Acute pancreatitis classification
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Joseph Nasr, M.D.[2]; Monish Thuvooru Muthu Kalyanaraman, M.B.B.S[3]
Overview
Acute pancreatitis may be classified according to four complementary features: clinical phase, clinical severity, morphologic subtype, and type of pancreatic or peripancreatic collection. The Revised Atlanta Classification (RAC) is the principal international framework and classifies severity as mild, moderately severe, or severe according to organ failure and local or systemic complications.[1] The Determinant-Based Classification (DBC) is an alternative four-tier system that combines organ failure with the presence and infection status of pancreatic or peripancreatic necrosis.[2]
These classifications describe different aspects of the same episode and should not be used interchangeably. Etiologic classification, prediction scores such as APACHE II, BISAP, and the Ranson criteria, and imaging severity indices are addressed in their respective microchapters.
| Classification axis | Categories | Principal clinical purpose |
|---|---|---|
| Clinical phase | Early phase and late phase | Distinguishes the predominantly systemic early response from the later course in which persistent organ failure and local complications must be described together |
| Clinical severity | Mild, moderately severe, or severe by the RAC; mild, moderate, severe, or critical by the DBC | Standardizes communication, outcome reporting, and clinical risk stratification |
| Morphology | Interstitial edematous pancreatitis or necrotizing pancreatitis | Describes the presence, location, and evolution of pancreatic or peripancreatic necrosis |
| Local collection | Acute peripancreatic fluid collection, pancreatic pseudocyst, acute necrotic collection, or walled-off necrosis | Standardizes the description of collections according to pancreatitis subtype, contents, encapsulation, and time from symptom onset |
Classification
Acute pancreatitis is classified below using the terminology and definitions of the Revised Atlanta Classification and the complementary Determinant-Based Classification.
Classification Based on Clinical Phase
Acute pancreatitis has two overlapping clinical phases: an early phase that usually lasts for the first week and a late phase that may continue for weeks to months.[1][3][4]
| Feature | Early phase | Late phase |
|---|---|---|
| Usual timing | First week after symptom onset | After the first week; may persist for weeks to months |
| Principal driver | Systemic response to pancreatic injury, including systemic inflammatory response syndrome and organ dysfunction | Persistent systemic inflammation, organ failure, and/or evolving local complications |
| Basis of severity assessment | Primarily clinical: presence and duration of organ failure | Clinical and morphologic: organ failure, local complications, and infection status |
| Role of imaging | Imaging may confirm an uncertain diagnosis or assess deterioration, but early CECT can underestimate evolving necrosis | Cross-sectional imaging is more reliable for characterizing necrosis, collection contents, and encapsulation |
| Patients affected | All patients with acute pancreatitis | Generally patients with moderately severe or severe acute pancreatitis |
- The phases overlap rather than changing at a rigid time point.
- The onset of acute pancreatitis is dated from the onset of abdominal pain, not from hospital admission.[1]
- Morphologic findings do not replace clinical assessment of organ failure in the early phase.
- Routine CT is not required solely to assign an early severity category when the diagnosis is established and the patient is improving. CT should be reserved for diagnostic uncertainty, clinical deterioration, or failure to improve after 48–72 hours.[5]
Classification Based on Severity
Acute pancreatitis severity is classified most commonly using the three-tier Revised Atlanta Classification; the four-tier Determinant-Based Classification may be used when the interaction between organ failure and infected necrosis needs to be emphasized.
Revised Atlanta Classification
Acute pancreatitis is classified by the RAC as mild, moderately severe, or severe according to the presence and duration of organ failure and the presence of local or systemic complications.[1][6][7]
| RAC severity grade | Organ failure | Local or systemic complications | Definition |
|---|---|---|---|
| Mild | None | None | No organ failure and no local or systemic complications |
| Moderately severe | Transient organ failure that resolves within 48 hours, or no organ failure | May be present | Transient organ failure and/or local or systemic complications, without persistent organ failure |
| Severe | Persistent organ failure involving one or more organ systems | May be present or absent | Organ failure that persists beyond 48 hours |
- Local complications include acute peripancreatic fluid collection, pancreatic pseudocyst, acute necrotic collection, walled-off necrosis, and other local manifestations such as gastric outlet dysfunction, splenic or portal vein thrombosis, and colonic necrosis.[1]
- Systemic complications are exacerbations of pre-existing comorbid disease precipitated by acute pancreatitis, such as worsening chronic lung disease or coronary artery disease.[1]
- Transient organ failure resolves within 48 hours and places the patient in the moderately severe category.
