Pancreatitis

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Caroline Collins

Fact Sheet

Fact Sheet

Disease/Medical Condition: Acute Pancreatitis (AP)


Usual Hospital Stay: 3-5 Days
Pathophysiology:
 Intra-acinar premature activation of pancreatic enzymes (trypsin, phospholipase A2, and elastase)
exocrine damage  autodigestion of pancreatic cells  destruction of pancreatic tissue. Enzymes released
by destroyed pancreatic cells  bloodstream =  amylase &  lipase  pancreatitis  edema,
autodigestion, hemorrhage of pancreatic tissue, fat necrosis
Etiologies:
 Gallstones (45% of cases), Alcohol use (35% of cases), Hyperlipidemia, Drug-induced, Post-procedural
(ERCP or abdominal surgery), Idiopathic, Genetic predisposition, Obstruction of Pancreatic Duct,
Pancreatic cancer, Hypercalcemia, Autoimmune disorders, Infections (viral, bacterial, fungal, and
parasitic), Trauma, Biliary Tract Disease, End Stage Renal Disease, Vasculitis
Symptoms:
 Upper abdominal pain, Abdominal pain that radiates to the back/feels worse after eating, Fever,
Tachycardia, Nausea, Vomiting, Tenderness when touching the abdomen, Abdominal distention,
Hypotension, Mild jaundice, Pleural effusion
Complications:
 10-30% with organ failure or complications
 Pancreatic Abscess  intra-ad pus/bacteria collection
 Pseudocyst  enclosed collection of pancreatic enzymes; debridement if nonhealing
 Pancreatic Necrosis  one/more pancreatic areas nonfunctioning or infected; debridement
 Others  Abdominal compartment syndrome, Acidosis, Acute renal failure, Acute respiratory distress
syndrome, Ascites, Bowel infarction, Development of chronic pancreatitis, Disseminated intravascular
coagulation, Gastric varices, Ileus, Mesenteric venous thrombosis, Splenic venous thrombosis
Severity of Acute Pancreatitis:
 Mild pancreatitis: absence of organ failure and local complications
 Moderately severe acute pancreatitis: transient organ failure lasting <48 hours and local complications.
 Severe acute pancreatitis: persistent organ failure lasting >48 hours from admission.
Diagnostic Criteria:
 Presence of at least 2 of 3 diagnostic criteria– abdominal pain, elevated serum amylase or lipase, and
radiological evidence
 Tests: Ultra-Sounds, CT, Magnetic Resonance Cholangiopancreatography (MRCP), Endoscopic
Retrograde Cholangiopancreatography (ERCP)
 Labs - amylase, lipase,  glucose,  WBC;  ALT/AST/bilis
Medical Goals:
 Rehydrate and correct fluid and electrolyte imbalances
 Maintain integrity of gut barrier in small intestine
 Reduce pain, fever, prevent shock, hypermetabolism, sepsis, and or compression of stomach or colon
 Achieve pancreatic rest and avoid pancreatic irritants (caffeine, alcohol)
 Avoid overfeeding
 Prevent metabolic complications
 Promote EN in patients requiring nutrition support, rather than PN
 Use CPN if abdominal pain is refractory  positive nitrogen balance
 Monitor hemodynamic/laboratory/serum parameters
Nutritional Concerns:
 Increased protein catabolism, abnormal lipid metabolism, possible malnutrition with increased metabolism
and poor PO intake
Medical Nutrition Therapy Goals:
 Adequate kcal and protein; minimize nitrogen losses; manage imbalances which may include
hypo-/hyperglycemia, hypertriglyceridemia, and imbalances of micronutrients such as calcium,
magnesium, and vitamins
Medical Nutrition Therapy:
Caroline Collins
Fact Sheet

• Energy: 25-30 kcal/kg


• Protein: 1.5-2.0 g/kg
• Low fat oral diet in absence of nausea/vomiting
• If alcohol abuse: supplement thiamin 100mg, folate 1mg, general multivitamin
• Pancreatic enzymes if steatorrhea
• EN/PN if indicated
• Feeding Progression:
• Initial status: NPO
• Mild: advance to small frequent oral low-fat feedings; MCT if steatorrhea; pancreatic enzyme
replacement with each meal. No nutrition support for mild AP (70-90% of cases) unless
malnourished and NPO 5-7 days expected.
• Moderate to Severe: nasogastric or nasojejunal feedings; Postpyloric TF is often well tolerated;
Formulas containing peptides and MCT and Omega 3’s can be helpful; EN at a trophic rate,
advanced to goal as fluid volume resuscitation is completed (w/in 24–48 hrs of admit); Standard
polymeric formula for severe acute pancreatitis; Consider IEF if complications
• If unable to feed enterally: parenteral nutrition indicated
Laboratory Tests/Values:
 Pancreatic panel: amylase, lipase, calcium, glucose, triglycerides

Pertinent Labs Normal Value AP Patients


Amylase 35 – 115 U/L , > 200-250 U/L
or 0-160 U/L depending on lab
Lipase 16–63 U/L , >110; more sensitive
or 23-85 U/L depending on lab than amylase
Ca++ 9.0- 10.5 mg/dl 
Glucose 70-110 mg/dL or <6.1 mmol/L 
Triglycerides <150 mg/dl – desirable 

Other Possible Labs Normal Value AP Patients


WBC Total 5000-10000/mm3 
ALT 4-40 U/L Males, 4-31 U/L Females 
AST 10-37 U/L Males, 10-31 U/L Females 
Bilirubin Direct <0.3 mg/dL, Total <1 mg/dL 
Triglycerides <150 mg/dl – desirable 
CRP .08-3.10 mg/L 
K+ 3.5-5.0 mEq/L 
Na 136-145 mEq/L 
Mg 1.3 – 2.1 mEq/L 

Food-Drug Interactions
 Drugs that may trigger AP: Lasix, azathioprine, dideoxyinosine, DDI, 6-mer-captopurine, ACE inhibitors,
dapsone, Acetaminophen, estrogens, methyldopa, steroids, nitrofurantoin, thiazides, cimetidine,
erythromycin, salicylates, Sulfonamides, tetracyclines,
 Limit alcohol, nicotine, and gastric stimulants such as peppermint and black pepper if not tolerated
Herbs, Botanicals, Supplements
 Antioxidants such as selenium may be beneficial
 Adequate calcium, magnesium, zinc, vitamin C, B-complex vitamins, folic acid for water-soluble vitamin,
fat-soluble vitamins in water-miscible form
 Probiotics may promote higher mortality
 Herbs and botanicals may have hepatotoxic properties
Patient Education: Signs/symptoms; omission of alcohol and gas-forming foods; tips for nausea and vomiting; if
home EN/PN needed, education and appropriate methods/monitoring; low fat, high protein, high calorie oral diet if
and when appropriate; antioxidant rich foods
Caroline Collins
Fact Sheet

References

Escott-Stump, S. (2015). Nutrition and diagnosis-related care. Philadelphia: Wolters Kluwer.

Gapp, J. (2019). Acute Pancreatitis. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK482468/.

Nelms M. (2011) Nutrition Therapy and Pathophysiology. 2nd Edition. Wadsworth, Cengage Learning.

Quinlan, J. D. (2014). Acute Pancreatitis. Retrieved from https://www.aafp.org/afp/2014/1101/p632.html.

Width, M., & Reinhard, T. (2018). Essential Pocket Guide for Clinical Nutrition (2nd ed.). Wolters Kluwer.

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