A broad differential diagnosis for the case of acute or recurrent epigastric abdominal pain includes, but is not limited to, the following:

In the United States, alcohol abuse continues to be the prominent risk factor for chronic pancreatitis, responsible for 45% of cases [17]. Chronic pancreatitis attributed to alcohol consumption usually presents in the fourth to sixth decades of life, and correlates with cumulative alcohol intake. While the patient in this case presented with a history of heavy alcohol intake, there is no safe level of alcohol consumption with regard to risk of chronic pancreatitis [18, 19]. A minority of alcoholics will develop alcoholic chronic pancreatitis, suggesting a genetic predisposition or other susceptibility in some patients [20].

A majority of cases of chronic pancreatitis not related to alcohol use are idiopathic. The presentation of idiopathic chronic pancreatitis has a bimodal age distribution, with an early onset group presenting during adolescence, and another late-onset group occurring at a mean age of 56 years. Pain is almost uniformly the first symptom in early onset chronic pancreatitis. Some cases can be attributed to an initial episode of severe acute pancreatitis, sometimes called the sentinel acute pancreatitis event, or SAPE. Late-onset disease is commonly associated with pain, however episodes of severe pain are less frequently reported [21].

The natural history of pain in all types of pancreatitis improves in severity and frequency in approximately two-thirds of cases. In a minority of cases, pain becomes worse over time. The course of progression in alcoholic chronic pancreatitis is reciprocal to the degree of alcohol abstinence. The pattern of recurrent pain also appears to follow two distinct patterns. In its early course, symptoms are akin to recurrent episodes of acute pancreatitis, with prolonged periods of absence between episodes. In later stages, many develop a “smoldering” pancreatitis, with episodes of exacerbation and associated endocrine dysfunction [22]. A sizable number of cases reach a terminal “burn out” of chronic pancreatitis, in which pain is improved or absent, and exocrine/endocrine deterioration comes to a halt [23, 24].

Long-standing chronic pancreatitis often leads to local complications responsible for significant additional morbidity. Intraductal calculi (pancreatolithiasis) and ductal stenosis are common and lead to duct dilation. Splenic vein thrombosis can occur due to its close proximity to the inflammatory process, and leads to hypersplenism and gastric varices. Pancreatic pseudocysts are common and frequently cause pain, portal vein compression, and sometimes even intestinal obstruction. Rarely, erosion into major vascular structures can lead to life-threatening hemorrhage. The risk of malignancy arising from a background of chronic pancreatitis is elevated four to six times that of the general population; however, the absolute risk is still low and may not warrant additional screening. In some cases, ductal dilation is accompanied by fibrosis and phlegmon of the pancreatic head. This can be concerning not only due to mass effect on surrounding structures, but also in shrouding the diagnosis of pancreatic head malignancies.

Eliciting a history of recurrent abdominal pain, anorexia, and nausea which is exacerbated by food intake should provoke an investigation toward pancreatitis as a possible diagnosis. Patients may also exhibit hyperglycemia, jaundice, steatorrhea, weight loss, and endorse a history of heavy alcohol use. Symptoms are variable, and up to 20% of patients with pancreatitis will present with “painless pancreatitis.” Initial laboratory testing should include serum amylase and lipase levels, however these markers may lose sensitivity after extensive glandular injury has impaired exocrine enzyme production. Extensive fibrosis and edema may lead to elevation of serum bilirubin and alkaline phosphatase in a minority of patients. Additionally, fecal fat excretion can be detected (alternatively Sudan staining of the feces can be utilized), although it is neither sensitive nor specific. Fecal chymotrypsin, trypsin, and elastase testing are now widely available, but suffer from low sensitivity in all but very late-stage disease. Enhanced pancreatic function tests have been studied, including MRCP and endoscopic-assisted secretin stimulation testing, but these techniques have yet to be widely adopted [25].

Endoscopic retrograde pancreatography (ERCP) was classically the reference imaging modality for the diagnosis of chronic pancreatitis, however, increasing consensus is developing around the use of endoscopic ultrasound (EUS) criteria. Studies comparing EUS to ERCP in the diagnosis of chronic pancreatitis have found good correlation between morphologic abnormalities seen on EUS with a sensitivity of 85–97% [26, 27]. However, in practice, computed tomography is almost always included as a powerful adjunct; modern CT scanning has 60–90% sensitivity, as well as 85–95% specificity in the diagnosis of chronic pancreatitis, with increasing sensitivity in more advanced disease [27, 28]. CT findings in chronic pancreatitis include parenchymal atrophy, inflammatory changes, calcifications, pseudocysts, and pancreatic and bile duct dilation. Irregular ductal contour, strictures, and side-branch abnormalities may be more prominent on ERCP and assist in classification and treatment planning. Transabdominal ultrasonography and plain films may detect large cysts, ductal dilation, and calcification, but are rarely used in guidance of treatment algorithms. Magnetic resonance imaging, while promising, is not clearly superior to ERCP and CT [5, 29].