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Abbreviations
NUTRITIONAL
MANAGEMENTIN
ACUTE AND CHRONIC
PANCREATITIS
Earnest Alexander Jr., Pharm.D.
Reviewed by Susan C. Fagan, Pharm.D., FCCP, BCPS; and Mark Newnham, Pharm.D., BCPS, BCNSP
Learning Objectives admissions. The remaining 20–30% of patients are admitted
with severe pancreatitis with reported mortality rates of up
1. Evaluate the classification, clinical manifestations, and to 25–30%. Therefore, the ratio of mild to severe acute
long-term risks associated with acute and chronic pancreatitis is about 4:1.
pancreatitis. Acute fluid collection occurs in 30–50% of acute
2. Assess common diagnostic tools used in acute and pancreatitis cases and typically resolves spontaneously. A
chronic pancreatitis and evaluate their usefulness. pseudocyst is a fluid collection that persists for 4–6 weeks
3. Analyze patient-specific characteristics in determining and becomes encapsulated by a wall of fibrous or
the nutritional support needs and goals of patients with granulation tissue. Asymptomatic pseudocysts do not
acute and chronic pancreatitis. require treatment. If symptomatic, pseudocysts can be
4. Demonstrate an understanding of the role of enteral and managed surgically, radiologically, or endoscopically. A
parenteral nutrition support in managing acute and small subset of patients with severe acute pancreatitis will
chronic pancreatitis. develop chronic pancreatitis or pancreatic necrosis. It is
5. Develop a plan to provide nutrition support through an estimated that about 5–15% of patients with acute and
appropriate route to a patient with acute and chronic chronic pancreatitis develop necrotizing pancreatitis.
pancreatitis. Necrotizing pancreatitis is a devastating disease with
reported mortality rates of up to 50–80%. Appropriate
surgical, antibiotic, and nutritional management reduces
Introduction to Acute and these rates to about 5–20%.
Chronic Pancreatitis Classifying and Diagnosing
Epidemiology of Acute and Chronic Pancreatitis Pancreatitis
Acute pancreatitis is defined as an acute inflammatory
process of the pancreas with variable involvement of other Many scoring systems have evolved to identify patients
regional tissues and remote organ systems. It is a relatively with severe pancreatitis who are at highest risk for organ
common disease, affecting 200,000 individuals annually in failure and/or local complications, such as necrosis, abscess,
the United States. Although it often runs a mild course, up or pseudocyst. Ranson criteria are scored based on
to 30% of acute pancreatitis cases will be associated with 11 clinical criteria with prognostic importance and is the
significant morbidity and mortality. Acute pancreatitis is most widely recognized system for classifying pancreatitis.
characterized by the sudden onset of severe epigastric pain, Five of these criteria are measured at the time of admission
which accounts for 3% of hospital admissions for abdominal and the other six in the first 48 hours after admission. The
pain. Mild attacks account for 70–80% of acute pancreatitis number of Ranson criteria present at the time of assessment
Fang J, DiSario JA. Nutritional management of acute pancreatitis. Curr Gastroenterol Rep 2002;4:120–7.
Rettally CA, Skarda S, Garza MA, Schenker S. The usefulness of laboratory tests in the early assessment of severity of acute pancreatitis. Crit Rev Clin Lab Sci
2003;40:117–49.
Pharmacotherapy Self-Assessment Program, 5th Edition 183 Nutritional Management in Acute and Chronic Pancreatitis
Abbreviations
Abbreviations in this during acute pancreatitis occur with a delay of 1–2 days, as
it reflects the stimulation of hepatic synthesis of the acute
Chapter phase reactants mediated by interleukin-6. Although the
release of inflammatory mediators such as interleukin-6 and
APACHE II Acute Physiology and Chronic polymorphonuclear elastase occurs more rapidly, serum
Health Evaluation II CRPdetermination is still the most widely used individual
CRP C-reactive protein marker for prognostic assessment of acute pancreatitis
EN Enteral nutrition because of ease of use and widespread availability.
