Acute Pancreatitis Flashcards
lDescribe the 2 main roles of the pancreas
Exocrine
Endocrine
What are the exocrine functions of the pancreas - how does it work?
Produces and releases digestive enzymes via the pancreatic duct into the duodenum in release to eating and drinking
What active enzymes does the pancreas produce and release? (6)
amylase
lipase
trypsin
chymotrypsin
elastase
carboxypeptidase
What are the 2 endocrine functions of the pancreas?
Makes and releases hormones. Mainly glucagon from alpha cells and insulin from beta cells.
What is the role of insulin?
Insulin transports glucose from blood stream into the cells.
What is the role of glucagon?
Glucagon helps release glucose from the liver stores by converting glycogen to glucose.
If there is disruption with either exocrine or endocrine functions of the pancreas - what are the nutritional implications?
- Disruption of blood glucose control. Hypoglycaemia = if not absorbing nutrition
Hyperglycaemia = if not enough insulin is released - Malabsorption
What is the role of the gall bladder ?
To store and release bile into the duodenum via the common bile duct bladder.
Bile and enzymes both work to break down food in the duodenum after chyme has been released into the duodenum via the pyloric sphincter from the stomach.
What digestive enzymes work on carbs, fat and protein from the saliva?
carb = amylase
fat = salivary lipase
protein - none
What digestive enzymes work on carbs, fat and protein from the gastric secretions?
carb = gastric amylase
fat = gastric lipase
protein = pepsin; rennin and gelatinase
What digestive enzymes work on carbs, fat and protein from the pancreas?
carb = pancreatic amylase
fat = lipase; steapsin
protein = trypsin; chymotrypsin; carboxypeptidase; elastase
What digestive enzymes work on carbs, fat and protein from the jejunal/ileal secretion?
carb = sucrase; maltase; isomaltase; lactase
fat = intestinal lipase
protein = brush border; proteases
What are the 3 phases of regulation and pancreatic secretion?
cephalic phase = triggered by sight, smell and taste of food
gastric phase = initiated by gastric distention; triggers release of enzymes and hormones
intestinal phase = in duodenum; when food is chyme - stimulates two hormones: secretin and cholecystokinin into blood circulation; triggers pancreas to release digestive enzymes
Summarise what acute pancreatitis is?
Pancreas becomes acutely inflamed.
A rapid and dynamic process which requires dietetic vigilance.
What are the main causes of acute pancreatitis? (7)
- gallstones
- excess alcohol intake
- idiopathic (unknown)
- Other = autoimmune, hypercalcaemia
- Post ECRP (endoscopic retrogade cholangio pancreatography) - an investigation with camera up through pancreatic ducts
- Drugs - medications
- Hypertriglyceridaemia
What are some of the consequences of moderate/severe acute pancreatitis?
What causes pancreatic tissue to necrose.
20% of all acute pancreatitis.
Infected necrosis = increased mortality rate. Occurs when there is bacterial translocation across the gut. barrier
Sterile necrosis = Not infected
Fluid can accumulate around the pancreas = necrotic tissue
What are the 3 signs and symptoms needed to diagnose acute pancreatitis? (2012 Atlanta Classification)
- abdominal pain consistent with pancreatitis
- serum amylase and/or lipase of at least 3x the normal upper limit
- Findings consistent with acute pancreatitis on CT, MRI and ultrasound.
Define mild acute pancreatitis
no organ failure.
no local or systemic complications
Define moderately severe acute pancreatitis
Organ failure that revolves within 48 hours (transient organ failure)
and/or local systemic complications without persistent organ failure
Define severe acute pancreatitis
persistent organ failure (> 48 hours)
Single or multiple organs. Often very unwell and need to go to ICU
Why is severity so important to dietetic care? (name 3)
1, Increasing severity = increased mortality risk
- accumulation of fluid in or around the pancreas can lead to necrosis and/or organ failure
- necrotic tissue can become infected from translocation of bacteria from the gut
Why is enteral nutrition important? (3 reasons)
- Starvation = associated with gut atrophy. This can cause bacterial translocation - can lead to necrotic pancreatic infection
- Oral/ enteral nutrition (NG or NJ) has been shown to reduce bacterial translocation from the gut and stimulates intestinal motility, reducing bacterial overgrowth and maintains the gut mucosal integrity
- This can reduce systemic infectious complications and benefits clinical outcomes.
Why should acute pancreatitis be considered at moderate to high nutritional risk?
because of the catabolic nature of the disease and the impact of nutritional status for disease development.
