Acute pancreatitis (AP) is an inflammatory condition causing abdominal pain, nausea, vomiting and an elevation of serum pancreatic enzymes. It is commonly caused by gallstones and alcohol consumption. The incidence of AP is rising due to increased rates of obesity and its relationship with gallstones (Vege, 2024). AP encompasses a spectrum of clinical features from mild cases with only transient abdominal pain to severe cases associated with multiorgan failure and/or complications such as infected or non-infected pancreatic necrosis. About 20% of patients with AP have the severe form, which is associated with a mortality rate of 25-30% (Vege, 2024). Management of AP is driven by its severity, therefore early recognition of patients with the severe form is critical for appropriate triage to the intensive care unit (ICU) and for optimizing outcomes. 
 
The diagnosis of AP requires at least two of the following three features: (1) acute onset epigastric abdominal pain, (2) serum amylase or lipase levels three times higher than the upper limit of normal, and (3) characteristic findings of AP on contrast-enhanced computed tomography (CT) or, less commonly, magnetic resonance imaging (MRI) or ultrasound (US). 
 
An early precise measurement of pancreatitis severity has been elusive despite the development of multiple scoring systems based on clinical, laboratory, and radiologic findings. Ranson’s criteria requires parameters assessed at admission and at 48 hours rendering it impossible to use in the emergency department for triage. The Imrie (Glasgow) score is a simplified version of Ranson’s criteria but has the same disadvantage. Other clinical scoring systems include acute physiology and chronic health evaluation (APACHEⅡ), bedside index for severity in acute pancreatitis (BISAP) and harmless acute pancreatitis score (HAPS). None of these scoring systems reliably predict the development of severe AP (Leal & Almeida, 2019).
 
Abnormally high levels of amylase and lipase have a high sensitivity for diagnosing AP but do not reliably differentiate the severity of the disease. Multiple other biomarkers have been studied, with blood urea nitrogen (BUN), serum creatinine, and C-reactive protein (CRP) showing the most promising results in predicting severity. In one study, BUN level of 20 mg/dL or higher at admission was associated with higher mortality, as was any increase in BUN at 24 hours. An elevated serum creatinine within the first 48 hours may predict the development of pancreatic necrosis. CRP levels rise steadily in relation to the severity of pancreatitis. At 48 hours, CRP above 150 mg/L is an accepted predictor of a worse prognosis, however current guidelines advise against the use of a single biomarker to triage patients (Vege, 2024).
 
Systemic inflammatory response syndrome (SIRS), a whole-body inflammatory response that can lead to organ failure, is common in patients with severe AP and is typically an early feature in AP regardless of severity. Early organ failure which persists for more than 48 hours is a reliable indicator of increased morbidity and mortality (Vege, 2024). Signs of organ failure on initial presentation, such as elevated creatinine, are always indicative of a severe form of AP. These patients should be monitored in step-down or intensive care units.
 
In 2013, multiple international pancreatic societies revised and updated the Atlanta classification of AP (Table 1) to provide standardized clinical and radiologic nomenclature based on 2 decades of research advances. Acute pancreatitis is now divided into two distinct subtypes, necrotizing pancreatitis and interstitial edematous pancreatitis (IEP), based on the presence or absence of necrosis on CT imaging. Two phases of AP were identified: early and late. Notably, the Atlanta Classification system incorporates the presence of organ failure rather than levels of biomarkers or scoring tools. Severity of the disease is classified as mild, moderately severe, and severe by the absence or presence of organ failure and local or systemic complications. Moderately severe AP has transient organ failure of < 48 hours, while severe AP is defined by the presence of persistent organ failure for ≥ 48 hours (Foster et al., 2016). Like the Ranson scoring criteria, the revised Atlanta classification of AP is unable to differentiate between moderately severe AP and severe AP before 48 hours after onset.
 