TPN Total parenteral nutrition C-reactive protein indicates pancreatic necrosis within
48–72 hours after disease onset with an accuracy of about
90%.
The Atlanta classification is an additional scoring system
is correlated with the incidence of systemic complications that uses information obtained by contrast-enhanced
and the presence of pancreatic necrosis. In addition to the computed tomography and clarified definitions of the
Ranson criteria, the Glasgow criteria are scored using a different complications likely to be encountered with acute
similar approach with only eight clinical criteria assessed pancreatitis. The Atlanta classification system categorizes
during the first 48 hours. These scoring systems are detailed disease under the general heading of pancreatic necrosis.
in Tables 1-1 and 1-2. Mild acute pancreatitis is associated Ultrasound or magnetic resonance pancreatography
with two or fewer criteria with both the Ranson and combined with this system aid in distinguishing among
Glasgow scoring systems. Despite some limitations in localized collections of necrotic tissues, acute pseudocysts,
sensitivity and specificity, studies suggest that patients with and fluid collections.
a Ranson or Glasgow criteria of 3 or higher have severe Evidence on computed tomography of hypoperfusion
pancreatitis. correlates well with pancreatic necrosis. Computed
The Acute Physiology and Chronic Health Evaluation II tomography is useful for diagnosing pancreatic necrosis
(APACHE II) is an illness severity score and prognostic after the first 24 hours of symptom onset with sensitivity
indicator based on 12 physiological variables, the patient’s further improving to about 100% between 4 and 10 days
age, and any history of severe organ system dysfunction or after symptom onset.
immunocompromised state. Traditionally, an APACHE II Interleukins (i.e., interleukin-6, interleukin-8, and
score of 10 or higher indicates the presence of severe interleukin-18), trypsin activation peptide, procalcitonin,
pancreatitis. However, many clinicians and researchers procarboxypeptidase-activation peptide, and phospholipase
currently use a lower APACHE II score (6 or higher) to A2also are markers of disease severity with proven validity,
differentiate mild acute pancreatitis from severe acute but they are either too expensive or too time-consuming for
pancreatitis. This lower APACHE II score has not yet been routine clinical practice. A single serological marker with
fully adopted by all practitioners because of the increased absolute reliability to predict a severe attack of acute
probability of erroneous classification of patients with mild pancreatitis at any time after onset of the disease is still not
acute pancreatitis as severe. The distinction between available.
APACHE II scoring cutoffs and the classification of mild Amylase and lipase are both enzymes released from the
and severe acute pancreatitis is important in properly pancreas during acute pancreatitis. Despite widespread use
evaluating the results of clinical data from recently of amylase and lipase concentrations for diagnosing acute
published studies. Studies that classify severe acute pancreatitis, the prognostic ability of either enzyme to
pancreatitis in patients with an APACHE II score of 10 or assess severity of disease has been consistently poor. The
greater than three Ranson criteria ensures the exclusion of reason plasma concentrations of the pancreatic enzymes
patients with mild disease. Unlike the Ranson or Glasgow have no value in predicting severity probably relates to the
system, the APACHE II score is more flexible, allows for rapid decline in concentrations after an early peak. The peak
classification of illness severity on admission, and may be occurs within the first 24 hours of symptoms, with amylase
recalculated daily. A combination of the APACHE II with having a shorter half-life compared to lipase. The decrease
either the Ranson or Glasgow scoring systems in research in concentrations over the course of several days limits the
and clinical practice ensures sensitivity and specificity in accuracy of these enzymes in measuring pancreatic severity
classifying acute pancreatitis and assessing progression of through the course of the disease. In addition, in the absence
the disease. To ensure the inclusion of patients with severe of pancreatitis, serum lipase may increase up to 2-fold
pancreatitis, studies should include only patients with three above normal in severe renal insufficiency (creatinine
or more Ranson criteria or an APACHE II score of 10 or clearance of 20 ml/minute or less). Pancreatic enzyme
more. concentrations also have limited value in diagnosing
In many institutions, measurement of biochemical chronic pancreatitis, with concentrations often normal or
markers has become a standard for prognostic assessment. low. The diagnosis of chronic pancreatitis is based on
An advantage of the markers is that they can be measured recurrent abdominal pain, radiographic abnormalities, and
repeatedly and thereby draw attention to the development of functional testing failures. Practitioners traditionally have
severe disease more simply than the complex scoring monitored daily enzyme concentrations instead of patients’
criteria. The use of C-reactive protein (CRP) can detect overall clinical picture in patients with chronic pancreatitis.
