ICM - Viva - Nutrition Flashcards

1
Q

What % of patients are malnourished on arrival to ICU

A

50%

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2
Q

Problems with malnutrition in ICU

A

Altered immunity - susceptible to infection

Prolonged MV

Increased LOS

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3
Q

How to assess nutritional status of patients

A
Clinical - weight and weight loss (recent)
           Co-morbid illnesses
           Severity of illness
           Evidence of GI dysfunction
           MUST scoring
           Upper arm circumf

Lab - anthropometry and albumin, confounded by oedema and acute phase changes

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4
Q

Ways to calculate energy needs

A

Indirect Calorimetry

Eqns - Harris-Benedict and Scholfied

Estimate based on IBW at 25-30kcal/kg/day (and add 20% in obesity)

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5
Q

Evidence on energy calculation strategy for feeding

A

TIACOS - targeted energy based on indirect calorimetry

(Vs 25kcal/kg/day)

Calorimetry received more calories, increased MV and LOS
Trend to reduced mort

EDEN trial - Trophic feed (25% of target) for first 6 days changed vent length

Received fewer calories, but outcomes were as good as full feed

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6
Q

Protein needs and rationale

A

Catabolism of protein is rapid.
Protein needs are higher than energy needs, and not met by provision
Open abdo is source of nitrogen loss, estimated at 2g nitrogen/litre fluid

Weight based - 1.2 - 2g/day

Negative N2 balance - excreting more N than taking in —> muscle loss

Balance = (Total protein in / 6.25) - (UUN +4)

Where UUN is nitrogen excreted in urine in 24 hours (+4 is insensible)

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7
Q

Calorie split

A

Of the non protein calories

60% carbs
40% lipid

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8
Q

Patients Requirements

A

Water. 30ml/kg
Sodium 1-2mmol
K 0.8 - 1.2
Ca. 0.1
Mg 0,1
Phos 0.4

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9
Q

Routes

A

Oral
NG
NJ
PN

Enteral is preferential unless a reason not to

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10
Q

Advantages of enteral

A

Physiological
Cheaper
No central line

GI tract integrity maintained - structure, perfusion, motility, less ulcers
Promotes immune function - mucosa assoc lymphoid, IgA

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11
Q

Advantages of parenteral

A

Don’t need a functioning GI tract

Can start early - no delay

Less interruptions

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12
Q

Disadvantage of Enteral

A

Needs a functioning tract
Diarrhoea
Risks with NG

Known to increase VAP risk
NG - sinusitis

Metabolic issues - electrolytes, high BM, refeeding

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13
Q

Disadvantages of parenteral

A

Not physiological

Hyper osmolar and irritant - central access

Systemic infection

Expensive

Hypercholesterolamia

Lipid emulsion - fatty liver

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14
Q

Evidence on route of feeding

A

CALORIES trial

No difference in mortality if fed enterally or parenteral lay

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15
Q

How to improve enteral delivery

A

Prokinetic - erythromicin/metoclop

Post pyloric feed - NJ/Jej

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16
Q

When to start feed

A

Enteral - within 24-48 hours of admission

After initial resus and haemodynamically stable

You don’t need flatus or bowel sounds to start

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17
Q

If EN is failing, what do the guidelines suggest

A

ESPEN - start TPN at 24 hours if EN not tolerated

ASPEN - after 7-10 days if unable to meet 60% of energy by enteral route

18
Q

Evidence for early / late initiation of PN

A

EPaNIC - day 3 or day 8 PN

Late - increased survival, shorter MV and RRT

19
Q

Components of TPN

A

Standard formulations

40% is non protein calories as lipid and 60% carbs

Amino acids/vitamins (B1, folate,; fat soluble ADEK)

Trace element (zinc, copper selenium)

Electrolytes

20
Q

Any evidence for Immunomodulation from nutrition supplements

A

Glutamine
Maybe good in burns and trauma,
Facilitates nitrogen transport and reduce protein loss

REDOX trial - early glutamine in MOF was harmful, higher mortality

Arginine
NO prescursor
Improves macrophage and NK cells cytotoxicity
Harmful in sepsis

Omega 3 - anti-inflammatory
OMEGA trial stopped for futility, less vent free days

Selenium - scavenges oxygen free radicals
Non significant reduction in mortality

21
Q

Any evidence for Glycaemic targets in non diabetic?

