Pancreatitis Flashcards
When does the incidence of pancreatitis peak?
Between 40-70 years old
Mortality for acute, necrotizing and severe?
5%, 17% and 30%
What are the costs of pancreatitis?
- Nearly $9,000 fo a 8-10 day hospital stay
- However, after hospital many cannot work (cost to individual)
Acute mortality due to gallstones or idiopathic?
10-25%
Chronic mortality due to alcoholism?
5%
What is the key concept to understand w/ pancreatitis?
The pancreas is an endocrine and an exocrine gland. When a blockage of the ducts leads to the build-up and subsequent digestion of the pancreas, this can also affect the exocrine function where insulin and glucagon are altered.
Which cells secrete NaHCO3, K+, Na+ and Cl- in the pancreas?
-Duct cells
Which cells secrete digestive enzymes in the pancreas?
Acinar cells
Provide 8 major digestive enzymes secreted from the acinar cells
- Trypsin
- Chymotrypsin
- Carboxypolypeptidase
- Deoxy/Ribonuclease
- Eleastrase
- Lipase
- Cholesterol esterase
- Alpha-Amylase
What normally activates trypsin?
Brush border enzymes, such as enterokinase
In the fasted state, is there secretions from the pancreas?
Yes, basal flow of secretion
What stimulates the pancreas in the cephalic/anticipatory state?
-Vagal nerve stimulation
What stimulates the pancreas in the fed state?
-Distention will stimulate the pancreas via vagal nerve
What stimulated the intestinal production of secretin and CCK?
Chyme
What does secretin stimulate?
- Release and contraction of pancreas in a negative-feedback loop fashion
- Allows for the neutralization of contents in the SI
What prevents further CCK production?
Active proteases which are released from the pancreas upon stimulation
What are other inhibitory factors in the intestinal phase?
- PPY
- Somatostatin
What is pancreatitis?
The inflammation of the pancreas and the ducts
-There are acute and chronic forms
What is pancreatitis characterized by?
- Edema, cellular exudate, fat necrosis
- Autodigestion, necrosis hemorrhage of pancreatic tissue
Signs/symptoms of pancreatitis?
- Nausea, vomiting, abdo distention, steatorrhea
- Hypotension and dehydration
What are common causes of acute pancreatitis?
- Biliary tract disease/cholelithiasis
- Alcoholism
- Idiopathic
Other causes of acute pancreatitis?
- Infection, drugs, surgery, cancer
- Obesity, hyperlipidemia
- Hyperparathyroidism, hypercalcemia
- Exposure to toxins
- Trauma, ERCP
Theories of acute pancreatitis?
- Autocatalytic digestion
- Rate formation of trypsin > inhibitors
___ with uncomplicated, mild to moderate pancreatitis will advance to oral diet within a week of admission
80%
___ of acute pancreatitis patients require nutrition support
20%
Why may alcohol cause pancreatitis?
May cause random spasms over the years which can cause idiopathic digestion
Which stress factor should be used with HB in acute pancreatitis?
As they are in catabolic state, try 1.39 x HB
Clinical symptoms/presentations of acute pancreatitis?
- Abdominal pain, nausea and vomiting
- SIRS/shock, fever, edema
- Exudate in peritoneal and pleural spaces
Biochemical presentations of acute pancreatitis?
- Elevated levels of pancreatic enzyme, amylase, lipase
- Elevated liver enzymes in biliary causes
- Low blood calcium
- Elevated serum TG
There is often elevated TGs, and fat necrosis around the pancreas during acute pancreatitis, what would we estimate their maximal fat clearance to be?
1 mg/kg/day
Recall lipid clearance in the critically ill patient
What is exudate?
Any fluid that has exuded from a tissue/capillary due to injury/inflammation
What is the pathogenesis of chronic pancreatitis linked to?
- Alcoholsim
- Cystic fibrosis
- Chemical exposures
- Recurrent acute
- –> Insult w/o symptoms
What is chronic pancreatitis exacerbated in? What does this cause?
- Alcohol intake
- Presents with acute like symptoms
How does alcohol elicit both acute/chronic pancreatitis?
-Damages the acinar cells, and will stimulate secretin with the induction of spasms within the ducts –> And cause a precipitation of protein within the ducts
How does cystic fibrosis lead to chronic pancreatitis?
-Mucus secretions and flow of enzymes is impaired, therefore enzymes collect and are activated in ducts –> Infections and digestion
What do the symptoms of chronic pancreatitis depend on?
Stage of disease and alcohol intake
Symptom of chronic pancreatitis?