pancreatic necrosis in the majority of patients with However, published data would suggest that this practice is
concentrations more than 120 mg/L. Increases in CRP unwarranted, and that patients’ overall clinical presentation
Nutritional Management in Acute and Chronic Pancreatitis 184 Pharmacotherapy Self-Assessment Program, 5th Edition
Abbreviations
Table 1-1. Ranson Criteria for Pancreatitis Severity Table 1-2. Glasgow Criteria for Pancreatitis Severity
Ranson Criteria Glasgow Criteria
Assessed at admission Assessed during initial 48 hours
Age 55 years or older Age 55 years or older
White blood cell count Greater than White blood cell count Greater than
3 3
16,000 cells/mm 15,000 cells/mm
Glucose Greater than 200 mg/dl Glucose Greater than 200 mg/dl
Lactic dehydrogenase Greater than 350 IU/L Albumin Less than 3.2 g/dl
Aspartate aminotransferase Greater than 250 IU/L Arterial PaO Less than 60 mm Hg
Assessed during initial 48 hours Calcium 2 Less than 8 mg/dl
Hematocrit decrease Greater than 10% Lactate dehydrogenase Greater than 600 IU/L
Blood urea nitrogen increase Greater than 5 mg/dl Blood urea nitrogen Greater than 45 mg/dl
Calcium Less than 8 mg/dl PaO = partial pressure of oxygen.
Arterial PaO Less than 60 mm Hg 2
Base deficit 2 Greater than 4 mEq/L Glasgow criteria is obtained by evaluating for the presence of eight clinical
Fluid sequestration Greater than 6 L criteria in the first 48 hours after symptom onset. The sum total of these
criteria is equal to the Glasgow criteria.
PaO = partial pressure of oxygen. Reprinted with permission from CRC Press, LLC. Rettally CA, Skarda S,
2 Garza MA, Schenker S. The usefulness of laboratory tests in the early
Ranson criteria is obtained by evaluating for the presence of 11 clinical assessment of severity of acute pancreatitis. Crit Rev Clin Lab Sci
criteria (five criteria are measured at the time of admission and the other six 2003;40:117–49.
in the first 48 hours after admission). Each criteria is given 1 point. These
criteria are added, with the sum total of these criteria equaling the Ranson
criteria. stimulate the pancreas and activate zymogen granules. This
Reprinted with permission from CRC Press, LLC. Rettally CA, Skarda S, process results in the activation of cytolytic enzymes, which
Garza MA, Schenker S. The usefulness of laboratory tests in the early initiate a cascade of inflammatory responses. These
assessment of severity of acute pancreatitis. Crit Rev Clin Lab Sci inflammatory responses lead to a spectrum of pancreatic
2003;40:117–49. injuries that range from mild edema to necrosis. The exact
should dictate chronic pancreatitis management. triglyceride concentration threshold associated with
Acombination of tools has been suggested as a strategy pancreatitis has not been definitely established. However,
to improve the distinction between mild and severe acute triglyceride concentrations of more than 1000 mg/dl are
pancreatitis, early after disease onset. A retrospective considered a risk factor for pancreatitis. It is important to
analysis performed in 72 nonconsecutive patients with acute note that triglyceride concentrations of 500–1000 mg/dl also
pancreatitis (32 severe) using a stepwise discriminant may induce acute pancreatitis.
