40. ICU Nutrition

Question 1

Why is nutritional support important in ICU patient

Answer 1

A significant number of patients admitted to hospital are malnourished, up to 40% according to McWhirter.

The majority of patients that are admitted to intensive care are catabolic and will have had a preceding period of starvation due to their surgery or underlying pathology

Question 2

Complications of poor nutritional support

Answer 2

Impaired wound healing

Reduced muscle bulk/strength and delayed mobilisation

Increased incidence of respiratory infection

Problems with weaning from mechanical ventilation

Question 3

How can you make an assessment of a patient’s nutritional status
on ICU?

Answer 3

There are objective markers that can be used in the assessment of
malnutrition, but many of these are flawed when faced with a patient with
multiorgan failure on intensive care. There are other methods that are more clinically orientated.

Question 4

Traditional objective assessment tools

Answer 4

Triceps skinfold thickness
Hand grip tests
Serum albumin (t1/2 14–20 days)
Serum prealbumin (t1/2 24–48 hours)
Serum transferrin
Total iron-binding capacity
Lymphocyte count

These are relatively insensitive and non-specific markers, e.g. albumin affected
by trauma, sepsis and excess extracellular water.

Question 5

Other methods

Answer 5

Subjective global assessment (SGA) – history and physical factors
Hill and Windsor (bedside nutritional assessment)

Question 6

Lean body mass assessment – experimental methods

Answer 6

Lean body mass assessment – experimental methods
Bioimpedence
Measuring total body water or potassium
Neutron activation
Muscle biopsy to measure muscle fibre area

These methods are similarly difficult to interpret in a critical care setting.

A nutritional history should be elicited (including normal weight and recent food intake) and there are formulae to derive ideal body mass and daily calorific requirements.

This question initially seems difficult to answer (as rarely formally done
on ICU).
Your answer should emphasise that a detailed history and examination
are still the mainstay of nutritional assessment.
However, you will need to be aware of the tests available.
Be wary of starting your answer with a negative comment about how
difficult it is to assess nutritional status on ICU – perhaps mention this at
the end, with the reasons why

Question 7

What routes can be used for nutritional support?

Answer 7

Enteral feeding Can be given by nasogastric, nasojejunal or
percutaneous gastrostomy/jejunostomy tubes.

Post-pyloric feeding is becoming more popular as
gastric atony can be a problem in critically ill patients
Side effects: diarrhoea, aspiration.

Parenteral feeding Often through a dedicated central venous catheter,
although peripheral polyurethane catheters or
peripherally inserted central catheters (PICC) can be
used.

Question 8

Some enteral feeding guidance

Answer 8

‘Underfeeding’ may provide a protective safety barrier (33%–65% of
calculated feed received led to less mortality than >65% of feed
received).

NICE recommend that, for the first 48 hours, parental nutrition should
be <50% of calculated requirement.

Nurse head-up 45%.

Accept gastric residual volumes of 200–250 ml.

Early use of prokinetics

Question 9

Some enteral feeding guidance

Answer 9

‘Underfeeding’ may provide a protective safety barrier (33%–65% of
calculated feed received led to less mortality than >65% of feed
received).

NICE recommend that, for the first 48 hours, parental nutrition should
be <50% of calculated requirement.

Nurse head-up 45%.

Accept gastric residual volumes of 200–250 ml.

Early use of prokinetics

Question 10

What problems are associated with parenteral nutrition?

Answer 10

Central venous catheter

Complications related to insertion
Catheter-related sepsis
Displacement
Occlusion / thrombosis

Metabolic

Hypo/hyperglycaemia
Metabolic acidosis
Potassium, sodium and phosphate imbalance
Excess CO2 production
Hypercholesterolaemia/hypertriglyceridemia
Essential fatty acid/vitamins / trace element
deficiencies

Intestinal
TPN fails to reverse intestinal villous atrophy
and bacterial translocation can occur

Hepatobiliary
Abnormal liver function tests.
This is multifactorial

Refeeding syndrome
↑Glu, ↓MgSO4, ↓K+, ↓PO4 seen when
refeeding malnourished patients

Question 11

What are the advantages of enteral nutrition?

Answer 11

More physiological route for digestion and absorption

Prevents mucosal atrophy – intestinal enterocytes receive a proportion of
their own nutrition directly from the gut lumen and enteral nutrition helps
maintain mucosal blood flow

Supports the normal gut flora

Reduction of bacterial translocation→↓risk of sepsis

Fewer metabolic complications

No catheter-associated complications of TPN – in particular, the risk of
central line sepsis.

Question 12

What can you tell me about immunomodulation and feeding?

