Classification of Acute Pancreatitis Andrzej Dąbrowski Andrzej Dąbrowski Department of Gastroenterology and Internal Medicine Medical University of Bialystok,

ClassificationClassificationof Acute Pancreatitisof Acute Pancreatitis

Andrzej DAndrzej Dąąbrowskibrowski

Department of GastroenterologyDepartment of Gastroenterologyand Internal Medicineand Internal Medicine

Medical University of Bialystok, PolandMedical University of Bialystok, Poland

Why do we need good AP classification?Why do we need good AP classification?

To improve clinical assessment of the AP

To facilitate communication between treating physicians

(uniformity)

For better reporting of clinical studies (common platform for

research)

IntroductionIntroduction – historical view – historical view

Pannala R et al. Pancreas 2009, 38, 355

Nicholaes Tulp (1593-1674) of Amsterdam is credited with the first description (1652) of acute pancreatitis.


Pannala R et al. Pancreas 2009, 38, 355

Reginald Fitz in 1889 described 3 forms of acute pancreatitis (hemorrhagic, suppurative, and gangrenous) and proposed that fat necrosis was a sequel of severe pancreatitis


Frey CF, Pancreas 1986, 1, 62

1942 – Lagerlof classified pancreatitis as acute and chronic based on clinical, functional, and pathologic observations from autopsy and operative findings.

Beginning in 1955, Joske, then Janowitz in 1957, Howard in 1960, and Dreiling in 1964 developed a comprehensive classification system of pancreatitis based on etiologic factors.

Blumenthal and Probstein in 1959 provided a classification system based on etiology in which they then categorized 163 patients from clinical and autopsy criteria.

1963 - Marseille Classification of pancreatitis

I. Acute pancreatitisII. Recurretnt acute pancreatitisIII. Recurrent chronic pancreatitisIV. Chronic pancreatitis

1983 – Cambridge classification

1984 – the second Marseille symposium


Frey CF, Pancreas 1986, 1, 62

1983 – Cambridge classification

The Cambridge group defined the severity and complications of acute pancreatitis.

An attack of acute pancreatitis was defined as “mild” if there was no multisystem failure and “severe” if multisystem failure occurred and/or there were early or late, local or systemic complications.

The complications identified for definition were (a) phlegmon, an inflammatory mass in and around the pancreas; (b) pseudocyst, a localized collection of fluid containing high concentrations of pancreatic enzymes within, adjacent to, or remote from the pancreas: and (c) abscess, pus in or around the pancreas.

Atlanta classification (1992)Atlanta classification (1992)

Bradley EL III, Arch Surg 1993, 128, 586

Definition

Acute pancreatitis

(AP)

An acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems

Associated with raised pancreatic enzyme levels in blood and/or urine

Severity

Mild AP Associated with minimal organ dysfunction and an uneventful recovery; lacks the features of severe acute pancreatitis. Usually normal enhancement of pancreatic parenchyma on contrast-enhanced computed tomography

Severe AP Associated with organ failure and/or local complications such as necrosis, abscess or pseudocyst

Predicted severity

Ranson score ≥3 or APACHE II score ≥8



Definition

Organ failure and systemic complications

Shock Systolic blood pressure < 90 mmHg

Pulmonary insufficiency

Pa O2≤60 mmHg

Renal failure Creatinine ≥177 µmol/l or ≤2 mg/dl after rehydration

Gastrointestinal bleeding

500 ml in 24 h

Disseminated intravascular coagulation

Platelets ≤100, 000/mm3, fibrinogen < 1·0 g/l and fibrin-split products > 80 µg/l

Severe metabolic disturbances

Calcium ≤1·87 mmol/l or ≤7·5 mg/dl



Definition

Local complications

Acute fluid collections

Occur early in the course of acute pancreatitis, are located in or near the pancreas and always lack a wall of granulation of fibrous tissue. In about half of patients, spontaneous regression occurs. In the other half, an acute fluid collection develops into a pancreatic abscess or pseudocyst

Pancreatic necrosis

Diffuse or focal area(s) of non-viable pancreatic parenchyma, typically associated with peripancreatic fat necrosis

Non-enhanced pancreatic parenchyma > 3 cm or involving more than 30% of the area of the pancreas



Definition

Local complications

Acute pseudocyst

Collection of pancreatic juice enclosed by a wall of fibrous or granulation tissue, which arises as a result of acute pancreatitis, pancreatic trauma or chronic pancreatitis, occurring at least 4 weeks after onset of symptoms, is round or ovoid and most often sterile; when pus is present, lesion is termed a pancreatic abscess

