1. METABOLIC
RESPONSE TO
TRAUMA

2. What is
trauma??
It is defined
as cellular
disruption
caused by an
exchange
with
environmental
energy that is
beyond the
body’s
resilience

3. Introduction

Altered homeostasis
The body system acts to maintain internal
constancy.
 The co-ordinated physiological process
which maintains most of the steady states
of organisms.
 Response is benificial,allows healing and
survival.


4. Response to Injury
Following elective surgery there is rise in
temp.,HR,RR,energy expenditure and
peripheral WBC.
 Following trauma/sepsis response is
accentuated causing SIRS,hypermetabolism,catabolism,shock and
MODS.


5. Mediators involved

Stress response is driven by afferent
nociceptive neurons,the spinal
cord,thalamus,hypothalamus and
pituitary.

6. PLASMA
ADIPOCYTE,
LIPOLYSIS
ACTH,GH
HEPATIC
GLUCONEIG
ENESIS
HYPOTHALAMUS
CRF
PITUITARY
ADRENAL
ADRENALINE,
CORTISOL
PANCREAS
GLUCAGON
ss
Injury
adaptive
immune
system
innate
immune
system
IL-1
TNFα
IL-6
IL-8
INSULIN
IGF-1
TESTOSTERONE
T3
SKELETAL
MUSCLE
DEGRADATI
ON
HEPATIC
ACUTE
PHASE
PROTEIN
SYNTHESIS,
PYREXIA,
HYPERMETA
BOLISM

7. Phases of response
The ‘ebb’ and ‘flow’ phases.
INJURY
ebb phase flow phase recovery

hours
days
weeks

8. The ebb phase
First 24-48 hrs.
 Hypovolaemia,decreased metabolic rate,
reduced cardiac output,hypothermia and
lactic acidosis.
 By catecholamines,cortisol and
aldosterone
 Degree on amt. of blood loss and somatic
afferent nerves at site of injury.(with acti

9. -vation of renin angiotensin system.
 ROLE—to conserve both circulatory
volume and energy stores for recovery.


10. The FLOW phase
Hypermetabolic phase corresponding to
SIRS.
 Involves mobilisation of body energy stores
recovery and repair,replacement of lost
tissues.
 Tissue oedema,incd basal metabolic
rate,cardiac output,temp.,o2
consumption,leucocytosis and
gluconeogenesis


11. CATABOLIC phase of flow
phase
Counter regulatory
hormones(catecolamines,cortisol,insulin,
glucagon) and inflammatory
mediators(IL-1,6,TNFα) causing fat and
protein metabolism leading to weight
loss and nitrogen excretion.
 Insulin resistance and poor glycaemic
control


12. Change in fluid composition
Loss of protein mass results in skeletal
muscle wasting and depletion of visceral
protein status.
 1gm of nitrogen has 6.25gm of protein ie.
About 36gm of wet tissue weight.
 In starvation nitrogen loss is
compensated by adaptive changes,but


13. during sepsis it fails and a state of
autocannibalism occurs causing loss of
10-20gm of nitrogen per day ie. 500gm
of wet tissue weight.
 Balance can be maintained by epidural
analgesia and early enteral feeding.


14. Effects of PAIN
Stimulates ADH release-acts directly on
kidneys causing fluid retentiondecreased pulse pressure stimulates JG
apparatus and activates R-A system in
turn causing inc. release of aldosterone.
 Aldosterone reabsorbs Na and water—
oliguria-peripheral oedema,visceral
oedema-delayed gastric emptying,food
intake.


15. Avoidable factors
Continuing haemorrage
 Hypothermia
 Tissue oedema
 Tissue underperfusion
 Starvation
 Immobility


16. 
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