- Persistent organ failure continues beyond 48 hours and defines severe acute pancreatitis, whether it involves one organ system or multiple organ systems.[8]
- Severity is dynamic. When organ failure is present but has not yet persisted for 48 hours, the episode should be considered potentially severe and reassessed rather than prematurely assigned a final category.[1]
- Local complications alone do not define severe acute pancreatitis; severe disease requires persistent organ failure.
Determinant-Based Classification
Acute pancreatitis is classified by the DBC according to two determinants: the systemic determinant of organ failure and the local determinant of pancreatic or peripancreatic necrosis and its infection status.[2][9][10]
| DBC severity grade | Local determinant | Systemic determinant | Definition |
|---|---|---|---|
| Mild | No pancreatic or peripancreatic necrosis | No organ failure | Neither determinant is present |
| Moderate | Sterile pancreatic or peripancreatic necrosis may be present | Transient organ failure may be present | Sterile necrosis and/or transient organ failure |
| Severe | Infected pancreatic or peripancreatic necrosis may be present | Persistent organ failure may be present | Infected necrosis or persistent organ failure, but not both together |
| Critical | Infected pancreatic or peripancreatic necrosis | Persistent organ failure | Both determinants are present |
The principal distinction between the systems is that the DBC reserves a separate critical category for the combination of infected necrosis and persistent organ failure. Comparative cohort studies have found that both the RAC and DBC stratify worsening outcomes effectively; neither system has shown a consistent overall performance advantage, although the DBC provides additional separation of the highest-risk combination.[11][12]
Original Atlanta Classification Versus Revised Atlanta Classification
Acute pancreatitis was classified by the original 1992 Atlanta system as either mild or severe; the 2012 revision introduced a three-tier clinical severity system and standardized morphologic terminology.[1][13]
| Feature | Original Atlanta Classification (1992) | Revised Atlanta Classification (2012) |
|---|---|---|
| Severity categories | Mild and severe | Mild, moderately severe, and severe |
| Organ-failure definition | Heterogeneous clinical thresholds | Modified Marshall score ≥2 in the respiratory, renal, or cardiovascular system |
| Duration of organ failure | Not incorporated consistently | Transient if it resolves within 48 hours; persistent if it continues beyond 48 hours |
| Clinical phases | Not formally separated | Early and late phases |
| Morphologic subtypes | Terminology was less standardized | Interstitial edematous pancreatitis and necrotizing pancreatitis |
| Collection terminology | Included terms such as acute pseudocyst and pancreatic abscess | APFC, pseudocyst, ANC, and WON, defined by contents, encapsulation, pancreatitis subtype, and timing |
The original Atlanta system used specific thresholds such as systolic blood pressure ≤90 mmHg, PaO2 ≤60 mmHg, serum creatinine ≥2 mg/dL after rehydration, and gastrointestinal bleeding >500 mL in 24 hours as manifestations of organ failure. The RAC replaced these heterogeneous criteria with the standardized modified Marshall system.[1][3]
Classification of Organ Failure
Acute pancreatitis organ failure is defined by a modified Marshall score of 2 or more in at least one of three organ systems: respiratory, renal, or cardiovascular.[1][14]
| Organ system | Score 0 | Score 1 | Score 2 | Score 3 | Score 4 |
|---|---|---|---|---|---|
| Respiratory: PaO2/FiO2 | >400 | 301–400 | 201–300 | 101–200 | ≤100 |
| Renal: serum creatinine, mg/dL | <1.4 | 1.4–1.8 | 1.9–3.6 | 3.7–4.9 | >4.9 |
| Cardiovascular: systolic blood pressure, mmHg | >90 | <90, fluid responsive | <90, not fluid responsive | <90 with pH <7.3 | <90 with pH <7.2 |
- A score of ≥2 in any one organ system defines organ failure.