Pancreatic abscess

Circumscribed, intra-abdominal collection of pus, usually in proximity to the pancreas, containing little or no pancreatic necrosis, which arises as a consequence of acute pancreatitis or pancreatic trauma

Often 4 weeks or more after onset

Pancreatic abscess and infected pancreatic necrosis differ in clinical expression and extent of associated necrosis

Definitions for organ failure and predicted Definitions for organ failure and predicted severe AP in guidelines published after 1993severe AP in guidelines published after 1993

Guideline Definitions for organ failure

Definitions for severe AP

UK 2005 Refers to Atlanta Classification 1992

At admission

Clinical assessment

BMI > 30 kg/m2

Pleural effusion

APACHE score > 8

At 24-48 h

Clinical assessment

Glasgow score ≥3

APACHE II score > 8

Persistent organ failure for 48 h (especially if multiple and progressive)

CRP > 150 mg/l

Note: Organ failure present within 1 week, which resolves within 48 h, should not be considered an indicator of a severe attack of acute pancreatitis

Bollen TL et al., Br J Surg 2008, 95, 6

Definitions for organ failure and predicted Definitions for organ failure and predicted severe AP in guidelines published after 1993severe AP in guidelines published after 1993

Guideline Definitions for organ failure

Definitions for severe AP

ACG 2006 Refers to Atlanta Classification 1992

Note: Criteria of organ failure will change in the future: gastrointestinal bleeding will undoubtedly be deleted

At admission

Age > 55 years

BMI > 30 kg/m2

Presence of organ failure

Pleural effusion/infiltrates

At 24-48 h

APACHE II score ≥ 8

Serum hematocrit ≥ 44%

Note: Ranson signs are no longer advocated, due to a comprehensive evaluation of 110 studies that concluded that Ranson signs provided very poor predictive power of severity of acute pancreatitis


Definitions of severe AP local complications Definitions of severe AP local complications need revisionneed revision


Contrast-enhanced computed tomography (CT) of a patient with acute pancreatitis 30 days after onset of symptoms. The fluid collection seems to be homogeneous and encapsulated (white arrows) and could be interpreted as a pseudocyst according to the Atlanta Classification. However, at operation the collection was found to contain large amounts of necrotic debris that CT had not shown.

Acute pseudocyst

(Atlanta 1992)

Collection of pancreatic juice enclosed by a wall of fibrous or granulation tissue, which arises as a result of acute pancreatitis, pancreatic trauma or chronic pancreatitis, occurring at least 4 weeks after onset of symptoms, is round or ovoid and most often sterile; when pus is present, lesion is termed a pancreatic abscess

CT findings in APCT findings in AP

Besselink MGH et al, Pancreas 2006, 33, 331

The interobserver agreement of the Atlanta classification for categorizing peripancreatic collections in acute pancreatitis on CT is poor. The Atlanta classification should not be used to describe complications of acute pancreatitis on CT.

CT findings in APCT findings in AP

Besselink MGH et al, Pancreas 2006, 33, 331

The use of the Atlanta classification on CT in necrotizing pancreatitis. A, Computed tomography scan 12 days after onset of disease. The definitions chosen for this collection were "pseudocyst" (n = 1), "pancreatic abscess" (n = 1), "pancreatic necrosis" (n = 1), and "mixture" (n = 2). B, Computed tomography scan 27 days after onset of disease. The definitions chosen for this collection were "pancreatic abscess" (n = 3) and "mixture" (n = 2). C, Computed tomography scan 31 days after onset of disease. The definitions chosen were "pancreatic necrosis" (n = 1), "pancreatic abscess" (n = 1), "pseudocyst" (n = 1), and "mixture" (n = 2).

Need for the revision Need for the revision

Although the Atlanta Classification has proved useful over the following 16 years, many of the definitions proved confusing (used inconsistently) and have not been accepted or utilized by the pancreatic community (pancreatic gastroenterologists, surgeons, and radiologists).

Revision of the AtlantaRevision of the Atlanta classification of classification of APAP

Acute Pancreatitis Classification Working Group. Revision of the Atlanta classification of acute pancreatitis (3rd revision) . www. pancreasclub.com/resources/AtlantaClassification.pdf

DEFINITION OF ACUTE PANCREATITIS

The clinical definition of AP, whether in the presence or absence of underlying chronic pancreatitis, requires two of the following three features:

1) abdominal pain suggestive strongly of AP,

2) serum amylase and/or lipase activity at least 3 times greater than the upper limit of normal, and

3) characteristic findings of acute pancreatitis on transabdominal ultrasonography or on CECT, which is considered to be the best, most universally available imaging modality.



