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Clasificacion pancreatitis aguda 2012.pdf

Clasificacion pancreatitis aguda 2012.pdf

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cation of acute pancreatitis
2012:revision of the Atlanta classi
cation and de
nitionsby international consensus
Peter A Banks,
Thomas L Bollen,
Christos Dervenis,
Hein G Gooszen,
Colin D Johnson,
Michael G Sarr,
Gregory G Tsiotos,
Santhi Swaroop Vege,
Acute Pancreatitis Classi
cation Working Group
Additional data are publishedonline only. To view these
lesplease visit the journal online(http://dx.doi.org/10.1136/ gutjnl-2012-302779).
Division of Gastroenterology,Hepatology, and Endoscopy,Harvard Medical School,Brigham and Women
sHospital, Boston,Massachusetts, USA
Department of Radiology,St Antonius Hospital,Nieuwegein, the Netherlands
First Department of Surgery,Agia Olga Hospital, Athens,Greece
Evidence-Based SurgeryResearch Unit, University of Nijmegen, Nijmegen,the Netherlands
University HospitalSouthampton, Southampton,UK
Department of Surgery, MayoClinic, Rochester, Minnesota,USA
Division of Digestive Surgery,Metropolitan Hospital, Athens,Greece
Department of Medicine,Division of Gastroenterologyand Hepatology, Mayo Clinic,Rochester, Minnesota, USA
Correspondence to
Michael G Sarr, Departmentof Surgery, Mayo Clinic(GU 10-01), 200 1st St SW,Rochester, MN 55905, USA;sarr.michael@mayo.eduRevised 29 August 2012Accepted 29 August 2012Published Online First25 October 2012
ABSTRACTBackground and objective
The Atlanta classi
cationof acute pancreatitis enabled standardised reporting of research and aided communication between clinicians.De
ciencies identi
ed and improved understanding of thedisease make a revision necessary.
A web-based consultation was undertaken in2007 to ensure wide participation of pancreatologists.After an initial meeting, the Working Group sent a draftdocument to 11 national and international pancreaticassociations. This working draft was forwarded to allmembers. Revisions were made in response tocomments, and the web-based consultation wasrepeated three times. The
nal consensus was reviewed,and only statements based on published evidence wereretained.
The revised classi
cation of acute pancreatitisidenti
ed two phases of the disease: early and late.Severity is classi
ed as mild, moderate or severe. Mildacute pancreatitis, the most common form, has no organfailure, local or systemic complications and usuallyresolves in the
rst week. Moderately severe acutepancreatitis is de
ned by the presence of transient organfailure, local complications or exacerbation of co-morbiddisease. Severe acute pancreatitis is de
ned bypersistent organ failure, that is, organ failure >48 h.Local complications are peripancreatic
uid collections,pancreatic and peripancreatic necrosis (sterile orinfected), pseudocyst and walled-off necrosis (sterile orinfected). We present a standardised template forreporting CT images.
This international, web-based consensusprovides clear de
nitions to classify acute pancreatitisusing easily identi
ed clinical and radiologic criteria. Thewide consultation among pancreatologists to reach thisconsensus should encourage widespread adoption.
The Atlanta Symposium in 1992 attempted to offera global
and a universally applicable clas-si
cation system for acute pancreatitis.
 Althoughthe Atlanta Classi
cation has been useful, some of the de
nitions proved confusing.
Better understand-ing of the pathophysiology of organ failure andnecrotising pancreatitis and their outcomes, as wellas improved diagnostic imaging, have made it neces-sary to revise the Atlanta Classi
cation. This revi-sion includes a clinical assessment of severity andprovides more objective terms to describe the localcomplications of acute pancreatitis.The goal of this report is to present the updatedrevision of the Atlanta Classi
cation of acute pan-creatitis in adults (>18 years). This revision wasdesigned to incorporate modern concepts of thedisease, to address areas of confusion, to improveclinical assessment of severity, to enable standardisedreporting of data, to assist the objective evaluationof new treatments, and to facilitate communicationamong treating physicians and between institutions.This consensus classi
cation de
nes criteria for thediagnosis of acute pancreatitis, differentiates the two
cance of this study What is already known on this subject?
The original Atlanta Classi
cation of acute pan-creatitis of 1992 is outdated.
Two types of acute pancreatitis have beendescribed: acute oedematous pancreatitis andacute necrotising pancreatitis.
The description of pancreatic and peripancreaticcollections is confusing and not universal.
