This document discusses homeostasis and the body's metabolic response to injury. It covers several key points: 1. Homeostasis aims to maintain constant internal conditions. Injury triggers a metabolic response involving hormones, cytokines, and cells to restore homeostasis. 2. The response has acute and chronic phases. The acute phase involves increased catabolism to provide energy, while the chronic phase sees increased anabolism to aid recovery. 3. Physiological changes include increased heart rate and breathing as well as weight loss. Clinical signs are fever, inflammation, and loss of appetite. Laboratory findings show immune cell changes and altered protein and glucose levels. 4. Factors like hypothermia, pain, starvation,

2. Homeostasis - Concept
Components of Responses
Mediators of Responses
Phases of Responses & Keyelements
Factors – Exacerbate & Avoidable

3.  Maintenance of nearly constant conditions
in the internal environment.
 Essentially all organs and tissues of the
body perform functions that help maintain
these constant conditions.

4. Homeostasis is the foundation of normal
physiology.
 Stress-free peri-operative care helps to restore
homeostasis following elective surgery.
 Resuscitation, surgical intervention & critical care
can return the severely injured patient to a
situation in which homeostasis becomes possible
once again.

5.  Metabolic response to injury is Gradedand
evolves with time
 the more severe the injury,
the greater the response Immunological
Hormonal
Cellular
response

8.  Physiological Consequences
 Metabolic Manifestations
 Clinical Manifestations
 Laboratory Changes

9. METABOLIC
 Hypermetabolism
 Acclerated
Gluconeogenesis
 EnhancedProtein
breakdown
 IncreasedFat
oxidation
PHYSIOLOGICAL
↑ Cardiac Output
↑ Ventilation
↑ Membrane
Transport
Weightloss
WoundHealing

10. CLINICAL
Fever
Tachycardia
Tachypnoea
Inflammation
Anorexia
LABORATORY
Leucocytosis/Leucopenia
Hyperglycemia
Elevated CRP/Alteredacute
Presenceof wound or phase reactants
Hepatic/Renaldysfunction

11. Mediators of Injury Response
Neuro – Endocrine [ Hormonal ]
Immune System [ Cytokines ]

12. Biphasic :
Acute phase - An actively secreting pituitary & elevated
counter regulatory hormones (cortisol, glucagon,
adrenaline).Changes are thought to be beneficial for shortterm
survival.
Chronic phase - Hypothalamic suppression & low serum levels
of the respective

14. CRF ACTH CORTISOL
ADRENALIN &
GLUCAGON
METABOLIC
RESPONSE
15

15.  Provide essential substrates for survival
 Postpone anabolism
 Optimize host defense

16. Proinflammatory
phase
Counter regulatory
phase
IL-1, IL-6, TNF-alpha
Hypothalamus → pyrexia
Hepatic acute phase protein
IL-1 receptor antagonist (IL-
1Ra) and TNFsoluble receptors
(TNF-sR-55 and 75)
Prevent excessive
proinflammatory activities
Restore homeostasis
COMP.ANTI-INFLAMMATORY
RESPONSESYNDROME
{CARS}
SIRS
MODS

17. EBB FLOW RECOVERY
SHOCK
CA
TABOL
ISM
ANABO
LISM
24-48 HRS
Hours
3-10 DAYS
Days Weeks
BREAKING DOWN
ENERGYSTORES
BUILDING UP

18. Phase Duration Role Physiological Hormones
Ebb 24 - 48
hrs
Conserve - blood
volume & energy
reserves - Repair
↓ BMR, ↓ temp, ↓
CO, hypovolaemia,
lactic acidosis
Catecholamines
, Cortisol,
aldosterone
Flow
Catabolic 3 – 10
days
Mobilisation of
energy stores –
Recovery & Repair
↑ BMR, ↑ Temp, ↑ O2
consump, ↑ CO
Cytokines + ↑
Insulin,
Glucagon,
Cortisol,
Catechol but
insulin
resistance
Anabolic 10 – 60 Growth
hormone, IGF
da1y4-s03-2016
Replacement of lost
tissue +ve Nitrogen balance
1
9

19. Hypermetabolism
Alterations in skeletal muscle
protein
Alterations in Liver protein
Insulin resistance

20. Majority of trauma patients - energy expenditureappr.
15-25% > predicted healthy resting values.
Factors which increases this metabolism :
* Central thermodysregulation
* Increased sympathetic activity
* Increased protein turnover
* Wound circulation abnormalities

21. 14-03-2016 Metabolic Responseto Injury-Dr.R.Durai
1. Muscle wasting – result of ↑ muscle protein degradation
+ ↓ muscle protein synthesis. (RS& GIT).Cardiac muscle is
spared.
2. Is mediated at amolecular level mainly by activation of
the ubiquitin-protease pathway.
3. Lead - Increased fatigue, reduced functional ability,
↓QOL & ↑ risk of morbidity & mortality.