- Abdominal pain, vomiting
- Malabsorption, steatorrhea
- Weight loss
Biochemical presentations in chronic pancreatitis?
High amylase and lipase followed by low concentrations as acinar cells atrophy
Other symptoms of acute pancreatitis?
-Pericardial effusions, ascites, psychosis, necrosis of bone, decreased insulin and glucagon
Chronic pancreatitis may have _____
recurrent acute episodes
What is nutrition support based on?
-Severity of scores and likelihood of not achieving oral intake within 7-days
Typical nutritional managements in more severe cases of acute pancreatitis?
-NPO, TPN or EN
Typical nutritional management for mild & moderate cases of acute pancreatitis?
- Oral feeds
- Low fat high CHO and PRO for some
- Clear fluids to begin, transition to full fluid diets (consider fat)
- No alcohol
- Frequent, small meals
Typical nutritional management for chronic pancreatitis?
- Replacement enzymes w/ meals
- Antacids
- Low fat/high-pro diet
- CHO depends on islet function
- MCT oil an EN
- No alcohol
- Vitamin supplement (fat soluble and B12)
Why are antacids key if we provide enzyme supplementation?
Too acidic of a PH will simply digest the enzymes.
Why is MCT oil desirable?
-Less reliant on bile, and may result in less of a stimulation of CCK
How is Ransons criteria determined?
- 5 observations on bloods are checked at admission or diagnosis
- 6 observations on bloods are re-checked during the initial 48 hrs
What happens when >/= 3 of ransons criteria are present?
> 60% of patients die in hosptialization
What is checked for increases in Ransons criteria?
-WBC
-Blood glucose
-Lactic dehydrogenase
-Aspartate transaminase
BUN
-Acid/Base deficit
-Fluid sequestration
What is checked for decreases in Ransons criteria?
- Hematocrit
- Arterial PO2
- Calcium
What does APACHE stand for?
Acute Physiology and Chronic Health Evaluation
What is inculded in the APACHE score?
- Age
- Rectal temo
- MAP
- HR
- PaO2
- Artetial pH
- Serum K, Na, Cr, Hct, WBC
- Glasgow comma Scale Score
- Chronic health status
What is the APACHE and RANSON which indicates mild/moderate pancreatitis?
APACHE II <9
Ransons <2
What will a CT scan indicate for mild/moderate pancreatitis? What is the mortality rate? How many will reach PO diet in 7 days?
- No necrosis
- 0%
- 81%
- -> Focus on supportive management
What is the APACHE and RANSON which indicates severe pancreatitis?
APACHE II >10
Ransons >3
What will a CT scan indicate for severe pancreatitis? What is the mortality rate? How many will reach PO diet in 7 days?
- Necrosis
- 19%
- 0%
- -> Focus on EN and PN Managements
In the case of a mild pancreatitis, and the oral diet is not tolerates, when should we progress to EN?
Only use EN if the oral diet fails over 4 days
What needs to be evaluated to establish disease severity?
-SIRS,APACHE, RANSONS and CT necrosis
Where are mild cases admitted? Moderate/severe? How are they fed?
- Admit to ICU
- Place NG tube and initiate standard EN
What happens if NG EN is not tolerated?
- Switch to N feeds
- Start PN if intolerant >5days.
Why should we use gastric feeds?
- Gastric as better stimulation which is not observed in the jejunum
- Gastric access is much easier to obtain
If a severe or moderate pancreatitis patient tolerates NG EN, how can we progress?
If appropriate, we may advance to oral diet per patient wishes
What are the nutritional goals in the mild and moderate case?
- Maintain or achieve optimal nutrition status
- Reduce steatorrhea
- Minimize pain
- Avoid alcohol
What does ASPEN recommend about low fat diet in mild states?
No evidece
- Use self-selection in context of standard nutrition therapy
- However, not for ICU patients
- If oral intake fails, initiate EN after 4 days
What are some important considerations in nutrition support regarding the acute, severe, pancreatic patient?
- Hyperglycemia and insulin resistance is common (40-90%)
- Hypertriglyceridemia in 12-15% of cases
- Electrolyte and micronutrient deficiencies
Why hyperglycemia?
-Critical illness and residual islet cell function
Why typerTG?
- Low LPL (cannot clear lipids)
- Hyperglycemia induced
Which electrolyte/micronutrient imbalance is present in 25% of cases
Hypocalcemia
Energy in AP nutrition support?
25 kcal/kg/day
-Avoid overfeeding
Why is HB x 1.39 (high) and 25 kcal/kg/day (low) recommended for NS?