- Organ failure may be single-organ or multiple-organ failure.
- In patients with pre-existing chronic kidney disease, the renal score must be interpreted according to deterioration from baseline because no formal correction exists for an elevated baseline creatinine.[1]
- For a non-ventilated patient, estimated FiO2 values are:
- Room air: 0.21
- 2 L/min supplemental oxygen: approximately 0.25
- 4 L/min: approximately 0.30
- 6–8 L/min: approximately 0.40
- 9–10 L/min: approximately 0.50
- The modified Marshall score is used to define current organ failure. Prognostic scores estimate the risk of a future severe course and are not substitutes for the RAC severity definition.
Classification Based on Morphology
Acute pancreatitis is divided into two morphologic subtypes: interstitial edematous pancreatitis and necrotizing pancreatitis.[1][3][13]
| Feature | Interstitial edematous pancreatitis | Necrotizing pancreatitis |
|---|---|---|
| Definition | Acute pancreatic and peripancreatic inflammation without recognizable tissue necrosis | Acute inflammation associated with necrosis of the pancreatic parenchyma, peripancreatic tissues, or both |
| Pancreatic enhancement on CECT | Relatively homogeneous enhancement | Nonenhancing pancreatic parenchyma when pancreatic necrosis is present; the gland may enhance normally in isolated peripancreatic necrosis |
| Peripancreatic findings | Fat haziness or stranding; an acute peripancreatic fluid collection may be present | Heterogeneous areas or collections containing variable amounts of necrotic tissue and fluid |
| Anatomic patterns | No necrosis | Combined pancreatic and peripancreatic necrosis is most common; isolated peripancreatic necrosis is less common; isolated pancreatic parenchymal necrosis is rare |
| Possible evolution | Resolution, APFC, or pseudocyst | Sterile or infected necrosis; ANC or WON |
- Interstitial edematous pancreatitis is the most common morphologic subtype and usually resolves during the first week.[1]
- Necrotizing pancreatitis occurs in approximately 5–10% of patients.[1][5]
- Early CECT may show patchy or heterogeneous enhancement before necrosis becomes clearly demarcated. When imaging is clinically indicated, a nonenhancing area after the first week is considered pancreatic parenchymal necrosis.[1][15]
- Pancreatic necrosis is defined by nonviable pancreatic parenchyma and/or peripancreatic tissue, not by a mandatory threshold of more than 3 cm or more than 30% of the gland.
- The extent of necrosis does not have an absolute relationship with the risk of infection.[1]
- Morphologic subtype and clinical severity are separate axes. Necrotizing pancreatitis may occur without persistent organ failure, while persistent organ failure defines severe acute pancreatitis regardless of the morphologic subtype.
Classification of Local Collections
Acute pancreatitis collections are classified according to the underlying morphologic subtype, the presence or absence of necrotic material, encapsulation, and time from symptom onset.[1][16]
| Collection | Associated morphology | Usual timing | Contents | Wall and location |
|---|---|---|---|---|
| Acute peripancreatic fluid collection (APFC) | Interstitial edematous pancreatitis | Within the first 4 weeks | Homogeneous fluid without a nonliquid component | No definable wall; confined by normal peripancreatic fascial planes; adjacent to the pancreas without intrapancreatic extension |
| Pancreatic pseudocyst | Interstitial edematous pancreatitis | Usually more than 4 weeks | Homogeneous fluid with no solid necrotic component | Well-defined, completely encapsulated inflammatory wall; usually outside the pancreas |
| Acute necrotic collection (ANC) | Necrotizing pancreatitis | Within the first 4 weeks | Variable amounts of fluid and necrotic tissue; may appear relatively homogeneous early | No definable wall; may be intrapancreatic and/or extrapancreatic |
| Walled-off necrosis (WON) | Necrotizing pancreatitis | Usually 4 weeks or more | Encapsulated pancreatic and/or peripancreatic necrotic material with variable fluid content | Mature, well-defined inflammatory wall; may be intrapancreatic and/or extrapancreatic |
- The 4-week threshold describes the usual evolution of a collection and should be interpreted with its contents and degree of encapsulation rather than used in isolation.
