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Critical Care

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  • Nutrition
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Branchial fistula

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Home | Critical Care

Nutrition

Requirements

  • Energy sources
  • Respiratory quotient: ratio of volume of CO2 produced to volume of oxygen consumed

  Energy Resp quotient RDA Notes
Fat 9.3kcal/g 0.7  
  • 50% total energy requirement must be provided by fat
  • Stored as triglycerides
  • Essential fatty acids (unable to be synthesized) - linoleic, linolenic, arachidonic acid: for synthesis of eicosanoids, PGs, LTs, TXAs
Glucose 4.1kcal/g 1.0  
  • Stress / critical illness renders patients hyperglycaemic and glucose intolerant
  • Excess glucose converted to lipid in liver; results in fatty liver
  • Excess CO2 produced increases ventilatory requirements
Protein 4.1kcal/g 0.8 0.8g/kg/day (nitrogen 0.15g/kg/day)
  • 6.25g of protein yields 1g of nitrogen
Amino acids      
  • Essentials: leucine, isoleucine, lysine, methionine, phenylalanine, threonine, tryptophan, valine
Minerals      
  • Essentials: Zinc, magnesium, manganese, selenium, copper, chromium
Vitamins      
  • Water soluble
  1. B1 - Thiamine: leads to wet (heart failure) or dry (neuropathy) beri-beri, Wernickes
  2. B2 - Riboflavin
  3. B3 - Niacin - Deficiency leads to pellagra (diarrhoea, dermatitis, dementia)
  4. B6 - Pyridoxine: stomatitis, peripheral neuropathy
  5. B7 - Biotin
  6. B12 - Cobalamine (contains cobalt): Megaloblastic anaemia
  7. C - Hydroxylases proline / lysine during collagen synthesis
  • Fat soluble
  1. A: Cell membrane stabilisation
  2. D: Calcium homeostasis
  3. E: Free-radical scavenger
  4. K: gamma-carboxylation of II, VII, IX, X

Starvation = Inadequate energy intake

Cachexia = Chronic deprivation of energy and nutrients irrespective of adequacy of intake (Maligant IL10)

Marasmus = Inadequate nutrients and energy

Kwashiokor =  Lack of protein (but some intake of energy)

Fasting = State of energy deprivation last no more than a few days

  • Glucose obtained from glycogen stores (liver, skeletal muscle)
  • Supply lasts +24hours
  • Then hepatic gluconeogenesis (from glycerol from fatty acids, amino acids from muscle protein, lactate) takes over
  • Increased generation of ketone bodies (acetone, acetoacetone, B-hydroxybutyrate) as source of energy during starvation
  • Hormones mobilised in starvation: Glucocorticoids, catacholamines, glucagon, thyroid hormone, insulin

 

Assessment

  1. Clinical
    • Physical appearance
    • Hand grip strenght
    • PFTs
  2. Anthropometric measurements
    • Height / weight - BMI
    • Fat: triceps skin fold
    • Lean fat: mid-arm circumference
  3. Biochemical measurements
    • Serum protein - Albumin
    • 24 hour creatinine
    • Immunological studies - total lymphocyte count, immune function

 

  Enteral
Parenteral
Indications Functionally intact gastro-intestinal system that cannot meet daily nutritional requirements Critical illness resulting in malnutrition with impaired gastrointestinal function (eg fistula, short bowel, IBD, enteritis)
Diet types
  1. Elemental
    • Reserved for those with malabsorption (short bowel syndrome)
    • Free amino acids, oligopeptides used
  2. Polymeric
    • Well functioning GIT
    • Whole protein used as source of nitrogen
  3. Modular
    • Enriched in particular nutrient
  4. Special formulation - arranged for special patients
    • Ventilated: high fat as energy source (opposed to glucose) to reduce CO2 generation

Components

  1. Water
  2. Carbs
  3. Protein
  4. Lipid / fat
  5. Vitamins
  6. Minerals
Mode of delivery
  • PO
  • Naso-gastric - bypassess oesophagus
  • Naso-jejunal - bypassess stomach/duodenum/biliary tree: reduces pancreatic secretions (esp for pancreatitis), reduces risk of aspiration
  • Gastrostomy: Enoscopic/fluroscopic placement
  • Jejunostomy: placed at lapartotomy (as above)
  • Via central vein (tunnelled subclavian line) - due to high osmolarity
Bowel effects
  • Continous feeding encourages bacterial colonisation of stomach (increased risk of pneumonia if there is aspiration)
  • Continous intragastric feeding causes secretory response from ascending colon leading to diarrhoea
  • Absence of enteral feeding leads to atrophic mucosa (local hormonal release from response to food stimulates release of enzymes necessary for mucosal integrity)
  • Leads to translocation of bacteria into systemic circulation
  • Leads to Sepsis / SIRS
Complications
  • Displacement of tube
  • Infection around gastrostomy
  • Refeeding syndrome: (switch from fat to carbohydrate feeding) - leads to hypophosphataemia
  • hyperkalaemia
  • Hyperglycaemia
  • Deranged LFT - enzyme induction due to AA imbalances
  • BM control
  • Hyperlipidaemia
  • Ventilatory problems (depending on feed)

 

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