Nutritional Support in Trauma Flashcards
What is the medical definition of trauma?
an injury or wound to living tissue caused by an extrinsic agent
What are examples of trauma?
- road traffic accident
- stabbing
- gunshot wound
- burns
- aneurysm repair
- tumour excision
- caesarean section
- amputation of diabetic foot
What are the immediate and later features of physical trauma?
immediate:
- intravascular fluid loss
- extravascular volume
- tissue destruction
- obstructed / impaired breathing
later:
- as above as well as:
- starvation
- infection
- inflammation
all of these factors have potential mortality
How might someone in a RTA be treated?
What may they die from if they do not recover?
if they cannot eat or drink, they are given IV fluids (3L 5% dextrose / day)
they may then rapidly lose weight
the death certificate cites “pneumonia” as the cause of death
What are the stages involved in someone dying from pneumonia after a RTA where they cannot eat or drink?
blood loss + impaired breathing + infection barrier penetration
- decreased circulating volume
- decreased red cells + O2
- decreased white cells + immune response
- decreased cardiac output / blood pressure
- decreased organ perfusion
- decreased energy substrate delivery to cells and tissues
this leads to major organ dysfunction (GI / heart / brain / renal) and infection barrier penetration (sepsis)
What do the following lines represent for causes of mortality after major trauma?
red = haematological shock
pink = head injury
green = acute respiratory distress syndrome
blue = multi-organ failure
What can cause shock?
interruption to the supply of substrates to the cell:
- oxygen, glucose, water, lipids, amino acids, micronutrients
interruption to the removal of metabolites from the cell:
- CO2, water, free radicals, toxic metabolites
What are the 3 stages involved in mortality from trauma?
phase 1 - clinical shock
someone may make a spontaneous recovery - physiological adaptation
or an intervention may be needed - resuscitation
phase 2 - hypercatabolic state
phase 3 - recovery (anabolic state)
When does shock (phase 1) tend to develop?
What is secreted?
- develops within 2-6 hours after injury
- lasts from 24-48 hours
- cytokines, cortisol and catecholamines are secreted
What happens to the body during phase 1 (shock)?
What are the primary aims in this phase?
- increased heart rate (tachycardia)
- increased respiratory rate
- peripheral vasoconstriction
- selective peripheral shut-down to preserve vital organs
- hypovolaemia
primary aims:
- stop bleeding
- prevent infection
When does phase 2 (catabolic state) develop?
What is secreted during this stage?
- develops around 2 days after injury
- it is necessary for survival but if it persists/is severe it increases mortality
- secretion of catecholamines, glucagon and ACTH leading to cortisol production
What are the effects on the body of phase 2 (catabolic state)?
What are the primary aims in this phase?
- increased oxygen consumption
- increased metabolic rate
- increased negative nitrogen balance
- increased glycolysis
- increased lipolysis
primary aims:
- avoid sepsis
- provide adequate nutrition
When does phase 3 (anabolic state) occur?
What does it coincide with?
occurs around 3-8 days after uncomplicated surgery
may not occur for several weeks after severe trauma and sepsis
coincides with beginning of diuresis and request for oral intake
What happens to the body during phase 3 (anabolic state)
What is most critical during this phase?
gradual restoration of:
- body protein synthesis
- normal nitrogen balance
- fat stores
- muscle strength
- adequate nutrition supply is critical in this phase
- risk of refeeding syndrome
- may last a few weeks / few months
- obesity paradox
What are the 6 stages involved in the inflammatory response at a trauma site?
- bacteria and pathogens enter the wound
- platelets release clotting factors
- mast cells secrete factors that mediate vasodilation to increase blood delivery to the injured area
- neutrophils & macrophages recruited to phagocytose pathogens
- macrophages secrete cytokines to attract immune cells + proliferate the inflammatory response
- inflammatory response continues until wound is healed
What are the endocrine effects of pro-inflammatory cytokines?
(e.g. IL-1, TNF-a)
increase in catabolic hormones:
- increased ACTH and cortisol
- increased glucagon
- increased catecholamines
decrease in anabolic hormones:
- decreased growth hormone
- decreased insulin
What are the effects of cytokines IL-1, IL-6 and TNF on the inflammatory response?
- fibroblast proliferation (repair)
- fever
- endocrine effects - catabolic & anabolic
- anorexia
- T cell activation & B cell proliferation
- acute phase proteins
- metabolic effects (catabolic)
- local effects
- chemotaxis
- vasodilation
- cell adhesion proteins
What are the 5 cardinal signs of inflammation?
