1B malnutrition and nutritional assessment Flashcards

1
Q

Define malnutrition

A

A state resulting from deficiency, excess or imbalance uptake/intake of energy, protein or other nutrition leading to measurable adverse affects on body composition, function and clinical outcome

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2
Q

What are causes of malnutrition in hospital?

A
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3
Q

What is disease related anorexia?

A

loss of appetite due to pathophysiology and modification of central regulation of feeding behaviour

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4
Q

What is metabolic response to illness/injury?

A

muscle breakdown to amino acids for gluconeogenesis and protein synthesis for immune response and tissue repair

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5
Q

What is the impact of malnutrition on postoperative mortality?

A

Post op mortality was 10x greater in those who had lost ≥20% body weight pre op compared with those who lost less

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6
Q

What does malnutrition increase?

A
  • Mortality
  • Septic and post surgical complications
  • Length of hospital stay
  • Pressure sores
  • Readmissions
  • Dependency
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7
Q

What does malnutrition decrease?

A
  • Wound healing
  • Response to treatment
  • Rehab potential
  • Quality of life
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8
Q

How does a dietitian assess patients for malnutrition?

A

A systematic process of collecting and interpreting info to determine nature and cause of nutrient imbalance:

  • Anthropometric measurements
  • Biochemical data
  • Medical history
  • Nutritional histories
  • Social history and physical exam
  • Nutritional exam
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9
Q

Why does BMI not play much of a role in a dietician’s assessment?

A
  • Influence of factors like gender, ethnicity and age are ignored
  • Can’t distinguish between fat mass and fat free mass
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10
Q

Which 2 types of people should nutrition support be considered for?

A
  • Malnourished
  • At risk of malnutrition
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11
Q

What are the requirements of malnourishment?

A
  • BMI <18.5 kg/m^2 or
  • Unintentional weight loss >10% for past 3 - 6/12 months or
  • BMI <20 kg/m^2 and unintentional weight loss >5% for past 3 - 6/12 months
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12
Q

What are the requirements to be at risk of malnutrition?

A
  • Have eaten little or nothing for >5 days and/or are likely to eat little or nothing for 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 like catabolism
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13
Q

Define artificial nutrition support

A

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

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14
Q

Is enteral feeding superior or inferior to parenteral nutrition?

A

EN (enteral nutrition) is superior to PN

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15
Q

What is the aim where PN is used?

A

To return to enteral → oral feeding as soon as clinically possible

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16
Q

What is the access for EN?

A

Is gastric feeding possible?

  • Yes → Nasogastric tube (NGT)
  • No → Nasoduodenal tube (NDT)/Nasojejunal tube (NJT)
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17
Q

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

A

Gastrostomy/jejunostomy

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18
Q

When is NGT contraindicated?

A
  • E.g. if there’s a gastric outlet obstruction
  • In that case NDT or NJT needed
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19
Q

What types of nutritional feeds are there?

A
  • Renal
  • Low sodium
  • Respiratory
  • Immune
  • Elemental
  • Peptide
  • High energy
  • High protein
20
Q

What types of complications are associated with EN?

A
  • Misplaced NGTs
  • Mechanical
  • Metabolic
  • GI
21
Q

When NGT is placed, what is needed to be taken?

A

Aspirate needs to be taken from tube showing pH ≤5.5 which shows acidity in stomach

If pH >5.5, CXR is performed

22
Q

What mechanical complications can occur with EN?

A
  • Misplacement
  • Blockage
  • Buried bumper
23
Q

What metabolic complications occur with EN?

A
  • Hyperglycaemia
  • Deranged electrolytes
24
Q

What GI complications occur with EN?

A
  • Aspiration
  • Vomiting
  • Diarrhoea
  • Nasopharyngeal pain
  • Laryngeal ulceration
25
Q

What is parenteral nutrition (PN)?

A

The delivery of nutrients, electrolytes and fluid directly into venous blood

26
Q

What are the indications for PN?