22. Cytokines – IL- 6 ↑ Synthesis of Positive
acute phase proteins : Fibrinogen & CRP
Negative acute reactants :Albumin decreases
Not Compensated

23. Hyperglycaemia is seen – ↑ glucose
production + ↓ glucose uptake – peripheral
tissues. ( transient induction of insulin
resistance seen )
Due – Cytokines & decreased responsiveness
of insulin- regulated glucose transporter
proteins.
The degree of insulin resistance is ∞ to
magnitude of the injurious process.

24. Main labile energy reserve in the body is
fat
Main labile protein reserve in the body is
skeletal muscle
While fat mass can be reduced without
major detriment to function, loss of
protein mass results not only in skeletal
muscle wasting, but also depletion of
visceral protein mass

26. 6.25 g of protein, which is contained in approximately 36
g of wet weight tissue.
Thus the loss of 1 g of nitrogen in urine is equivalentto
the breakdown of 36 g of wet weight leantissue.
Protein turnover in the whole body is of the order of150-
200 g per day.
A normal human ingests 70-100 g of protein per day,
which is metabolized and excreted in urine as ammonia
and urea(14 g N/day)

27. During total starvation, urinary loss of nitrogen is rapidly
attenuated by a series of adaptive changes
Loss of body weight follows a similar course , thus
accounting for the survival of hunger strikers for a period of
50-60 days
Following major injury, and particularly in the presence of
ongoing septic complications , this adaptive change fails to
occur, and there is a state of auto cannibalism , resulting in
continuing urinary nitrogen losses of 10-20 g/day(500 g lean
tissue/day)
As with total starvation, once loss of body protein mass has
reached 30-40 % of the total, survival is unlikely

28. resuscitation,
<24 hrs – Body weight increases due to extracellular water
expansion by 6-10 litres.
This can be overcome by careful intra operative management
of fluid balance
1-10 days –Total body protein will diminish by 15% and body
weight will reach negative balance asthe expansion of extra
cellular space resolves
This can be overcome by blocking Neuro endocrine response
with epidural analgesia and early enteral feeds

29. Factors - ↑ response to injury
30
Hypothermia
Pain
Starvation
Immobilisation
Sepsis
Hypotension

30. 31

31.  Continuing haemorrhage
 Hypothermia
 Tissue oedema
 Tissue underperfusion
 Starvation
 Immobility
Avoidable factors that compound the response to
injury

32. Volume loss : Careful limitation of intra operative
administration of colloids and crystalloids so that
there is no net weight gain.
Hypothermia : RT – maintaining normothermia by
an upper body forced air heating cover ↓ wound
infection, cardiac complications and bleeding and
transfusion requirements.
eeding and

33. Administration of activated protein C - to critically ill
patients has been shown to ↓ organ failure and death.
It is thought to act, in part, via preservation of the
micro circulation in vital organs.
Maintaining the inormoglycemia with insulin infusion
during critical illness has been proposed to protect the
endothelium and thereby contribute to the prevention
of organ failure and death.

34. Starvation :During starvation, the body is faced
with an obligate need to generate glucose to
sustain cerebral energy metabolism(100g of
glucose per day).
Provision of at least 2Lof IV 5%dextrose for
fasting patients provides glucose as above.

35. Tissue oedema : is mediated by the variety of
mediators involved in the systemic inflammation.
Careful administration of anti-mediators & reduce
fluid overload during resuscitation reduces this
condition.
Immobility : Has been recognized as a potent
stimulus for inducing muscle wasting. Early
mobilization is an essential measure to avoid muscle
wasting.

36. Minimal access techniques
Minimal periods of Starvation
Epidural analgesia
Early mobilization