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.
• These changes are intended to restore the body to its pre-
injury condition.
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
Two phases:
the ‘ebb’ and the ‘flow’
Ebb:
- usually comprised the first few hours after injury
- cold and hypotensive
1.
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
FACTORS MEDIATING THE METABOLIC
RESPONSE TO INJURY
• The metabolic response is a complex interaction between
many body systems.
Injury response
Neurohormonal
+
Inflammatory
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.
SOME CYTOKINES INVOLVED IN THE
ACUTE
INFLAMMATORY RESPONSE
• TNF-a
• IL-1
• IL-8
• IL-6
• IL-10
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
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
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
• 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
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
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
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
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
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
• Patient-Related factors:
- Genetic predisposition
- Coexisting disease
- Drug treatments
- Nutritional status
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
TO SUMMARIZE
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