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SHOCK IN TRAUMA
PATIENT
Dr. Md. Sabbir Ahamed
Honorary Medical Officer
Surgery Casualty Block-02
Dhaka Medical College Hospital
SHOCK
Shock is a systemic state of low tissue
perfusion that is inadequate for normal
cellular respiration
Pathophysiology of Shock
Cellular:
Reduced tissue perfusion
From aerobic to anaerobic metabolism
Systemic metabolic acidosis
Intracellular lysosomes release autodigestive enzymes
Cell lysis
Pathophysiology of Shock
Microvascular:
Tissue ischaemia progress
Activation of immune & coagulation system
Hypoxia & acidosis activate complement & prime neutrophil
Generation of oxygen free radical & cytokine release
Injury to capillary endothelium leads to
loss of it’s integrity & it becomes leaky
Pathophysiology of Shock
Systemic:
1. Cardiovascular
2. Respiratory
3. Renal
4. Endocrine
5. Ischaemia- Reperfusion Syndrome
Pathophysiology of Shock
Ischaemia-reperfusion syndrome:
Tissue Hypoperfusion, Hypoxia
Activation of cellular & humoral elements
(complement, neutrophil, microvascular thrombi)
When normal circulation is restored these are flushed back into circulation & causes further
endothelial injury and organ damage
acute lung injury
acute renal injury
multiple organ failure
Death
Types of Shock
1. Hypovolaemic shock
2. Cardiogenic shock
3. Obstructive shock
4. Distributive shock –
* septic shock
* anaphylactic shock
* neurogenic shock
5. Endocrine shock
Stages of Shock
 Initial Stage
 Compensatory Stage
 Progressive Stage
 Irreversible Stage
Stages of Shock
 Initial Stage
 Compensatory Stage
 Progressive Stage
 Irreversible Stage
Stages of Shock
Initial Stage:
• Initially, the body compensates with the onset of shock.
• No changes are noted clinically.
• Changes are beginning to occur on the cellular level.
Stages of Shock
 Initial Stage
 Compensatory Stage
 Progressive Stage
 Irreversible Stage
Stages of Shock
Compensatory Stage:
• Fluid shift from interstital to intravascular space.
• Activation of SNS - activation of epinephrine and norepinephrine.
• Kidneys release renin into blood, formation of angiotension & release of
aldosterone, ADH.
Stages of Shock
 Initial Stage
 Compensatory Stage
 Progressive Stage
 Irreversible Stage
Stages of Shock
Progressive Stage:
• Vicious circle of compensation eventually leads to decompensation.
• Blood pressure starts to fall - SBP below 80 is considered danger signal.
Tachycardia;
Tachypnea;
Decreased urine output;
Decreased body temperature; cold, pale clammy skin.
Stages of Shock
 Initial Stage
 Compensatory Stage
 Progressive Stage
 Irreversible Stage
Stages of Shock
Irreversible Stage:
• Body attempts at compensation have failed
• Pooling and sludging of blood; thrombosis of small vessels occurs.
• Tissue hypoxia and anoxia occur - lactic acid accumulation contributes
to cell death.
Severity of Shock
Shock in Trauma Patients
Shock is a common and frequently treatable cause of death in
injured patients and is second only to traumatic brain injury as
the leading cause of death from trauma.
ATLS (ADVANCED TRAUMA LIFE SUPPORT)
When a Patients Arrives
PRIMARY SURVEY- cABCDE
c- Exsanguinating external haemorrhage from massive arterial bleeding needs to be controlled even
before the airway is managed.
A- Airway with cervical spine control (maintain cervical spine stabilization when appropriate)
B- Breathing and ventilation assessment (maintain adequate oxygenation)
C- Circulation and haemorrhage (control haemorrhage and maintain adequate end-organ perfusion)
D- Disability assessment (perform basic neurologic evaluation by GCS)
E- Exposure, with environmental control (undress patient and search everywhere for possible injury,
while preventing hypothermia
Is the patients in Shock??
Blood pressure- Not reliable ….
