NUTRITIONAL SUPPORT IN TRAUMA Flashcards

1
Q

Trauma:

A

an injury/wound to living tissue caused by an extrinsic agent

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2
Q

profounder effects trauma has on biochemistry

A
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)
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3
Q

SHOCK:

A

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

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4
Q

Phase 1 (shock

A

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

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5
Q

Phase 2 (catabolic state)

A

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

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6
Q

Phase 3 (anabolic state)

A

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.

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7
Q

Inflammatory response at a trauma site

A

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.

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8
Q

Reduced circulating load –> anaerobic respiratiion –> lactate build up –> hypoxia

A

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

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9
Q

Nutritional support should consider:

A

demands of hypermetabolic phase

pre-trauma nutritional state

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10
Q

Primary Malnutrition

A

Protein-calorie undernutrition (starvation)

Dietary deficiency of specific nutrients (e.g. trace elements, water soluble vitamins / fat soluble vitamins)

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11
Q

Secondary Malnutrition

A

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

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12
Q

Consequences of Malnutrition

A

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%.

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13
Q

Cystic fibrosis

A

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

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14
Q

CF Lung disease:

A

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

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15
Q

CF GI disease

A

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.

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