triaged to an intensive care unit for more careful monitoring.
Nutrition is another key therapeutic component. As opposed to delayed nutrition, early initiation of nutrition has shown improved outcomes, preferably using oral feeding.11 In patients with mild pancreatitis, early initiation of a low‐fat diet (versus a clear liquid diet) has been shown to reduce length of hospital stay. Patients with moderate or severe pancreatitis may not be in a clinical condition to tolerate oral feeding within 48–72 hours, so enteral feeding using a nasogastric or nasojejunal tube is recommended and should be initiated within 72 hours when possible. Several randomized controlled trials and meta‐analyses report no differences in pre‐pyloric versus post‐pyloric feeding.12 Parenteral nutrition is considered the last option for nutrition if caloric goals cannot be met through enteral means. Compared to enteral feeding, parenteral nutrition is associated with a significantly higher risk of infection in this patient population, including bacteraemia and infected necrosis.
Routine antibiotic therapy in severe acute pancreatitis is not recommended unless there is evidence of infected necrosis or persistent clinical instability concerning sepsis.13 In patients with bile duct stones, endoscopic duct clearance by ERCP is recommended, although this need not be performed urgently except in cholangitic patients. There is now clear data that patients with gallstones who develop mild acute pancreatitis should undergo cholecystectomy during their index admission to reduce the likelihood of repeated attacks and subsequent complications.14
Acute pancreatic fluid collections and pancreatic necrosis, which may develop in the first four weeks, are generally best managed conservatively. If these collections persist beyond four weeks, they can become walled off as pseudocysts (fluid) or walled‐off pancreatic necrosis (solid debris) (see Figure 21.1). Walled‐off collections can be drained/debrided endoscopically if symptomatic using a variety of well‐supported techniques. Radiologic drainage or surgery should be uncommonly required in the modern era. In particular, surgery performed for pancreatic necrosis is associated with high morbidity and mortality and should be performed only by surgical teams with strong experience in this area.
Figure 21.1 Acute necrotizing pancreatitis, with a bilobed walled‐off necrosis occupying the body and tail of the pancreas.
Chronic pancreatitis
Chronic pancreatitis is a progressive inflammatory condition that leads to histological changes, including an increase in intralobular fibrous tissue, atrophy of the acini, and a chronic inflammatory infiltrate.15 Macroscopically, ductal changes can occur, mainly ductal irregularity with intermittent strictures and dilatation. Calcifications and pancreatic atrophy may also be present (Figure 21.2). In clinical practice, the diagnosis of chronic pancreatitis relies on a combination of symptoms, pancreatic function testing, and morphological appearance of the pancreas, rather than biopsy confirmation.
Figure 21.2 Atrophied pancreas with dilated, irregular pancreatic duct and intraductal stone.
In the United States, the prevalence of chronic pancreatitis is 40–50 per 100,000 population.16 The incidence of chronic pancreatitis in the elderly is uncertain, but it is unusual for symptomatic chronic pancreatitis to be diagnosed for the first time after the age of 65. Post‐mortem examinations reveal that pancreatic stones/calcifications occur in ∼15% of patients over the age of 90 and that changes of chronic pancreatitis are seen. The significance of these findings is uncertain as there may be no correlation with clinical disease.14
Causes of chronic pancreatitis
Drinking alcohol and smoking cigarettes are the commonest causes of chronic pancreatitis. In the elderly, autoimmune pancreatitis can also be considered. Pancreatic insufficiency of unknown cause can occur uncommonly in older persons without other symptoms of pancreatitis. Chronic pancreatitis changes may also be present due to chronic ductal obstruction such as that caused by a pancreatic or periampullary tumour; therefore, a careful history and good‐quality imaging evaluation are required to exclude mass lesions, particularly in patients without other risk factors for chronic pancreatitis
Clinical presentation of chronic pancreatitis
Abdominal pain, a characteristic of chronic pancreatitis in younger patients, may be less severe or even absent in the elderly.17 Weight loss, new‐onset diabetes, and steatorrhea (representing fat malabsorption) are often the presenting symptoms in elderly patients. Occasionally, chronic pancreatitis is recognized as an incidental finding when pancreatic calcifications are noted on abdominal CT or, more rarely, abdominal X‐rays.
Clinical examination is usually normal, although there may be localized tenderness in the epigastrium. Signs of malnutrition occur late in the disease.
Diagnosis of chronic pancreatitis
Establishing a diagnosis is often challenging, especially early in the disease course. Serum amylase and lipase levels are usually normal or only slightly elevated. If there is associated obstruction of the intrapancreatic bile duct, bilirubin and alkaline phosphatase levels may be elevated. Diagnosis relies on clinical signs and symptoms, pancreatic function tests, and radiologic evaluation.
Both direct and indirect pancreatic function tests can be used to evaluate steatorrhea resulting from exocrine insufficiency. Direct tests are those that require hormonal stimulation as part of the test protocol, whereas indirect tests do not.
Our opinion is that the best and most widely available indirect test of pancreatic function is the faecal pancreatic elastase. Faecal elastase levels fall with ageing and are a sensitive diagnostic test for malabsorption. However, faecal elastase can be falsely positive in unformed stool, and sensitivity is low early in the disease.18 Measurement of serum vitamin A and β‐carotene can be used to screen for fat malabsorption.19 Steatorrhea can potentially be recognized by Sudan staining of the stool, although this test has very limited specificity. The 72‐hour faecal fat collection can be more effective in quantifying steatorrhea if performed correctly, but this test is rarely ordered in practice due to its very cumbersome nature, requiring a daily diet of 100 g of fat and appropriate stool collection by the patient.
Among the direct function tests, the most sensitive are the cholecystokinin and secretin stimulation tests, which typically require upper endoscopy to collect duodenal aspirates (to measure the concentration of pancreatic enzymes or bicarbonate) as part of the test protocol. Although highly sensitive, direct function tests are limited by their invasive nature and are performed only in specialized centres.
Imaging procedures
Radiologic evaluation has generally superseded function studies in the diagnosis of chronic pancreatitis. Other than the rarely‐used abdominal X‐ray, abdominal ultrasound is the least expensive and most widely available modality for assessing the pancreas; however, the sensitivity of ultrasound for detecting chronic pancreatitis changes is less than that of CT or MRCP. In about two‐thirds of chronic patients, ultrasonography may show swelling of the gland or duct dilatation, but abdominal ultrasound may not be able to view the entire pancreas because of intervening bowel gas.
CT scanning provides similar information and is more sensitive