pancreatitis Rule out other intra abdominal conditions as cause of abdominal pain or other symptoms Bowel obstruction, infarction or perforation; acute cholecystitis; appendicitis Confirm diagnosis and Identify causes (e.g. gallstones) Evaluate and stage local pancreatic morphology Identify and manage complications Menu of Tests: US, Plain Film, CT, MR

Back to Our Patient R

Patient R: Ranson s Criteria Ranson s Score 3 (Threshold) At Presentation Age > 55 BG > 200 WBC > 16,000 LDH > 350 ALT > 250 Within 48 Hours Hct > 10% decrease Serum Ca < 8 Base Def > 4 BUN > 5 increase Fluid Sequestration > 6L PaO 2 < 60 PATIENT X PRESENTATION WBC 19.1 BG 235 Age 52 ALT 10 LDH 15

We are less concerned about our patient progressing down an more severe path based on him having only 2/5 Ranson s criteria at presentation.

However, we can use radiology to assess whether his acute pancreatitis is due to one of the commonest etiologies: gallstones. We therefore proceed to abdominal Ultrasound

Use of Abdominal Ultrasound in Acute Pancreatitis Indicated early in acute pancreatitis Pros Inexpensive Excellent for identifying gallbladder pathology, sludge and gallstones (Most common cause of pancreatitis!) Evaluate bile duct dilation May visualize masses and follow up of pseudocyst Cons Not optimal for pancreas; retroperitoneal location easily obscured by bowel gas distension Less sensitive for stones in distal CBD Limited in early assessment of pancreatitis Balthazar, E J, Acute Pancreatitis: Assessment of Severity with Clinical and CT Evaluation. Radiology 2002

Patient R Abdominal US: Liver,GB Liver parenchyma: no gross intra-hepatic ductal dilitation Gallbladder: anechoic cystic region with increased throughtransmission Abdominal Ultrasound: RUQ Image from: PACS, BIDMC

Patient R Abdominal US: GB Absence of hyperechoic foci Non-distended GB with normal wall thickness Abdominal Ultrasound: RUQ No signs of acute cholecyctitis: lack of gallbladder wall thickening, pericholecystic fluid or cholelithiasis Image from: PACS, BIDMC

Happily, our suspicion of gallbladder pathology as the cause of our patient R s acute pancreatitis is now greatly lowered. So we continue supportive management with bowel rest, IVF and analgesics.

On Hospital Day 5 our Patient R develops bowel distension and abdominal pain. We proceed immediately to Abdominal Plain Film

Use of Abdominal Plain Film in Acute Pancreatitis Pros Screen for/exclude separate or accompanying abdominal process Signs of peritonitis or bowel ischemia Free air Bowel Obstruction Ascites Inexpensive, readily available and fast Cons Poor visualization of the pancreas and retroperitoneum May see calcifications due to chronic process

Patient R: Abdominal Plain Film HD 5 Transverse colon shows no marked distention but with no contrast spasm of the desc. colon just distal to splenic flexure residual contrast in asc. and desc. colon ----- isolated segments of dilated sm. bowel, up to 3cm luminal diameter Abdominal Plain Film: Supine Image from: PACS, BIDMC

Patient R Abdominal Plain Film HD 5 Air fluid levels Abdominal Plain Film: L Lat Decubitus Image from: PACS, BIDMC

The presence of distension in the along with air fluid levels concern us for small bowel obstruction. We decide to closely follow our patient.

On Hospital Day 6 Our patient has worsening abdominal pain and distension. We quickly perform a repeat abdominal plain film.

Patient X Abdominal Plain Film HD 6 Distended stomach arrest of contrast (2 days) 8.5 cm Marked distension of transverse colon, still with no contrast in lumen. 3.3 cm Increased focal distension of small bowel Abdominal Plain Film: Supine Image from: PACS, BIDMC

We are certainly more concerned about obstruction now. Before we continue, let s review some possible causes of obstruction in this patient.

Possible Causes of Bowel Obstruction in Our Patient R Functional Focal ileus/sentinel loops (Transverse colon and segments of small bowel) due to adjacent pancreatic inflammatory process Mechanical Pancreatic mass Developing fluid collections or pseudocyst GB unseen on U/S

We are more concerned about yet unseen causes of any mechanical obstruction. We now proceed to Abdominal CT to further evaluate the cause of the increasing abdominal distension and to have a better look at the inflamed pancreas.

