NUTRITIONAL SUPPORT IN TRAUMA Flashcards
Trauma:
an injury/wound to living tissue caused by an extrinsic agent
profounder effects trauma has on biochemistry
Circulating volume Red cells (O2) White cells (Immune response) Cardiac output / BP Organ perfusion Energy substrate delivery to cells and tissues Major organ dysfunction (GI/Heart/Brain/Renal) Infection barrier penetration (sepsis)
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
Phase 1 (shock
Develops within 2-6 hours after injury. Lasts 24 – 48h.Cytokines, Catecholamines and cortisol secreted. Heart rate (tachycardia), respiratory rate. Peripheral vasoconstriction (selective peripheral shut-down to preserve vital organs) & Hypovolaemia.
In this phase, Primary aims= 1) stop bleeding 2) prevent infection
Phase 2 (catabolic state)
Develops approx 2 days after injury. Necessary for survival but if persists / is severe, mortality.
Catecholamine’s, Glucagon, ACTH Cortisol
Oxygen consumption, metabolic rate, Negative nitrogen balance (skeletal muscle breakdown to release amino acids), Glycolysis (skeletal energy reserve depleted), Lipolysis (adipose tissue breakdown to release fatty acids). In this phase, Primary aims= 1) Avoid sepsis 2) Provide adequate nutrition
Phase 3 (anabolic state)
Occurs approx 3-8 days after uncomplicated surgery. May not occur for weeks after severe trauma and sepsis
Coincides with beginning of diuresis and request for oral intake.
Gradual restoration of: body protein synthesis, Normal nitrogen balance, Fat stores, Muscle strength
Adequate nutrition supply is critical in this phase. Refeeding syndrome risk. May last a few weeks / a few months. Obesity paradox.
Inflammatory response at a trauma site
Bacteria and pathogens enter 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.
Reduced circulating load –> anaerobic respiratiion –> lactate build up –> hypoxia
Lactate production in hypoxia: 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). [Lactate] Tissue hypoxia
Nutritional support should consider:
demands of hypermetabolic phase
pre-trauma nutritional state
Primary Malnutrition
Protein-calorie undernutrition (starvation)
Dietary deficiency of specific nutrients (e.g. trace elements, water soluble vitamins / fat soluble vitamins)
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
Consequences of Malnutrition
Negative Nitrogen balance, Muscle wasting
Widespread cellular dysfunction, Associated with
Infection, poor wound healing, changes in drug metabolism, prolonged hospitalization, and increased mortality. The overall incidence of malnutrition in hospitalized patients is approximately 50%.
Cystic fibrosis
affects 1 in 2,500 new-born infants in UK. Common disease associated with malnutrition. Localises to the apical membrane of secretory and absorptive epithelial cells within the airways, pancreas, liver, intestine, sweat glands and the vas deferens. 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
CF Lung disease:
increases bacterial colonisation, Neutrophils accumulate, elastase is secreted which digests lung proteins causing tissue damage; dead neutrophils release DNA which increases the viscosity of CF sputum –> Infection + Persistent inflammatory state
TREATMENT
Physiotherapy, Exercise, Bronchodilators, Antibiotics
(oral / nebuliser / iv), Steroids, Mucolytics (DNase)
Decrease Infection and Inflammation
CF GI disease
Meconium ileus at birth (~15%) – may require surgical resection (associated risk of intestinal failure)
Severe hepatobiliary disease – hepatic metabolism of lipids, steroid hormones, drugs and toxins compromised.
Pancreatic cysts, exocrine insufficiency, decreased Insulin–> Diabetes. decreased Lipase –> Lipid malabsorption, steatorrhoea, fat soluble vitamin deficiency decreased Proteases: protein malnutrition = Poor appetite, failure to thrive, low weight.
TREATMENT
Pancreatic enzyme replacement (Creon), Nutritional supplements, Fat-soluble vitamins, High calorie diet, Ursodeoxycholic acid
-Maintain body weight
-Avoid catabolic state
-Introduce artificial feed early if sick.