Theme 11 L6: Nutritional support in trauma Flashcards
1
Q
What is trauma?
A
an injury or wound to living tissue caused by an extrinsic agent
2
Q
Following trauma, what is the first phase of injury?
A
Clinical shock
onset: immediate to 2-4 hours)
3
Q
What are the clinical features of shock?
A
- decreased circulating volume
- decreased red cells –> cellular hypoxia
- anaerobic metabolism –> lactate accumulation
- decreased white cells
- decreased cardiac output / BP / organ perfusion
- decreased energy substrate delivery to cells and tissues
- toxic and inflammatory products in circulation + infection barrier penetration (sepsis)
4
Q
What are the primary aims of phase 1 (shock) ?
A
- stop haemorrhage
2. prevent infection
5
Q
What is the second phase response after trauma?
A
hypercatabolic state
24-48 hours
6
Q
Following phase 1 response to trauma (clinical shock), what two things could occur?
A
- Spontaneous recovery (physiological adaptation)
2. Resuscitation (intervention) leading to phase 2 –> hypercatabolic state
7
Q
What is the pathogenesis of the hypercatabolic state (phase 2)?
A
- catecholamines secretion –> increased glucagon, ACTH
- increase in oxygen consumption and metabolic rate
- increase in glycolysis –> glucose
- increase in lipolysis –> free fatty acids
- increase in proteolysis –> amino acids
- negative nitrogen balance develops
- stress / pain, inflammatory cascade activation
8
Q
What are the primary aims of phase 2, the hypercatabolic state?
A
- avoid sepsis
- provide adequate nutrition
- immune modulation
9
Q
What is the phase 3 response following trauma?
A
Anabolic state (recovery) occurs approx 3-8 days after uncomplicated surgery
10
Q
During recovery (phase 3: anabolic state), there is gradual restoration of?
A
- body protein synthesis
- normal nitrogen balance
- fat stores
- muscle strength
11
Q
What is critical during the anabolic state?
A
adequate nutrition supply
12
Q
What is the main risk during phase 3, the anabolic state?
A
refeeding syndrome
13
Q
What is the obesity paradox
A
more obese patients with more reserves might have better outcomes during phase 3, the recovery phase
14
Q
Explain the inflammatory response at a trauma site (6 steps)
A
- Bacteria and pathogens enter wound
- Platelets release clotting factors
- Mast cells secrete factors that mediate vasodilation to increase blood delivery to the injured areas
- Neutrophils + macrophages recruited to phagocytose pathogens
- Macrophages secrete cytokines to attract immune cells + proliferative inflammatory response
- Inflammatory response continues until wound is healed
15
Q
What are the two main pro inflammatory cytokines?
A
IL-1, TNF-a
16
Q
What are the endocrine effects of pro inflammatory cytokines (IL-1, TNF-a)?
A
- increase catabolic hormones
- increase ACTH –> increase cortisol
- increase catecholamines –> increase glucagon
- decrease anabolic hormones (growth hormone and insulin)
- decrease appetite
17
Q
What are the catabolic hormones?
A
adrenaline, cortisol and glucagon
18
Q
Which inflammatory modulators can be given?
A
glutamine and omega-3-FA
19
Q
What is catabolism?
A
- ‘break down’ state
- starvation
- stored nutrients put to use - glycogen broken down via adrenaline in muscle or glucagon in liver
- viscious cycle - decreased appetite, increased inflammation
20
Q
In catabolic response to trauma, what is phase 1?
A
Glycogenolysis:
- in muscle, adrenaline stimulates breakdown of glycogen to glucose
- in liver, glucagon stimulates break down of glycogen to glucose
21
Q
What receptor does adrenaline act on?
A
B-adrenergic receptor on cell surface
22
Q
In catabolic response to trauma, what is phase 2?
A
Gluconeogenesis:
- skeletal + secreted protein breakdown
- amino acid break down to glucose + lactate production
- nitrogen loss
23
Q
In catabolic response to trauma, what is phase 3?
A
Lipolysis and Ketogenesis:
FFA (free fatty acids) –> acetyl coA –> acetoacetate & hydroxybutyrate
24
Q
In health, how long can glycogen stores maintain glucose?
A
24hrs
25
As the brain has no glycogen store, what does it use as an energy substrate for adaptation during the catabolic state
ketones
26
Why can the kidneys and liver survive hours of interruption of blood supply?
capable of gluconeogenesis
27
Which substrates do the liver and kidney use for gluconeogenesis?
fatty acids/ amino acids
28
Which substrates do skeletal muscle use for gluconeogenesis?
glycogen stores/ fatty acids
29
How does lipolysis occur (the 3rd phase to the catabolic response to trauma)?