(BP falls when 30% blood volume is lost )
Look for-
Pulse Rate
Respiratory rate
Urinary output
Conscious level
ANY INJURED PATIENT WHO IS COOL & HAS TACHYCARDIA IS
CONSIDERED TO BE IN SHOCK UNTIL PROVEN OTHERWISE
Haemorrhagic Shock??
• Try to find source----
Chest
Abdomen
Pelvis
Extremities
Any external bleeding
What to do?
First we resuscitate the patent. Then-
1. Focussed Assessment Sonography in Trauma (FAST)
2. X-ray chest, abdomen & pelvis
3. USG
4. Whole body CT scan (WBCT) –It is the gold standard
investigation for trauma patient.
Haemorrhagic Shock
• Advanced Trauma Life Support (ATLS) manual describes four classes
of hemorrhage to emphasize the early signs of the shock state.
• The adult human has approximately 5 litres of blood ( 70ml/kg children
& adults, 80ml/kg neonates)
• Volume replacement is determined by patient’s response to initial
therapy
• Haemorrhage control & balanced fluid resuscitation must be initiated
when early S/S of blood loss are apparent or suspected- NOT WHEN BP
IS FALLING OR ABSENT.
• Bleeding patients needs blood- BLOOD FOR BLOOD
Class I Haemorrhage
● Blood volume loss upto 15 percent.
• The heart rate is minimally elevated or
normal, and there is no change in blood
pressure, pulse pressure, or respiratory rate.
• Usually don’t require blood
Class II Haemorrhage
• 15 to 30 percent blood volume loss
• Manifested clinically as Tachycardia (heart rate of 100 to 120),
Tachypnea (respiratory rate of 20 to 24),
• Decreased pulse pressure, although systolic blood pressure changes
minimally if at all.
• Skin may be cool and clammy, and capillary refill may be delayed.
• Mx- most stabilized with crystalloid, few may require blood.
Class III Haemorrhage
• 30 to 40 percent blood volume loss, resulting in a significant
drop in blood pressure and changes in mental status.
• Any hypotension (SBP less than 90 mmHg) or drop in BP
greater than 20 to 30 percent of the measurement at
presentation is cause for concern.
• Heart rate (≥120 and thready) and RR are markedly elevated,
while urine output is diminished. Capillary refill is delayed.
• Mx- Stop BLEEDING & BLOOD TRANSFUSION.
Class IV Haemorrhage
• More than 40 percent blood volume loss
• LIFE THREATENING….
• Patients are hypotensive ( SBP less than 90 mmHg).
• Pulse pressure is narrowed (≤25 mmHg) and tachycardia is
marked (>120).
• Urine output is minimal or absent.
• The skin is cold and pale, and capillary refill is delayed.
• Mx- Rapid fluid transfusion and surgical intervention
depending on initial fluid response
Fractures & Soft Tissue Injuries
How to Use It?
If a 70 kg patient come to us with clinically femur fracture-
• Estimated blood loss???
• Classification of shock??
• Fluids??
• Estimated blood volume- 70ml/kg*70kg= 4900ml
• Blood loss = 1500 ml
• % of blood loss = (4900×100÷1500)
=32.6%
• Class III Haemorrhage
• crystalloids+ blood products
Management of Shock
Resuscitation:
If there is initial doubt about the cause of shock, it is safer to
assume the cause is hypovolaemia and begin with fluid
resuscitation and then assess the response
Fluid therapy:
In all cases of shock, regardless of classification,
hypovolaemia and inadequate preload must be addressed
before other therapy is instituted
Types of Fluid
Crystalloids
*Normal saline (0.9% NaCl)
*Hartmann’s solution
*Ringer’s lactate
Colloids: albumin or commercially available products.
Blood & Blood products.
Remember
Oxygen carrying capacity of crystalloid
and colloids are zero. If blood is being lost
the ideal replacement fluid is blood,
although crystalloid therapy may be
required while awaiting blood products.
Permissive Hypotension
The initial aim of resuscitation is to maintain the
blood supply to the vital organs- brain, heart,
kidneys.
