Nutritional support in Trauma

Question 1

What is Trauma?

Answer 1

Injury/would caused by an extrinsic agent

Question 2

What are the immediate possible outcomes of trauma?

Answer 2

Intravascular/extravascualr fluid loss

Obstructed or impaired breathing

Tissue destruction

Question 3

What are the later possible outcome son trauma?

Answer 3

Starvation
Infection
Inflammation

Question 4

If you survive initial blood loss/head injury, what other conditions can potentially kill you?

Answer 4

Acute respiratory distress syndrome - weakness of resp muscles

Multi organ failure

Nutrition can prevent this!

Question 5

What is haematological shock?

Answer 5

Disruption to supply of substrates to cell e.g. O2, glucose, lipids, AA, H2O

Disruption ot removal of metabolites e.g. CO2, H2O, free radicals, toxic metabolites

Question 6

What are the 3 phases following trauma?

Answer 6

1. Clinical shock (haematological)
2. (if spontaneous recovery/intervention) Hypercatabolic state
3. Recovery phase (anabolic state)

Question 7

When and for how long does phase I last for?

Answer 7

Starts 2-6 hrs following injury

Lasts 24-48 hrs

Question 8

What are the clinical characteristics of phase I? What cause these?

Answer 8

Increased HR, RR, peripheral vasoconstriction
Hypovolaemia

Increased catecholamine, cortisol and cytokine secretion

Question 9

What are the main aims in phase I

Answer 9

Stop bleeding and prevent infection

Question 10

When does Phase II occur ?

Answer 10

Approx 2 days after injury

Question 11

What are the characteristics of phase II? What cause these?

Answer 11

Increased metabolic rate and oxygen consumption

• Increased negative nitrogen balance (increased skeletal muscle breakdown and increased AA)
• increased lipolysis and glycolysis
• due to catecholamine, glucagon and ACTH to cortisol secretion

Question 12

What are the primary clinical aims of phase II?

Answer 12

• Prevent sepsis

- Provide adequate nutrition

Question 13

When does phase 3 occur? How long for?

Answer 13

Between 3-8 days following trauma

May last weeks!

Question 14

What are the clinical characteristics of phase 3?

Answer 14

Anabolic state
- coincides with diuresis and request for food/drink

• Restoration of body protein synthesis, normal nitrogen balance, fat stores, muscle strength

Question 15

What are the clinical aims of phase 3?

Answer 15

Adequate nutrition = key

• avoid referring syndrome

Question 16

What is the obesity paradox?

Answer 16

Those who are more obese are likely to recover from trauma quicker

Question 17

What can the inflammatory response at the trauma site cause? what is its effect?

Answer 17

Systemic capillary leak

Loss of H2N NaCl, Albumin, and energy substrates

Question 18

What are the 3 main cytokines involved in the inflammatory response?

Answer 18

IL-1, IL-6, TNF alpha

Question 19

What are the effects of the cytokines in the inflammatory response?

Answer 19

Local effects - chemotaxis, vasodilation, cell adhesion

• metabolic effects ( catabolic)
• endocrine effects (catabolic/anabolic states)
• Fever

T cell activation and B cell proliferation

Question 20

What are the endocrine effects of cytokines?

Answer 20

Up-regulation of catabolic hormones (ACTH and cortisol), catecholamines, glucagon

Down regulation of anabolic hormones (insulin and GH)

Question 21

What is glucogenolysis?

Answer 21

Glycogen breakdown to glucose

Question 22

What is gluneogdnesis?

Answer 22

Glucose generation from skeletal and secreted protein breakdown

Not very efficient!

Produce lactate, loss of skeletal muscle and nitrogen loss

Question 23

What is lipolysis and ketoacidosis?

Answer 23

FFA > acetyl CoA . acetoacetate + hydroxybutyrate

Question 24

When/why is lipolysis and ketogenesis used?

Answer 24

Gradual change from gluconeogenesis to ketone metabolism to spare protein/skeletal muscle loss

Question 25

How does hypoxia result in increased cell death?

Answer 25

Increased use of anaerobic metabolism (only 2ATP generated and lactic acid produced) - Cell death results from metabolic acidosis (LA) and metabolic failure (insufficient energy provided)

Question 26

There is a protein synthesis/proteolysis imbalance with trauma. Why is this?

Answer 26

Reduced synthesis of new protein - use to generate proteins important for inflammation e.g. CRP, haptoglobin, clotting factors Increased proteolysis - increased free AA; gluconeogenesis and inflammatory protein synthesis - increased plasma albumin - increased nitrogen loss

Question 27

Protein turnover - what i the difference between starvation and sepsis?

Answer 27

Starvation - administration of CHO/fats will stop muscle wasting Sepsis - cytokines (from macrophages) stimulate protein breakdown (not energy deficit), resulting in increased proteolysis of essential structural/secreted proteins (life threatening e.g. resp muscles)

Question 28

What blood marker, resulting from anaerobic metabolism, can be used as a prognostic marker of trauma?

Answer 28

Blood lactate

Question 29

What is the difference between primary and secondary malnutrition?

Answer 29

PRIMARY - Protein-calorie malnutrition, dietary deficiency of specific nutrients e.g. vitamins, trace elements SECONDARY - adequate nutrition but inadequate absorption, appetite, utilisation - increased demands not met by intake

Question 30

What are the consequences of malnutrition?

Answer 30

Negative nitrogen balance Muscle wasting Cellular dysfunction

Question 31

How is refeeding syndrome caused?

Answer 31

Rapid switch from catabolic to anabolic state with refeeding Increase insulin secretion and down reg of glucagon, ACTH, catecholamines etc - increased glycogen synthesis and protein synthesis - This results in hypokaleamia, hypomagnesaemia, thiamine deficiency and oedema

Question 32

What is cystic fibrosis?

Answer 32

Defective Cystic fibrosis transmembrane regulator protein (cAMP dependent chloride channel)

Question 33

What is the function of CFTR?

Answer 33

Production of thin, watery, free flowing mucus Lubricates airways/secretory ducts Protects lining of airways, digestive system and reproductive system

Question 34

What happens with CFTR dysfunction?

Answer 34

Failure of maintain hydration of macromolecules in the lumen of ducts of lungs, pancreas, intestine, liver and vas deferent - causes secretions to precipitate and obstructions MALNUTIRITION Persistent inflammatory state - catabolic state

Question 35

What are the manifestations of GI disease in CF?

Answer 35

Meconium ileus Hepatobiliary disease - reduced lipid, steroid hormone, drug and toxin metabolism Pancreatic cysts - exocrine insufficiency - reduced lipase, protease and insulin

Question 36

What are the treatments for CF

Answer 36

Respiratory - reduce inflammation/infection - physio/exercise - bronchodilators - antibiotics - mucolytics GI - avoid catabolic state - Pancreatic enzyme replacement - creon - vitamin/nutrition supplements - high calorie diet