Nutritional Support in Trauma Flashcards
What are the 3 phases of trauma
- Clinical Shock
- Hypercatabolic state
- Recovery- anabolic state
When does phase 1: shock occur and how long does it last for?
2-6 hrs after injury. Lasts 24-48hrs
What chemical modulators are released into the blood in phase 1: shock
Cytokines, catecholamines, cortisol
4 clinical effects of phase 1: shock
Tachycardia
Increased resp. rate
Peripheral vasoconstriction
Hypovolaemia
Aims during phase 1
Stop bleeding
Prevent infection
When does phase 2 present
2 days after injury
What chemical modulators are released into the blood during phase 2
Catecholamines, glucagon, ACTH
4 clinical effects of phase 2
Increase in O2 consumption
Increase in metabolic rate
Increase in glycolysis
Increase in lipolysis
When does phase 3 present
Coincides with beginning of diuresis and requenst for oral intake. May not occur for weeks after severe trauma and sepsis
What is the obestiy paradox
Obesity is survival advantage in the recovery of trauma
What are the 3 cytokines that play the biggest roles after trauma
IL-1, IL-6 and TNF
What endocrine effects to cytokines have, after trauma
Cytokine mediated secretion of catabolic hormones (increase in ACTH, glucagon, catecholamines)
Cytokine mediated inhibition of anabolic hormones (less growth hormone, less insulin)
How many grams of glucose/day/kg does the brain require?
120g
What does the brain use as an energy substrate when glucose is not available?
Ketones
How do the kidneys and liver adapt to less glucose availibility?
Gluconeognesis
What substrates does the liver and kidney use for gluconeogenesis?
Fatty acids/amino acids
What substrates does skeletal muscle use for gluconeogenesis?
Glycogen stores/amino acids
What are the 3 main metabolic responses to trauma, i.e. what happens when the supply of glucose and oxygen is interrupted?
Glycogenolysis
Gluconeogeneis
Lipolysis and ketogenesis
How are lipids used to make ketones simultaneously?
FFA>Acetyl CoA>Acetoacetate+Hydroxybutyrate
What are the cellular effects of anaerobic respiration
Loss of membrane Na/K pump>cellular swelling and loss of membrane integrity>lysosomal enzyme release
What pH, H+conc. and lactate conc. is considered lactic acidosis
60mmol/L
>5.0mmol/L
What are the 2 main metabolic effects of anaerobic respiration, and how do they come about?
Metabolic failure (inadequate energy production) Metabolic acidosis (lactic acid production)
What are the effects of trauma on levels of: inflammatory modulators albumin free amino acids ammonia conc. in plasma N2 loss
Inflammatory modulators increase Albumin decreases free amino acids increase Ammonia concentration in plasma increases Nitrogen loss increases
What is the difference in administering adequate calories in patients who are starving and in trauma/sepsis patients?
In starvation, this will reverse muscle wasting. This is not true for trauma/sepsis patients
Why does providing calories not reverse muscle wasting in trauma/septic patients?
Because primary stimulation for protein breakdown is cytokine secretion from activated macrophages
What concentration of lactate in the blood has a 100% mortality?
> 5mmol/L
At what time after trauma does N2 losses peak?
4-8 days
Protein calorie undernutrition (starvation)
Primary malnutrition
Nutrients present in adequate amounts by appetite is suppressed, or absorption and utilization are inadequate or increased demand for specific nutrients to meet physiological needs
Secondary malnutrition
Describe refeeding syndrome
Triggers insulin release, which results in cellular uptake of potassium, phosphate and magnesium- lowers the concentrations of these in the blood as well as thiamine deficiency and salt and water retention (oedema)
How common is CF?
1 in 2500 newborns
Describe the cystic fibrosis transmembrane regulator (CFTR) protein
cAMP dependent chloride channel that facilitates the production of mucus
4 main effects of CF
Malnutrition-digestive enzyme deficiencies
Infection and persistent inflammatory state
Meconium ileus at birth
Severe hepatobiliary disease
Pancreatic cysts, decreased exocrine insufficiency
How common is meconium ileus?
15%
What are the results of exocrine insufficiency in CF?
less insulin- diabetes
less lipase-lipid malabsorption, steatorrhoea, fat soluble vit.deficiency
less proteases
Pancreatic enzyme replacement
Creon
Name 4 commensal flora of gut
Bacteroides
Clostridium perfringens
Escherichia coli
Enterococcus faecalis
Anaerobic gram -ve bacilli -commensal flora of the gut
Bacteroides
Anaerobic gram +ve bacilli
Clostridium perfringens
Faculative gram -ve bacilli
Escherichia coli
faculative gram +ve cocci
Enteroccocus faecalis
Common bacterial causes of diarrhoea
Salmonella Shigella E.coli Campylobacter Vibrio cholerae C.diff Staph A Bacillus cereus
Common parasitic causes of diarhhoea
Entamoeba hist.
giardia lamblia
cryptosporidium
Common viral causes of diarrhoea
norovirus
rotavirus
Complications of diarrhoea
Dehydration renal failure
Haemolytic urinary sundrome (HUS)
Toxic megacolon
Guillian barre syndrome- associated with campylobacter
Which 4 bacteria act by adhering to the gut wall and cause gastroenteritis this way, rather than by producing enterotoxins?
Shigella
E.coli (enteroadherent forms)
Campylobacter
Salmonellae
Which bacteria can cause gastroenteritis and grows on undercooked meat?
Campylobacter
How does E.Coli 0157 cause gastroenteritis
Enterotoxin production. 10-15% patients develop haemolytic uraemic syndrome
Toxin mechanism of action for E.coli 0157
Activates G protein, increases cAMP, activates ion channels which over-excrete Cl- and water follows by osmosis (opposite of CF)
What is the danger of killing E.coli bacteria
Release more of the toxin and can make the disease worse
In what circumstances would you give antibiotics with someone with gastroenteritis
Very young and v.cold
Camplylbacter-prolonged or severe symptoms
Invasion e.g positive blood cultures
What bacteria accounts for 99% pseudomembranous colitis?
C.Diff
Current C.Diff infection therapy
Oral metronidazole/oral vancomycin
