Metabolic Response to Trauma

1. Metabolic Response to Trauma Dr. Dalal AL-Matrouk

2. Introduction • Following accidental or deliberate injury, a characteristic series of changes occurs, both locally at the site of injury and within the body generally. • These changes are intended to restore the body to its pre-injury condition.

3. Introduction • Many of these physiological changes can be modified or corrected by treatments. • Although the metabolic response aims to return an individual to health, it can sometimes have harmful effects. For example, a major response can damage organs distant to the injured site itself.

4. Phases of the metabolic response to trauma Two phases: the ‘ebb’ and the ‘flow’ • Ebb: • usually comprised the first few hours after injury • cold and hypotensive 2. flow: • initial catabolic phase high metabolic rate, breakdown of proteins and fats, a net loss of body nitrogen and weight loss. • followed by an anabolic phase  protein and fat stores were restored and weight gain

5. Ebb or shock phase • Immediately following injury • Usually brief in duration; 12 to 24 hours • Reduced: Blood pressure, cardiac output, body temperature and oxygen consumption • Often associated with hemorrhage, resulted in hypoperfusion and lactic acidosis

6. Flow phase • Hypermetabolism • increase in basal metabolic rate • increased oxygen consumption & cardiac output • increased urinary nitrogen losses, altered glucose metabolism, accelerated tissue catabolism

7. 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

8. FACTORS MEDIATING THE METABOLICRESPONSE TO INJURY • The metabolic response is a complex interaction between many body systems.

9. Injury response + Neurohormonal Inflammatory

10. THE ACUTE INFLAMMATORY RESPONSE • Physical damage to tissues results in local activation of cells such as tissue macrophages. • These cells release a variety of cytokines.

11. SOME CYTOKINES INVOLVED IN THE ACUTEINFLAMMATORY RESPONSE • TNF-a • IL-1 • IL-8 • IL-6 • IL-10

13. THE ACUTE INFLAMMATORY RESPONSE • The effects of the inflammatory response mediators can be localized (paracrine effect) or become generalized in the body (endocrine effect). • This cascade of events results in rapid amplification of the initial stimulus  large numbers of inflammatory cells at the injured site  mediating the inflammatory response via cytokines.

14. THE ACUTE INFLAMMATORY RESPONSE • Other pro-inflammatory substances are released in association with tissue injury. • These include prostaglandins, kinins, complement and free radicals. • Anti-inflammatory substances and mechanisms also exist, such as antioxidants (e.g. glutathione, vitamin A and vitamin C) and protease enzyme inhibitors (e.g. a2macroglobulin)

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

16. Neurohormonal response

17. Neuro Response Stimulation of the sympathetic nervous system: • results in tachycardia and increased cardiac output. • Noradrenaline release from sympathetic nerve endings and adrenaline release from the adrenal gland increase circulating catecholamine concentrations.

18. ENDOCRINE RESPONSE • Hormonal changes are mainly involved in maintaining the body’s fluid balance and in the changes to substrate metabolism that occur following injury.

20. Consequences of metabolic response to injury Hypovolemia: Due to fluid loss/sequestration neuroendocrine response to restore normal fluid status Fluid conserving measures: - ADH: promotes water retention - Aldosterone: reabsorbtion of sodium & excretion of potassium & hydrogen - Duration of high ADH & Aldosterone:48-72 hrs

22. Blood conserving measures: Hypovolemia low C.O  decreased blood flow to organs  neuroendocrine response to increase C.O (SV X HR)

23. Consequences of metabolic response to injury INCREASED ENERGY METABOLISM : • Following severe trauma, resting energy expenditure is increased by 50%. • Thermogenesis: metabolic rate is increased by 6-10% for each 1C increase in T • Catabolism is mediated by catecholamines & cytokines  changes in carbohydrate, protein & fat metabolism

25. Consequences of metabolic response to injury Changes in RBC synthesis & coagulation: 1. Anemia : - bleeding - hemodilution - impaired BM function (less erythropoitin) - changes in iron metabolism (less available iron) 2. Hypercoagulability: • Activation of plts by epinephrine & cytokines • Dehydration & immobility • Increased procoagulants (fibrinogen) & decreased anticoagulants (protein C)

26. Consequences of metabolic response to injury Changes in RBC synthesis & coagulation: 3.Hypercoagulability: • Rare • Assocaited with shock, massive blood transfusion or sepsis • Exteme form: DIC

27. Factors modifying the metabolic response to injury • Patient-Related factors: • Genetic predisposition • Coexisting disease • Drug treatments • Nutritional status

28. Factors modifying the metabolic response to injury • Surgical/trauma-Related factors: • Severity of injury • Nature of injury ( e.g burn) • Ischemia-reperfusion injury • Tempreture/infection • Anesthetic technique

29. To summarize

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