- heat
- redness
- swelling
- pain
- loss of function
In health, how long do glycogen stores maintain glucose concentration?
in health, glycogen stores can maintain [glucose] for up to 24 hours
How long does the brain survive after circulatory failure?
How does it store glycogen and what is its requirement?
the brain has NO glycogen store
obligate substrate is glucose and oxygen
(requirement = 120g/day which is equivalent to 1kg muscle)
it will not survive for more than 2 minutes of circulatory failure
it adapts to using ketones as an energy substrate
How long can the kidneys and liver survive after interruption of blood supply?
the kidneys and liver are capable of gluconeogenesis
they can survive for hours after interruption of blood supply
What substrates are used by the liver/kidney and skeletal muscle?
different tissues use different substrates
the liver & kidneys use fatty acids / amino acids
skeletal muscle uses glycogen stores / fatty acids
What are the first 2 phases that occur when the supply of oxygen and glucose is interrupted?
Phase 1 - glycogenolysis:
- glycogen is converted to glucose
- this lasts for 24 hours maximum
Phase 2 - gluconeogenesis:
- involves skeletal + secreted protein breakdown
- amino acids are converted to glucose + lactate production
How much glucose can be produced from 1kg of muscle in gluconeogenesis?
What is the nitrogen loss during this phase?
1 kg of muscle contains 200g protein which produces 120g glucose
nitrogen loss is around 60-70 g/day but it can be up to 300g
What happens in phase 3 when the supply of oxygen and glucose is interrupted?
Phase 3 - lipolysis + ketogenesis:
- free fatty acids are converted to acetyl CoA
- this is converted to acetoacetate & hydroxybutyrate
- there is a gradual change to ketone metabolism by the CNS which spares protein stores and muscles
What is the main problem associated with ketogenesis?
ketones are acids and cause a diuresis with loss of water and electrolytes
What happens to skeletal muscle proteolysis as part of trauma protein turnover?
How does this happen?
skeletal muscle proteolysis INCREASES
- increase in [free amino acids]
- these are transported to the liver for gluconeogenesis + protein synthesis
- increased plasma [ammonia]
- increased nitrogen loss
- via urinary excretion of urea
How does the amount of new protein synthesised change in trauma protein turnover?
How does this happen?
amount of new protein synthesised REDUCES and the profile of proteins synthesised changes
- increase in inflammatory modulators and scavengers
- e.g. CRP, haptoglobin, clotting actors, modulators of clotting such as protease inhibitors
- this leads to decreased albumin
What will administration of adequate calories do in starvation?
In what type of patients is this not true?
in starvation, administration of adequate calories as carbohydrate/lipid will stop muscle wasting
this is not true in trauma/sepsis patients
as the primary stimulation for protein breakdown is cytokine secretion from activated macrophages
After starvation, what may further proteolysis lead to?
How can this lead to pneumonia?
further proteolysis results in life-threatening damage to essential structural and secreted protein
structural respiratory muscle weakness results in poor cough, retention of secretions (pneumonia)
Why does lactate production happen in hypoxia?
What is the result of this?
due to decreased aerobic metabolism and increased anaerobic metabolism
- pyruvate does not undergo oxidative phosphorylation via the TCA cycle but is reduced to lactate
- anaerobic metabolism can only continue until [lactate] becomes toxic
- H+ inhibits enzymes
- increased [lactate] is equivalent to tissue hypoxia
How can blood lactate act as a prognostic marker in trauma?
failure of blood lactate to return to normal following trauma resuscitation carries a poor prognosis
What is the vicious cycle involved in lactate metabolism?
- mitochondrial failure due to hypoxia
- decreased oxidative phosphorylated
- NADH > NAD+
- anaerobic glycolysis continues
What should nutritional support consider?
- demands of hypermetabolic phase
- pre-trauma nutritional state
When does nitrogen loss peak?
How much muscle protein is lost in fractures and severe burns?
nitrogen loss peaks at 4-8 days
in fracture of long bone - 60-70g muscle protein
in severe burns - 300g muscle protein
How does immobilisation affect recovery?
immobilisation increases losses
calcium, phosphate, magnesium, etc.