function analysis, selected a polymorphonuclear elastase Acute pancreatitis usually has a rapid onset manifested
value on day 1 and CRP value on day 2 as the best by upper abdominal pain, vomiting, fever, tachycardia,
diagnostic combination. Researchers described 97% leukocytosis, and elevated serum concentrations of
accuracy in predicting severe cases with this approach. pancreatic enzymes. The most prevalent feature of chronic
However, their report does not clearly define specific cutoff pancreatitis is abdominal pain. This pain typically increases
values for polymorphonuclear elastase and CRP at these after a meal as a result of pancreatic acinar cell secretion
time points. Although polymorphonuclear elastase appears activated by the hormone cholecystokinin.
to be a useful tool for diagnosing acute pancreatitis, the Significant ischemia of the gland predisposes it to severe
availability of the test currently is limited to major research hemorrhage and necrosis. Necrotic pancreatic tissue
centers with limited availability in the community hospital presents a welcoming environment for microorganisms,
setting. with necrotizing pancreatitis leading to secondary infections
in 40–60% of cases. Early studies reported mortality rates of
50–80% with necrotizing pancreatitis, but modern intensive
Etiology and Clinical care management has reduced mortality rates to about 20%.
The high mortality rates associated with necrotizing
Manifestations of pancreatitis are attributed to a severe systemic inflammatory
response triggered by an intense cytokine reaction resulting
Pancreatitis in multiple organ failure. The organs most commonly
affected are the lungs (e.g., adult respiratory distress
The causes of acute pancreatitis can be divided into syndrome) and kidneys (e.g., acute renal failure).
several broad categories, including biliary obstruction,
toxins, trauma, infections, vascular and metabolic Nutritional Pathophysiology
abnormalities, and miscellaneous causes. The vast majority
of cases are caused by biliary obstruction secondary to in Pancreatitis
gallstone formation or toxins such as ethanol. In fact, biliary
obstruction by gallstones accounts for about 45% of cases, Nutritional Pathophysiology in Acute Pancreatitis
and ethanol accounts for another 35%. The remaining 20% Knowledge of the metabolic pathophysiology of acute
of cases are idiopathic or have miscellaneous causes.
Obstruction leads to increased pressure and distention in pancreatitis is the foundation of appropriate nutritional
the pancreatic duct. Direct toxins (e.g., ethanol and other management. Acute pancreatitis starts within the pancreas,
drugs), hypertriglyceridemia, and hypercalcemia can all with severe disease leading to extensive tissue destruction
Pharmacotherapy Self-Assessment Program, 5th Edition 185 Nutritional Management in Acute and Chronic Pancreatitis
Abbreviations
generating profound systemic and metabolic derangements. Table 1-3. Metabolic Changes in Acute Pancreatitis
These changes occur because of the release of hydrolytic Increased Decreased
enzymes, toxins, and cytokines, which damage several Energy expenditure Insulin response
organ systems and promote hypermetabolism with a Gluconeogenesis Glutathione
negative energy balance. Metabolism in patients with acute Proteolysis Vitamins A, C, and E
pancreatitis typically behaves in a similar fashion to patients Urea turnover Selenium
with sepsis, with hyperdynamic changes, hypermetabolism, Lipolysis Methionine
and catabolism. Patients with severe acute pancreatitis may BCAAoxidation Glutamine
develop hyperdynamic states, with increased cardiac output, Glutamine oxidation
decreased systemic vascular resistance, and mild to severe BCAA= branched-chain amino acid.
deficiencies of oxygen extraction.
Alterations in measured energy expenditure have been
determined by indirect calorimetry and compared to increased uptake of endogenous amino acids by the skeletal
predicted energy expenditure estimated using the Harris- muscle mass, have been reported clinically and
Benedict equation in a prospective, case-referent study in 48 experimentally. The exact reason for this catabolism is not
patients with pancreatitis (eight mild acute, five severe fully understood; however, the process of nitrogen loss and
acute, 24 chronic, seven acute with sepsis, and four chronic use closely resembles that which occurs during sepsis.