Answer 12

…

Question 13

Typical daily nutritional requirements

Answer 13

Water 30 ml/kg

Na+ 1.2 mmol/kg

K+ 0.8 mmol/kg

Calories 30 kcal/kg

Protein 0.25 g nitrogen/kg

(10 g nitrogen ∼ 60 g protein)

Fat 2 g/kg
Glucose 2 g/kg

Question 14

Indications for nutritional support

Answer 14

cachectic patients with a preoperative
weight loss of 15% or more, or who have effectively been starved for more than
10 days (for example, because of dysphagia), have improved outcomes if they
receive nutritional support before surgery. There are numerous other indications,
including malabsorption owing to small bowel resection, small bowel fistulas,
radiation enteritis, intractable diarrhoea and vomiting, and hyperemesis
gravidarum.

Question 15

Starvation

Answer 15

: this can be defined as the result of a severe or total lack of nutrients
needed for the maintenance of life. In the absence of adequate intake, hepatic
glycogen stores are depleted within 24–48 hours, after which adipose tissue becomes
the source of fatty acids for use as an energy substrate

A small number of cell types,
amongst which are erythrocytes and cells in the renal medulla, can utilize only
glucose, and this has to be provided via amino acids that are produced from protein
breakdown. The CNS normally depends on glucose but can function using ketones as
an energy substrate.

Question 16

Nutritional requirements energy

Answer 16

– : basal expenditure can be judged from the Harris–Benedict equation
(which links weight, height and age)
or from nomograms.

Kilocalorie needs range from around
30 kcal kg1 in the non-stressed ambulatory state to

60 kcal kg1 in sepsis or following major trauma

After severe thermal injury,
which exemplifies an accelerated catabolic state, patients may require 80 kcal kg

Question 17

Nutritional requirements - protein

Answer 17

– protein: this can be estimated empirically.

Demands may range from 0.5–1.0 g kg1 in the non-stressed state

to 2.5 g kg1 under conditions of extreme stress.

Question 18

Assessment of nitrogen balance

Answer 18

: each gram of nitrogen is equivalent to 6.2 g of
protein or 30 g of muscle. In catabolic states patients are in negative balance. Losses
can be determined over each 24-hour period by measuring urinary urea and incorporating
the value into a formula, a typical example of which is 24-hour nitrogen
loss

Question 19

Nutritional requirements – fluids:

Answer 19

a simple formula for basal requirements in a
temperate climate is 100 ml kg1 for the first 10 kg body weight, 50 ml kg1 for the
next 10 kg and then 20 ml kg1 thereafter. To this total must be added the various
losses as appropriate. (This formula can also be used to approximate normal kilocalorie
requirements.)

Question 20

Calorie sources:

Answer 20

carbohydrate (glucose) and protein (amino acids) provide 4 kcal of
energy per gram, fat provides 9 kcal

Glucose-rich solutions are associated with hyperglycaemia and fatty infiltration of the liver,
with excess CO2 production which increases the respiratory quotient (RQ) to unity,
with hyperinsulinaemia and fluid retention, with hypophosphataemia
causing reduced tissue oxygenation, and with decreased immune function.

Lipid administration (10% or 20% emulsion) reduces reliance on glucose as a calorie source with its attendant problems and provides essential fatty acids.

Hyperlipidaemia can complicate its administration.

Protein is given in the form of crystalline amino acids

Question 21

Additives:

Answer 21

these include extra electrolytes, where appropriate, together with phosphate
and magnesium; trace elements, including zinc, copper, manganese, chromium
and selenium; and the full range of fat-soluble and water-soluble vitamins.

Question 22

Other supplements

Answer 22

Glutamine appears to improve energy utilization and protein
synthesis in skeletal muscle as well as enhancing both gut immunity and lymphocyte
function.

Question 23

The Refeeding Syndrome

Answer 23

severe metabolic derangements that can occur when nutrition
is reintroduced to individuals who have been starved or severely malnourished,

to patients with severe illness who are profoundly catabolic

presents typically within 4 days of the start of replenishment and is characterized by
metabolic derangement and acidosis, together with variable symptoms and signs.

Question 24

Symptoms + Signs

Answer 24

These include gastrointestinal symptoms,

muscle weakness and myalgia,

impaired cerebration,
cardiac arrhythmias
myocardial dysfunction.

It is because these are relatively non-specific that the condition may go unrecognized

Question 25

Individuals at risk include patients

Answer 25

with cachexia due to malignancy;
those with malabsorption due, f
or example, to inflammatory bowel disease;

and those with long term nutritional deficiencies

including chronic alcoholics and those with anorexia nervosa.

