Complications
Overall, exocrine insufficiency is present in 8% to 22% at time of diagnosis, 44% to 48% after 13-26 years, and 91% to 100% after 14-36 years.[11] No therapy is proven to prevent development and/or deterioration of exocrine pancreatic function.
Occurs due to injury, atrophy, and loss of pancreatic exocrine tissue, which in turn are due to inflammation and fibrosis of the gland. Patients develop bulky, greasy stools with or without weight loss and nutritional deficiencies.
Treated with pancreatic enzyme supplementation. Failure of enzymes to reduce steatorrhoea raises several possibilities: insufficient dose, non-compliance, enzyme degradation and/or bile acid precipitation (treated with acid-reducing agent), or non-pancreatic causes of steatorrhoea.
Small intestinal bacterial overgrowth is more common in patients with chronic pancreatitis associated with alcoholic and non-alcoholic aetiologies than in healthy subjects. Treatment may improve digestive function and symptoms but rigorous studies are needed in this population.[253]
Glucose intolerance is common. The accumulated prevalence over decades ranges between 28% and 76% (mean 45%).[92]
May occur early in the course of chronic pancreatitis due to insulin resistance, but clearly occurs in severe chronic pancreatitis due to insulinopenia (due to injury, atrophy, and loss of pancreatic islets).
Treated with insulin supplementation, but patients are at risk of hypoglycaemia due to hypoglucagonaemia and impaired hepatic gluconeogenesis.
No therapy is proven to prevent development and/or deterioration of endocrine insufficiency.
Overall, the prevalence of calcifications ranges between 0% to 4% at onset of symptoms and 80% to 91% after 14-36 years.[10][11] The accumulated prevalence over decades is around 65%.[92]
Cause unknown. It occurs most commonly with alcoholic chronic pancreatitis, can also occur in hereditary pancreatitis and tropical pancreatitis, and is much less common in idiopathic pancreatitis.[136]
Occasionally present in other conditions (e.g., neuroendocrine tumour, intraductal papillary mucinous neoplasm), but overall specificity is high for chronic pancreatitis and correlates with intrapancreatic distribution: parenchymal (67%), intraductal (88%), diffuse parenchymal (91%), and coexisting intraductal and parenchymal calcifications (100%).[254]
Extracorporeal shock wave lithotripsy (ESWL) can be offered to patients with pancreatic duct calcifications with a minimal diameter of 2-5 mm.[82][181]
Caused by pancreatic fibrosis, intraductal calculus, pancreatic pseudocyst, and malignant obstruction.
Treatment is with ductal decompression.
Prevalence of 4.8%, likely due to decreased bone mineral density, malnutrition, micro-nutrient deficiencies, increased systemic inflammation, and the high pooled prevalence rates for osteopenia (39.8%) and osteoporosis (23.4%).[98][99] Fracture risk is greater if alcohol is an underlying risk factor for chronic pancreatitis and patients have cirrhosis.[100]
Patients, particularly high-risk patients (i.e., post-menopausal women, men over the age of 50 years, previous history of low-trauma fracture) and those with malabsorption, should be screened with a dual-energy x-ray absorptiometry scan. Surveillance exams should be offered if osteopenia is detected. Those with osteoporosis should start appropriate medication and/or see a bone specialist for further evaluation.[135]
All patients with chronic pancreatitis should have an adequate daily intake of calcium and vitamin D, perform weight-bearing exercise, and cease alcohol and tobacco use.
Overall affects 5% to 10% of patients.[90][203] Frequency varies with aetiology. Caused by pancreatic fibrosis and pancreatic pseudocyst.
Patients experience jaundice and continuous or recurrent pain. Up to 72% of those with biliary dilation and cholestasis develop obstructive liver disease.[255]
Surgery is the recommended treatment of choice. Decompression can reverse secondary biliary fibrosis.[256] Non-surgical candidates may benefit from endoscopic decompression.
Frequency varies with aetiology: alcoholic chronic pancreatitis, 5%; juvenile idiopathic chronic pancreatitis, 5%; and other groups, 0%.[10] Caused by pancreatic fibrosis in the proximal duodenum.
Patients experience nausea, vomiting, anorexia, and weight loss.
Treatment is by surgical bypass.