How many acute pancreatitis patients be nutrition screened and why? What method used?
All patients with predicted mild to moderate acute pancreatitis should be screened using validated methods (Nutritional Risk Screening, 2002)
All patients with severe AP should always be considered at nutritional risk
Why are all moderate AP patients be considered high nutritional risk?
Because of the catabolic nature of the disease because of the impact of nutritional status in disease development
When should oral nutrition be offered to AP patients?
as soon as clinically tolerated and independent of serum lipase concentrations in patients with predicted mild AP.
Why should AP patients not be made nil by mouth?
Unless a clear reason for nil by mouth (i.e. severe vomiting) enteral feeding should be offered (oral or tube) to anyone with severe or moderately severe AP.
How quickly should enteral nutrition be offered to anyone with severe or moderately severe AP?
Within 72 hours of presentation.
When should parenteral nutrition be offered to AP patients?
Only if enteral nutrition has failed or is contraindicated.
Why is feeding orally or via NG preferred over PN?
Oral and EN reduces bacterial translocation and is better for gut health
How soon into hospital admission should EN be started? and why?
within 24 - 72 hours in case of intolerance to oral feeding.
When AP patient requires nutrition support which methods are the preferred order administration? and when/why?
- NG
- NJ is preferred in case of digestive intolerance.
- PN for those not tolerating EN or are unable to tolerate targeted nutritional requirements, or if contraindications to EN exist.
What are signs of an AP patient not tolerating EN?
- feeling very sick
- delayed gastric emptying
- if they need a rhyles tube to drain the stomach of excess fluid
What impact on nutritional intake can accumulation of fluid around the pancreas?
Can reduce appetite, induce vomiting (delayed gastric emptying), early satiety, duodenum/gastric stricturing or obstruction because it can press on the stomach or early part of the small intestine.
Why would you opt for a NJ tube for AP patients?
steatorrhea or diarrhoea (10-12 x/day) = can cause a lot of weight loss
Narrowing of GI tract. can make placing NJ difficult
Why would you do NJ feeding in addition to PN? What rate of feed would you use for this?
may need PN + NJ feed still try to do tropic feeding (10 - 20 ml/hour) to keep gut microbiome integrity and keep it working
Why challenge Nil By Mouth by medical team?
Oral nutrition benefits and maintains gut integrity
In mild AP: outline clinical practice (7)
- challenge nil by mouth
- oral fluids allowed throughout
- Avoid very high fat options BUT in practice it is better to eat more due to malnutrition risk impacting disease progression.
- Revert to oral fluids if pain worsens upon eating (soups, ONS etc)
- Consider ONS: Fat free/ medium chain triglycerides
- be vigilant for changes in severity = pro-active approach
- be aware of the cause of pancreatitis i.e. risk of excess alcohol intake increases risk of malnutrition.
Why are MCT supplements preferred over general ONS?
Muedium chain triglycerides are sometimes better tolerated. Although have a higher glucose content, recommend to sip over a couple of hours to prevent blood glucose dysregulation (hyperglycaemia)
what impact can one episode of severe pancreatitis have on future nutritional status (even after recovery)?
need insulin and pancreatic enzyme because of destruction of many pancreatic cells = this changes pancreatic function long term/indefinitely
Energy requirements for severe acute pancreatitis stage and recovery phase?
severe (often in ICU) = 15-25 kcal/kg/day
Recovery phase = 25 - 35 kcal/kg/day
When would recovery phase of SAP need more energy than those stated in PENG?
If severe with a long stay in ICU - likely been very catabolic therefore higher needs.
- if they’re being drained with a rhymes tube
- are they losing a lot of fluid via rhyles tube or very loose stools or vomiting?
- Malabsorption; are they absorbing everything = often unable to digest or produce enough enzymes
What are signs of fat malabsorption?
steatorrhea
- many bowel movements a day (up to 12x)
- yellow stools
- oily stools
- floating stools, difficult to flush
- very smelly
Dietetic assessment; What anthropometry? (3)
- weight and height
- weight history
- muscle and fat stores = middle upper arm circumference and hand grip strength
Dietetic assessment; What Biochemistry? (12)
- regular blood glucose
- renal profile
- liver function tests
- bone profile: magnesium, phosphate and calcium
- C-reactive protein
- full blood count
- Truglycerides - upon diagnosis and weekly when on PN
- HbA1c
- Fat soluble vitamins (ADEK)
- B12
- Parathyroid hormone
- Selenium and zinc
Dietetic assessment; What Clinical? (8)
- bowels (malabsorption, constipation)
- pain
- nausea
- vomiting
- bloating, wind
- anorexia, satiety
- As acute phase?
