THE PHYSIOLOGICAL IMPACT OF TRAUMA AND INFECTION The...
Transcript of THE PHYSIOLOGICAL IMPACT OF TRAUMA AND INFECTION The...
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JP Pretorius Head: Department of Critical Care
Head: Clinical Unit Surgical/Trauma ICU
University of Pretoria &
Steve Biko Academic Hospital
THE PHYSIOLOGICAL IMPACT
OF TRAUMA AND INFECTION
=
The Metabolic Response to
Stress
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Characteristics of Surgical Stress
• Hypermetabolism
• Protein catabolism
• Insulin resistance
• Salt and water sequestration
The metabolic response to stress ……
and much, much MORE !!!!!
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Metabolic Response
• BMR
• Negative Nitrogen balance
• Increased gluconeogenesis
• Increased synthesis of acute phase proteins
BUT.......how does this reaction or process evolve or develop ?
WHAT stimulates or initiates this change ?
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PEARLS!.....
• Injury and infection invoke a constellation of changes in the host
• A transitory ebb or shock or hypometabolic phase develops first (conservation, protection)
• This is followed by a flow or hypermetabolic phase
(mobilisation, preparation, self-preservation )
• The magnitude of the response is proportional to the extent of the injury
• Comorbid conditions will impact on the response
• Therapeutic procedures will impact on the response
Will modulation of the stress response benefit or improve survival ?
A Constellation of Changes in the Host
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How are the different components of this
composite and intricate process related ?
… the “psycho-”
to the “neuro-”
to the “endocrine-”
to the “metabolic-”
to the “immunologic” component ????
Does it reflect order or chaos?
What does getting sick means?
A Constellation of Changes in the Host
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The
Psycho-neuro-endocrino-immune
response
=
A total body, all systems, all cells
compensatory response intent on
self-preservation
= Host defense!
= Maintenance of HOMEOSTASIS
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Schema of the metabolic response to stress
Cellular
metabolism
Acute
Phase
Response
Intermediary
metabolism
receptors
Glucocorticoids
adrenal
pituitary
Hypothalamus Afferent
Neuronal
impulses
ILLNESS
INJURY
INFECTION
Cytokine
release
endocrine
effects
paracrine
metabolism
Catecholamines
sympathetic
nervous
system
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Components involved in the development of
the Coagulopathy of Trauma
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Visceral
Humoral
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Cytokine link to Metabolic + Immune reactions
= metabolic fuel
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BUT……..
The process can go the wrong way !
(Murphy’s 1st law ?)
TIME TO SOURCE CONTROL !!!!!
Prevention is the best cure for MODS + MOF
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C H A O S
INITIAL INSULT
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HOST DEFENSE
“Psycho-neuro-endocrino-immunology”
Controlled, Balanced Integration of:
• Neuro-endocrine response
• Metabolic and biochemical adaptation
• Inflammatory response
• Immunological reactions in blood and tissue
“General Adaptation Syndrome”
Hans Selye
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STRESS RESPONSE
The Threat:
Shock Resuscitation Hypermetabolism MODS MOFS
The Solution:
Tissue oxygen delivery Cell metabolic regulation
= perfusion deficit = substrate deficit
Cardiopulmonary resuscitation Metabolic resuscitation
Cell metabolic regulation Tissue oxygen delivery
Resuscitation in progress
Early…………Transition in emphasis over time………...Later
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HOMEOSTASIS
SUCCESSFUL SUPPORTIVE THERAPY
FOR CRITICALLY ILL PATIENTS
DEPENDS ON METABOLIC
RESUSCITATION
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Characteristics of Metabolic Phases Occurring After
Severe Injury
Ebb Phase Response
“Conservation”
Flow Phase: Acute
Response
“Preparation”
Flow Phase: Adaptive
Response
“Rebuilding”
Hypovolemic Shock
↓ tissue perfusion
↓ metabolic rate
↓ oxygen consumption
↓ blood pressure
↓ body temperature
Catabolism predominates
↑ glucocorticoids
↑ glucagon
↑ catecholamines
Release of cytokines,
lipid mediators
Production of acute
phase proteins
↑ excretion of nitrogen
↑ metabolic rate
↑ oxygen consumption
Impaired utilization of fuels
Anabolism predominates
Hormonal response
gradually diminishes
↓ hypermetabolic rate
Associated with recovery
Potential for restoration
of body protein.