Catecholamines trigger c-AMP cascade that results in free fatty acid and glycerol release.
Glucocorticoids also fuel this response
30
In the fed state, how does insulin have a negative role in proteolysis?
if insulin is around, proteolysis doesnt occur
31
Why does proteolysis increase in the fasting state/ diabetes?
insulin is not available so there is protein degradation which results in atrophy of muscles and high protein turnover in the cells
32
What occurs in a state of high protein turnover?
- amount of protein synthesis reduces and profile of proteins synthesised changes
- inflammatory modulates e.g CRP, clotting factors increase
- albumin decreases
- skeletal muscle proteolysis increases
33
In trauma and sepsis, what is the primary stimulation for protein breakdown?
cytokine secretion from activated macrophages
34
What is the main prognostic marker in trauma?
lactate - failure of blood lactate to return to normal following trauma resuscitation carries a poor prognosis
35
What are the effects of a raised lactate?
-
- anaerobic metabolism - tissue hypoxia
- pyruvate does not undergo oxidative phosphorylation via the TCA cycle but is reduced to lactate
- mitochondrial failure due to hypoxia
- decreased oxidative phosphorlyation
- NADH accumulates rather than NAD+
- anaerobic metabolism can only continue until lactate becomes toxic
36
Can adequate nutrition reverse the catabolic state?
no - prognosis is better with nutrition but provision of adequate nutrition cannot reverse the catabolic state - cytokine driven pro inflammatory state
37
What is primary malnutrition?
- protein / calorie undernutrition (starvation)
| - dietary deficiency of specific nutrients
38
What is secondary malnutrition?
-nutrients present in adequate amounts but appetite is suppressed OR absorption / utilization are inadequate
39
What are the consequences of malnutrition?
- negative nitrogen balance
- muscle wasting
- widespread cellular dysfunction - infection, poor would healing, changes in drug metabolism, prolonged hospitalisation, increased mortality
40
Explain the pathogenesis of refeeding syndrome
-increased insulin secretion --> glucose uptake
-increased proteins and glycogen synthesis
-uptake of magnesium, phosphorus, potassium leads to hypophosphataemia, hypokalaemia, hypomagnesaemia
-thiamine use leads to thiamine deficiency
= refeeding syndrome
41
What are the signs and symptoms of RFS?
- convulsions
- delirium
- ataxia
- wernicke's encephalopathy
- hypotension
- arrhythmias
- heart failure
- renal failure
- paralytic ileus
- anaemia
- hyperglycaemia
- peripheral oedema
- paraesthesia
- rhabdomyolysis
- fasciculation
42
Which autosomal recessive condition is associated with malnutrition?
cystic fibrosis
43
How does CFTR dysfunction cause malnutrition?
- failure to maintain hydration of macromolecules in the lumen of the ducts of the pancreas and intestine - secretions precipitate - obstruction
- digestive enzyme deficiencies --> malnutrition
44
In bacterial colonisations of lungs, neutrophils accumulate and secrete what to cause structural lung damage?
elastase
45
Which nutritional deficits are seen in CF?
- meconium ileus at birth
- cannot produce insulin - diabetes
- cannot produce lipase - lipid malabsorption, steatorrhoea, fat volume vitamin deficiency
- proteases - protein malnutrition
- poor appetite, failure to thrive, low weight
46
What treatments can you give for the respiratory disease associated with CF?
-exercise
-bronchodilators
-anti biotics (oral/ nebuliser / iv)
-steroids
-mucolytics (DNase)
reduce infection and inflammation
47
What treatments can you give for the GI disease associated with CF?
- pancreatic enzyme replacement (creon capsules contain lipase, protease and amylase)
- nutritional supplements
- fat-soluble vitamins
- high calorie diet
- ursodeoxycholic acid
48
Which syndrome is associated with a thiamine (B1) deficiency?
Wernicke-Korsakoff syndrome
49
What is thiamine a co-factor for?
transketolase, PDH, a-KGDH
50
What is thiamine important for?
glycolysis, citric acid cycle, synthesis of nucleic acid, neurotransmitter glutathione, steroids
51
What occurs cellularly during a thiamine deficiency?
mitochondrial damage, cellular necrosis, oxidative stress, purkinje cells in cerebellum
52
What are the signs of Wernickes encephalopathy?
confusion
ataxia (unsteady gait)
neural oculomotor disturbances
53
Who is at risk of Wernicke Korsakoff syndrome?
1. Alcoholics
- decreased thiamine absorption and stores in the liver
2. Cancer chemotherapy
- appetite decreased
- demand for nucleic acid synthesis
3. Anorexia nervosa
4. Refeeding syndrome
