Initial treatment for CP is lifestyle modification with alcohol and smoking cessation, along with elimination of other metabolic or exogenous toxins. Further treatment is divided into 3 categories: medical, endoscopic, and surgical. Appropriate selection of therapeutic measures depends on the overall health of the patient, as well as the etiology and severity of CP.5
Pain control is the established mainstay of treatment, yet pain management is one of medicine’s most elusive therapeutic measures. In the past, mechanical dysfunction due to pancreatic duct obstruction and resultant ductal hypertension was thought to be responsible for most of the pain associated with CP. More recently, however, neurobiologic mechanisms have been implicated. In theory, recurrent damage to the pancreas results in inflammation of intrapancreatic nerves triggering abnormal pain as organized in the central nervous system.5,6 Concepts based on nerve inflammation support inclusion of neuropathic pain medications to existing treatment regimens. Such novel regimens could prove beneficial in pain control as well as in reduction of opioid use and dependence. Patients with CP are often responsive to medications such as tricyclic antidepressants, gabapentin, pregabalin, and selective serotonin reuptake inhibitors. Therapeutic success with such regimens lends biologic plausibility to the concept of pancreatic neuropathy.5,6 Some patients, in contrast, achieve adequate pain relief with nonsteroidal anti-inflammatory drugs and acetaminophen. Antioxidant therapy and pancreatic enzyme replacement are available but are of unpredictable efficacy in reducing pain.5
Another medical essential is management of pancreatic exocrine dysfunction. Abdominal pain, malabsorption, weight loss, and steatorrhea are indicative of exocrine insufficiency. Treatment is advisable for patients with these signs and symptoms. Most patients begin therapy with digestive enzyme replacement such as 40,000 units of lipase with meals. Severe insufficiency may require up to 90,000 units 3 times daily. Lesser amounts are appropriate for lighter meals or snacks.5,9 Typical enzyme preparations contain amylase and protease. Histamine-2 receptor antagonists and proton pump inhibitors provide benefit in addition to enzyme supplementation. These agents act by minimizing premature enzymatic breakdown of pancreatic enzymes by stomach acid. Reduction of fat intake and consumption of multiple small meals throughout the day are also effective for some patients. Response to enzyme replacement can be monitored by frequently checking serum levels of fat-soluble vitamins, especially vitamin D.9
A third goal of medical therapy is management of pancreatic endocrine deficiency. Labelled as “pancreatic diabetes,” or “type 3C diabetes,” this entity must be distinguished from type 1 or type 2 diabetes mellitus, although it is treated similarly in early stages.5,9,10 Until insulin is necessary for euglycemia, type 3C diabetes may be successfully treated with metformin. In addition to antidiabetic effects, metformin has antineoplastic properties and has been reported to reduce the risk of pancreatic cancer by as much as 70%.10 Sulfonylurea preparations may also be considered an appropriate choice, but care must be taken to avoid hypoglycemia. If endocrine insufficiency ensues and first-line management is ineffective, insulin will be necessary.5,10 Incretin-based therapies, such as glucagon-like peptide-1 (GLP-1) analogues and dipeptidyl peptidase 4 (DPP-4) inhibitors, are not recommended due to concomitant increased risk of medication-induced pancreatitis and problematic side effects. Likewise, thiazolidinediones should also be avoided.10
Endoscopy may be necessary when medical therapy fails. Careful patient selection is prudent to avoid endoscopic complications, such as acute pancreatitis and exacerbation of CP.5 ERCP is usually definitive in removal of obstructing intraductal stones, dilation of intraductal strictures, and drainage of pseudocysts.5,9
Interventional surgery is reserved for patients for whom medical and endoscopic therapies are unsuccessful. Certain cases of severe CP require surgery as first-line therapy. Surgical indications include poor pain control; duodenal, biliary, and pancreatic duct obstruction; symptomatic pseudocysts (complex or large); extensive necrosis; and suspicion of pancreatic cancer.5 Four common surgical techniques are used:
- Pancreaticojejunostomy, for obstructive ductal disease, can be performed using the Frey or Puestow techniques.5
- Pancreaticoduodenectomy, for cases with significant disease of the pancreatic head, can be performed using the Whipple or Beger approaches.5
- Distal pancreatectomy is preferred for disease in the pancreatic tail.5
- Total pancreatectomy with islet auto-transplantation can be performed in patients with nonobstructive disease and atrophy of the acini involving the entire pancreas.5
This review has discussed the complex nature of CP and serves to raise awareness of the disease among all providers. It is important to be familiar with risk factors, clinical presentation, diagnostic workup, and treatment. Early recognition of CP is paramount in preserving quality of life for patients with the condition.
Anna Walker, PA-C, is a physician assistant in the department of medicine, division of gastroenterology, at Augusta University Medical Center, in Augusta, Georgia. Michael Felz, MD, is an associate clinical professor in the department of physician assistant studies at Augusta University, in Augusta, Georgia.
- Lew D, Afghani E, Pandol S. Chronic pancreatitis: current status and challenges for prevention and treatment. Dig Dis Sci. 2017;62(7):1702-1712.
- Juel J, Olesen SS, Olesen AE, et al. Study protocol for a randomised, double-blinded, placebo-controlled, clinical trial of S-ketamine for pain treatment in patients with chronic pancreatitis (RESET trial). BMJ Open. 2015;5(3):e007087.
- Conwell DL, Lee LS, Yadav D, et al. American Pancreatic Association practice guidelines in chronic pancreatitis: evidence-based report on diagnostic guidelines. Pancreas. 2014;43(8):1143-1162.
- Stevens T, Conwell DL, Zuccaro G. Pathogenesis of chronic pancreatitis: an evidence-based review of past theories and recent developments. Am J Gastroenterol. 2004;99(11):2256-2270.
- Majumder S, Chari ST. Chronic pancreatitis. Lancet. 2016;387(10031):1957-1966.
- Poulsen JL, Olesen SS, Malver LP, Frøkjær JB, Drewes AM. Pain and chronic pancreatitis: a complex interplay of multiple mechanisms. World J Gastroenterol. 2013;19(42):7282-7291.
- Huffman J, Wehbi M, Obideen K. Chronic pancreatitis treatment & management: approach considerations, behavior modification, pharmacologic alleviation of abdominal pain Medscape website. https://emedicine.medscape.com/article/181554-treatment#d10. Updated November 11, 2019. Accessed June 10, 2019.
- D’Souza SL, Anderson MA, Korsnes SJ, et al. EUS diagnostic criteria for chronic pancreatitis: a comparison of conventional versus Rosemont criteria. Dig Dis Sci. 2015;60(12):3782-3787.
- Nair RJ, Lawler L, Miller MR. Chronic pancreatitis. Am Fam Physician. 2007;76(11):1679-1688.
- Ewald N, Hardt PD. Diagnosis and treatment of diabetes mellitus in chronic pancreatitis. World J Gastroenterol. 2013;19(42):7276-7281.
This article originally appeared on Clinical Advisor