Acute Pancreatitis: the revised Atlanta Classificationh24-files.s3.amazonaws.com/110213/692960-qQpMQ.pdf · Acute Pancreatitis: the revised Atlanta Classification Bruce Lehnert MD

10.05.2015

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Acute Pancreatitis: the revised Atlanta Classification

Bruce Lehnert MD

Background

• Acute pancreatitis: inflammatory process of the pancreas

– May involve adjacent or remote tissues

– High clinical variability

• 300,000 hospital admissions in the US per year

– 1‐3% overall mortality

• May be as high as 50% among patients with severe disease

– $2.2 billion

Background• Numerous causes (GETSMASHED)

– Gallstones‐ most common– EtOH– Trauma– Steroids– Mumps– Autoimmune– Scorpion Sting

• Tityus genus: central and south America

– Pancreatitis after up to 80% of stings

– Hyperlipidemia– Hypothermia– Hyperparathyroidism– ERCP– Drugs

• Azathioprine• Valproic acid

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Presentation

• Epigastric pain• Nausea, vomiting• Fever• Grey Turner sign: Bluish discoloration of flanks• Cullen Sign: Perumbilical discoloration

• Diagnostic criteria (2 out of 3 required):– Sudden onset upper abdominal pain– Serum amylase and/or lipase 3X upper limit of normal

• Levels are not markers for severity

– Findings on CT , MRI, or US characteristic of acute pancreatitis• Morphologic appearance of the pancreas and disease severity at this stage may not correlate.

• Imaging typically reserved for equivocal cases (i.e. amylase/lipase not 3X normal)

Revised Atlanta classification

• Atlanta classification for acute pancreatitis:– Introduced in 1992.– universally applicable classification system for acute pancreatitis.

– This system was designed to improve correlation and communication of findings by gastroenterologist, surgeons, and radiologists

– No therapy guidelines.

• Revised in 2008– Improve uniformity and objectivity of accepted terminology • Evolution of peripancreatic fluid, necrosis

– Assessments of clinical severity

Phases of acute pancreatitis

• Early phase (first week)– Time of disease onset defined as start of symptoms, not presentation to hospital

– Severity of acute pancreatitis primarily related to systemic inflammatory response (SIRS)• Mortality related to multi organ dysfunction.• Degree of gland necrosis typically does not influence disease at this stage.– Typically too early for infected necrosis.

• Treatment decisions during this phase are based on clinical parameters, not imaging appearance

– Disease progresses from early pancreatic inflammation and peripancreatic edema• Resolution• Necrosis• Organ failure resolves or continues to worsen

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Phases of acute pancreatitis

• Late phase (>1 week)–May extend for weeks to months

– Necrosis

– Infection • Bacteremia

• Sepsis

– Persistent multiorgan failure

– Treatment often directed by imaging findings (drain placement, necrosectomy) • Local complications: infection of necrotic tissue

– Mortality for sterile necrosis: 5‐10%

– Mortality for infected necrosis: 20‐30%

Early phase severity grading• Based on presence and duration of organ failure

• Marshall scoring system• Respiratory (paO2): 0‐4

• Cardiovascular (BP): 0‐4

• Renal (Creatinine): 0‐4

– Organ failure is defined as score ≥ 2for at least one system

• Mild pancreatitis:– Organ failure that resolves < 48 hours

– 0% Mortality

• Severe pancreatitis:– Organ failure lasting > 48 hours

Late phase classification• Morphologic Imaging Based Classification– Applied after the 1st week (or at least 72hrs) • < 5 days: gland edema and early necrosis may be difficult to distinguish.