Uncommon in patients aged under 45 years, except in patients with hereditary pancreatitis. Cumulative risk of 2% per decade.[92] Risk typically <5%, although a true risk has been questioned.[10][11][92][257][258]
Some forms are inherited (7% to 8%). Others may be associated with one or more risk factors: obesity, smoking, diabetes mellitus, chronic pancreatitis.
Patients develop pain, weight loss, and insulin resistance or diabetes.
Treatment is with curative resection and adjuvant chemo-radiation (if detected early). Otherwise, palliative treatments with chemotherapy, surgery, and/or endoscopy.
The American College of Gastroenterology states that there is no definitive benefit to screening patients with chronic pancreatitis for pancreatic ductal adenocarcinoma, even in those at high risk for pancreatic malignancy due to genetic or environmental risk factors.[85]
The American Gastroenterological Association recommends that pancreatic cancer screening should be considered in patients with hereditary pancreatitis; screening should be initiated at age 40 years in CKDN2A and PRSS1 mutation carriers with hereditary pancreatitis.[259]
International and UK guidelines recommend that patients with hereditary pancreatitis with inherited PRSS1 mutations should undergo surveillance for pancreatic cancer.[260][261]
Recommended screening and surveillance tests are endoscopic ultrasonography (EUS) or magnetic resonance imaging (MRI)/magnetic resonance cholangiopancreatography (MRCP).
Opioids are commonly used to treat pain. Patients demonstrate a strong desire to take the drug after repeated use, combining behavioural, cognitive, and physiological phenomena.[234] The high frequency of alcohol addiction increases the risk for opioid addiction.
Long-acting opioid agonists (e.g., methadone) have been shown to decrease illicit or non-prescribed opioid use.[235][236] Buprenorphine, a partial opioid agonist, is an alternative for maintenance therapy in opioid addiction. Compared with methadone, patients taking buprenorphine had significantly lower rates of illicit opioid use, but had lower completion rates.[237] Naltrexone, an opioid antagonist, has also been used to combat opioid addiction.
Overall frequency is approximately 25%, but varies with aetiology.[238]
Occurs due to disruption of pancreatic duct rather than walling off of peri-pancreatic fluid collections.
Most are asymptomatic, but they can cause pain. Pancreatic pseudocysts expand and compress local structures, leak or fistulise to other structures, become infected, and erode into vascular structures causing a pseudoaneurysm and bleeding.
Rarely resolve spontaneously.[239] Most may be treated with conservative management. Drainage may be required for rapid enlargement, pain, infection, or compression of surrounding structures.
Frequency is considered to be <1%.[240][241][242]
Around 15% of patients with pseudocysts may have ascites and 60% of patients with ascites have a pseudocyst.[240][241][242] Cause is likely to be related to disruption of pancreatic duct or rupture of a pseudocyst.
Presentation is usually subacute with symptoms of abdominal swelling and/or mild abdominal pain, nausea and vomiting, and weight loss. Ascites contains high concentrations of protein and amylase, typically >16.7 microkat/L (>1000 international units/L).[243][244]
Initially treated by stopping oral intake and use of parenteral nutrition, intermittent large-volume paracentesis, and octreotide for 2-3 weeks.[245][246] If persistent, anatomy should be clarified with imaging, including a pre-operative endoscopic retrograde cholangiopancreatography.
Occurs in 1% to 2% of patients.[11] Cause is likely to be related to disruption of pancreatic duct or rupture of a pseudocyst. Fistulas may form with adjacent viscera, the pleural space, or the pericardium.
Most close spontaneously with conservative management, but some require endoscopic or surgical treatment.[247][248]
Occurs in 3% to 8% of patients.[10][249][250] Caused by peptic ulcer disease, or pseudocyst compression or erosion into an artery. Peptic ulcer disease is related to decreased bicarbonate secretion and increased duodenal acidity. Pseudocyst compression is largely responsible for thrombosis of the splenic vein and portal vein, leading to portal hypertension and gastric or oesophageal variceal bleeding in 8% to 16%.[249][250][251] Treatment includes splenectomy for splenic vein thrombosis and variceal bleeding.
Erosion of pseudocyst into an artery (splenic, hepatic, gastroduodenal, and pancreaticoduodenal) can lead to development of a pseudoaneurysm in around 3%.[252] Treatment is by embolisation.
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