CLINICAL CLASSIFICATION (1st week)

DEFINITION OF SEVERITY OF ACUTE PANCREATITIS

The definition of the severity of acute pancreatitis (during the first week) is based on clinical rather than morphologic parameters (thereafter; over the first week) .

Initially at presentation and over the first 48 hours, patients should be classified temporarily as having severe acute pancreatitis based on the presence of the persistent systemic inflammatory response syndrome (SIRS) and/or developing organ failure.

Several potential risk factors of severity and measurements related to the acute pancreatitis that may reflect severity should be recorded ideally and evaluated prospectively, including age, BMI, hematocrit, APACHE II scores, and serum levels of C-reactive protein.

It should be stressed that serum amylase and lipase activities, while important in the diagnosis of “acute pancreatitis,” are not of any clinical importance in defining the severity of acute pancreatitis.



OVER THE FIRST WEEK

Over the first week, the distinction between non-severe old term: mild and severe acute pancreatitis depends ultimately on the development of organ failure.

Non-severe acute pancreatitis is defined as the absence of organ failure or the presence of organ failure that does not exceed 48 hours in duration.

The definition of severe acute pancreatitis is the persistence of organ failure that exceeds 48 hours duration (i.e., organ failure recorded at least once during each of three consecutive days).

OF>48 hrs Severe AP



DEFINITION OF ORGAN FAILURE

Three organ systems should be assessed to define organ failure: respiratory, cardiovascular, and renal.

Organ failure is best and most easily defined in accordance with the Marshall scoring system as a score ≥2 for at least one of these three organ systems: respiratory (pO2/FIO2); renal (serum creatinine in μmol/l or mg/dl); and cardiovascular (systolic blood pressure in mm Hg).

Multi-system organ failure is defined as two or more organs failing over the same 2- to 3-day period.



Marshall Scoring System

FIO2 = fraction of inspired oxygen



MORPHOLOGIC IMAGING-BASED CLASSIFICATION (used AFTER the first week)

This new classification proposes the use of morphologic CECT criteria to diagnose the specific type of acute pancreatitis:

• Acute interstitial edematous pancreatitis (IEP)

• Acute necrotizing pancreatitis.

A. Presence/absence and site(s) of necrosis, 3 subtypes:

• normal pancreatic parenchyma enhancement with peripancreatic fluid collections (fat necrosis)

• one or more focal areas of nonenhancing pancreatic parenchyma with peripancreatic fluid collections

• without peripancreatic fluid collections

B. Evidence for the presence/absence of infection (FNA, gas within nonenhancing retroperitoneal tissue)



NECROTIZING PANCREATITIS

Pancreatic Parenchyma:

About 80% of patients with necrotizing pancreatitis have a variable extent of pancreatic parenchymal necrosis on CECT.

The extent of necrosis is quantified in three categories: <30%, 30-50%, and >50% of the total pancreatic parenchyma.

The presence of pancreatic parenchymal non-enhancement differentiates necrotizing pancreatitis from IEP.

gland enlargement on CECT

minimal

diffuse

localized




Peripancreatic Tissues:

The presence or absence of necrosis in the peripancreatic tissues is more difficult to evaluate by CECT, especially early in the course of the disease.

While the presence or absence of necrosis in the peripancreatic tissues is not always possible to diagnose definitively with CECT, CECT may suggest the presence of peripancreatic necrosis by the presence of “thickening” of the paracolic gutters and of the base of the small bowel mesentery, fat stranding and involvement of the anterior pararenal spaces, or especially the presence of non-homogeneous fluid collections containing solid components in one or more areas.


Characteristics of Necrosis:

The relative amount of liquid vs semi-solid components within areas of necrosis varies with the time since onset of necrotizing pancreatitis.

As time evolves, the initially solid necrosis liquefies by a process of liquefaction necrosis. Complete resolution of necrosis (weeks to months later) may occur through liquefaction necrosis and eventual reabsorption of the liquefaction. In some patients, complete reabsorption may never occur.

If resorption does not take place, the area of liquefaction necrosis may persist as an area of walled-off pancreatic necrosis (WOPN; organized necrosis, necroma, or pancreatic sequestration) without symptoms or may cause pain or mechanical obstruction of the duodenum and/or bile duct.

solid necrosis

<1 week

semi-solid necrosis(PNPFC)>4 weeks

liquefied necrosis (WOPN)

liquefaction liquefaction(no resorption)




Infection:

Depending on the stage of the necrosis (primarily solid, semi-solid, or liquefaction) and the organism(s) involved, the infected necrosis will have varying amounts of suppuration (pus).