– Differentiate between:• Acute interstitial edematous pancreatitis (IEP)

• Acute necrotizing pancreatitis

– Addresses fluid collections and peripancreatic necrosis

Day 1

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Day 3





Day 10





Day 20

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Day 120

Imaging the pancreas

• Contrast enhanced CT is modality of choice– EUS, MRI to be used for

troubleshooting, identify gallstone disease, clarify peripancreatic fluid collections

• CT Technique:– Negative oral contrast– Weight based IV contrast

dosing– Noncontrast‐ abdomen– Arterial‐ abdomen– Venous‐ abdomen and pelvis

• Morphologic Imaging Based Classification

– Acute interstitial edematous pancreatitis (IEP)

• Diffuse or localized gland enlargement

• Homogeneous/ mildly heterogeneous enhancement

• Mild peripancreatic and retroperitoneal fat stranding and simple fluid

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• Morphologic Imaging Based Classification

– Acute interstitial edematous pancreatitis (IEP)

• Diffuse or localized gland enlargement

• Homogeneous/ mildly heterogeneous enhancement

• Mild peripancreatic and retroperitoneal fat stranding and simple fluid

Morphologic Imaging Based Classification• Necrotizing pancreatitis

– Pancreas• One or more areas of gland nonenhancement (<30HU)

• Develops 24‐48 hrs after onset of symptoms

• Initially homogeneous non enhancement, later becoming more heterogeneous– Liquefying pancreatic parenchyma

• Extent of necrosis (Imaging severity)– <30%– 30‐50%– >50%

Morphologic Imaging Based Classification

• Necrotizing pancreatitis

– Peripancreatic

• Necrosis more difficult to identify

• Peripancreatic necrosis without gland necrosis

– Relatively uncommon

– Lower mortality than gland necrosis

• Heterogeneous areas of nonenhancement

– Non liquid components

– Retroperitoneum

– Lesser sac

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Morphologic Imaging Based Classification

• Necrotizing pancreatitis– Combined pancreatic and peripancreatic necrosis is most common manifestation.

– Early (<1 week)necrosis may appear solid and nonenhancing

– Late necrosis (>4 weeks) becomes more heterogeneous• Mixed liquid and solid components

• May be found with IEP and necrotizing pancreatitis:

– APFC: Acute peripancreatic fluid collections

– ANC: Acute necrotic collection

– Pseudocyst

–WON: Walled of necrosis

Fluid collections

• APFC: Acute peripancreatic fluid collection– 1st 4 weeks after disease onset

– Typically found in patients with IEP• Typically remain sterile and reabsorb spontaneously

• Intervention not necessary‐may introduce infection

– CT findings:• No solid component• No wall enhancement• Follow normal fascial planes

Fluid collections

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• ANC: Acute necrotic collection– 1st 4 weeks after disease

onset• Easiest to diagnose after first 1‐2 weeks

– Found in patients with necrotizing pancreatitis• Ini al solid necrosis → liquefied necrosis

– CT findings:• Variable amounts of fluid and necrosis

• No definable wall • Intra or extra pancreatic• May have direct connection with disrupted pancreatic duct

Fluid collections

• Pseudocyst– >4 weeks after disease onset– Develop from persistent APFC

• 20% of cases• May develop in necrotizing

pancreatitis due to duct disruption

– Fluid contains amylase and lipase• Communication with pancreatic ducts

– CT findings• Well circumscribed

– Round/oval– Well defined, enhancing wall

• Homogeneous fluid– No solid or necrotic component

• Pancreatic duct communication or dilated main pancreatic duct may be visible

• Gas within lesion suggests infection– Imaging not reliable: FNA necessary

for confirmation

Fluid collections

• WON: Walled off necrosis– >4 weeks after disease onset

– Develops from maturing ANC (60%)• Thickened wall develops

– May involve pancreas and/or peripancreatic tissue• Any fluid replacing pancreas

parenchyma after 4 weeks

– CT findings• Low attenuation, heterogeneous

fluid collection– Often irregular in shape– Loculations

• Well defined enhancing rim• Presence of gas concerning for

infection– FNA necessary for diagnosis

Fluid collections

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• WON: Walled off necrosis– >4 weeks after disease onset