- bone density assessment
Dietetic assessment; What dietary? (3)
- 24 hour diet recall
- anticipated periods of nil by. mouth
- 3 day food charts, diet history and food diaries
Why is EN preferred (NG or NJ) to PN if unable to eat adequately orally? (4)
- Lower mortality. Early EN = 82% less likely to die than those on exclusive PN.
- Maintains gut microbiome integrity as well as gut function
- reduced rates of multi organ failure
- reduced rates of infection and translocation of bacteria across gut barrier
What circumstances would you place NJ before access required? (3)
- risk of gut obstruction from fluid accumulation
- unable to tolerate NG or food, or likely to
- Vomiting and delayed gastric emptying
What is the step progress of feeding in severity of AP?
- First line NG - close monitoring
- Delayed gastric emptying/ gastric compression/ gastric outlet obstruction - nausea/ vomiting pain = NG unlikely effective
- Attempt NJT (with NG rhymes tube for drainage)
- fitness for endoscopy/radiology to assess?
- Think ahead before deterioration
What is NJT ?
nasal jejunum set below the ligament go Treitz
Why are polymeric formulas generally preferred for feeds?
no evidence to support preference however, AP patients likely to have malabsorption - peptide feeds reduce digestive efforts and increase ease of absorption
Which patient would have polymeric and which would start straight on peptide?
polymers = mild AP
peptide = moderate/severe
on a feed HN stands for?
higher nitrogen = helps achieve nitrogen balance and alleviate rate of catabolism
if a feed has higher ratio (%) of MCT - why is this relevant?
Don’t need lipase or as much bile to digest therefore more passively absorbed.
why is osmolality important?
higher osmolality worsens diarrhoea, or can help support adequate bowel movements.
Lower osmolality = helps reduce diarrhoea
When should PN be administered?
when EN is not tolerated targeted nutritional requirements or if contraindications to EN exist.
PN should be given after adequate fluid resuscitation and when full haemodynamic stabilisation has occurred.
PN - why monitor blood glucose closely? Why is it preferred carbohydrate source?
- it is cheap, readily available and easy to monitor
- must monitor meticulously to avoid hyperglycaemia
PN carbohydrate infusion does not affect pancreatic secretion and function
PN - why administer lipids and when should they be temporarily stopped?
- efficient source of kcal
- IV lipids are safe in pancreatitis of hypertriglyceridaemia is avoided
- lipids should be stopped if plasma triglycerides >12 mmol/L
- to be avoided completely in case of hypertriglyceridaemia-associated AP
Blood glucose Monitoring: why and what impact on nutritional status?
- severe AP can destroy p pancreatic cells and present with hyperglycaemia (lack of insulin production)
Pain Monitoring: why and what impact on nutritional status?
- impacts ability to eat
Anthro: Monitoring: why and what impact on nutritional status?
weight changes, handgrip strength, mid upper arm circumference - esp helpful is there is excess fluid accumalation.
GI symptoms: Monitoring: why and what impact on nutritional status?
Discomfort, vomiting, nausea, bowel frequency
Fluid balance Monitoring: why and what impact on nutritional status?
do they need extra water flushes?
Bowels Monitoring: why and what impact on nutritional status?
steatorrhea
Micronutrients (long stay patients); Monitoring: why and what impact on nutritional status?
more needed in long stay patients (chronic pancreatitis)
TAG: Monitoring: why and what impact on nutritional status?
triglycerides
severity score: Monitoring: why and what impact on nutritional status?
Affects treatment plan and risk. Can change incredibly quickly
What are 8 key aspects of dietetic care for AP patients?
- Daily reviews in early stages to assess severity
- Pro-active - be ready to change direction of care
- feed early
- use EN over PN
- Is using PN, aim to continue using EN (place NG first for quicker feeding access)
- Unless contraindicated use NG route first
- In tertiary cases use peptide feed (better tolerated)
- Monitor intervention - change accordingly
If someone is on PN should you continue EN?
Yes. Use trophic EN feeding.
If at risk of referring what should you do?
prescribe thiamin and B12.
When CRP is high micronutrient readings can be inaccurate so difficult to determine what is actually going on.
What are protein requirements for AP?
1 - 1.5 g/kg actual body weight