Table 1:  2013 Revision of Atlanta Classification of Acute Pancreatitis (Banks et al., 2013)
Severity of Acute Pancreatitis	Definition
Mild	No organ failure No local or systemic complications
Moderately severe	Local complications* and/or transient organ failure (<48 hours duration)
Severe	Persistent single or multiple organ failure (>48 hours duration)

*Local complications of acute pancreatitis include acute peripancreatic fluid collection, pancreatic pseudocyst, acute necrotic collection, and walled-off necrosis.
 
The bedside nurse plays a key role in monitoring for early signs of organ failure to assist in triage, imaging and treatment decisions (Table 2). The common initial manifestations of SIRS related organ dysfunction are non-specific and may include fever, chills, fatigue, malaise, anxiety, or confusion. In severe AP, pulmonary decompensation is most common, followed by renal, cardiovascular, hepatic, and neurologic. Multiorgan failure occurs in 20% of patients with severe AP (Vege, 2024). It is important to intervene early, at the first sign of decompensation of even a single organ system. Rapid deterioration may occur which requires the activation of the rapid response or critical care team. AP patients with severe organ failure are at higher risk of mortality. 
 

Table 2:  Organ failure criteria for patients with acute pancreatitis and/or systemic inflammatory response syndrome (Fujishima, 2016)
Organ System	Mild Criteria	Severe Criteria
Pulmonary	Tachypnea Hypoxia or hypercarbia Requiring positive pressure ventilation for up to 5 days	Requiring positive pressure ventilation for > 5 days Refractory hypoxemia (partial pressure of oxygen [PaO2]:fraction of inspired oxygen [FiO2] <100)
Renal	Oliguria (< 500 mL/day) Increasing creatinine (2-3 mg/dL)	Requiring hemodialysis
Cardiovascular	Mild hypotension Tachycardia Demand cardiac ischemia	Shock
Hepatic	Bilirubin 2-3 mg/dL or other liver function tests >2 × normal PT elevated to 2 × normal	Jaundice with bilirubin 8-10 mg/dL Severe coagulopathy with bleeding complications
Neurologic	Confusion	Coma
Gastrointestinal	Intolerance of gastric feeding for more than 5 days	Stress ulceration with need for blood transfusion Acalculous cholecystitis

 
So how should your ED patient with acute pancreatitis be triaged? Should he/she be sent home, admitted to a med-surg floor, or admitted to the ICU? Getting the decision right is important for instituting the right treatment but predicting your patient’s clinical course is difficult using existing biomarkers, radiographic findings, and severity scoring tools. Early detection of the presence of organ failure is vital to appropriate triage to ICUs. Frequent assessment of the AP patient’s symptoms, vital signs, and physical exam findings is a critical component of early identification of patients who require a higher level of care, imaging to identify complications such as pancreatic necrosis, and supportive measures for the management of SIRS. 

References:

Banks, P. A., Bollen, T. L., Dervenis, C., Gooszen, H. G., Johnson, C. D., Sarr, M. G., Tsiotos, G. G., Vege, S. S., & Acute Pancreatitis Classification Working Group (2013). Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus. Gut, 62(1), 102–111. https://doi.org/10.1136/gutjnl-2012-302779

Foster, B., Jensen, K., Bakis, G. Shaaban, A., & Coakley, F. (2016). Revised Atlanta classification for acute pancreatitis: A pictorial essay. Radiographics, 36(3): 675-687. https://doi.org/10.1148/rg.2016150097

Fujishima S. (2016). Organ dysfunction as a new standard for defining sepsis. Inflammation and regeneration, 36, 24. https://doi.org/10.1186/s41232-016-0029-y

Leal, C., & Almeida, N. (2019). Predicting Severity in Acute Pancreatitis: A Never-Ending Quest…. GE Portuguese journal of gastroenterology, 26(4), 232–234. https://doi.org/10.1159/000499680

Vege, S. (2024, March 18). Etiology of Acute Pancreatitis. UpToDate. https://www.uptodate.com/contents/etiology-of-acute-pancreatitis

Vege, S. (2024, March 20). Predicting the severity of acute pancreatitis. UpToDate. https://www.uptodate.com/contents/predicting-the-severity-of-acute-pancreatitis