A
  • An inadequate or unsafe oral and/or EN intake

or

  • A non-functioning, inaccessible or perforated GI tract
27
Q

What is the access for PN?

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
28
Q

What is the composition of the nutrient bags?

A
  • Ready made or bespoke ‘scratch’ bags
  • MDT confers to set fluid and electrolyte targets for that day
29
Q

What are the metabolic complications of PN?

A
  • Hyperglycaemia
  • Deranged electrolytes
  • Abnormal liver enzymes
  • Oedema
  • Hypertriglyceridaemia
30
Q

What are the mechanical complications of PN?

A

Tend to be around when line is inserted for use for PN

  • Pneumothorax
  • Haemothorax
  • Thrombosis
  • Cardiac arrhythmias
  • Catheter occlusion
  • Thrombophlebitis (inflammatory process causing blood clot to form and block veins, usually in legs)
  • Extravasation (leakage of fluids from vein into surrounding tissues)
31
Q

Does nutrition support benefit the malnourished patient?

A
  • Yes because in a study, patients receiving nutritional support compared with patients in the control group had significantly lower levels of mortality
  • Nutritional support also associated with reduction in nonelective hospital readmissions, higher energy and protein intake and weight increase
32
Q

What is albumin?

A

Most abundant circulating protein in plasma of healthy people and is synthesised in liver

33
Q

What is low plasma albumin associated with?

A

Poor prognosis

34
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
35
Q

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

A

No

  • Albumin synthesis decreases during inflammation so it’s not a valid marker for nutritional status
  • Best evidence is hypoalbuminaemia in obese trauma patients
  • Dietitian focussed on aetiology/impact of inflammatory state on nutrition status
36
Q

What is refeeding syndrome?

A

A group of biochemical shifts and clinical symptoms that can occur in the malnourished individual on reintroduction of oral, EN or PN

37
Q

What changes happen in the body in starvation?

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 of these electrolytes are maintained while intracellular stores are depleted
  • Micronutrient stores deplete and thiamine deficiency is likely as it’s water soluble and body has limited stores
38
Q

What happens when carbs 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+, Mg+ 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
39
Q

What clinical problems can low electrolyte concs and thiamine result in?

A

Carb reduces sodium and fluid excretion, expanding extracellular fluid compartment leading to refeeding oedema and fluid overload

40
Q

What are consequences of RFS?

A
  • Arrhythmia, tachycardia, CHF → cardiac arrest, sudden death
  • Respiratory depression
  • Encephalopathy, coma, seizures, rhabdomyolysis (breakdown of muscle tissue leading to release of muscle fibre contents into blood that harm the kidney)
  • Wernicke’s encephalopathy
41
Q

What are the criteria for defining AT risk of RFS?

A

Very little or no food intake for >5 days

42
Q

What are the criteria for defining HIGH risk of RFS?

A

≥1 of the following:

  • BMI <16 kg/m^2
  • Unintentional weight loss > 15% for 3-6/12 months
  • V little/no nutrition for >10 days
  • Low K+, Mg2+, PO4 prior to feeding

or ≥2 of the following:

  • BMI < 18.5 kg/m^2
  • Unintentional weight loss >10% for 3-6/12 months
  • V little/no nutrition for >5 days
  • PMHx alcohol abuse or drugs (insulin, chemo, antacids, diuretics)
43
Q

What are the criteria for defining EXTREMELY high risk of RFS?

A
  • BMI <14 kg/m^2
  • Negligible intake > 15 days
44
Q

What is the management of RFS?

A

1) 10-20kcal/kg of nutrition given of which 40-50% of energy is carbs. Micronutrients from onset of feeding

2) Correct and monitor electrolytes daily following Trust policy

3) Administer thiamine from onset of feeding following Trust policy

4) Monitor fluid shifts and minimise risk of fluid and Na+ overload

45
Q

What oral nutritional support options are there?

A
  • Fortification of meals and snacks
  • Altered meal patterns
  • Practical Support
  • Oral Nutritional Supplements (ONS)
  • Tailored dietary counselling