Wound healing depends in
part on nutrient intake
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+110
+80
+100
+50
-20
+90
+20
+70
+60
+30
+10
Normal
-40
+40
-10
-30
Third degree burns
>20% BSA
Head injury
Severe infection
Multiple fractures
Postoperative
Partial starvation
Effects of injury, sepsis and nutritional depletion on
resting energy expenditure
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Pro-& anti
Inflammatory
Cytokine biology
Heat
Shock
proteins
Immune
function
Transcription
factors
Oxidant/
Antioxidant
balance
Interorgan
Substrate flow
Clinical
outcome
Effect of genotype
Modulation by nutrients
Genetic Influences
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The Latest on Inflammation !
• Human genome project
• Baseline level of preconditioning
= ability of the host to tolerate and respond
to an insult without severe disturbance to homeostasis
• Degree of preconditioning
• Simultaneous pro- and anti-inflammatory responses
Suliburk et al Eur Surg Res 2008; 40: 184 - 189
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Gut as Motor of MODS - A Vicious Circle?
Intra-abdominal
Pressure
Mucosal
Breakdown
(Multi-System Organ Failure)
Bacterial translocation
Acidosis
Decreased O2 delivery
Anaerobic metabolism
Capillary leak
Free radical formation
MSOF
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The Mucosal Barrier: Is It the Motor
for MOF ?
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The Latest on Inflammation !
• Despite improvement in care, Multiple Organ Failure
continues to cause significant morbidity + mortality
• “Shock” >>>organ ischaemia>>>critical for
development of MODS + MOF
• MOF is a gut-derived phenomenon
70’s+80’s > improved resuscitation > ICU > MOF epidemic
• 90’s > understanding of MOF improves outcome – still
the prime cause of ICU deaths + prolonged stay
• Roles of Trauma + Sepsis > early and late MOF
Suliburk et al Eur Surg Res 2008; 40: 184 - 189
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View of MOF in the 1990s: dysfunctional inflammation causes MOF.
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Current evolving view of MOF: unbalanced early pro-inflammation.
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Alternative intervention to balance anti-inflammation will enhance preconditioning,
Leading to improve healing that will enable patients to recover. Alternative treatments
include use of ketamine as a sedative/analgesic agent, immune enhancing nutritional
modulation, liberal use of fresh frozen plasma, and body temperature maintenance
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Global view of shock. Shock is common to trauma, bleeding and sepsis, with each
sharing some common biologic pathways with the other as well as a possessing their own
unique characteristics and treatments.
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The “psycho-neuro-immuno-endocrine response” to injury
or infection functions to enhance the possibility of survival
without treatment
CONCLUSION
RF Grimble
1
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Survival of an individual often depends on the effectiveness
of regulatory systems in changing the priority given to
different physiologic processes, particularly those that exert
a large metabolic demand
2
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For the infected individual, marshalling of resources to
combat invading pathogens must assume a priority over
all other physiologic demands.
3
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After the invasion has been repulsed and the damaged
done by the invader repaired, priorities normally given
to other physiological processes can be restored.
4
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The high priority given to combating pathogens is
necessary because of the speed with which pathogens
multiply after they are established within the host.
5
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Clearly, the provision of nutrients to allow the immune
system to function correctly cannot be left to chance.
Thus, cytokines act as modulatory agents by which the
activity of the system is changed and metabolic activity of
the host is direct toward providing nutrients for the system.
6
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The enhanced production of cytokines and oxidants, which
follows pathogenic invasion and injury, although designed
to combat the invader, carries the potential to damage the
host. Damage is limited by concurrent enhancement of the
antioxidant defenses of the host and activation of systems
for retaining cytokine production within healthful confines,
as discussed earlier.
7
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The future challenge for the clinician and scientist
working within the field of nutrition will be in
determining how the nature of the nutrient-cytokine
interactions, identified in the experimental context, can
be used to achieve a healthful diet and clinical benefit.
8
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MUST READ’s !!!
1. The Gut in Systemic Inflammatory Response Syndrome and
Sepsis - Enzyme Systems Fighting Multiple Organ Failure
J. Suliburk et al
Eur Surg Res 2008;40:184–189
2. Damage Control Resuscitation: The New Face of Damage
Control
Juan C. Duchesne et al
The Journal of TRAUMA® Injury, Infection, and Critical Care •
Volume 69, Number 4, October 2010
3. Enhanced Recovery After Surgery: The Future of Improving
Surgical Care
Krishna K. Varadhan et al
Crit Care Clin 26 (2010) 527–547