For a short time, this can be achieved with a
target systolic blood pressure of 70-90 mmHg,
although a higher blood pressure of >90mmHg
should be the target if a head injury is suspected.
Excessive intravenous crystalloid or colloid
solutions should be avoided because they cause
- Haemodilution
- Increase Coagulopathy.
- Increase the risk of ARDS
Remember
Dynamic Fluid Response
If 250-500ml of fluid is rapidly given over 5-10minutes
Observe HR, BP, CVP
Responders: patients is not actively loosing blood but require filling to a
normal volume status.
Transient responders: patients have moderate ongoing fluid loss
Non- responders: severe volume depleted & major ongoing loss of
intravascular volume, usually through persistent uncontrolled haemorrhage.
Monitoring for patients in Shock:
Minimum-
* ECG
* Pulse oximetry
* Blood pressure
* Urine output
Additional modalities-
* Central venous pressure
* Invasive blood pressure
* Cardiac output
* Base deficit & serum lactate
End point of resuscitation
• It is much easier to know when to start resuscitation than when
to stop.
• Traditionally patients have been resuscitated until they have a
normal BP, Pulse & Urine output.
• A patients therefore may be resuscitated to restore central
perfusion to brain, lungs & kidneys and yet continue to under-
perfuse gut & muscle beds.
• This state of normal vital signs and continued under-perfusion is
termed as
-Occult Hypoperfusion.
End point of resuscitation
Resuscitation algorithms directed at
correcting global perfusion end points-
1. Base deficit.
2. Lactate.
3. Mixed venous oxygen saturation.
Further investigations
After resuscitate the patients i.e when the patient is
hemo-dynamically stable-
Patient may be send for further investigations like
1. X-ray chest, abdomen & pelvis
2. USG
3. Whole body CT scan (WBCT) –It is the gold
standard investigation for trauma patient.
Consequences
 Unresuscitatable shock
 Multiple organ failure-
Lungs-ARDS
Kidney- acute renal insufficiency
Clotting- coagulopathy
Cardiac- cardiovascular failure
ThankYou…

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Shock in Trauma Patient by Dr. Sabbir.pptx

  • 1. SHOCK IN TRAUMA PATIENT Dr. Md. Sabbir Ahamed Honorary Medical Officer Surgery Casualty Block-02 Dhaka Medical College Hospital
  • 2. SHOCK Shock is a systemic state of low tissue perfusion that is inadequate for normal cellular respiration
  • 3. Pathophysiology of Shock Cellular: Reduced tissue perfusion From aerobic to anaerobic metabolism Systemic metabolic acidosis Intracellular lysosomes release autodigestive enzymes Cell lysis
  • 4. Pathophysiology of Shock Microvascular: Tissue ischaemia progress Activation of immune & coagulation system Hypoxia & acidosis activate complement & prime neutrophil Generation of oxygen free radical & cytokine release Injury to capillary endothelium leads to loss of it’s integrity & it becomes leaky
  • 5. Pathophysiology of Shock Systemic: 1. Cardiovascular 2. Respiratory 3. Renal 4. Endocrine 5. Ischaemia- Reperfusion Syndrome
  • 6. Pathophysiology of Shock Ischaemia-reperfusion syndrome: Tissue Hypoperfusion, Hypoxia Activation of cellular & humoral elements (complement, neutrophil, microvascular thrombi) When normal circulation is restored these are flushed back into circulation & causes further endothelial injury and organ damage acute lung injury acute renal injury multiple organ failure Death
  • 7. Types of Shock 1. Hypovolaemic shock 2. Cardiogenic shock 3. Obstructive shock 4. Distributive shock – * septic shock * anaphylactic shock * neurogenic shock 5. Endocrine shock
  • 8. Stages of Shock  Initial Stage  Compensatory Stage  Progressive Stage  Irreversible Stage
  • 9. Stages of Shock  Initial Stage  Compensatory Stage  Progressive Stage  Irreversible Stage
  • 10. Stages of Shock Initial Stage: • Initially, the body compensates with the onset of shock. • No changes are noted clinically. • Changes are beginning to occur on the cellular level.
