T11-L6: Nutritional Support in Trauma

Question 1

At what stage of trauma do most deaths occur?

Answer 1

The initial stage of shock due to haematological shock or brain injury.

Question 2

What are the 3 stages of response to trauma?

Answer 2

Phase 1: Clinical Shock
Phase 2: Hypercatabolic stage
Phase 3: recovery (anabolic state)

Question 3

Describes the features of phase 1 (shock) in trauma.

Answer 3

• Circulating volume drops
• Cellular hypoxia and so a switch to aerobic metabolism and so the build up of lactate
• Loss of white cells leads to susceptibility of infection
• Cardiac output leads to reduced organ perfusion
• Toxic and inflammatory cells products build up
• Loss of barrier to infection penetration

In this stage the primary aim is to stop haemorrhage and prevent infection

Question 4

Describes the features of phase 2 (catabolism) in trauma.

Answer 4

• Catecholamines and glucagon drive glycolysis and proteolysis
• Increase in oxygen consumption
• Negative protein balance
• Adrenaline release
• Stress and pain
• Inflammatory cascade activated
• Higher metabolic state

The primary aims of this stage is to avoid sepsis, provide adequate nutrition an immune modulation to clam the inflammatory response

Question 5

Describes the features of phase 3 (anabolism) in trauma.

Answer 5

With uncomplicated surgery this can occur 3-8 days after. If not, it may happen after several weeks. This coincides with beginning of diuresis and request for oral intact
Gradual restoration of:
- Body protein synthesis
- Normal nitrogen balance
- Fat stores
- Muscle strength
- Adequate nutrition supply is critical in this phase
- Refeeding syndrome risk
- May last a few weeks / a few months
Obesity paradox - patients who are thin, even with no sign of malnutrition, tend to do worse than patients who are heavier

Question 6

What are the 3 phases of catabolism?

Answer 6

Phase 1: Glyogenolsis stimulated by glucagon and adrenaline (catecholamines)

Phase 2: Gluconeogenesis stimulated by glucagon, growth hormone, epinephrine, and cortisol

Phase 2: Lipolysis and Ketogenesis

Question 7

What is driving the lack of appetite catabolism?

Answer 7

Cytokine driven proinflammatory state

Question 8

What supply does the brain switch to to adapt to more than 2 minutes of circulatory failure?

Answer 8

Ketones

Question 9

What are the drivers for lipid degeneration in a catabolic state?

Answer 9

• Catecholamines e.g. adrenaline

- Glucocorticoids e.g. cortisol

Question 10

Give features of the hyper catabolic state that follows trauma (4).

Answer 10

• Negative nitrogen balance
• Insulin resistance
• Increased energy requirements
• Fluid retention

Question 11

How can lactate be used as a prognostic marker in trauma?

Answer 11

<1 mmol/L = 18% mortality
2-4 mmol/L= 74% mortality
> 5 mmol/L = 99.9% mortality

Question 12

True/False: Provision of adequate nutrition can reverse a hypercatabolic state.

Answer 12

False - Prognosis is Bette with adequate nutrition it provision of adequate nutrition cannot reverse the catabolic state. You need to address the cytokine driven pro inflammatory state:

• Support vital functions
• Maintian electrolyte and fluid balance
• Immune modulators may be needed
• Glutamine and Omega-3 fatty acids are anti-inflammatory

Question 13

What is the difference between primary and secondary malnutrition?

Answer 13

Primary malnutrition:
• Protein/calorie undernutrition (starvation)
•Dietary deficiency of specific nutrients (e.g. trace elements, water soluble vitamins / fat soluble vitamins)

Secondary malnutrition:
• Nutrients present in adequate amounts but appetite is suppressed
• Nutrients present in adequate amounts but absorption and utilization are inadequate
• Increased demand for specific nutrients to meet physiological needs

Question 14

Give consequences of malnutrition.

Answer 14

• Negative nitrogen balance
• Muscle wasting
• Widespread cellular dysfunction e.g. infection ,poor wound healing, changes in drugs metabolism, prolonged hospitalisation and increased mortality

Question 15

Describe referring syndrome.

Answer 15

1. There is chronic malnutrition
2. Insulin levels reduce and glucagon and cortisol increase
3. This leads to glycogenolysis, gluconeogenesis and protein catabolism
4. The effect of this is depletion go electrolytes, proteins, fats, minerals and vitamins.
5. Upon referring there is insulin secretion which leads to protein and glycogen synthesis. In addition there is glucose outage, uptake of phosphorus, magnesium and potassium and increased thiamine use.
6. This can lead to hypophosphateaemia, hypokalaemia, hypomagnesaemia, thiamine deficiency and sodium and water retention if given rapidly.
7. This is known as referring syndrome. This can lead to convulsions, delirium, ataxia, hypotension, oedema, parasthesia etc.

Question 16

Why can cystic fibrosis lead to malnutrition?

Answer 16

There is a mutation in the cAMP dependent chloride channel - CFTR. This channel is localised to the apical membrane of secretory and absorptive epithelial cells within airways, pancreas, liver, intestine, sweat glands and the vas deferens. As a result in CF that macromolecules (e.g. digestive enzymes) cannot be secreted smoothly out of secretory ducts leading to malnutrition. They therefore need to be given exogenous enzymes.

• Decrease in insulin can lead to diabetes
• Decreased in lipase can cause lipid malabsorption, steatorrhoea, fat soluble vitamin deficiency etc.
• Decrease in proteases can lead to protein malnutrition

Question 17

What is Wernicke-Korakoff syndrome?

Answer 17

Thiamine deficiency. Thiamine (B1) is a cofactor for many enzymes involved in glycolysis, citric acid cycle and synthesis of important compounds such as nucleic aid. Thiamine deficiency leads to risk of Mitochondrial damage, cellular necrosis, oxidative stress particularly in the Purkinje cells in cerebellum.

This can lead to Wernicke encephalopathy - confusion, ataxia and neural oculomotor disturbances. If this persists, it can progress to Korakoff psychosis where there is disproportionate memory loss.

Question 18

What are the risk factors for Wernicke-Korakoff syndrome?

Answer 18

• Alcohol dependency
- this is as alcohol reduces thiamine absorption and reduces thiamine stores in liver. Other factors include having a poor diet and genetic predisposition as not everyone who is alcohol dependent gets it
• Cancer chemotherapy - due to reduced appetite and increased demand for nucleic acid synthesis
• Anorexia nervosa
• Refeeding syndrome