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BODY RESPONSE TO INJ

URY
Mr. Nazim Jat
FRCS
 Body response to injury
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LEARNING OBJECTIVES
 Classical concepts of homeostasis

 Mediators of the metabolic response to injury

 Physiochemical & biochemical changes that occu

r during injury and recovery

 Changes in body composition that accompany su

rgical injury
 Avoidable factors that compound the metabolic r

esponse to injury
 Concepts of behind optimal perioperative care
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Injury response

Neural Response
+ Inflammatory Response

Hormonal Response
 Response Based on Time
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 2 distinct periods of the post-traumatic respon

ses(Hormonal/General Response)
 Ebb phase (Immediate Response)
 Flow phase (Late Response)
 Ebb or shock phase
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 Immediately following injury

 Usually brief in duration; 12 to 24 hours
 Reduce: Blood pressure, cardiac output, body
temperature and oxygen consumption
 Often associated with hemorrhage, resulted in
hypoperfusion and lactic acidosis
 With restoration of blood volume  more acce
lerated responses
 Flow phase
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 Hypermetabolism
 increase in basal metabolic rate
 increased oxygen consumption
 degree related to severity of inflammatory respon
se
 temperature: reasonable indicator
 Flow phase
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 Increased cardiac output, increased urinary nit

rogen losses, altered glucose metabolism, acce
lerated tissue catabolism
 Accidental injury similar to elective operation,
but much more intensive and extend over a lo
ng period
 Altered glucose metabolism(Hormonal Respons
e)
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 Hyperglycemia
 Ebb phase
 parallelseverity 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
 Alteration in protein metabolism
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 Extensive urinary nitrogen loss

 related to extent of trauma
 but also depend on previous nutritional status, ag
e, sex (muscle mass)
 Unfed patients
 protein breakdown < synthesis: negative nitrogen
balance
 Exogenous calories and nitrogen  increase p
rotein synthesis, nitrogen loss not attenuated
 Alteration in fat metabolism
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 Stored triglyceride: mobilized

 Oxidized at accelerated rate (lipolysis)
 Ketosis is blunted
 Difference between elective and accidental injury
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 Inflammation
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 Inflammatory response
 Primitive
 Complex
 Nonspecific immune system
 Inflammatory  change in body composition
 acute challenge to homeostasis
 Inflammation
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 Localized
 rubor(redness)
 tumor(swelling)
 calor(pain)
 dolor(heat)
 function laesa
(loss of function)
 Inflammation
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 Systemic
 hypermetabolism
 body protein catabolism
 insulin resistance
 fever
 acute phase protein response (Catabolism)
 Dysregulation  Septic multiple organ failure
(major cause of death in ICU)
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 Advantages of inflammatory response
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• Mobilization of fuel and substrates from muscle and adipose tissue

to maximize visceral functions

(gluconeogenesis, glutamine synthesis, acute phase protein synthe

sis)
• Initiation of process of local control and elimination of offending ag

ent
(fever response, 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, fluid resuscitatio

n and antibiotic therapy*
 Neural Response
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 Neural Response
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 Mediated by host biochemicals

 hormones, growth factors, enzymes, kinins, comp
lement, cytokines and eicosanoid
 Initial injury  local mast cells release nume
rous mediators (chief:cytokines and eicosanoid
s)
 Pro-inflammatory forms
 and anti-inflammatory forms
 Neural Response
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• Early
• TNF, IL-1, IL-6,PGE2, LT4 (leukotriene-4)
• TNF +PG+IL-1: acute phase response
▫ fever, acute phase protein synthesis, insulin resistan
ce
▫ Peak early and disappear from plasma
• Stimulate IL-6 release: reduce level of insulin-lik
e growth factor (IGF-1) proteolysis and amino
acid release from muscle, acute phase proteins
 Anti-inflammatory forms
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 Inflammatory stimulus controlled and eliminat

ed
 Anti-inflammatory cytokines
 IL-4, IL-10, IL-13, ecosanoids (PGE2,LT5)
 Bring inflammatory response to conclusion
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 Neurohormonal response
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 Neurohormonal response
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• Afferent stimuli to vagus nerve

▫ Cytokine (e.g. TNF-alpha, IL-1)
▫ Baroreceptors
▫ Chemoreceptors
▫ Thermoreceptors
• CNS: hypothalamus
• Parasympathetic: acetylcholine
▫ Reduces tissue macrophage activation
▫ Release of proinflammatory mediators (Anti-inflamma
tory pathways)
 Neurohormonal response
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• Glucagon, glucocorticoids and epinephrin

• Ebb phase
▫ Epinephrine: sympthoadrenal axis help to maintain pre
ssure, blood flow
• Flow phase
▫ Glucagon: glycogenolytic and gluconeogenesis
▫ Cortisol: mobilized amino acids from skeletal muscle an
d increases gluconeogenesis
▫ Catecholamines: glycolysis and gluconeogenesis, incre
ase lactate production form skeletal muscle, increase me
tabolic rate and stimulate lipolysis
 Acute phase proteins
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 Fibrinogen
 C-reactive protein
 Inhibit generalized tissue destruction from infl
ammation
 Volume loss and tissue hypoperfusion
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 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 acidosis
 Tissue damage, Pain and Fear
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 Injury of body tissue: most important factor ini

tiating stress response
 Afferent neural pathways from wound  hypot
halamus: injury occurred
 Tissue destruction sensed in conscious patient
as pain
 Stress response (pain and fear) Efferent path
ways from brain  catecholamine ”fight or fl
ight” response
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THE END
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