- Within the first week, APFC and ANC may both appear predominantly fluid and may be difficult to distinguish. Sequential CT, MRI, ultrasound, or endoscopic ultrasound may better demonstrate a solid necrotic component.[1]
- A true pseudocyst contains fluid without necrotic debris. A mature collection containing necrotic material is WON, even if it appears predominantly cystic on CT.[13]
- WON usually matures after approximately 4 weeks, although demarcated necrotic collections may occasionally form earlier.[17]
- Infection is a modifier rather than a separate collection type. Necrosis and collections should be described as sterile or infected when this is known or strongly suspected.
- Extraluminal gas within pancreatic or peripancreatic necrosis strongly suggests infection, but the absence of gas does not exclude infected necrosis.[1][12]
Standardized Terminology and Reporting
Acute pancreatitis should be reported using standardized RAC terminology so that the clinical severity grade, morphologic subtype, and collection type remain distinct.
| Avoid or qualify | Preferred terminology | Reason |
|---|---|---|
| Acute pseudocyst | APFC or ANC, depending on contents and morphologic subtype | A pseudocyst is an encapsulated fluid-only collection that usually requires more than 4 weeks to mature |
| Pancreatic abscess | Infected ANC or infected WON | The older term does not adequately describe whether necrotic material or a mature wall is present |
| Phlegmon | Describe the specific inflammatory change, necrosis, or collection | The term is nonspecific and is not part of the RAC lexicon |
| Organized pancreatic necrosis or necroma | WON | WON is the standardized term for mature encapsulated necrosis |
| Severe pancreatitis based on CT appearance alone | State the morphologic subtype and assign RAC severity according to organ failure | Persistent organ failure, not the extent of imaging abnormalities alone, defines severe acute pancreatitis |
A complete description should include:
- Time from onset of abdominal pain
- RAC severity category and whether organ failure is transient or persistent
- Organ system or systems involved
- Interstitial edematous or necrotizing morphology
- Location of necrosis: pancreatic, peripancreatic, or both
- Collection type, location, contents, and degree of encapsulation
- Sterile or infected status when known or strongly suspected
- Relevant additional local complications
Clinical Pearls and Pitfalls
Acute pancreatitis classification is dynamic and must be updated as organ failure resolves or persists and as local complications evolve.
High-yield principles
- The duration of organ failure is the key distinction between moderately severe and severe acute pancreatitis.
- A modified Marshall score of ≥2 in any assessed organ system defines organ failure; persistence beyond 48 hours defines severe acute pancreatitis.
- Mild acute pancreatitis requires all three of the following: no organ failure, no local complications, and no systemic complications.
- A local complication without persistent organ failure is classified as moderately severe, not severe.
- Morphologic subtype, collection type, and clinical severity should each be stated separately.
- The DBC adds a critical category for infected necrosis combined with persistent organ failure.
Common pitfalls
- Assigning a final severity category at admission when the duration of organ failure is not yet known
- Omitting systemic complications from the definition of moderately severe acute pancreatitis
- Treating a prognostic score as though it were the RAC severity classification
- Equating necrotizing pancreatitis with severe acute pancreatitis
- Defining pancreatic necrosis by an obsolete size or percentage threshold
- Calling every mature pancreatic collection a pseudocyst without assessing for solid necrotic debris
- Applying the 4-week threshold without considering collection contents and encapsulation
- Using early CECT to exclude necrosis when perfusion abnormalities have not yet fully evolved
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 Banks PA, Bollen TL, Dervenis C; et al. (2013). "Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus". Gut. 62 (1): 102–111. doi:10.1136/gutjnl-2012-302779.