- What someone NEEDS is not necessarily wha they should be fed
- We are often aiming for 80% of the target
- 25 kcal/kg/day likely more appropriate, but try both and use clinical judgement
Protein in AP?
1.5 g/kg/day
What should be used in terms of energy for a septic, AP patient?
HB x (1.39 + 1.15)
Goals in providing adequate kcal and protein in AP patient?
- Support acute phase protein
- Minimize nitrogen losses
- Manage imbalances
Why is enteral nutrition the preferred method in AP?
- Maintain gut integrity, decrease septic and metabolic complications, decrease cost
- Reduced stress response compared to PN
- Reduced infection
- Reduced LOS by 4 days
- Reduced surgical intervention
- Reduced organ failure
Which organs are likely to fail in pancreatitis?
- Respiratory system (PENN state, may be sedated, propofol)
- Kidney (Higher protein, CRRT, hypotension)
Which mode of feeding will provide pancreatic rest while using the GIT?
Enteral support below the ligament of Treitz (LOT) via nasojejunal tube
If there is pain, where should we feed?
Below LOT
How should EN be administered?
- Initiate within 48-72 hours of admission
- Continuous infusion over 24 hours a day
- Initiate feeding 25 ml/hour and advance to reach 25 kcal/kg over 24-48 hours
EER in pancreatitis?
25 kcal/kg/day or indirect calorimetry
Estimated protein in pancreatitis?
- 5 k/kg/day
- Up to 2g/kg/day (MUHC)
Formulation of EN in pancreatitis?
-Standard polymeric formula, mixed protein, fat CHO
What kind of formula should we use if intolerance in expected?
- Semi-elemental or elemental or very low-fat formulas
- R/o C.Diff and sorbitol containing meds first
What type of formula should we use if steatorrhea?
Semi-elemental with mCT
CHO limit in pancreatitis on EN? Why?
5 mg/kg/min
- Due to hyperglycemia and hyperTG
- -> On exam, use both 5 and 3 then rationalize whether it is a severe or mild case
When can we advance EN feeds to oral diet? When do we switch to PN?
- Advance to oral diet when no pain for 24 hours
- Switch to PN if there is intolerance
When is PN only considered?
In patients for whom enteral access is not possible or not tolerate or the most SEVERE cases
What are the severe cases where PN is warranted?
- Persistent ileus
- Small intestinal obstruction
When can we initiate PN?
5 days after admission, even if high risk (already at high risk for infection, risk outweighs benefit)
Type of PN?
Mixed fuel
PN energy?
Increase slowly to reach 25-35 kcal/kg
CHO limit in PN?
-5 mg/kg/min or 3 mg/kg/min
Protein in PN?
1.2-1.5 g/kg/day
Intralipid in PN?When?
Less than 15-30% of kcal
-When TG <400 mg/dL or 4.52 mmol/L
Lipid of _____ does not cause hyperTG
1 mg/kg/day
When is pancreatitis chronic?
When there is pancreatitis insufficiency
Overarching goal in nutrition support of chronic pancreatitis?
Restore and maintain weight
Meals in chronic pancreatitis?
- Frequent, small meals moderate to low in fat
- However, low fat ay exacerbate malnutrition, and tolerance is the goal
- MCT may be used
What must be taken in chronic pancreatitis?
Pancreatic enzymes taken with food (no more than 30 mins prior, or smaller amounts during meals)
What should be avoided in diet in chronic pancreatitis?
-Alcohol, coffee, tea, spices, irritant condiments
What should be monitored in chronic pancreatitis?
- Monitor fat, water-soluble vitamins
- Medical management of pH
- Treat with insulin if hyperglycemia or diabetes
Lipase dosages per meal?
500-2500 U lipase/kg/meal
Lipase dosages per day?
<10000 U lipase/kg/day
Lipase per g of dietary fat per day at meals and snacks?
1000-4000 U lipase/1 g dietary fat per day
Guidelines for pancreatic enyzmes?
- Swallow without crushing
- The enteric coating will become activated at > pH 5, therefore consider adding something to increase/neutralize the pH, such as antacids
When will the pH in the SI be <5?
When bile acid not active, in pancreatitis
What are the two functions of antacids?
- Enteric coat activation of pancreatic enzyme replacements
- Aid in fat malabsorption
In failure of oral diet, what is preferred in terms of NS in chronic pancreatitis?
- EN preferred
- Semi-elemental and elemental best given pancreatic insufficiency (enzymes do not lend to tube feeding)