What are the new
This current global consensus classi
cation ofacute pancreatitis offers a comprehensive clas-si
cation of acute pancreatitis, severity andperipancreatic collections.
New information of aetiology, pathophysiology,severity and radiologic descriptions of pancre-atic and peripancreatic collections are provided.
This classi
cation differentiates acute peripan-creatic
uid, pancreatic pseudocyst, acute nec-rotic collections and walled-off necrosis.
How might it impact on clinical practice inthe foreseeable future?
This classi
cation of acute pancreatitis willallow a consistent, worldwide classi
The description of pancreatic and peripancreaticcollections on cross-sectional imaging will allowa consistent terminology across all studies.
This classi
cation of acute pancreatitis shouldavoid the confusion in terminology seen overthe last 20 years.
111. doi:10.1136/gutjnl-2012-302779
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types of acute pancreatitis (interstitial oedematous pancreatitisand necrotising pancreatitis), classi
es the severity of acute pan-creatitis into three categories, and de
nes the morphology seen onimaging of pancreatic and peripancreatic collections that arise ascomplications of acute pancreatitis. This revision is not intendedto be a management guideline.
This classi
cation was generated by an iterative, web-based con-sultation process led by a working group and incorporatingresponses from the members of 11 national and internationalpancreatic societies. All responses were reviewed by the workinggroup, and the process was repeated by a web-based approachuntil the current fourth draft, which was then
nalised for sub-mission. A full description of the methods is shown in onlinesupplementary appendix 1. There are many substantial andimportant differences in the current document when comparedto our preliminary working draft that appeared on the PancreasClub website
and which has been referred to by otherauthors.
Revised de
nitions and classi
cation of acute pancreatitis
The following de
nitions and classi
cations are proposedfor use in clinical and research communications.
nition of diagnosis of acute pancreatitis
The diagnosis of acute pancreatitis requires two of the followingthree features: (1)
abdominal pain
consistent with acute pancrea-titis (acute onset of a persistent, severe, epigastric pain often radi-ating to the back); (2) serum
lipase activity (or amylase activity) atleast three times greater than the upper limit of normal
; and (3) charac-teristic
ndings of acute pancreatitis on contrast-enhancedcomputed tomography (CECT) and less commonly magnetic res-onance imaging (MRI) or transabdominal ultrasonography.
If abdominal pain suggests strongly that acute pancreatitis ispresent, but the serum amylase and/or lipase activity is less thanthree times the upper limit of normal, as may be the case withdelayed presentation, imaging will be required to con
rm thediagnosis.
13 14
If the diagnosis of acute pancreatitis is establishedby abdominal pain and by increases in the serum pancreaticenzyme activities, a CECT is not usually required for diagnosisin the emergency room or on admission to the hospital.
nition of onset of acute pancreatitis
The onset of acute pancreatitis is de
ned as the time of onsetof abdominal pain (not the time of admission to the hospital).The time interval between onset of abdominal pain and
rstadmission to the hospital should be noted. When patients withsevere disease are transferred to a tertiary hospital, the intervalsbetween onset of symptoms,
rst admission and transfershould be noted. Data recorded from a tertiary care hospitalshould be strati
ed to allow separate consideration of theoutcomes of patients who were admitted directly and thoseadmitted by transfer from another hospital (see online supple-mentary appendix 2 for suggested recording of data).
nition of types of acute pancreatitis
 Acute pancreatitis can be subdivided into two types: interstitialoedematous pancreatitis and necrotising pancreatitis.
 Interstitial oedematous pancreatitis
The majority of patients with acute pancreatitis have diffuse(or occasionally localised) enlargement of the pancreas due toin
ammatory oedema. On CECT, the pancreatic parenchymashows relatively homogeneous enhancement, and the peripan-creatic fat usually shows some in
ammatory changes of hazi-ness or mild stranding. There may also be some peripancreatic
uid (see below, De
nition of pancreatic and peripancreatic col-lections) (
gures 1 and 2). The clinical symptoms of interstitialoedematous pancreatitis usually resolve within the
rst week.
