Metabolic response in injury

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Metabolic response in injury
• 1930s, Cuthbertson • 2 distinct periods of the post-traumatic responses
– Ebb phase – Flow phase

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cardiac output. body temperature and oxygen consumption • Often associated with hemorrhage. 12 to 24 hours • Reduce: Blood pressure. resulted in hypoperfusion and lactic acidosis • With restoration of blood volume  more accelerated responses 3 .Ebb or shock phase • Immediately following injury • Usually brief in duration.

Flow phase • Hypermetabolism – increase in basal metabolic rate – increased oxygen consumption – degree related to severity of inflammatory response – temperature: reasonable indicator 4 .

but much more intensive and extend over a long period 5 . increased urinary nitrogen losses. accelerated tissue catabolism • Accidental injury similar to elective operation.Flow phase • Hypermetabolism • Increased cardiac output. altered glucose metabolism.

Altered glucose metabolism • Hyperglycemia – Ebb phase • parallel severity of stress • low insulin levels • glucose production only slightly elevated – Flow phase: hyperglycemia persist • insulin levels-normal or elevated • increase hepatic glucose production • profound insulin resistance 6 .

Alteration in protein metabolism • Extensive urinary nitrogen loss – related to extent of trauma – but also depend on previous nutritional status. nitrogen loss not attenuated 7 . sex (muscle mass) • Unfed patients – protein breakdown > synthesis: negative balance • Exogenous calories and nitrogen  increase protein synthesis. age.

Alteration in fat metabolism • Stored triglyceride: mobilized • Oxidized at accelerated rate (lipolysis) • Ketosis is blunted 8 .

Difference between elective and accidental injury 9 .

Injury response Neurohormonal + Inflammatory 10 .

Inflammation • Inflammatory response – Primitive – Complex – Nonspecific immune system • Inflammatory  change in body composition  acute challenge to homeostasis 11 .

Inflammation • Localized – rubor(redness) – tumor(swelling) – calor(pain) – dolor(heat) – function laesa (loss of function) 12 .

Inflammation • Systemic – hypermetabolism – body protein catabolism – insulin resistance – fever – acute phase protein response  Dysregulation  Septic multiple organ failure (major cause of death in ICU) 13 .

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Inflammation 15 .

glutamine synthesis. neutrophil and macrophage recruitment) • Signals to specific immune system to elimination of offending agent • Reduction of fluid loss to maintain hydration * Inflammatory response: internal nutrition support.Advantages of inflammatory response • Mobilization of fuel and substrates from muscle and adipose tissue to maximize visceral functions (gluconeogenesis. fluid resuscitation and antibiotic therapy* 16 . acute phase protein synthesis) • Initiation of process of local control and elimination of offending agent (fever response.

growth factors. kinins. enzymes. complement.Inflammation • Mediated by host biochemicals – hormones. cytokines and eicosanoid • Initial injury  local mast cells release numerous mediators (chief:cytokines and eicosanoids) – Pro-inflammatory forms – and anti-inflammatory forms 17 .

PGE2. acute phase proteins 18 . IL-6. insulin resistance ▫ Peak early and disappear from plasma • Stimulate IL-6 release: reduce level of insulinlike growth factor (IGF-1) proteolysis and amino acid release from muscle.Pro-inflammatory forms • Early • TNF. IL-1. acute phase protein synthesis. LT4 (leukotriene-4) • TNF +PG+IL-1: acute phase response ▫ fever.

Anti-inflammatory forms • Inflammatory stimulus controlled and eliminated • Anti-inflammatory cytokines • IL-4. IL-13. IL-10.LT5) • Bring inflammatory response to conclusion 19 . ecosanoids (PGE2.

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Neurohormonal response 21 .

Neurohormonal response • Afferent stimuli to vagus nerve ▫ ▫ ▫ ▫ Cytokine (e. TNF-alpha.g. IL-1) Baroreceptors Chemoreceptors Thermoreceptors • CNS: hypothalamus • Parasympathetic: acetylcholine ▫ Reduces tissue macrophage activation ▫ Release of proinflammatory mediators (Antiinflammatory pathways) 22 .

glucocorticoids and epinephrin • Ebb phase ▫ Epinephrine: sympthoadrenal axis help to maintain pressure. blood flow • Flow phase ▫ Glucagon: glycogenolytic and gluconeogenesis ▫ Cortisol: mobilized amino acids from skeletal muscle and increases gluconeogenesis ▫ Catecholamines: glycolysis and gluconeogenesis. increase metabolic rate and stimulate lipolysis 23 .Neurohormonal response • Glucagon. increase lactate production form skeletal muscle.

Acute phase proteins • Fibrinogen • C-reactive protein • Inhibit generalized tissue destruction from inflammation 24 .

Volume loss and tissue hypoperfusion • Hemorrhage or plasma loss  compensate to maintain adequate organ perfusion • Pressure receptors (aortic arch. carotid artery) • Volume receptors (wall of left atrium) • Signal to brain • Heart rate and stroke volume increase • Stimulate release of ADH and aldosterone • Prolonged shock  oxygen delivery inadequate  anaerobic metabolism  lactic 25 .

Tissue damage. Pain and Fear • Injury of body tissue: most important factor initiating stress response • Afferent neural pathways from wound  hypothalamus: injury occurred • Tissue destruction sensed in conscious patient as pain • Stress response (pain and fear) Efferent pathways from brain  catecholamine ”fight or flight” response 26 .

THE END 27 .

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