HORMONAL & METABOLIC RESPONS

TO TRAUMA

RONNY B,drg*,
DAVID B. K.drg.SpBM**
During Trauma ~ Tissues maybe
Injured :
Directly by mechanical forces,
physical factors (extreme heat,cold
&radiation)
Indirectly by distrurbances of blood
supply
Physiologic Response to Injury
Metabolic response :
CUTHBERTSONS TWO PHASE
(Ebb phase, Flow phase ( catabolic
& anabolic )
4 Phase metabolic response
shock phase resuscitation phase
hyper metabolic phase (post injury)
- MODS
* otmar L.T.:AO principles of fracture
management 2000 Thieme-sthgart
newyork p 662
Stress
Fear Cortex
Pain

Endotoxin
Temperature Hypot
Pituitary

Blood volume
fluid shifts
Hypoxemia
Hypercapnea Acidosis Receptors Brain Stem
Autonomic

Tissue Injury
Cortex
Hypothalamus Pituitary
Brain Stem Autonomic Centers
Efferent Stimuli :
efferent response to re establish homeostasis
by restitution of :
The effective circulating plasma volume
To provide fuel
To maintain vital organ function

Autonomic Nervous System catecholamines :
Non epinephrine
Epinephrine
A1 mediated peripheral vasoconstrictor

B1 mediated heart rate & contractility

Hormonal response : ant pituitary
Insulin
Glucagon
Corticotropin
Vasopressin ( antidiuretic hormone)
Growth hormone
Thyroxine

Systemic mediators :
(mediators release after injury w/ local & systemic effect ,as
result of reperfusion, lead to aplification of the inflammatory
response)

Complement
Oxygen radicals
Cytokines
Eicosanoids
Nitrit oxide (NO)
METABOLIC RESPONSE
CUTHBERTSONS TWO PHASE :
EBB PHASE :
Occurs initially after injury
Characterized by : physiologic response to restore
tissue perfusion & circulating blood volume
FLOW PHASE :
Begins once the patient is successfully
resuscitated
Sub divided :2 phases
* CATABOLIC PHASE:
- From days week
- Characterized by : hyperdynamic response to
trauma
* ANABOLIC PHASE :
- begins after wounds have closed
- characterized by return of normal homeostasis

4 PHASE METABOLIC RESPONSE :
1. Shock phase : characterized by hypoperrfusion secondary to
hemorrhage & tissue injury

2. Resuscitation phase :
Is seen w/ active vol. resuscitation &
operation to control hemorrhage
Characterized by : elaboration of many inflammatory mediators.

3. Hyper metabolic phase (post injury) :
Similar to catabolic phase
Characterized by sympathetic & adrenal response
Acutely , this serves to protect the individual
Prolonged & sustained this phase SIRSMODS

4. MODS :
Over expression of injury induced inflammatory mediators or
development of infections complications
most cause of late death in trauma ICU
The Journal of Bone & Joint., JBJS.ORG
Vol 87A,No2 Feb 05
Diagnosa :
Two or more following clinical finding
1. Body themperature > 38
0
C or < 36
0
C
2. Tachycardia ( HR >90 beats/min)
3. Tachypnea ( RR>20/min)
( Pa CO
2
<32 mm HG)
4. Leucocytonis / WBC > 12.000 cell/mm
3
5. Leucopenia ( WBC 4000 cells/mm
3
)
or significant bondemia>10% immature
neutrophil Sepsis SIRS + this result of
confirmed infection process.
FOLLOWING TRAUMA :
Px anegic post traumatic
sepsis
( Immunosepsis effect of
trauma )
Prod. of immunoglobulin
Neutrophil chemotaxis
Phagocytosis
Lysosomal enzyme content
CYTOKINES THAT ARE IMPORTANT
INFLAMATORY MEDIATORS
Interleukin(IL) ----- IL
1
, IL
2
, IL
3
, IL
4
, IL
5
, IL
6
, IL
7
, IL
8
, IL
9
, IL
10
,
IL
11
, IL
12
, IL
13
, IL
18


Tumor Necrosis Factors (TNF)---TNF
,Lymphotoxin (LT)

Interferon (IFN)--------- IFN , IFN , IFN

Colony Stimulating Factors (CSF)---
GCSF,MCSF,GM,CSF
the Journal of Bone & Joint
.,.JBJS.ORG,Vol 87A,No2,Feb 05

During the Struggle Lethal Triad
for surgical control - metabolic acidosis
of - bleeding - hypothermia
- repeated bouts of - coagulopathy
hypotension
- physiologic instability

ICU for physiologic
restoration


Level I
Trauma Center
Late definitive repair
Damage
Control
Damage Control : 3 distinct phase
1. Abbreviated Surgical Control of
hemorrhage and contamination
2. Continued and complex
resuscitation in the ICU
3. Definitive repair and reconstruction
Technical Consideration of Damage Control
Phase I : Establishing control & knowing when to stop

1. Hemorrhage control ( vascular clamps, suture ligature, temporary
vascular shunting, Avoid complex repair of bleeding solid injuries,
interventional radiology for complex bleeding.

2. Contamination Control
Control bellow viscus injuries for ligament
Simple repair
Gastro story or jejunostomy tubes
Debridemant open fractures.

3. Packing
Apply laparotomy pads over all dissected surfaces and any solid organ injuries (over
pack off abd.carity)

4. Abdominal Closure
Towel clip closure, continuous suture
Bogota bags
Phase II Secondary Resuscitation : Breaking the
vicious cycle
1. Maximization of hemodynamics
2. Core Re warning
3. Coagulopathy correction

Phase III : second operation
Re inspection and reconstruction

Damage control :
require exquisite surgical judgment
When attempting to resuscitate PX in ICU :
Recognition of failed surgical control of bleeding
and the need for re exploration is essential
Priorities and Timing of Surgery Depending on
Physiological Status
Physiological Status Surgical Intervention Timing
Responds to
Resuscitation
(-)live saving surgery
(?)DAMAGE
CONTROL
(+) Delayed
Primary Surgery
Day I
Hyper inflammation Second look only Day 2-3
Window of Opportunity Scheduled definitive
surgery
Day 5-10
Immunosuppression No Surgery !
Recovery Secondary reconstructive
surgery
Week 3
Thank You