Flashcards in Nutritional support in Trauma Deck (36):
What is Trauma?
Injury/would caused by an extrinsic agent
What are the immediate possible outcomes of trauma?
Intravascular/extravascualr fluid loss
Obstructed or impaired breathing
What are the later possible outcome son trauma?
If you survive initial blood loss/head injury, what other conditions can potentially kill you?
Acute respiratory distress syndrome - weakness of resp muscles
Multi organ failure
Nutrition can prevent this!
What is haematological shock?
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
What are the 3 phases following trauma?
1. Clinical shock (haematological)
2. (if spontaneous recovery/intervention) Hypercatabolic state
3. Recovery phase (anabolic state)
When and for how long does phase I last for?
Starts 2-6 hrs following injury
Lasts 24-48 hrs
What are the clinical characteristics of phase I? What cause these?
Increased HR, RR, peripheral vasoconstriction
Increased catecholamine, cortisol and cytokine secretion
What are the main aims in phase I
Stop bleeding and prevent infection
When does Phase II occur ?
Approx 2 days after injury
What are the characteristics of phase II? What cause these?
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
What are the primary clinical aims of phase II?
-Provide adequate nutrition
When does phase 3 occur? How long for?
Between 3-8 days following trauma
May last weeks!
What are the clinical characteristics of phase 3?
- coincides with diuresis and request for food/drink
- Restoration of body protein synthesis, normal nitrogen balance, fat stores, muscle strength
What are the clinical aims of phase 3?
Adequate nutrition = key
- avoid referring syndrome
What is the obesity paradox?
Those who are more obese are likely to recover from trauma quicker
What can the inflammatory response at the trauma site cause? what is its effect?
Systemic capillary leak
Loss of H2N NaCl, Albumin, and energy substrates
What are the 3 main cytokines involved in the inflammatory response?
IL-1, IL-6, TNF alpha
What are the effects of the cytokines in the inflammatory response?
Local effects - chemotaxis, vasodilation, cell adhesion
- metabolic effects ( catabolic)
- endocrine effects (catabolic/anabolic states)
T cell activation and B cell proliferation
What are the endocrine effects of cytokines?
Up-regulation of catabolic hormones (ACTH and cortisol), catecholamines, glucagon
Down regulation of anabolic hormones (insulin and GH)
What is glucogenolysis?
Glycogen breakdown to glucose
What is gluneogdnesis?
Glucose generation from skeletal and secreted protein breakdown
Not very efficient!
Produce lactate, loss of skeletal muscle and nitrogen loss
What is lipolysis and ketoacidosis?
FFA > acetyl CoA . acetoacetate + hydroxybutyrate
When/why is lipolysis and ketogenesis used?
Gradual change from gluconeogenesis to ketone metabolism to spare protein/skeletal muscle loss
How does hypoxia result in increased cell death?
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)
There is a protein synthesis/proteolysis imbalance with trauma. Why is this?
Reduced synthesis of new protein - use to generate proteins important for inflammation e.g. CRP, haptoglobin, clotting factors
- increased free AA; gluconeogenesis and inflammatory protein synthesis
- increased plasma albumin
- increased nitrogen loss
Protein turnover - what i the difference between starvation and sepsis?
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)
What blood marker, resulting from anaerobic metabolism, can be used as a prognostic marker of trauma?
What is the difference between primary and secondary malnutrition?
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
What are the consequences of malnutrition?
Negative nitrogen balance
How is refeeding syndrome caused?
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
What is cystic fibrosis?
Defective Cystic fibrosis transmembrane regulator protein (cAMP dependent chloride channel)
What is the function of CFTR?
Production of thin, watery, free flowing mucus
Lubricates airways/secretory ducts
Protects lining of airways, digestive system and reproductive system
What happens with CFTR dysfunction?
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
Persistent inflammatory state - catabolic state
What are the manifestations of GI disease in CF?
Hepatobiliary disease - reduced lipid, steroid hormone, drug and toxin metabolism
Pancreatic cysts - exocrine insufficiency - reduced lipase, protease and insulin