22 Nutrition and trauma

Question 1

What are the immediate features of physical trauma?

Answer 1

Intravascular fluid loss.
Extravascular volume.
Tissue destruction.
Obstructed/impaired breathing.

Question 2

What are the causes of mortality after major trauma? (3)

Answer 2

0-5 days: haematological shock and head injury.
5-15 days: Acute Respiratory Distress Syndrome.
10-35 days: Multi organ failure.

Question 3

What is shock?

Answer 3

Interruption to the supply of substrates to the cell and removal of metabolites.

Question 4

What are the three physiological phases after trauma?

Answer 4

1. Clinical shock.
2. Hypercatabolic state.
3. Recovery (anabolic state).

Question 5

Describe phase 1 (SHOCK) after trauma.
Chemicals released? (3)
Effects (4)
What do doctor aim to do then?

Answer 5

2-6hrs later, lasts 24-48hrs.
Cytokines, catecholamines + cortisol release.
High hr + rr. Peripheral vasoconstriction. Hypovolaemia.
Stop bleeding + prevent infection.

Question 6

Describe phase 2 (catabolism) after trauma.
Chemicals released? (3) Effects (5).
What do doctor aim to do then?

Answer 6

2 days after.
Catecholamines, glucagon + ACTH release.
Increase O2 + metabolic rate. -ve N balance. Increased glycolysis + lipolysis.
Avoid sepsis, provide nutrition.

Question 7

Describe phase 3 (anabolism) after trauma.
Features (5)
What do doctor aim to do then?

Answer 7

3-8 days after, weeks if severe.
Restoration of N balance, protein synthesis, fat stores + muscle strength. Coincides with diuresis.
Nutrition, refeeding syndrome risk.

Question 8

What mediates the inflammatory response after trauma? (3)

What are the endocrine effects of these cytokines?

Answer 8

IL-1, IL-6, TNF.
Increased catabolic hormone secretion: ACTH, glucagon, catecholamines.
Inhibition of anabolic hormones: growth hormone, insulin.

Question 9

In health, how long can glycogen stores maintain blood glucose?

Answer 9

24 hours.

Question 10

What is the metabolic response to trauma? (3)

Answer 10

1. 24hrs glycogenolysis.
2. Skeletal + secreted protein breakdown. N loss 60-300g/day. Lactate produced.
3. Lipolysis + ketogenesis. Causes diuresis. Acetoacetate + hydroxybutyrate produced.

Question 11

How does anaerobic metabolism lead to cell death?

Answer 11

Inadequate energy produced (1mol glucose-2mol ATP) -> metabolic failure.
Lactic acid production -> metabolic acidosis.

Question 12

How does protein turnover change after trauma?

Answer 12

Decreased albumin synthesis. Increased inflammatory modulator and clotting factor synthesis
Increased skeletal muscle proteolysis - increase free AA (for gluconeogenesis), increased plasma [ammonia], increased N2 loss.

Question 13

Do adequate calories prevent muscle wasting after trauma?

Why?

Answer 13

No.

Breakdown mediated by cytokine secretion from activated macrophages.

Question 14

How is lactate used as a prognostic marker in trauma?

Answer 14

Failure to return to normal = poor prognostic marker. >5mml/l = 100% mortality.

Question 15

What is the vicious cycle of lactate production after trauma?

Answer 15

Hypoxic mitochondrial failure. Oxidative phosphorylation decreases. NADH > NAD+. Anaerobic glycolysis continues.

Question 16

When does nitrogen loss peak after trauma?

What amounts are lost following fracture of long bone vs sever burns.

Answer 16

4-8days.
Bone: 60-70g.
Sever burns: 300g.

Question 17

Distinguish between primary and secondary malnutrition.

Answer 17

1: protein/calorie/nutrient undernutrition.
2: suppressed appetite, absorption + utilisation inadequate, increased demand.

Question 18

How does referring syndrome occur?

Answer 18

Refeeding switches body to anabolism. CHO is energy source, insulin section.
Increase in protein/glycogen synthesis, increase in glucose/ thiamine/ K+/ Mg2+/ PO4- uptake.
Results in blood deficiency of these.
Leads to cardiac arrhythmia and failure

Question 19

What does the exocrine insufficiency in cystic fibrosis cause? (3 enzymes + effects)

Answer 19

Low insulin - diabetes.
Low lipase - lipid malabsorption, steatorrhoea, fat soluble vitamin deficiency.
Low proteases - protein malnutrition.

Question 20

How are the GI components of cystic fibrosis treated? (4)

Answer 20

Creon (enzyme replacement - lipase, protease, amylase).
Nutritional supplement.
High calorie diet.
Ursodeoxycholic acid.