Manual of Clinical Nutrition

Pancreatitis

Manual of Clinical Nutrition Management III- 90 Copyright © 2013 Compass Group, Inc.

Data Reference Range Discussion

Serum bilirubin 0.2 to 0.9 mg/dL Elevated values may be due to compression of the distal common
duct within the pancreas, biliary stones, or inflammation of the
liver and bile ducts

Serum lipase <1.5 IU/mL Elevated with liberation of lipase from the pancreas into the
bloodstream

Blood glucose 70 to 110 mg/dL Elevated with impaired secretion of insulin in response to glucose
load because of inflammatory destruction of Islets of
Langerhans
Glucagon released from alpha cells may contribute to the
elevation of blood glucose

Fecal fat 5 to 6 g/100 g of
stool

Elevated with fat malabsorption secondary to impaired digestion

of fat due to impaired secretion of pancreatic lipase

Value may reach 50 g/24 hours

Serum carotene (^) 90 to 280 g/dL
100 to 300 IU/dL
Decreased secondary to fat malabsorption associated with
steatorrhea
This test is rarely done.
Serum Total
calcium
Ionized calcium
9 to 11 mg/dL
4.5-5.6 mg/dL
Decreased due to saponification of calcium with unabsorbed fatty
acids, or as result of increased calcitonin, decreased magnesium
levels, hypoalbuminemia, and/or decreased parathyroid
hormone release.
Recommended for critically ill patients or patients with
hypoalbuminemia. Ionized calcium levels are unaffected by
changes in serum albumin levels providing a more accurate
assessment of calcium status in critically ill and patients
receiving specialized nutrition support (14).
Hematocrit 42 to 52% (males)
37 to 47% (females)
Elevated due to hemoconcentration when serum exudes into the
abdomen
Decreased in severe hemorrhagic pancreatitis
CT scan Identifies level of necrosis of pancreas
Physical
examination
Subjective Hypoactive bowel sounds
Abdominal pain,
Nausea, vomiting
Diarrhea or bulky foul-smelling stools and flatulence indicate fat
malabsorption.
Nutrition Intervention in Acute Pancreatitis
Treatment of acute pancreatitis has drastically changed over the past decade (1). Parenteral nutrition (PN)
and bowel rest has traditionally been the primary management approach based on the hypothetical reasons
that enteral feeding may stimulate the synthesis of pancreatic enzymes and worsen the severity of disease.
However, current evidence suggests that the provision of enteral nutrition (EN) has a dramatic impact on
patient outcome compared to the provision of parenteral nutrition (PN) (15-16). Two landmark meta-analyses
demonstrated that use of EN reduces infection by as much as 52%, hospital length of stay by as much as 4
days, need for surgical intervention by as much as 52%, and trend toward reduced organ failure by as much
as 41% when compared to use of PN (15-16). Experience from the literature suggests that efforts to promote
pancreatic rest as the sole management strategy to treat pancreatitis is ineffective and does not have impact
on patient outcome (1,17).
The choice of nutrition therapy should be determined by disease severity, anticipated length of
intervention, and tolerance to the intervention (1,17). Current standards of care indicate that patients with
mild to moderate pancreatitis should initially be prescribed NPO with intravenous hydration support and