- ↑ 2.0 2.1 Dellinger EP, Forsmark CE, Layer P; et al. (2012). "Determinant-based classification of acute pancreatitis severity: an international multidisciplinary consultation". Ann Surg. 256 (6): 875–880. doi:10.1097/SLA.0b013e318256f778.
- ↑ 3.0 3.1 3.2 Thoeni RF (2012). "The revised Atlanta classification of acute pancreatitis: its importance for the radiologist and its effect on treatment". Radiology. 262 (3): 751–764. doi:10.1148/radiol.11110947.
- ↑ Expert Panel on Gastrointestinal Imaging, Porter KK, Zaheer A; et al. (2019). "ACR Appropriateness Criteria® Acute Pancreatitis". J Am Coll Radiol. 16 (11S): S316–S330. doi:10.1016/j.jacr.2019.05.017.
- ↑ 5.0 5.1 Tenner S, Vege SS, Sheth SG; et al. (2024). "American College of Gastroenterology guidelines: management of acute pancreatitis". Am J Gastroenterol. 119 (3): 419–437. doi:10.14309/ajg.0000000000002645.
- ↑ Mederos MA, Reber HA, Girgis MD (2021). "Acute pancreatitis: a review". JAMA. 325 (4): 382–390. doi:10.1001/jama.2020.20317.
- ↑ Wu BU, Banks PA (2013). "Clinical management of patients with acute pancreatitis". Gastroenterology. 144 (6): 1272–1281. doi:10.1053/j.gastro.2013.01.075.
- ↑ Trikudanathan G, Yazici C, Evans Phillips A, Forsmark CE (2024). "Diagnosis and management of acute pancreatitis". Gastroenterology. 167 (4): 673–688. doi:10.1053/j.gastro.2024.02.052.
- ↑ Boxhoorn L, Voermans RP, Bouwense SA; et al. (2020). "Acute pancreatitis". Lancet. 396 (10252): 726–734. doi:10.1016/S0140-6736(20)31310-6.
- ↑ Aaron AE, Amabile A, Andolfi C; et al. (2021). Gastrointestinal Surgical Emergencies. American College of Surgeons.
- ↑ Bansal SS, Hodson J, Sutcliffe RS; et al. (2016). "Performance of the revised Atlanta and determinant-based classifications for severity in acute pancreatitis". Br J Surg. 103 (4): 427–433. doi:10.1002/bjs.10088.
- ↑ 12.0 12.1 Trikudanathan G, Wolbrink DRJ, van Santvoort HC; et al. (2019). "Current concepts in severe acute and necrotizing pancreatitis: an evidence-based approach". Gastroenterology. 156 (7): 1994–2007.e3. doi:10.1053/j.gastro.2019.01.269.
- ↑ 13.0 13.1 13.2 Foster BR, Jensen KK, Bakis G, Shaaban AM, Coakley FV (2016). "Revised Atlanta classification for acute pancreatitis: a pictorial essay". Radiographics. 36 (3): 675–687. doi:10.1148/rg.2016150097.
- ↑ Garg PK, Singh VP (2019). "Organ failure due to systemic injury in acute pancreatitis". Gastroenterology. 156 (7): 2008–2023. doi:10.1053/j.gastro.2018.12.041.
- ↑ Milano RV, Morneault-Gill K, Kamal HY, Barkin JA, Chadwick CB (2024). "Pancreatitis in cystic fibrosis: presentation, medical and surgical management, and the impact of modulator therapies". Pediatr Pulmonol. 59 (Suppl 1): S53–S60. doi:10.1002/ppul.26958.
- ↑ Muthusamy VR, Chandrasekhara V, Acosta RD; et al. (2016). "The role of endoscopy in the diagnosis and treatment of inflammatory pancreatic fluid collections". Gastrointest Endosc. 83 (3): 481–488. doi:10.1016/j.gie.2015.11.027.
- ↑ Maurer LR, Fagenholz PJ (2023). "Contemporary surgical management of pancreatic necrosis". JAMA Surg. 158 (1): 81–88. doi:10.1001/jamasurg.2022.5695.