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Year 2 - BRS > 6.9 - Malnutrition and nutritional assessment > Flashcards

6.9 - Malnutrition and nutritional assessment Flashcards

1
Q

Define malnutrition.

A

A state in which deficiency, excess or imbalance, of energy, protein or other nutrients, results in a measurable adverse effect on body composition, function and clinical outcome

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2
Q

How does prevalence of malnutrition change by age?

A
  • curvilinear relationship where highest rates of malnutrition are in youngest and oldest age groups
  • more common in women than men
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3
Q

How does prevalence of malnutrition differ in wards?

A

Oncology and care of elderly wards have highest rates

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4
Q

How many people on admission to hospital have malnutrition?

A

1 in 3 –> shows a lot of malnutrition occurs in community

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5
Q

What % of people have lost weight at discharge and what is the weight loss in?

A
  • 70% have lost weight at discharge - mainly lost muscle mass
  • most weight loss seen in those who were initially malnourished at admission
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6
Q

What does hospitalisation exacerbate in relation to malnutrition?

A

Hospitalisation exacerbates nutrition risk

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7
Q

Generally, which groups are affected by malnutrition? (5)

A
  • older people over 65, particularly if admitted to hospital
  • people with long term conditions like diabetes, kidney disease and chronic lung disease
  • people with chronic progressive conditions like cancer, dementia
  • those who abuse drugs or alcohol
  • patients with GI dysfunction
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8
Q

What can the causes of malnutrition in hospital be divided into? (3)

A
  • reduced intake
  • maldigestion, malabsorption
  • altered metabolism
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9
Q

What can cause reduced intake related malnutrition in hospital? (9)

A
  • contraindicated
  • disease-related anorexia (loss of appetite due to pathophysiology and modification of central regulation of feeding behaviour)
  • taste changes
  • nil by mouth
  • food options
  • depression
  • inactivity
  • oral health
  • fatigue
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10
Q

What can cause maldigestion/malabsorption related malnutrition in hospital? (4)

A
  • function
  • length
  • losses
  • drug-nutrient interactions
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11
Q

What can cause altered metabolism related malnutrition in hospital?

A
  • injury
  • shock (1-2 days) - nutrition goal: survival, reduced % energy expenditure
  • catabolism (2 days-weeks) - nutrition goal: cover metabolic needs, energy expenditure rises and falls
  • anabolism (after weeks) - nutrition goal: muscle recovery, energy expenditure stable
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12
Q

What is the impact of malnutrition on postoperative mortality?

A
  • 1936: post-op mortality was 10x greater in those who had lost >20% bodyweight preoperatively, compared to those who had lost less (perforated duodenal ulcer surgery)
  • 2022 - malnutrition directly caused 77 hospital deaths, and contributory factor to 436 hospital deaths
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13
Q

What does malnutrition cause overall?

A

Physical and functional decline, and poorer clinical outcomes

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14
Q

What does malnutrition increase? (6)

A
  • mortality
  • septic and post-surgical complications
  • length of hospital stay
  • pressure sores
  • readmissions
  • dependency
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15
Q

What does malnutrition decrease? (4)

A
  • wound healing
  • response to treatment
  • rehabilitation potential
  • quality of life
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16
Q

How much does malnutrition cost England per year?

A
  • £19.6 billion –> 15% of total expenditure on health and social care
  • most of costs are in secondary healthcare
  • health costs said to be 3x greater for malnourished than well nourished patients
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17
Q

What is the order for diagnosing malnutrition?

A
  • screen - a simple tool to identify risk, not assessment or diagnosis
  • assess (dietitian) - a systematic process of collecting and interpreting information to determine the nature and cause of the nutrient imbalance
  • diagnose - nutrition diagnosis
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18
Q

How can we screen for malnutrition?

A
  • MUST (Malnutrition Universal Screening Tool) - based on BMI, unplanned weight loss and presence of acute disease
  • categorises patients as being low, medium or high risk and gives guidelines for treating each
  • carried out by any HCP
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19
Q

What is a limitation for using MUST as a screening tool for malnutrition?

A

Can miss malnourished populations e.g. where overhydration is common like in ascites and oedema, or where specific screening for functional impairment is desired

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20
Q

What does a dietitian look at when assessing patients for malnutrition? (9)

A
  • anthropometry
  • body composition
  • function
  • biochemistry
  • clinical
  • dietary
  • social history
  • physical exam
  • requirements
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21
Q

Which two groups of people should nutrition support be considered for?

