The term “pancreas” derives its name from the Greek words pan (all) and kreas (flesh). Understanding pancreas physiology was first attempted in the 17th century by Regnier de Graaf1. Giovanni Morgagni is credited with the first description of the syndrome of acute pancreatitis (AP) in 17612. Reginald Huber Fitz proposed the first classification of AP into hemorrhagic, gangrenous, and suppurative types in 18893. The distinction of acute from chronic pancreatitis was not well described until the middle of the 20th century when Mandred W. Comfort gave a detailed account of chronic relapsing pancreatitis in 19464.
Diagnosis and classification of severity
The diagnosis of AP is based on the presence of two of the three following criteria: typical abdominal pain (severe, upper abdominal pain frequently radiating to the back), serum amylase and/or lipase levels greater than 3 times the upper limit of normal, and/or characteristic imaging findings.
The original 1992 Atlanta classification provided the first blueprint to standardize how severity of AP was defined5. Over the years, better understanding of AP pathophysiology and its complications led to a greater focus on local and systemic determinants of severity6 and eventually the Revised Atlanta Classification (RAC) in 2013 (Table 1).
Management of acute pancreatitis
Determination of etiology
The most common causes of AP are gallstones and alcohol, accounting for more than two-thirds of all cases13. Other etiologies include hypertriglyceridemia, ERCP, drugs induced, familial/hereditary, and post-traumatic. Initial work up includes a thorough history to quantify alcohol consumption and assess for recently started medications, measurement of liver injury tests14 and triglyceride levels, and performance of a transabdominal ultrasound to evaluate for biliary dilation, chole- and choledocholithiasis15.
Assessment of disease severity
Despite extensive research and trials using medications such as ulinastatin, octreotide, pentoxifylline, gabexate, N-acetyl cysteine, steroids, IL-10, and antibiotics20, no pharmacologic agent has been shown to significantly alter the clinical course/outcomes of AP.
Adequate intravenous hydration remains the cornerstone of early management in AP21. Studies have demonstrated that increased intestinal permeability, secondary to reduced intestinal capillary microcirculation, leads to bacterial translocation and development of SIRS22. Intestinal microcirculation does not become as readily impaired, and there is a certain “latency” to its onset, from the insult that triggers pancreatitis. This gives rise to the concept of a “golden window” of 12-24 hours from the insult to potentially reverse such changes and prevent organ dysfunction. It has been shown that patients who are adequately resuscitated with intravenous fluids have lower risk for local and systemic complications23.