2. Factors affecting metabolic
response to trauma
• Severity of the injury
• Additional damage caused by subsequent
immune reactions
• Inadequate response / treatment
3. What is Metabolic response to injury?
TRAUMA SEPSIS SURGERY
METABOLIC
RESPONSE
Afferent neuronal input
>cytokines/modulators
4. Metabolic Response to
The Aim
Maintain Critical Organ function
Restore Homeostasis
Mobilize Energy reserves
Provide substrate for tissue repair
Repair of dysfunctional tissue
Eradicate sepsis
5.
6. Metabolic Response to Trauma- Fourth year Lecture- 1423-1424
Response to Injury
Cuthbertson
Ebb Phase Flow Phase
Injury
Catabolism
Anabolic
Death
Minutes Hours Days…………………Weeks
Energy
Temperature
O2 Consumption
7. Metabolic response to trauma
SUMMARY unmodified response
Phase Duration Role Physiological Hormones
Ebb 48 hrs maintenance of
blood volume;
catecholamines
decr. BMR, decr. Temp,
decr. O2 consumption;
vasoconstriction; incr.
CO, incr. HR; acute
phase proteins
Catecholamines
, Cortisol,
Aldosterone
Flow
Catabolic 3-10 days maintenance of
energy
incr. BMR, incr. Temp.,
incr. O2 consumption,
negative nitrogen
balance
Incr. glucagon,
insulin, cortisol,
catecholamines
- but insulin
resistance
Anabolic 10-60 days replacement of lost
tissue
positive nitrogen
balance
Growth
hormone, IGF
9. Mediators of Metabolic response
Endocrine
• Catecholamines
• Glucagon
• Insulin
• Cortisol
• Endorphins
• Growth hormone etc
Cytokins
• SOME CYTOKINES INVOLVED IN THE ACUTE
INFLAMMATORY RESPONSE
Cytokine Relevant actions
• TNF-a Pro-inflammatory; release of leucocytes
by bone marrow; activation of leucocytes and
• endothelial cells
• IL-1 Fever; T-cell and macrophage activation
• IL-6 Growth and differentiation of lymphocytes;
activation of the acute-phase protein response
• IL-8 Chemotactic for neutrophils and T cells
• IL-10 Inhibits immune function
• Others
• Complement factors
10. Metabolic Response to Trauma- Fourth year Lecture- 1423-1424
Factors influencing the Extent and Duration of the
Metabolic Response
Pain and Fear
Surgical Factors:
Type of surgery
Region
Duration
Preoperative support
Extent of the trauma and degree of resuscitation
Post traumatic complications:
Hemorrhage
Hypoxia
Sepsis and Fever
StarvationIleus
Re-operation
Pre-existing nutritional status
Age and sex
11. Metabolic response to trauma
• LOCAL RESPONSE
• Tissue damage leads to the activation
of neutrophils and macrophages
• SYSTEMIC RESPONSE
• Hemorrhagic shock induces ischemia
and this causes the tissue to change
its metabolism to anaerobic.
• During resuscitation, thus
reperfusion, oxygen is transported to
the ischemic area in the tissue and
radical oxygen species (ROS) are
formed. These ROS are chemo-
attractants and activators of
neutrophils .
• Polymorphonuclear granulocytes
(PMNs) have an important role in the
defense and debridement of the
injured tissue from the first 10
minutes until 3 days after injury
12. Clinical Spectrum of SIRS(T)
• Infection
– Identifiable source of
microbial insult
• SIRS = 2 or more:
– Temp ≥38˚C or ≤36˚C
– HR ≥ 90 bpm
– RR ≥ 20 breaths/min or
PaCO2 ≤ 32 mmHg or
mechanical ventilation
– WBC ≥ 12,000/µL or ≤
4000/µL or ≥ 10% band forms
• Sepsis/Trauma
– Infection + SIRS
• Severe Sepsis
– Sepsis + Organ Dysfunction
• Septic Shock
– Sepsis + Cardiovascular Collapse
(requires vasopressors)
14. Mediators of Metabolic response
• Cytokines and chemokines
• Complement factors
• Endocrine response
• 1st & 2nd Hit
15. What is the ‘CARS’
Like the systemic inflammatory response
syndrome (SIRS), the compensatory anti-
inflammatory response syndrome (CARS) is a
complex pattern of immunologic responses to
severe infection or injury. The difference is
that while SIRS is a proinflammatory response
tasked with killing infectious organisms
through activation of the immune system,
CARS is a global deactivation of the immune
system tasked with restoring homeostasis
16. The magnitude of the metabolic response is generally
proportional to the severity of tissue injury, but can be modified
by additional factors