  • 11. Stages of Shock  Initial Stage  Compensatory Stage  Progressive Stage  Irreversible Stage
  • 12. Stages of Shock Compensatory Stage: • Fluid shift from interstital to intravascular space. • Activation of SNS - activation of epinephrine and norepinephrine. • Kidneys release renin into blood, formation of angiotension & release of aldosterone, ADH.
  • 13.
  • 14. Stages of Shock  Initial Stage  Compensatory Stage  Progressive Stage  Irreversible Stage
  • 15. Stages of Shock Progressive Stage: • Vicious circle of compensation eventually leads to decompensation. • Blood pressure starts to fall - SBP below 80 is considered danger signal. Tachycardia; Tachypnea; Decreased urine output; Decreased body temperature; cold, pale clammy skin.
  • 16. Stages of Shock  Initial Stage  Compensatory Stage  Progressive Stage  Irreversible Stage
  • 17. Stages of Shock Irreversible Stage: • Body attempts at compensation have failed • Pooling and sludging of blood; thrombosis of small vessels occurs. • Tissue hypoxia and anoxia occur - lactic acid accumulation contributes to cell death.
  • 19. Shock in Trauma Patients Shock is a common and frequently treatable cause of death in injured patients and is second only to traumatic brain injury as the leading cause of death from trauma. ATLS (ADVANCED TRAUMA LIFE SUPPORT)
  • 20. When a Patients Arrives PRIMARY SURVEY- cABCDE c- Exsanguinating external haemorrhage from massive arterial bleeding needs to be controlled even before the airway is managed. A- Airway with cervical spine control (maintain cervical spine stabilization when appropriate) B- Breathing and ventilation assessment (maintain adequate oxygenation) C- Circulation and haemorrhage (control haemorrhage and maintain adequate end-organ perfusion) D- Disability assessment (perform basic neurologic evaluation by GCS) E- Exposure, with environmental control (undress patient and search everywhere for possible injury, while preventing hypothermia
  • 21.
  • 22. Is the patients in Shock?? Blood pressure- Not reliable …. (BP falls when 30% blood volume is lost ) Look for- Pulse Rate Respiratory rate Urinary output Conscious level ANY INJURED PATIENT WHO IS COOL & HAS TACHYCARDIA IS CONSIDERED TO BE IN SHOCK UNTIL PROVEN OTHERWISE
  • 23. Haemorrhagic Shock?? • Try to find source---- Chest Abdomen Pelvis Extremities Any external bleeding
  • 24. What to do? First we resuscitate the patent. Then- 1. Focussed Assessment Sonography in Trauma (FAST) 2. X-ray chest, abdomen & pelvis 3. USG 4. Whole body CT scan (WBCT) –It is the gold standard investigation for trauma patient.
  • 25. Haemorrhagic Shock • Advanced Trauma Life Support (ATLS) manual describes four classes of hemorrhage to emphasize the early signs of the shock state. • The adult human has approximately 5 litres of blood ( 70ml/kg children & adults, 80ml/kg neonates) • Volume replacement is determined by patient’s response to initial therapy • Haemorrhage control & balanced fluid resuscitation must be initiated when early S/S of blood loss are apparent or suspected- NOT WHEN BP IS FALLING OR ABSENT. • Bleeding patients needs blood- BLOOD FOR BLOOD
  • 26.
  • 27. Class I Haemorrhage ● Blood volume loss upto 15 percent. • The heart rate is minimally elevated or normal, and there is no change in blood pressure, pulse pressure, or respiratory rate. • Usually don’t require blood
  • 28. Class II Haemorrhage • 15 to 30 percent blood volume loss • Manifested clinically as Tachycardia (heart rate of 100 to 120), Tachypnea (respiratory rate of 20 to 24), • Decreased pulse pressure, although systolic blood pressure changes minimally if at all. • Skin may be cool and clammy, and capillary refill may be delayed. • Mx- most stabilized with crystalloid, few may require blood.