Pros Use of Abdominal CT in Acute Readily available and Fast Pancreatitis Aid in diagnosis and staging of pancreatitis Depict, quantify pancreatic parenchymal injury Ability to assess the presence or absence of: Edema (focal or diffuse) Peripancreatic fluid and inflammation Fluid collections Pseudocysts Necrosis Evaluate common bile duct for stones or other obstructions Cons Our Patient R is in ARF and this may be exacerbated by IV contrast administration

Patient R Delayed Phase axial CT: Supra pancreatic fluid collection 4x7cm fluid collection just superior to the pancreas Delayed Phase CT: Axial Image from: PACS, BIDMC

Normal vs. Acute Pancreatitis Acute pancreatitis: swollen, edematous gland with indistinct edges blurred into those of surrounding structures Normal pancreas: Fluffy, macronodular gland texture distinct from surrounding organs Axial Delayed Phase CT: Companion Pt. 1 Axial Delayed Phase CT: Patient R Images from: PACS, BIDMC

Patient R: Abdominal CT peripancreatic fat stranding and peripancreatic fat stranding patent splenic vein patent splenic vein Axial Delayed Phase CT: Patient R Axial Delayed Phase CT: Patient R Images from: PACS, BIDMC

Patient R Abdominal CT: Focal Transverse Ileus and Arrest of adynamic transverse colon arrest of contrast Contrast Axial Delayed Phase CT: Patient R Axial Delayed Phase CT: Patient R Images from: PACS, BIDMC

Patient R Abdominal CT: Suspicious hyperattenuating lesion There is a round hyperdensity measuring 1.4cm with similar attenuation as the adjacent aorta. We can also visualize the IVC posterior and the GDA adjacent and just superior to the lesion. This could represent: 1.Pseudoaneurysm of GDA 2.Gallstone 3.Reactive lymph node. Delayed Phase CT: Axial Image from: PACS, BIDMC

What Now??? We need to further explore this lesion as our last study was limited by the lack of both a non contrast and arterial phase. Luckily, we have another tool in our arsenal.

Use of MR in Acute Pancreatitis Increasingly used in diagnosis and management of acute pancreatitis Pros Non invasive and no use of IV contrast Ability to better characterize fluid collections (acute collection vs. abscess, necrosis, hemorrhage, pseudocyst) Ability to delineate pancreatic and bile ducts (detect choledocholithiasis missed on U/S ) and other complications comparable to ERCP Greater sensitivity vs. CT in detecting mild pancreatitis Cons Expensive and in many less severe cases not necessary for diagnosis and management Less readily available in non tertiary medical centers

Patient R: Abdominal MR Our lesion has high signal distinct from the absence of signal (flow-void sequence) in the other three vessels of interest: GDA, IVC and aorta. In particular, the lesion is distinct from the GDA, significantly reducing our suspicion for pseudoaneurysm. T2 MRI: flow-void sequence Image from: PACS, BIDMC

Patient R: High signal lesion on MR In this sequence, gallstones would demonstrate no signal and our lesion is consistent with a reactive lymph node. T2 MRI: flow-void sequence Image from: PACS, BIDMC

Patient R: Comparison of CT versus MRI findings Delayed Phase CT: Axial T2 MR: flow-void sequence The suspicious lesion on CT was further evaluated on MR and found to be benign consistent with a reactive lymph nose Images from: PACS, BIDMC

A word about Pleural Effusions

Pleural Effusions: a common complication of Acute Pancreatitis Patient R: Delayed Phase CT Low lung volumes, Bibasilar atelectasis and pleural effusions Patient R: Frontal CXR Images from: PACS, BIDMC Approx. 1/3 patients with acute pancreatitis will have will have abnormal CXRs. The typical findings include elevated hemidiaphragm, pleural effusions, atelectasis and in more severe cases ARDS Patient R: Lateral CXR

Patient R: Remaining Course HD 6 Emesis and large BM that largely relieved abdominal pain Started on TPN Diet slowly advanced until tolerated regular diet Continued on supportive measures as labs normalized and symptoms resolved Discharged to Home on HD 16

Patient R Remaining Course cont d PRESENTATION WBC 19.1 ARF: Cr 3.2 (baseline 1.0) BG: 235 Lipase: 2211(0 60) Amylase: 804 (0 100) ALT:10 (0 40) AST:9 (0 40) AP:79 (39 117) Ca: 7.9 (8.4 10.2) TGs: 511 (0 149) DISCHARGE WBC 7.4 Cr 0.9 BG: 95 Lipase: 59*(0 60) Amylase: 50* (0 100) ALT:18 AST:29 AP:79* Ca: 8.7 (8.4 10.2) TGs: 112 (0 149) * Last labs drawn before date of discharge

Summary Acute Pancreatitis is a common illness with many potential highly morbid complications. Many cases are diagnosed clinically and managed supportively with bowel rest, aggressive fluid administrations and analgesics. Radiology plays important role in confirming diagnoses, evaluating severity and identifying and managing complications of acute pancreatitis.

References Whitcomb, D C, Acute Pancreatitis. N Engl J Med 2006;354:2142 50. Balthazar, E J, Acute Pancreatitis: Assessment of Severity with Clinical and CT Evaluation. Radiology 2002; 223:603 613 Textbook of Gastrointestinal Radiology / [edited by] Richard M. Gore, Marc S. Levine. London : W. B. Saunders Co., c2000. Up-To-Date, Clinical manifestations and diagnosis of acute pancreatitis, etiologies of acute pancreatitis

Acknowledgements Ernest Yeh, MD Maria Levantakis, Course Co ordinator Gillian Lieberman, MD