A

NICE-SUGAR
Tight very conventional glucose control (tight 4.5 to 6) (convention less than 10

90 day mortality higher in tight group
More hypos

Previous small studies suggested tight might be better

22
Q

Refeeding pathophysio

A

Happens when nutrition is restarted in patients have starved

Chronic malnutrition - protein and fat metabolism, and phosphate loss

Reintroduce carbs - anabolic state, insulin surge,
Re uptake of phosphate, magnesium and potassium

23
Q

Effect of carb load in refeeding

A

Insulin release

Glycogen synthesis , Fat Synth, Protein Synth, (these need K, Mg, PO3)
PO3 uptake into cells

Hypophophate, Mg lost in urine

Form phosphorylated carb compounds —deplete ATP
Cellular dysfunction, decreased o2 delivery

24
Q

Presentation of refeeding

A

CVS - heart failure and arrhythmia

GI - Vomiting, constipation, anorexia

Resp - resp muscle weakness

MSK - weak, osteomalacia

Neuro - ataxia delirium’s, coma, Wernickes (thiamine)

Metabolic - Low PO, MG, K, Ca, Thiamine

25
Q

Risk factors for Refeeding Sybdrome NICE criteria

A

One of:
BMI <16.
Weight loss 15% in 3-6/12.
Little intake 10 days.
Low K, PO, Mg before.

Two of
BMI < 18.5
Loss of 10%
5 day Poor intake
Alcohol abuse

26
Q

Comorbidities that are Risk factors for refeeding

A

Decreased intake - eating disorder, alcohol,depression, NBM,

Decreased absorption - Malabsorption, IBD, CF, panc, short bowel

Increased catab - malignancy, inflammation

27
Q

Tx of refeeding

A

Monitor and look out for it
Risk assess

Electrolytes, vitamins and trace elements
Pabrinex for 3 days, then thiamine and vit B

Avoid fluid overload

Cautious re-institution of feed 10kcal/kg/day

28
Q

Vitamin A role and deficiency

A

Vision, growth

Night blindness, Xeropthalmia

29
Q

B1
What is it
Role
Deficiency

A

Thiamine
Co-enzyme in ATP production

Dry beri beri - wasting and paralysis, damaged nerves
Wet beri berry - high out put cardiac failure
Wernickes - ataxia, confusion, opthalmoplegia
Korsakoff - memory loss

30
Q

B2
What is it
Role
Deficiency

A

Riboflavin

Red cell production, anti-oxidant

Ariboflavinosis - Stomatitis, sore tongue and throat, fissured lips

31
Q

B3
What is it

Role

Deficiency

A

Niacin

Skin formation, Metabolism

Pellagra - diarrhoea, dermatitis, dementia

32
Q

What is vitamin B9? needed for? deficiency?

A

Folate

DNA/RNA production
RBC production

Glossitis, diarrhoea, confusion, anaemia

Foetal neural tube

33
Q

B12

A

Cobalamin

DNA and RNA
RBC

Pernicious anaemia
Subacute combined degeneration of the cord

34
Q

C

A

Collagen production, wound healing, teeth and bond maintain acne

Weakness, weight loss,
Scurvy

35
Q

D

A

Calcium absorption
Immune system

Rickets and osteomalacia

36
Q

Vit E

A

Anti ox, free radical scavenger

Dysarthria
Loss of tendon reflexes
Ataxia
Anaemia
Retinopathy
37
Q

Vit K

A

Coag, bone metabolism

Hypercoagulable

38
Q

Selenium

A

Converts T4 into T3

Hypothyroid
Osteochondropathy (Kasin Beck disease)

39
Q

Zinc deficiency

A

Hormone production

Diarrhoea
Acne
Motor disorder

40
Q

Role of Copper

A

Iron transport
Maintain bone, cardiac and connective tissue

Myelopdysplasia,
Anaemia

41
Q

Zinc

A

Bone production
Skin integrity
BM control

Bone demineralisation
Altered carb/fat metab
Impaired glucose tolerance