What techniques are used to help patients through the hypermetabolic phase?
nutrition is crucial in helping patients through the hyper-metabolic phase and preparing for anabolic recovery
- ambient temperature
- use the gut if possible (nasogastric tubes)
- TPN (trace elements, fat soluble vitamins)
What is meant by primary malnutrition?
- protein-calorie undernutrition (starvation)
- dietary deficiency of specific nutrients (e.g. trace elements, water soluble vitamins / fat soluble vitamins)
What is meant by 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
What are the consequences of malnutrition?
What is it associated with and what is the incidence in hospitalised patients?
- negative nitrogen balance
- muscle wasting
- widespread cellular dysfunction
- associated with:
- infection
- poor wound healing
- changes in drug metabolism
- prolonged hospitalisation
- increased mortality
the overall incidence of malnutrition in hospitalised patients is approximately 50%
What are the stages that can lead to refeeding syndrome?
- starvation / malnutrition
- glycogenolysis, gluconeogenesis and protein catabolism
- protein, fat, mineral and electrolyte/vitamin depletion - salt and water intolerance
- refeeding (switch to anabolism)
- fluid, salt, nutrients (CHO major energy source)
- insulin secretion
- increased protein and glycogen sysnthesis
- hypokalaemia, hypomagnesaemia, hypophophataemia, thiamine deficiency, salt/water retention (oedema) lead to refeeding syndrome
What actually is refeeding syndrome?
a metabolic disturbance that occurs as a result of reinstitution of nutrition to people who are starved, severely malnourished or metabolically stressed due to severe illness
What is a common disease associated with malnutrition that affects 1 in 2,500 newborn infants in the UK?
cystic fibrosis
What is the cystic fibrosis transmembrane regulator (CFTR) protein?
What is its function and where is it found?
a cAMP dependent chloride channel
localises to the apical membrane of secretory and absorptive epithelial cells within the:
- airways
- pancreas
- liver
- intestine
- sweat glands and the vas deferens
What is the role of the CFTR protein?
CFTR faciliates the production of thin, watery, free-flowing mucus
this lubricates airways and secretory ducts
and protects the lining of the airways, digestive system and reproductive system
so that macromolecules (e.g. digestive enzymes) can be secreted smoothly out of secretory ducts
What is the main cause of CFTR dysfunction?
failure to maintain hydration of macromolecules in the lumen of the ducts of the lungs, pancreas, intestine, liver and vas deferens causes secretions to precipitate and cause obstruction
What do digestive enzyme deficiencies lead to in CFTR dysfunction?
malnutrition
What happens in lung disease where there is CFTR dysfunction?
- increased bacterial colonisation
- neutrophils accumulate
- elastase is secreted which digests lung proteins causing tissue damage
- dead neutrophils release DNA which increases the viscosity of the CF sputum
infection + persistent inflammatory state
What are the 3 main gastrointestinal diseases in cystic fibrosis?
What do they result in?
- meconium ileus at birth
- severe hepatobiliary disease
- pancreatic cysts , exocrine insuffiency
leads to poor appetite, failure to thrive and low weight
What is the treatment for meconium ileus?
occurs in around 15% of births with CF
may require surgical resection as there is an associated risk of intestinal failure
What are the consequences of severe hepatobiliary disease in CF?
hepatic metabolism of lipids, steroid hormones, drugs and toxins is compromised
What is the result of pancreatic cysts and exocrine insufficiency in CF?
- decreased insulin - diabetes
- decreased lipase - lipid malabsorption, steatorrhoea, fat soluble vitamin deficiency
- decreased proteases - protein malnutrition
What is the treatment for respiratory disease due to cystic fibrosis?
- physiotherapy
- exercise
- bronchodilators
- antibiotics (oral / nebuliser / IV)
- steroids
- mucolytics (DNase)
the aim is to reduce infection and inflammationn
What is the treatment for GI disease caused by cystic fibrosis?
- pancreatic enzyme replacement (Creon)
- nutritional supplements
- fat-soluble vitamins
- high calorie diet
- ursodeoxycholic acid
- maintain body weight
- avoid catabolic state
- introduce artifical feed early if sick
What is contained within Creon delayed release capsules?
lipase, protease and amylase
they are made from pig pancreas
What is a nebuliser used for in cystic fibrosis treatment?
drug delivery into the lungs
What are the 3 main stages in cystic fibrosis treatment?
- prompt use of appropriate antibiotics
- lifelong nutritional supplements
- early use of nutritional support in acute illness