– Develops from maturing ANC (60%)• Thickened wall develops

– May involve pancreas and/or peripancreatic tissue• Any fluid replacing pancreas

parenchyma after 4 weeks

– CT findings• Low attenuation, heterogeneous

fluid collection– Often irregular in shape– Loculations

• Well defined enhancing rim• Presence of gas concerning for

infection– FNA necessary for diagnosis

Fluid collections

• Local complications

– Infection

– Disconnected duct syndrome

– Portal/splenic vein thrombosis

– Hemorrhage

– Pseudoaneurysm

– Biliary obstruction

– Bowel obstruction

– Enteric fistula

Management/Complications

• Infection– All four types of fluid

collections can become infected

– Most common in necrotic collections containing nonliquified material• 20% of necrotizing pancreatitis cases

– Most common 2‐4 weeks after presentation

– Gas is collection is relatively specific• Present in minority of cases (12‐22%)

– Management• Drainage/necrosectomynecessary due to high associated mortality

Complications

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Complications

Images courtesy of Dr Bryan Balmadrid, University of Washington, Division of

Gastroenterology







Complications

Images courtesy of Dr Bryan Balmadrid, University of Washington, Division of

Gastroenterology







Complications

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Complications

• Disconnected duct– Necrosis of the central pancreas that disrupts main pancreatic duct• 40% of cases

– Residual upstream gland continues to function and excrete pancreatic juices• Growing peripancreatic fluid collection

• Pancreatic ascites

– Management• Prolonged percutaneous or transmural drainage

• ERCP stent placement for short segment disruptions.

Complications






Complications

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Complications

• Pseudoaneurysm

– Arterial wall weakened by pancreatic digestive enzymes

• Splenic artery is most common (up to 10%)

• GDA second most common

– At risk for catastrophic hemorrhage

• Stenting/embolization typically performed

Complications

• Pseudoaneurysm






Complications

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• Pseudoaneurysm






Complications

• Hemorrhage

– Spontaneous hemorrhage may results from vascular erosion/digestion, pseudoaneurysmrupture, varices

– Relatively uncommon

• 1‐5% necrotizing pancreatitis cases

Complications

• Venous Thrombosis

–Multifactorial

• Inflammation

• Mass effect on vessel lumen

• Slow flow

– Splenic vein most commonly affected

• Splenomegaly, splenic infarcts may result

Complications

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• Venous Thrombosis

–Multifactorial

• Inflammation

• Mass effect on vessel lumen

• Slow flow

– Splenic vein most commonly affected

• Splenomegaly, splenic infarcts may result

Complications

• IEP vs Necrotizing pancreatitis– Degree of gland necrosis

• <30%• 30‐50%• >50%

– Presence of peripancreatic necrosis

• < 4 weeks– APFC

• Sterile• Infected

– ANC• Sterile• Infected

• >4 weeks– Pseudocyst

• Sterile• Infected

– WON• Sterile• Infected

Summary: The radiology report

Suggested Reading• Thoeni RF. The revised Atlanta classification of acute pancreatitis: its importance

for the radiologist and its effect on treatment. Radiology 2012; 262:751‐764

• Shyu JY, Sainani NI, Sahni VA, et al. Necrotizing pancreatitis: diagnosis, imaging, and intervention. Radiographics : a review publication of the Radiological Society of North America, Inc 2014; 34:1218‐1239

• Zaheer A, Singh VK, Qureshi RO, Fishman EK. The revised Atlanta classification for acute pancreatitis: updates in imaging terminology and guidelines. Abdominal imaging 2013; 38:125‐136

• Shanbhogue AK, Fasih N, Surabhi VR, Doherty GP, Shanbhogue DK, Sethi SK. A clinical and radiologic review of uncommon types and causes of pancreatitis. Radiographics : a review publication of the Radiological Society of North America, Inc 2009; 29:1003‐1026

• Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis‐‐2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013; 62:102‐111

Acute Pancreatitis: the revised Atlanta Classificationh24-files.s3.amazonaws.com/110213/692960-qQpMQ.pdf · Acute Pancreatitis: the revised Atlanta Classification Bruce Lehnert MD

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