In the setting of chronic alcohol use, this patient has had RAP attacks. A prior CT scan noted pancreatic calcifications, and the patient has had baseline chronic pancreatitis-type pain for the past year. Based on the clinical presentation, this patient had alcoholic chronic pancreatitis. A key concern in the history is recurrent AP despite alcohol cessation. The CT revealed evidence of a PD stone with ductal obstruction, which likely represents the cause for this patient’s current acute on chronic pancreatitis.

CP represents the progression of chronic pancreatic inflammation to irreversible fibrosis, which ultimately can lead to chronic upper abdominal pain and the compromise of pancreatic endocrine and exocrine function [1]. Progressive fibrosis can lead to both pancreatic parenchymal changes and duct abnormalities leading to impaired ductal outflow. CP can be further sub-stratified into large and small pancreatic duct disease with and without calcifications. Standard labs including lipase are often normal in symptomatic CP patients.

Endocrine dysfunction manifests typically as diabetes mellitus (DM). Management includes initiation of oral hypoglycemics and insulin supplementation as needed. New onset diabetes in the setting of chronic pancreatitis is associated with an increased risk for pancreatic cancer [2]. In this scenario, follow-up cross-sectional imaging may be recommended.

Exocrine pancreatic insufficiency (EPI) is due to the impaired synthesis and/or pancreatic secretion of luminal bicarbonate and digestive enzymes (lipase-protease-amylase) [3]. Patients develop steatorrhea as well as vitamin B12 and fat-soluble vitamin (K-A-D-E) deficiencies. The gold standard for EPI is quantitative fecal fat testing where patients are subjected to a high-fat diet (100 g of fat/day), with subsequent stool collection. A fecal fat excretion greater than 7 g/day is diagnostic of EPI. A qualitative stool fat test (Sudan red staining) is no longer recommended due to poor specificity. Elastase is a pancreatic enzyme, excreted via the gut. In EPI, fecal elastase concentrations decline, and a concentration less than 200 mg/g of stool can suggest the EPI diagnosis [4]. In an effort to detect early EPI, pancreatic function tests (PFTs) can be performed. For example, patients can be given IV secretin followed by direct aspiration of peri-ampullary pancreatic secretions [5]. EPI is diagnosed with duodenal aspirate bicarbonate concentrations less than 80 mEq/L. Endoscopic PFTs demonstrate a sensitivity and specificity of 82% and 86%, respectively, for the EPI diagnosis.

Abdominal imaging is necessary for the CP diagnosis. Abdominal X-ray can reveal pancreatic calcifications which are pathognomonic for CP. In progressed disease, the CT abdomen will note calcifications along with an atrophic pancreas (Fig. 6.2). EUS is an increasingly utilized modality to evaluate chronic pancreatitis and can characterize both parenchymal disease (lobularity, hyperechoic foci and strands, calcifications, cysts) and ductal disease (hyperechoic pancreatic duct walls, irregular pancreatic duct, dilated pancreatic duct, visible side branches) [6]. When five or more criteria are met, CP becomes increasingly more likely. MRCP can also be a valuable imaging modality to characterize ductal-based disease.

The classic triad of pancreatic calcifications, steatorrhea, and diabetes mellitus is highly specific but often occurs very late in the progression of chronic pancreatitis. Typically there is evidence of CP on imaging (abdominal X-ray, CT, MRCP, and EUS) along with pancreatitis pain, diabetes, and/or fat malabsorption.

Pancreatitis-type abdominal pain is the most common clinical manifestation of CP. Type A pain refers to frequent severe episodic pain versus type B pain, which can be more prolonged and persistent. Over time, CP pain can become debilitating and lead to a severely impaired quality of life [7].

The exact pathogenesis related to CP pain is not completely understood. It has been proposed that ductal hypertension and microvascular ischemia contribute to the development of CP pain. Ductal hypertension refers to the sequelae of reduced pancreatic duct outflow which leads to pancreatic ductal reflux and chronic pancreatic injury.

In the acute pain exacerbation setting, the first consideration is to identify if there is evidence of acute on chronic pancreatitis. If this is the case, then management involves admission for IV hydration and pain control.

The necessity for CP medical management is predicated on the presence of debilitating symptoms resulting in impaired functionality. Initial management involves the elimination of modifiable risk factors such as smoking and alcohol intake. Dietary modification with small, low-fat meals can contribute to pain relief by moderating pancreatic enzyme secretion and reducing fat malabsorption. For patients with EPI, pancreatic enzyme supplementation allows for fat digestion which can decrease postprandial dyspepsia and steatorrhea.

Analgesic management employs a stepwise approach, beginning with nonnarcotics such as acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs). Neuropathic agents such as tri-cyclic antidepressants (TCAs—nortriptyline, amitriptyline), serotonin and norepinephrine reuptake inhibitors (duloxetine), and GABA agonists (pregabalin) can offer pain relief and afford an opportunity to avoid or delay the use of narcotics [8]. If pain symptoms persist, a trial with a low-dose narcotic such as tramadol can be considered, followed in succession by more potent narcotics such as fentanyl or hydromorphone.

Pancreatic enzyme replacement therapy for pain control has been investigated. In theory, exogenous pancreatic enzyme supplementation reduces endogenous pancreatic duct secretions and ductal hypertension. Numerous randomized controlled trials evaluated the efficacy of pancreatic enzyme supplementation for chronic pancreatitis pain relief. A meta-analysis summarizing these trials revealed no significant pain benefit from enzyme supplementation [9].