 Necrotising pancreatitis
 About 5
10% of patients develop necrosis of the pancreaticparenchyma, the peripancreatic tissue or both (see below,De
nition of pancreatic and peripancreatic collections) (
gures 3,4, 5). Necrotising pancreatitis most commonly manifests asnecrosis involving both the pancreas and peripancreatic tissuesand less commonly as necrosis of only the peripancreatic tissue,and rarely of the pancreatic parenchyma alone.The impairment of pancreatic perfusion and signs of peripan-creatic necrosis evolve over several days,
which explainswhy an early CECT may underestimate the eventual extent of pancreatic and peripancreatic necrosis. In the
rst few days of the illness, the pattern of perfusion of the pancreatic paren-chyma as seen on CECT may be patchy, with variable attenu-ation before the area of impaired enhancement becomes moredemarcated and/or con
uent. After the
rst week of thedisease, a non-enhancing area of pancreatic parenchyma shouldbe considered to be pancreatic parenchymal necrosis.In peripancreatic necrosis, the pancreas enhances normally onCECTas it does with interstitial oedematous pancreatitis, but theperipancreatic tissues develop necrosis. Patients with peripancrea-tic necrosis alone have increased morbidity and interventionrates compared to patients with interstitial oedematouspancreatitis.
15 17 20
The natural history of pancreatic and peripancreatic necrosisis variable, because it may remain solid or liquefy, remainsterile or become infected, persist, or disappear over time.
Infected pancreatic necrosis
Pancreatic and peripancreatic necrosis can remain sterile orbecome infected; most of the evidence suggests no absolute cor-relation between the extent of necrosis and the risk of infectionand duration of symptoms.
Infected necrosis is rare duringthe
rst week.
21 25
Figure 1
A 63-year-old man with acute interstitial oedematouspancreatitis. There is peripancreatic fat stranding (arrows) without anacute peripancreatic
uid collection; the pancreas enhances completelybut has a heterogeneous appearance due to oedema.
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The diagnosis of infected pancreatic necrosis is importantbecause of the need for antibiotic treatment and likely activeintervention.
The presence of infection can be presumedwhen there is extraluminal gas in the pancreatic and/or peri-pancreatic tissues on CECT (
gure 6) or when percutaneous,image-guided,
ne-needle aspiration (FNA) is positive for bac-teria and/or fungi on Gram stain and culture.
There may be avarying amount of suppuration (pus) associated with theinfected pancreatic necrosis, and this suppuration tends toincrease with time with liquefaction. The original AtlantaClassi
cation proposed the term
pancreatic abscess
to de
ne a
localised collection of purulent material
without signi
 cant nec-rotic material
nding is extremely uncommon, andbecause the term is confusing and has not been adoptedwidely,
the term
pancreatic abscess
is not used in thecurrent classi
cation.The development of secondary infection in pancreatic necro-sis is associated with increased morbidity and mortality.
Complications of acute pancreatitis
nition of organ failure
Three organ systems should be assessed to de
ne organ failure:respiratory, cardiovascular and renal. Organ failure is de
ned asa score of 2 or more for one of these three organ systems usingthe modi
ed Marshall scoring system
(table 1). The modi
edMarshall scoring system has the merit of simplicity, universalapplicability across international centres, and the ability tostratify disease severity easily and objectively.
The modi
edMarshall scoring system is preferred to the SOFA scoringsystem,
which is for patients managed in a critical care unitand which takes into account the use of inotropic and respira-tory support. Both scoring methods have the advantage of being able to be used on presentation and repeated daily.
30 31
They also allow strati
cation of the severity of organ failure,although that is not part of the current classi
Figure 3
(A) Acute necrotic collections (ANC) in a 44-year-old manwith acute necrotising pancreatitis involving only the peripancreatictissues. Note enhancement of the entire pancreatic parenchyma (whitestars) and the heterogeneous, non-liquid peripancreatic components inthe retroperitoneum (white arrows pointing at the borders of the ANC).(B) The ANC in the same patient as (A) but imaged a few weeks laterdemonstrate a heterogeneous collection with areas of fat (black arrowheads) surrounded by
uid density, and areas which have aslightly greater attenuation (black arrows) than seen in collectionswithout necrosis such as shown in
gure 7. This
nding is typical forperipancreatic necrosis. White arrows denote border of ANC; whitestars denote enhancement of pancreatic parenchyma. The ANC are notyet fully encapsulated.
Figure 2
(A) A 38-year-old woman with acute interstitial oedematouspancreatitis and acute peripancreatic
uid collection (APFC) in the leftanterior pararenal space (white arrows showing the borders of theAPFC). The pancreas enhances completely, is thickened, and has aheterogeneous appearance due to oedema. APFC has
uid densitywithout an encapsulating wall. (B) A few weeks later, a follow up CTshows complete resolution of the APFC with minimal residualperipancreatic fat stranding.
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