Specific mineral depletion can occur such as the

hypophosphataemia associated with chronic antacid use
(aluminium and magnesium bind to phosphate and prevent its absorption),

or the hypokalaemia in patients on long-term diuretic therapy.

Question 26

Individuals at risk include patients

Answer 26

with cachexia due to malignancy;
those with malabsorption due, f
or example, to inflammatory bowel disease;

and those with long term nutritional deficiencies

including chronic alcoholics and those with anorexia nervosa.

Specific mineral depletion can occur such as the

hypophosphatemia associated with chronic antacid use
(aluminium and magnesium bind to phosphate and prevent its absorption),

or the hypokalaemia in patients on long-term diuretic therapy.

Question 27

When a subject is starved,

Answer 27

When a subject is starved,

hepatic glycogen is fully depleted within 24–48 hours
(depending on energy expenditure),

after which the body becomes dependent on
fatty acids and amino acids as the primary energy source.

The brain is able to use ketones as an energy source
and blood levels do rise as muscle preferentially switches
to fatty acid utilization

intracellular depletion of various essential substances, including
potassium, magnesium and phosphate, whose serum concentrations, however, may
remain within the normal range. Insulin secretion is suppressed and glucagon release
is increased. The basal metabolic rate decreases by up to 25% in order to conserve
energy stores.

Question 28

Nutrition is reintroduced

Answer 28

As soon as nutrition is reintroduced (either enterally or parenterally) there is sharp
rise in metabolic rate as the increase in blood glucose stimulates release of insulin,

which as an anabolic hormone increases the synthesis of glycogen, fat and protein.

anabolism requires various minerals,

in particular phosphate and magnesium, together with co-factors of which thiamine (vitamin B1) is probably the most important.

Insulin drives potassium and glucose into the cells via the Na+-K+
ATP-ase symporter.

Phosphate and magnesium also move into the intracellular compartment.

These processes reduce the plasma concentrations of all these substances
whose total body levels are likely to be substantially depleted.

It is these fluid and electrolyte shifts superimposed
on total body mineral depletion that are responsible
for the clinical features of the syndrome.

Question 29

Glucose:

Answer 29

the glycaemia that occurs with refeeding stimulates insulin release with the
suppression of gluconeogenesis. Acute hyperglycaemia may follow with predictable
sequelae of osmotic diuresis and metabolic (ketotic) acidosis.

Question 30

Sodium and water:

Answer 30

the sudden return of carbohydrate metabolism is accompanied
by sodium and water retention. If the relative oliguria is then treated with fluid
restoration, there is the risk of circulatory overload with a myocardium that may
already be impaired by depleted ATP.

Question 31

Phosphate

Answer 31

Phosphate:

this mineral is essential for all intracellular process,

for maintaining the structure of the cell membrane
and for activating a large number of enzymes and
second messenger systems.

In its incorporation in 2,3-DPG
it controls oxygenhaemoglobin affinity
and is central to energy storage as part of ATP.

Severe ATP depletion can affect myocardial contractility,
and is also associated with rhabdomyolysis. Normal cerebration can be
impaired. Severe hypophosphataemia is defined as a plasma concentration less than
0.3 mmol l–1. Initial acute replacement can be initiated with 18 mmol intravenously
over 12 hours.

Question 32

Potassium

Answer 32

: this is the major intracellular cation, and the rapid uptake by cells and
consequent fall in plasma concentration can provoke potentially fatal cardiac
arrhythmias.

Question 33

Magnesium

Answer 33

: this is another important intracellular cation
which is a co-factor in numerous enzyme systems,

including those involved in oxidative phosphorylation and ATP production.

It is described in more detail under ‘Magnesium Sulphate’ in
Chapter 4.

Severe hypomagnesaemia is defined as a plasma concentration less than
0.5 mmol l–1.

Acute replacement can be achieved by giving 24 mmol intravenously
over 24 hours

Question 34

Thiamine

Answer 34

: this is an essential co-factor in carbohydrate metabolism. Its deficiency
can cause acute neurological disturbance, including Wernicke’s encephalopathy with
confusion and ataxia.

Question 35

Guidelines, including those from NICE, recommend

Answer 35

slow repletion at a maximum initial rate of 10 kcal kg–1 24 h–1 and increasing to full
energy requirements over 4–7 days. This will depend on the degree of malnutrition
or the period of starvation; if this is severe, the initial rate should be halved to 5 kcal
kg–1 24 h–1. There is no need for correction of electrolyte and mineral concentrations
before refeeding begins. Vitamin supplementation should also be started
immediately.