  • 29. Class III Haemorrhage • 30 to 40 percent blood volume loss, resulting in a significant drop in blood pressure and changes in mental status. • Any hypotension (SBP less than 90 mmHg) or drop in BP greater than 20 to 30 percent of the measurement at presentation is cause for concern. • Heart rate (≥120 and thready) and RR are markedly elevated, while urine output is diminished. Capillary refill is delayed. • Mx- Stop BLEEDING & BLOOD TRANSFUSION.
  • 30. Class IV Haemorrhage • More than 40 percent blood volume loss • LIFE THREATENING…. • Patients are hypotensive ( SBP less than 90 mmHg). • Pulse pressure is narrowed (≤25 mmHg) and tachycardia is marked (>120). • Urine output is minimal or absent. • The skin is cold and pale, and capillary refill is delayed. • Mx- Rapid fluid transfusion and surgical intervention depending on initial fluid response
  • 31. Fractures & Soft Tissue Injuries
  • 32. How to Use It? If a 70 kg patient come to us with clinically femur fracture- • Estimated blood loss??? • Classification of shock?? • Fluids?? • Estimated blood volume- 70ml/kg*70kg= 4900ml • Blood loss = 1500 ml • % of blood loss = (4900×100÷1500) =32.6% • Class III Haemorrhage • crystalloids+ blood products
  • 33. Management of Shock Resuscitation: If there is initial doubt about the cause of shock, it is safer to assume the cause is hypovolaemia and begin with fluid resuscitation and then assess the response Fluid therapy: In all cases of shock, regardless of classification, hypovolaemia and inadequate preload must be addressed before other therapy is instituted
  • 34. Types of Fluid Crystalloids *Normal saline (0.9% NaCl) *Hartmann’s solution *Ringer’s lactate Colloids: albumin or commercially available products. Blood & Blood products.
  • 35. Remember Oxygen carrying capacity of crystalloid and colloids are zero. If blood is being lost the ideal replacement fluid is blood, although crystalloid therapy may be required while awaiting blood products.
  • 36. Permissive Hypotension The initial aim of resuscitation is to maintain the blood supply to the vital organs- brain, heart, kidneys. For a short time, this can be achieved with a target systolic blood pressure of 70-90 mmHg, although a higher blood pressure of >90mmHg should be the target if a head injury is suspected.
  • 37. Excessive intravenous crystalloid or colloid solutions should be avoided because they cause - Haemodilution - Increase Coagulopathy. - Increase the risk of ARDS Remember
  • 38. Dynamic Fluid Response If 250-500ml of fluid is rapidly given over 5-10minutes Observe HR, BP, CVP Responders: patients is not actively loosing blood but require filling to a normal volume status. Transient responders: patients have moderate ongoing fluid loss Non- responders: severe volume depleted & major ongoing loss of intravascular volume, usually through persistent uncontrolled haemorrhage.
  • 39. Monitoring for patients in Shock: Minimum- * ECG * Pulse oximetry * Blood pressure * Urine output Additional modalities- * Central venous pressure * Invasive blood pressure * Cardiac output * Base deficit & serum lactate
  • 40. End point of resuscitation • It is much easier to know when to start resuscitation than when to stop. • Traditionally patients have been resuscitated until they have a normal BP, Pulse & Urine output. • A patients therefore may be resuscitated to restore central perfusion to brain, lungs & kidneys and yet continue to under- perfuse gut & muscle beds. • This state of normal vital signs and continued under-perfusion is termed as -Occult Hypoperfusion.
  • 41. End point of resuscitation Resuscitation algorithms directed at correcting global perfusion end points- 1. Base deficit. 2. Lactate. 3. Mixed venous oxygen saturation.
  • 42. Further investigations After resuscitate the patients i.e when the patient is hemo-dynamically stable- Patient may be send for further investigations like 1. X-ray chest, abdomen & pelvis 2. USG 3. Whole body CT scan (WBCT) –It is the gold standard investigation for trauma patient.
  • 43. Consequences  Unresuscitatable shock  Multiple organ failure- Lungs-ARDS Kidney- acute renal insufficiency Clotting- coagulopathy Cardiac- cardiovascular failure