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Metabolic Response to Trauma. Dr. Dalal AL- Matrouk. Introduction. Following accidental or deliberate injury, a characteristic series of changes occurs, both locally at the site of injury and within the body generally.

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metabolic response to trauma

Metabolic Response to Trauma

Dr. Dalal AL-Matrouk

introduction
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.
introduction1
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.
phases of the metabolic response to trauma
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
ebb or shock phase
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
flow phase
Flow phase
  • Hypermetabolism
    • increase in basal metabolic rate
    • increased oxygen consumption & cardiac output
    • increased urinary nitrogen losses, altered glucose metabolism, accelerated tissue catabolism
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
factors mediating the metabolic response to injury
FACTORS MEDIATING THE METABOLICRESPONSE TO INJURY
  • The metabolic response is a complex interaction between many body systems.
slide9

Injury response

+

Neurohormonal

Inflammatory

the acute inflammatory response
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.
the acute inflammatory response1
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.
the acute inflammatory response2
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)
acute phase proteins
Acute phase proteins
  • Fibrinogen
  • C-reactive protein
  • Inhibit generalized tissue destruction from inflammation
neuro response
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.
endocrine response
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.
consequences of metabolic response to injury
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

slide22

Blood conserving measures:

Hypovolemia low C.O  decreased blood flow to organs  neuroendocrine response to increase C.O (SV X HR)

consequences of metabolic response to injury1
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
consequences of metabolic response to injury2
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)
consequences of metabolic response to injury3
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
factors modifying the metabolic response to injury
Factors modifying the metabolic response to injury
  • Patient-Related factors:
    • Genetic predisposition
    • Coexisting disease
    • Drug treatments
    • Nutritional status
factors modifying the metabolic response to injury1
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