In the later stages of infected necrosis, the content may be predominantly pus (in addition to some solid components) as the process of liquefaction necrosis matures.

“Pancreatic abscess” according to the Atlanta Classification in 1992 is a “localized collection of purulent material without significant necrotic material;” most agree that the latter Atlanta definition of “pancreatic abscess” is an exceedingly uncommon finding in necrotizing pancreatitis. The current imaging-based classification does not use the term “pancreatic abscess” in order to avoid this confusion.



Both acute IEP and necrotizing pancreatitis can be associated with

PANCREATIC AND PERIPANCREATIC FLUID COLLECTIONS



ACUTE PERIPANCREATIC FLUID COLLECTIONS (APFCs) (1st 4 weeks after onset of IEP)

a. Sterile

b. Infected

These fluid collections arise in patients with IEP, have no solid components, and result from parenchymal and/or peripancreatic inflammation in the absence of necrosis. Resolve spontaneously within 6 weeks 40%, 80% if <6 cm; communication with pancreatic duct seen in 70%.

They exist predominantly adjacent to the pancreas, have no definable wall, and are confined by the normal peripancreatic fascial planes, primarily the anterior pararenal fascia.

APFCs arise presumably from rupture of the main duct or a small peripheral pancreatic ductal side branch or they result from local edema related to the pancreatic inflammation and have no connection with the ductal system.

Old term: acute fluid collections



POST-NECROTIC PANCREATIC/PERIPANCREATIC FLUID COLLECTIONS

a. Sterile

b. Infected

Fluid collections arising in patients with acute necrotizing pancreatitis are termed PNPFCs to distinguish them from APFCs and pseudocysts.

PNPFCs contain both fluid and necrotic contents to varying degrees.

In PNPFCs, a continuum exists from the initial solid necrosis to liquefaction necrosis, depending on duration of the disease since onset.

PNPFC may or may not have a connection with the pancreatic ductal system.

NecrosisPNPFC

(necrosis+fluid)WOPN (infected or sterile)

late stage

Old term: acute fluid collections



PANCREATIC PSEUDOCYST

Non-infected

Pseudocysts on CECT become defined >4 weeks after onset of pancreatitis as a well-circumscribed (clearly evident wall; capsule), usually round or oval, homogeneous fluid collection surrounded by a well-defined wall with no solid necrotic debris within the fluid collection.

Pseudocysts develop from an APFC that persists for >4 weeks after onset of pancreatitis. Prior to 4 weeks, these collections are categorized as APFC.

Old term: pancreatic pseudocyst


Acute Pancreatitis Classification Working Group. Revision of the Atlanta classification of acute

pancreatitis (3rd revision) . www. pancreasclub.com/resources/AtlantaClassification.pdf

PANCREATIC PSEUDOCYST

Infected (suppurative)

Determination of presence or absence of infection in a pancreatic pseudocyst is also potentially important.

An infected pancreatic pseudocyst contains purulent liquid without an associated solid component (necrosis).

This definition differentiates pseudocyst from infected PNPFC and infected WOPN. As with all peripancreatic fluid collections, image-guided FNA with Gram stain and culture or the presence of extraluminal gas are necessary to confirm the pre-interventional diagnosis of infection.

Old term: pancreatic abscess

http://www.laurentbrouat.com/wp-content/uploads/2009/10/boring-class.jpg

Acute pancreatitis has been described for the first time by:A.Reginald FitzB.David DreilingC.Nicholaes TulpD.Hippokrates of Kos

What is the uncommon complication of acute pancreatitis:A.RespiratoryB.RenalC.CardiovascularD.Gastrointestinal bleeding

The true statement about acute peripancreatic fluid collections is:A.Fluid collections arising in patients with acute necrotizing pancreatitis, but not in patients with acute interstitial edematous pancreatitis.B.Have no solid components, and result from parenchymal and/or peripancreatic inflammation in the absence of necrosis.C.Become defined >4 weeks after onset of pancreatitis as a well-circumscribed, usually round or oval, homogeneous fluid collection surrounded by a well-defined wall with no solid necrotic debris within the fluid collection.D.Contain both fluid and necrotic contents to varying degrees.

Documents

Classification of Acute Pancreatitis Andrzej Dąbrowski Andrzej Dąbrowski Department of Gastroenterology and Internal Medicine Medical University of Bialystok,