A
  • malnourished
  • at risk of malnutrition
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22
Q

What are the requirements for being malnourished? (3)

A
  • BMI <18.5 kg/m2 OR
  • unintentional weight loss >10% past 3-6 months out of last 12 months OR
  • BMI <20kg/m2 + unintentional weight loss >5% past 3-6 months out of last 12 months
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23
Q

What are the requirements to be at risk of malnutrition? (2)

A
  • have eaten little or nothing for >5 days and/or are likely to eat little or nothing for the next 5 days or longer OR
  • have a poor absorptive capacity, and/or have high nutrient losses and/or have increased nutritional needs from causes such as catabolism
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24
Q

What is the algorithm of treatment of malnutrition? (Look at image on slide)

A
  • is oral nutrition possible & safe?
  • Y = oral nutrition support - counselling, supplements, texture modification, thickeners; consider need for modified diet according to clinical condition e.g. reduced Na+, MCT, peptides
    • regularly monitor intake, if inadequate –> enteral tube feeding - short term (fine bore naso-enteral tube) or long term, regularly monitor adequacy
  • N = is GI tract functional & accessible?
    • Y = enteral tube feeding
    • N = parenteral nutrition (if limited tube feeding possible, enteral tube feeding)
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25
Q

What nutritional options are available via the oral nutrition support route? (5)

A
  • fortification of meals and snacks
  • altered meal patterns
  • practical support
  • oral nutritional supplements (ONS)
  • tailored dietary counselling
26
Q

When do we consider oral nutrition support?

A

Consider for any patient with inadequate food and fluid intakes to meet requirements, unless they cannot swallow safely, have inadequate gastrointestinal function or if no benefit is anticipated e.g. end of life care

27
Q

Define artificial nutrition support.

A

The provision of enteral or parenteral nutrients to treat or prevent malnutrition

28
Q

Is enteral nutrition (EN) superior or inferior to parenteral nutrition (PN)?

A

EN is superior to PN

29
Q

What is the aim where parenteral nutrition is used?

A

To return to enteral –> oral feeding as soon as clinically possible

30
Q

What is the access for enteral nutrition (EN)?

A

Is gastric feeding possible?

  • Y = naso-gastric tube (NGT)
  • N = naso-duodenal tube (NDT) / naso-jejunal tube (NJT)
31
Q

What is the access for enteral nutrition (EN) for long term (>3 months)?

A

Gastrostomy / jejunostomy

32
Q

When is NGT contraindicated?

A

E.g. if there is a gastric outlet obstruction, in which case NDT or NJT needed

33
Q

What types of nutritional feeds in enteral nutrition are there? (8)

A
  • renal
  • low sodium
  • respiratory
  • immune
  • elemental
  • peptide
  • high energy
  • high protein
34
Q

What complications are associated with enteral nutrition (EN)? (4)

A
  • misplaced NGTs - caused 21 deaths and 79 cases of harm from 2005-2011
  • mechanical - misplacement, blockage, buried bumper
  • metabolic - hyperglycaemia, deranged electrolytes
  • GI - aspiration, vomiting, diarrhoea, nasopharyngeal pain, laryngeal ulceration
35
Q

When NGT is placed, what needs to be taken?

A
  • aspirate needs to be taken from tube showing pH<5.5 which shows acidity in stomach
  • if pH>5.5, chest X-ray is done
36
Q

What is parenteral nutrition (PN)?

A

The delivery of nutrients, electrolytes and fluid directly into venous blood (bypassing GI tract)

37
Q

What are the indications for parenteral nutrition (PN)? (2)

A
  • an inadequate or unsafe oral and/or enteral nutritional intake OR
  • a non-functioning, inaccessible or perforated gastrointestinal tract
38
Q

What is the access for parenteral nutrition?

A
  • central venous catheter (CVC) in subclavian, femoral or jugular veins with tip at superior vena cava and right atrium
  • peripherally inserted catheter with tip still at SVC but catheter inserted from antecubital fossa and pushed into central vein
  • different CVCs for short/long term use
39
Q

What is the composition of the nutrient bags in parenteral nutrition?

A
  • ready-made or bespoke ‘scratch’ bags
  • MDT confers to set fluid and electrolyte targets for the day
40
Q

What are the complications of parenteral nutrition? (3 types)

A
  • metabolic - hyperglycaemia, deranged electrolytes, abnormal liver enzymes, oedema, hypertriglyceridemia
  • mechanical - pneumothorax, haemothorax, thrombosis, cardiac arrhythmias, catheter occlusion, thrombophlebitis (blood clot to form and block veins, usually legs), extravasation (leakage of fluids from vein into surrounding tissues)
  • catheter-related infections
41
Q

Does nutrition support benefit the malnourished patient?

A
  • yes - study showed patients receiving nutritional support had significantly lower levels or mortality vs control group
  • also associated with reduction in non-elective hospital admissions, higher energy and protein intake and weight increase
42
Q

What is albumin?

A

The most abundant circulating protein in plasma of healthy people, and is synthesised in liver

43
Q

What is albumin synthesis stimulated by?

A

Hormones like insulin, cortisol and growth hormone

44
Q

What is hypoalbuminaemia associated with?

A

Poor prognosis

45
Q

What is albumin inhibited by?

A
  • inflammation - it is a negative acute phase protein
  • inflammatory factors specifically include IL-6 and TNF
46
Q

What is the acute phase response?

A
  • inflammatory stimulus –> activation of monocytes and macrophages –> release cytokines
  • cytokines act on liver to stimulate production of some proteins whilst downregulating others e.g. albumin
  • degradation and transcapillary losses of albumin also increase in this state
47
Q

Is albumin a valid marker of malnutrition in the acute hospital setting?

