Manual of Clinical Nutrition Management III- 89 Copyright © 2013 Compass Group, Inc.
PANCREATITIS
Discussion
The pancreas is a major organ involved in the digestion and absorption of food. The pancreas is comprised of
two major glands each providing a unique function. The endocrine gland known as the Islets of Langerhans is
responsible for producing insulin, glucagon, and somatostatin. The exocrine portion of the gland (referred as
the ductal system) is responsible for secretion of multiple digestive enzymes including amylase, lipase,
carboxypeptidase, phospholipase-alpha, chymotrypsin, aminopeptidase, trypsinogen, and cholesterase (1).
Acute pancreatitis involves a systematic immunoinflammatory response to a localized process of
autodigestion of the pancreatic gland and can include the involvement of other tissues and organ systems (1-3).
The onset of pain usually occurs 24 to 36 hours after the peak of cytokine production which leads to the
inflammatory response (4). Distant organ failure can occur in 1 to 3 days (4).
The etiology of acute pancreatitis in the U.S. involves alcohol abuse in 75% of cases (1,5). Approximately
15% of case are either idiopathic or caused by biliary tract diseases (passage of common bile duct stone),
while 10% is accounted for by a variety of disorders such as pancreas divisum, trauma, hypoparathyroidism,
hyperclacemia, hyperlipidemia, post-endoscopic retrograde cholangiopancreatography (ERCP), medications,
and biliary dyskinesia (1,5). Treatment often depends on severity which is identified by objective scoring
systems such as Acute Physiology and Chronic Health Evaluation (APACHE) II score and Ranson Criteria (1,6-9),
and the presence of necrosis on CT scan (1,6). In addition, disease severity is determined by the adequacy of
fluid resuscitation, the presence and extent of necrosis within the gland, the presence of obesity, infection
within the gland, failure of at leaset one organ system, and the route of nutrition support (1). For severe cases
the anticipated hospital length of stay is approximately 1 month with a high percentage of patients
developing complications such as infection, sepsis, and organ failure (1). For mild to moderate cases, there is a
low risk for complications (< 5%), with the chance for 80% to advance to an oral diet successfully within 1
week (1, 6- 9 ).
Nutritional Assessment and Diagnosis
Acute pancreatitis produces a hypermetabolic response that alters carbohydrate protein, fat, and energy
metabolism leading to rapid deterioration of nutritional status (1). Reduced oral intake can occur from
abdominal pain, food aversion, nausea, vomiting, gastric atony, paralytic ileus, or partial obstruction of the
duodenum from enlargement of the pancreatic gland (1). Pancreatitis can also produce a hemodynamic
response, which is similar to that of sepsis (1). This response includes increased cardiac output, decreased
peripheral resistance, and increased oxygen consumption, currently known as the systemic inflammatory
response syndrome (SIRS) (1). Energy expenditure reportedly increases by 139% of that predicted by the
Harris-Benedict equation and can further be increased by 15% if the pancreatitis is complicated by sepsis
(1,10),. Patients with acute pancreatitis are more hypermetabolic when compared to those with chronic
pancreatitis (10).
Nutrient losses are often increased because of maldigestion from reduced enzyme output, malabsorption of
luminal nutrients, or excessive protein loss caused by diarrhea or pancreatic fistulas (1). Protein catabolic rate
and urea production rates are significantly increased. Errors in carbohydrate metabolism leading to
hyperglycemia and insulin resistance occur in 40% to 90% of patients (1,11). Errors in fat metabolism with
hypertriglyceridemia occur in 12% to 15% of cases (1,12,13). Hypocalcemia has been shown to be prevalent (13)
and occurs as a result of reduced calcium levels related to decreased parathyroid hormone release, increased
calcitonin, decreased magnesium levels, hypoalbuminemia, and saponification of calcium with unabsorbed
fatty acids (1). Since long-term alcohol use is a primary cause of acute pancreatitis, decreases in zinc,
magnesium, thiamin, and folate levels are often observed and should be evaluated (1,11-13). Table III- 24
provides common assessment parameters that may be altered as a result of pancreatitis and can be used in
diagnosing nutrition related problems.
Table III- 24 : Common Assessment Parameters for Pancreatitis
Data Reference Range Discussion
Serum amylase 30 to 95 IU Elevated with pancreatic dysfunction, due to liberation of
digestive enzymes from pancreas into neighboring tissues and
bloodstream