Traumatic shock

1. TRAUMATIC SHOCK

AISYAH DAHIYAH BINTI AB WAHAB
GROUP 19
PATHOPHYSIOLOGY DEPARTMENT

2. definition

DEFINITION
• Shock it is a severe disturbance of hemodynamic in
which the circulatory system fails to maintain
adequate perfusion of vital organ.
• Traumatic shock is characterized by severe tissue.
damage, such as multiple fractures, severe
contusions, or burns.

3. Shock in trauma

SHOCK IN TRAUMA
• Classification
1. Hypovolemic
2. Distributive
3. Cardiogenic

4. Hypovolemic shock

HYPOVOLEMIC
SHOCK
MOST COMMON CAUSE OF SHOCK IN
T H E T R A U M A PAT I E N T
1. DUE TO HEMORRHAGE ( LOSS OF
R B C S I M PA I R S O X Y G E N
T R A N S P O R TAT I O N
2 . I N A N Y T R A U M A PAT I E N T W I T H
SHOCK, ASSUME HAEMORRHAGE IS
CAUSE UNTIL PROVEN OTHERWISE

5. Distributive shock

DISTRIBUTIVE
SHOCK
• NEUROGENIC SHOCK
1 . D E C R E A S E D S Y S T E M I C VA S C U L A R
R E S I S TA N C E D U E T O VA S O D I L AT I O N
2. MOST COMMON CAUSE IN SPINAL
CORD INJURY

6. Cardiogenic shock

CARDIOGENIC SHOCK
• INTRINSIC
1. BLUNT CARDIAC TRAUMA LEADING
TO MUSCLE DAMAGE AND
DYSRHYTHMIA
2 . VA LV U L A R D I S C R U P T I O N
EXTRINSIC
1 . P E R I C A R D I A L TA M P O N A D E
2. TENSION PNEUMOTHORAX

7. Traumatic shock mechanism

TRAUMATIC SHOCK MECHANISM
• Microcirculation –Systemic vascular resistance rises to maintain a level of systemic
pressure that is adequate for perfusion of the heart and brain at the expense of other
tissue. Arteriolar vascular smooth cells has both α- and β–adrenergic receptors.
Norepinephrine release - acting on α 1 -receptors as vasoconstrictor - is the
fundamental compensatory response in shock. –Reduced filtration because of
decreased capillary surface area across which filtration occurs.
• Consequence: increased interstitial and intravascular volume at the expense of
intracellular volume.

8. Traumatic shock mechanism

TRAUMATIC SHOCK MECHANISM
• Cellular response –Decline of intracellular high energy phosphate stores (decreased
amount of ATP) because of the mitochondrial dysfunction.
• Consequences: Accumulation of hydrogen ions, lactate (products of anaerobic
metabolism) As shock progresses, these vasodilatation metabolites cause further
hypotension and hypo perfusion

9. Traumatic shock mechanism

TRAUMATIC SHOCK MECHANISM
• Cardiovascular response –Decreased ventricular filling (decreased preload). The
increased heart rate is a useful but limited compensatory mechanism to maintain the
adequate stroke volume –Impaired myocardial contractility which reduces the stroke
volume –Elevated systemic vascular resistance (except of hyper dynamic stage of
septic shock) increases the afterload

10. Traumatic shock mechanism

TRAUMATIC SHOCK MECHANISM
• Pulmonary response –Increased pulmonary vascular resistance (particularly in septic
shock) –Tachypnoe, but restricted ventilation, reduced functional residual capacity –
atelectasis. –Acute respiratory distress syndrome characterized by noncardiogenic
pulmonary oedema secondary to pulmonary capillary endothelial and alveolar
epithelial injury

11. Traumatic shock mechanism

TRAUMATIC SHOCK MECHANISM
• Renal response –Consequences of hypo perfusion: reduced renal blood flow,
increased afferent arteriolar resistance – reduced glomerular filtration rate together
with the increased aldosterone and vasopressin production will cause reduced urine
volume –Acute tubular necrosis as a result of interaction of shock, sepsis and
administration of nephrotoxic agents

12. Traumatic shock mechanism

TRAUMATIC SHOCK MECHANISM
• Inflammatory responses –Activation of an extensive network of proinflammatory
mediator systems plays a significant role in the progression of shock and contributes to
the development of organ injury Activation of classic and alternative pathways of
complement cascade causing cell damage Activation of coagulation cascade causes
microvascular thrombosis Tumour necrosis factor-α, produced by activated
macrophages contributes to hypotension, lactic acidosis, and respiratory failure IL-8
upregulate adhesion molecules on the neutrophil to enhance aggregation, and damage
to the vascular endothelium Increased Thromboxane A 2 levels is potent
vasoconstrictor that contributes to the pulmonary hypertension

13. Clinical manifestation

CLINICAL
MANIFESTATION
1. PRESENCE OF PERIPHERAL AND
PULMONARY EDEMA
2. INFUSION OF LARGE VOLUME FLUID
W H I C H M AY B E A D E Q U AT E F O R P U R E
H Y P O V O L E M I C S H O C K I S U S U A L LY
I N A D E Q U AT E F O R T R A U M AT I C S H O C K
3 . TA C H Y C A R D I A A N D TA C H Y P N E A
4. WEAK, THREAD PULSES
5. HYPOTENSION
6. COOL AND CLAMMY SKIN
7 . M E N TA L S TAT U S C H A N G E S
8. DECREASES URINE OUTPUT (DARK
A N D C O N C E N T R AT E D )

14. Treatment and management

TREATMENT AND
MANAGEMENT
P R E - H O S P I TA L C A R E :
1. EXTERNAL BLEEDING SHOULD BE
CONTROLLED BY DIRECT PRESSURE
2 . I M M O B I L I Z AT I O N PAT I E N T
3 . S E C U R I N G A D E Q U AT E A I R W AY S
4 . E N S U R I N G V E N T I L AT I O N
5 . M E D I C AT I O N T O I N C R E A S E T H E
HEART PUMPING ABILITIES
( D O B U TA M I N E , E P I N E P H R I N E , N O R E P I
NEPHRINE)

15. Thank you

THANK YOU