with sepsis). Ranson criteria of three or more were used to Gluconeogenesis increases, whereas glucose clearance
classify severe acute pancreatitis. Researchers found a great and oxidation diminish, leading to glucose intolerance in
deal of variability in measured energy expenditure with 10% 40–90% of cases. As a consequence, insulin can be required
of all patients hypometabolic (less than 90% of predicted in up to 81% of patients. Reduced lipid clearance also has
energy expenditure), 38% normal metabolic (90–110% of been documented in 12–15% of cases. A summary of
predicted energy expenditure), and 52% hypermetabolic metabolic changes that occur with acute pancreatitis is
(more than 110% of predicted energy expenditure). There provided in Table 1-3.
was a higher mean measured energy expenditure, expressed Some studies indicate pancreatic damage occurs from
as percentage of predicted energy expenditure, for patients activation of oxygen-derived free radicals in acute
with sepsis with pancreatitis (120 ± 11%) compared with pancreatitis. Data suggest that glutathione and other
patients with chronic pancreatitis (105 ± 14%; p<0.05). sulfhydryl compounds are depleted and lipid peroxidation is
However, there was no significant difference in the mean increased in patients with acute and chronic pancreatitis. A
measured energy expenditure for patients with sepsis recently published study assessed the contribution of
compared with patients with acute pancreatitis (112 ± 17%; oxidative stress in 320 patients with acute pancreatitis
p=NS). In addition, patients with severe acute pancreatitis (90 severe) compared with 263 healthy controls.
had a significantly higher mean measured energy Statistically significant reductions of glutathione were noted
expenditure (126 ± 10%) compared with patients with mild at 24 and 48 hours from diagnosis in patients with both mild
acute pancreatitis 111 ± 15%; p<0.03). The variability acute and severe acute pancreatitis compared with controls.
makes it somewhat difficult to pinpoint the optimum caloric The clinical significance of this level of depletion in
requirements of these patients, particularly with the antioxidant defenses has not been concretely established and
Harris-Benedict equation. Therefore, recommendations for questions linger regarding the amounts of antioxidants
total caloric intake range from 25 kcal/kg/day to required for repletion.
35 kcal/kg/day in most patients. The upper limit of this Hypocalcemia is related to the severity of the disease and
calorie range is best in patients with sepsis coinciding with has been observed in 40–60% of patients with acute
severe acute pancreatitis. The most accurate means of pancreatitis. Serum concentrations are maximally depressed
determining caloric requirements is through indirect during the first 3 days of the attack. The pathogenesis likely
calorimetry. is multifactorial, involving saponification of calcium with
Acute pancreatitis increases the catabolism and free fatty acids, hypoalbuminemia, hypomagnesemia,
proteolysis of skeletal muscle by as much as 80% in increased calcitonin release, and decreased parathyroid
comparison with healthy controls. Further nitrogen losses hormone secretion. The first step for managing
increase to as much as 20–40 g/day. Decreased hypocalcemia should be to verify that the reduced serum
concentrations of total plasma proteins, rapid turnover of calcium is not caused by hypoalbuminemia. If the ionized or
proteins, and a marked decrease of the ratio of branched- corrected calcium is low (based on local laboratory
chain to aromatic amino acid further characterize this standards), an attempt at correction should be made with
hypercatabolic state. Theories regarding this ratio have led calcium supplementation.
to a handful of small studies evaluating exogenous
administration of branched-chain amino acids (e.g., L- Nutritional Pathophysiology in Chronic
arginine) with no role defined. Therefore, exogenous Pancreatitis
standard amino acid mixture administration is the mainstay Chronic pancreatitis may lead to maldigestion and
of therapy in patients with pancreatitis. Significant malnutrition in some patients. This process is secondary to
decreases in plasma essential amino acids, with marked long-standing inflammation and fibrosis in the pancreas that
reductions of almost all amino acids in the liver and destroys exocrine tissue, leading to inadequate delivery of
Dickerson RN, Vehe KL, Mullen JL, Fuerer ID. Resting energy expenditure in patients with pancreatitis. Crit Care Med 1991;19:484–90.
Nutritional Management in Acute and Chronic Pancreatitis 186 Pharmacotherapy Self-Assessment Program, 5th Edition
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