How sick is my pancreatitis patient?

Acute pancreatitis (AP) is an inflammatory condition that causes abdominal pain, nausea, vomiting, and elevated serum pancreatic enzymes. It is often brought on by gallstones and alcohol consumption. The incidence of AP is increasing on account of the increased prevalence of obesity and its association with gallstones (Vege, 2024). AP encompasses a spectrum of clinical manifestations from mild cases with only transient abdominal pain to severe cases related to multi-organ failure and/or complications corresponding to infected or non-infected pancreatic necrosis. Approximately 20% of patients with AP have a severe form, which is related to a mortality rate of 25-30% (Vege, 2024). The treatment of AP is dependent upon its severity, so early recognition of patients with severe disease is crucial for appropriate triage to the intensive care unit (ICU) and optimal outcomes.

The diagnosis of OA requires at the least two of the next three features: (1) severe epigastric pain, (2) serum amylase or lipase levels which are thrice the upper limit of normal, and (3) characteristic findings of OA on contrast-enhanced computed tomography (CT) or, less regularly, magnetic resonance imaging (MRI) or ultrasonography (US).

Early, precise measurement of the severity of pancreatitis has been elusive despite the event of multiple scoring systems based on clinical, laboratory, and radiological findings. The Ranson criteria require parameters assessed on admission and after 48 h, which prevents their use within the emergency department for triage. The Imrie rating (Glasgow) is a simplified version of the Ranson criteria but has the identical shortcoming. Other clinical scoring systems include the Acute Physiology and Chronic Health Evaluation (APACHEⅡ), the Bedside Index of Acute Pancreatitis Severity (BISAP), and the Harmless Acute Pancreatitis Score (HAPS). None of those scoring systems reliably predict the event of severe AP (Leal & Almeida, 2019).

Abnormally high levels of amylase and lipase have high sensitivity for diagnosing AP but don’t reliably differentiate disease severity. Many other biomarkers have been studied, with blood urea nitrogen (BUN), serum creatinine, and C-reactive protein (CRP) showing probably the most promising ends in predicting severity. In one study, a BUN level of 20 mg/dL or higher at admission was related to increased mortality, as was any increase in BUN after 24 hours. Elevated serum creatinine in the primary 48 hours may predict the event of pancreatic necrosis. CRP levels rise steadily with the severity of pancreatitis. After 48 hours, CRP > 150 mg/L is an accepted predictor of poor prognosis, but current guidelines recommend against using a single biomarker to triage patients (Vege, 2024).

Systemic inflammatory response syndrome (SIRS), a systemic inflammatory response that may result in organ failure, is common in patients with severe AP and is frequently an early symptom of AP, whatever the severity. Early organ failure that persists for greater than 48 hours is a reliable indicator of increased morbidity and mortality (Vege, 2024). Early signs of organ failure, corresponding to elevated creatinine, all the time indicate severe AP. These patients must be monitored in intensive care units or critical care units.

In 2013, multiple international pancreatic societies revised and updated the Atlanta AP classification (Table 1) to offer a standardized clinical and radiological nomenclature based on 2 a long time of research progress. Acute pancreatitis is now divided into 2 distinct subtypes, necrotizing pancreatitis and interstitial edematous pancreatitis (IEP), based on the presence or absence of necrosis on CT imaging. Two phases of AP have been identified: early and late. Interestingly, the Atlanta classification system takes into consideration the presence of organ failure fairly than biomarker levels or scoring tools. Disease severity is assessed as mild, moderate, and severe based on the absence or presence of organ failure and native or systemic complications. Moderately severe AP is characterised by transient organ failure lasting <48 hours, whereas severe AP is defined by the presence of persistent organ failure lasting ≥48 hours (Foster et al., 2016). Like the Ranson scoring criteria, the revised Atlanta OA classification doesn't distinguish between moderately severe OA and severe OA until 48 hours after symptom onset.

The bedside nurse plays a key role in monitoring for early signs of organ failure to help in triage, imaging, and treatment decisions (Table 2). Typical initial symptoms of SIRS-related organ dysfunction are nonspecific and should include fever, chills, fatigue, malaise, anxiety, or confusion. Pulmonary decompensation is commonest in severe AP, followed by renal, cardiovascular, hepatic, and neurologic decompensation. Multiple organ failure occurs in 20% of patients with severe AP (Vege, 2024). It is very important to intervene early at the primary sign of decompensation in even a single organ system. Rapid deterioration may occur, requiring activation of a rapid response team or intensive care unit. AP patients with severe organ failure are at increased risk of mortality.

So how do you have to triage a patient with acute pancreatitis within the ED? Should they be sent home, admitted to a medical-surgical unit, or admitted to the ICU? Making the proper decision is very important for implementing appropriate treatment, but predicting the patient’s clinical course is difficult using existing biomarkers, radiological findings, and severity assessment tools. Early detection of organ failure is critical for appropriate ICU triage. Frequent assessment of the patient’s symptoms, vital signs, and physical examination findings is essential to early identification of patients who require a better level of care, imaging to discover complications corresponding to pancreatic necrosis, and supportive measures for SIRS.

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

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

Fujishima S. (2016). Organ dysfunction as a brand new standard for outlining sepsis. , , 24. https://doi.org/10.1186/s41232-016-0029-y

Leal, C. and Almeida, N. (2019). Predicting the severity of acute pancreatitis: the never-ending search…, (4), 232–234. https://doi.org/10.1159/000499680

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

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