Clinical Pearls & Morning Reports
Chronic pancreatitis is associated with increased mortality from any cause. Read the NEJM Clinical Practice Article here.
Q: What imaging findings characterize chronic pancreatitis?
A: Classic chronic pancreatitis, usually associated with alcohol use, smoking, or certain gene mutations, typically begins with recurrent painful bouts of pancreatitis, followed by the insidious development of chronic, debilitating pain during the next 3 to 5 years after an initial episode. Classic imaging findings of one or more of the triad of pancreatic ductal calcifications, ductal dilatation, and parenchymal atrophy indicate progression to chronic pancreatitis.
Q: Describe complications of chronic pancreatitis.
A: Complications include pseudocysts, bile-duct stricture, duodenal stricture, splanchnic venous thromboses, and pancreatic cancer. Loss of islet mass and insulin causes glucose intolerance and eventually diabetes (type 3c); loss of counterregulatory hormones can cause wide swings in blood glucose levels. Exocrine pancreatic dysfunction can progress from a “pancreas sufficient” phase to pancreatic exocrine insufficiency characterized by steatorrhea; the latter occurs with near total (>90%) loss of pancreatic exocrine function. Prolonged steatorrhea leads to weight loss, sarcopenia, and deficiencies of fat-soluble vitamins, vitamin B12, and other micronutrients. The chronic inflammatory state and deficiency of vitamin D and possibly vitamin K often result in osteopenia or osteoporosis, with bone pain and low-impact fractures.
A: Histologic analysis is not needed for diagnosis and is often not available; definitive diagnosis rests heavily on imaging findings. Imaging methods include computed tomography (CT), magnetic resonance cholangiopancreatography (MRCP), and endoscopic ultrasonography (EUS). In a large meta-analysis, the sensitivity and specificity of CT, magnetic resonance imaging (MRI), and EUS did not differ significantly, but EUS is invasive, observer-dependent, and prone to false positive results. Assessment should include the nature and severity of upper abdominal pain, imaging findings, nutritional status, substance abuse, disability due to disease, resilience and motivation for behavioral change, and effect of the disease on psychosocial function. Pancreatic exocrine function is evaluated by history taking and laboratory testing. Measurement of the fecal elastase level is simple, inexpensive, and widely available. A fecal fat test should be performed to confirm pancreatic insufficiency if fecal elastase levels or vitamin A or E levels are very low in the absence of the classic complex of symptoms of steatorrhea.
A: For acute and chronic pain, medical therapies include analgesic agents, antioxidants, and neuromodulators (e.g., gabapentinoids and tricyclic antidepressants). Regular use of opioids should be avoided. Endoscopic therapy, predominantly involving the removal of stones in a pancreatic duct, dilatation of strictures, or both, is often the first intervention for moderate-to-severe pain that does not respond to medical therapy. Options for surgery for pain relief include pancreatic resection for persistent focal inflammation, drainage of an obstructed duct, or a combination of both, or, in the most refractory cases, total pancreatectomy with or without autologous islet-cell transplantation. Three randomized trials have compared surgery with endoscopic therapy for painful chronic pancreatitis; all showed higher percentages of patients having pain relief with surgery than with endoscopy, with similar complication rates and mortality and a greater use of reinterventions in the endoscopy group. Endoscopic intervention is typically preferred as the initial option. However, patients with persistence of pain despite endoscopic therapy should be reevaluated for surgery.