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Clinical Pathology > CP11-8 Nutritional Support in Trauma > Flashcards

CP11-8 Nutritional Support in Trauma Flashcards

1
Q

What is the definition of trauma?

A

An injury or wound to living tissue caused by an extrinsic agent

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2
Q

What percentage of global mortality is caused by trauma?

A

9%

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3
Q

What are some potential features of physical trauma?

A

Bleeding (intravascular fluid loss)
Extra vascular volume increases
Tissue destruction
Obstructed/impaired breathing
Infection
Inflammation
Starvation due to metabolic changes

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4
Q

What changes due to trauma can cause shock?

A

Blood loss
Poor blood flow
Low O2 supply

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5
Q

What are the three phases of metabolic change following trauma?

A

Shock
Hypercatabolism
Anabolic phase

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6
Q

What is involved in the hypercatabolism phase after trauma?

A

Increase in basal metabolic rate
Increase in anaerobic metabolism
Excessive metabolic breakdown of fat and protein

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7
Q

What is involved in the anabolic phase following trauma?

A

Macromolecule synthesis
Onset of recovery including improved appetite and diuretics.

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8
Q

What most commonly causes immediate death after trauma?

A

Haematological shock
Brain injury

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9
Q

What most commonly causes early death after trauma?

A

Haemorrhage
CNS injury

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10
Q

What most commonly causes late death after trauma?

A

Infection
Multi-organ failure

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11
Q

How does loss of circulating volume affect the body?

A

Decrease in red cells = decrease in O2 causing cellular hypoxia, anaerobic metabolism and lactate accumulation
Decrease in white cells and immune response
Decrease in cardiac output, BP and organ perfusion
Decrease in energy substrate deliver to cells and tissues

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12
Q

After trauma what are the endocrine effects of pro inflammatory cytokines (IL-1 and TNF-alpha)?

A

Increase in catabolic hormones include ACTH (cortisol) and catecholamines (e.g. glucagon)

Decrease in anabolic hormone secretion including growth hormone and insulin

This decreases appetite

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13
Q

After trauma, how long can glucose stores in the body last without eating?

A

24 hours

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14
Q

What happens to the brain in states of stress?

A

It has no glycogen store so has to use ketones in place as an energy substrate

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15
Q

What is a danger in the catabolic phase?

A

Stress-induced hyperglycaemia and increased blood lactate - both reduce prognosis

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16
Q

What are some catabolic responses to trauma?

A

Glycogenolysis
Lipolysis and ketogenesis
Proteolysis and gluconeogenesis

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17
Q

How much glucose can be gained from a 1kg of muscle when the body is in a state of proteolysis?

A

Only 120g

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18
Q

How much nitrogen is lost on average per day when the body is in a state of proteolysis?

A

60-70 g/day

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19
Q

What are some qualitative protein changes after trauma?

A

Increase in inflammatory modulators and scavengers
Increased CRP
Increase haptoglobin
Increase in clotting factors
Decrease in albumin

20
Q

What are some quantitative protein changes that can occur as a result of trauma?

A

Decrease in synthesis of protein
Decrease in skeletal protein
Decrease in structural protein
Decrease in secreted protein

21
Q

How can unchecked proteolysis lead to death?

A

Causes life-threatening damage to essential structural and secreted proteins so can no longer prevent the development of infections like pneumonia for examples as can no longer cough to expel infection so retains secretions leading to inflammation.

22
Q

How long does the anabolic phase after trauma usually last?

A

3-8 days

23
Q

When does the anabolic phase after trauma happen?

A

Sometimes not until several weeks after severe trauma and coincides with beginning of dieuresis and request for oral intake.

24
Q

What is a risk during the anabolic phase?

A

Reseeding syndrome risk

25
Q

What is the obesity paradox?

A

People who are obese tend to do better after trauma as have more energy reserves

26
Q

What is restored in the anabolic phase after trauma?

A

Body proteins
Nitrogen balance
Fat stores
Muscle strength

27
Q

True or false - provision of adequate nutrition can reverse a hypercatabolic state?

A

False - strongly catabolic patients cannot achieve a positive nitrogen balance by nutritional intervention until the peak of the catabolic drive has passed, instead it is important to support vital functions, maintain electrolyt and fluid balance.

28
Q

What is important to consider in nutritional support following trauma?

A

Timing
Route - enteral/parental
Constituents
Monitoring

29
Q

When determining the constituents of nutritional support following trauma, what should be considered?

A

The demands of the hypermetabolic phase
Pre-trauma nutritional state
The amount of nitrogen lost
What will be lost by immobilisation
Refeeding syndrome

30
Q

What is refeeding syndrome?

A

When a patient has been deprived of nutrition for so long that they are in starvation mode so upon refeeding will cause rapid uptake of glucose.

31
Q

What are some consequences of malnutrition?

A

Negative nitrogen balance
Muscle wasting
Widespread cellular dysfunction - including infection, poor wound healing, changes in drug metabolism, prolonged hospitalisation and increased mortality.

32
Q

What is the incidence of malnutrition in hospitalised patients?

A

50%

33
Q

How do you nutritionally treat patients with CF?

A

With pancreatic enzyme replacement (Creon)
Nutritional supplements
Fat-soluble vitamins
High calorie diet
Ursodeoxycholic acid

34
Q

What is the aim of nutritional treatment in CF patients?

A

Maintain body weight
Avoid catabolic state
Introduce peritoneal nutrition early when get sick

35
Q

What is Wernicke’s-Korsakoff syndrome?

A

A thiamine (B1) deficiency affecting glycolysis, the citric acid cycle, synthesis of nucleic acids, neurotransmitters, formation of gluathione and steroids.

36
Q

What drugs increase breakdown of thiamine?

A

Anti neoplastic drugs
Contraceptives
Diuretics

37
Q

What is a consequence of acute B1 (thiamine) deficiency?

A

Wernicke encephalopathy

38
Q

What is the classic triad that characterises Wernicke’s encephalopathy present in 17% of affected patients?

A

Encephalopathy, occulomotor dysfunction and gait ataxia

39
Q

What is korsakoff syndrome?

A

Chronic B1 deficiency

40
Q

What criteria is used to diagnose Wernicke’s encephalopathy?

A
41
Q

What are symptoms of Wernicke’s encephalopathy?

A
42
Q

What are symptoms of korsakoff syndrome?

A
43
Q

How do you treat Wernicke’s encephalopathy?

A
44
Q

What are risk factors for thiamine deficiency?

A

Alcohol dependency
Cancer chemotherapy
Anorexia nervosa
Bariatric surgery
Refeeding syndrome

45
Q

What modulates the metabolic response to trauma?

A

Catecholamines
Hormones
Cytokines

Clinical Pathology (65 decks)

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