A
  • no
  • albumin synthesis decreases during inflammation so not a valid marker of nutritional status
  • best evidence is hypoalbuminaemia in obese trauma patients
  • dietitian focused on aetiology/impact of inflammatory state on nutrition status
48
Q

What is refeeding syndrome?

A

A group of biochemical shifts & clinical symptoms that can occur in the malnourished or starved individual on the reintroduction of oral, enteral or parenteral nutrition

49
Q

What changes happen in the body in starvation? (7)

A
  • reduction in insulin and increase in glucagon secretion to increase glucose
  • liver glycogen stores and amino acids in skeletal muscle are metabolised into glucose
    • once these stores are depleted in 1-3 days, metabolism shifts to derive energy from ketone production due to free fatty acids being released from fat stores (used instead of amino acids)
    • this shift spares skeletal muscle breakdown and fat free mass is preserved to an extent
  • decreased metabolic rate and brain adapts to use ketone bodies instead of glucose, resulting in loss of fat mass
  • action of cellular pumps is reduced to reduce energy expenditure, with electrolytes leaking across cell membrane instead
  • increase in extracellular water, total body water and sodium (sodium and fluid leak into cells leading to sodium and fluid intolerance)
  • depletion of total body potassium, magnesium and phosphate (serum concs maintained, IC stores depleted)
  • micronutrient stores deplete and thiamine deficiency is likely (water soluble and body has limited stores)
50
Q

What features are seen in refeeding syndrome? (5)

A
  • hypokalaemia
  • hypomagnesaemia
  • hypophosphataemia
  • thiamine deficiency
  • salt and water retention –> oedema
51
Q

What happens when carbohydrates are introduced into a starving body?

A
  • insulin secretion occurs, stimulating sodium-potassium ATPase pump, requiring Mg as a cofactor
  • drives K+ into cells and Na+ and fluid out of cells into extracellular space
  • phosphate driven into cells as it’s required for energy storage as ATP
  • results in increased cellular uptake in glucose, K+, Mg2+ and phosphate and reduction in extracellular concs
  • thiamine is a coenzyme in carb metabolism and deficiency can occur on refeeding in a vit B depleted patient
52
Q

What problems does refeeding carbohydrates into a starving body cause?

A
  • low electrolyte concentrations and thiamine deficiency = clinical problems
  • carbohydrates reduce sodium and fluid excretion, expanding ECF compartment –> refeeding oedema and fluid overload
53
Q

What are the consequences of refeeding syndrome (RFS)? (4)

A
  • arrhythmia, tachycardia, CHF –> cardiac arrest, sudden death
  • respiratory depression
  • encephalopathy, coma, seizures, rhabdomyolysis (breakdown of muscle tissue = release of muscle fibre contents into blood = harms kidney)
  • Wernicke’s encephalopathy
54
Q

Who can refeeding syndrome also occur in?

A
  • refeeding syndrome can occur in overweight individuals particularly those who have eaten nothing for protracted periods
  • patients with normal levels of K+, Mg2+ and PO4(3-) can still develop refeeding syndrome
55
Q

What is the criteria for defining risk of refeeding syndrome?

A
  • at risk
  • high risk
  • extremely high risk
56
Q

Who is at risk of refeeding syndrome?

A

Very little or no food intake for >5 days

57
Q

Who is at high risk for refeeding syndrome?

A

> /=1 of the following:

  • BMI<16kg/m2
  • unintentional weight loss >15% for 3-6/12 months
  • very little/no nutrition for >10 days
  • low K+, Mg2+, PO4 prior to feeding

OR >/=2 of the following:

  • BMI<18.5kg/m2
  • unintentional weight loss >10% for 3-6/12 months
  • very little/no nutrition for >5 days
  • PMHx alcohol abuse or drugs (insulin, chemo, antacids, diuretics)
58
Q

Who is at extremely high risk for refeeding syndrome?

A
  • BMI<14kg/m2
  • negligible intake >15 days
59
Q

What is the management of refeeding syndrome?

A
  1. administer thiamine 30 minutes before and for the first ten days of feeding following Trust policy
  2. correct and monitor electrolytes daily following Trust policy
  3. start: 10-20kcal/kg of nutrition given of which 40-50% of energy is carbs, micronutrients from onset of feeding
  4. monitor fluid shifts and minimise risk of fluid and Na+ overload
60
Q

What is an acute disease that can cause malnutrition?

A

Severe acute pancreatitis –> can also cause disease-related anorexia

61
Q

What is the difference between clear and free fluids?

A
  • clear fluids: transparent fluids with minimal fats (and sometimes minimal protein) - trying to avoid gut stimulation and the need to digest nutrients
  • free fluids: liquid at room temperature - can contain fat, proteins and carbohydrates
62
Q

How should patients with severe acute pancreatitis receive nutrition support?

A
  • bedside nasogastric (NG) tube - feed into stomach and see whether this is tolerated
  • progressive pancreatitis = collections in and around gland can obstruct stomach –> patients unable to release food from stomach
  • in this situation may need to place tube further down e.g. trial naso-jejunal tube (NJT) feeding

Year 2 - BRS (84 decks)

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