Lecture By: management of hemorrhagic shock by ESSAM A. SALEMICU REGISTRARE

2. ‫الرحيم‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬
management of hemorrhagic
shock

3. points
1. Shock is hypoperfusion not hypotension
2. Rapid identification of HS and initiation of
ttt before hypotension occur is essential to
minimize morbidity

4. Class I
A. Loss of up to 15% of total blood volume (0 to
750 ml in 70 kg person).
B. Characterized by normal blood pressure, urine
output, slight tachycardia, tachypnea, slight
anxiety.

5. Class II
A. Loss of 15 % to 30% of total blood volume
(750 to 1,500 ml )
B. Characterized by normal blood pressure,
tachycardia, mild tachypnea, decrease urine
output and mild anxiety.

6. Class III
A. Loss of 30% to 40% of total blood volume
(1,500 to 2,ooo)
B. Characterized by hypotension, tachycardia,
tachypnea, decreased urine output , anxiety
and confusion.

7. Class IV
A. Loss of > 40% of total blood volume
(>2,ooo)
B. Characterized by severe hypotension and
tachycardia, tachypnea, negligible urine
output and lethargy

8. Notes that
BP is normal until significant blood loss occur.
( class III )
Tachycardia is the earliest reliable sign of
shock.

10. 1. Replace three times the volume of blood lost
with warm crystalloids. (1L of blood lost
should be replaced with 3L of crystalloid.
2.Patient need Massive transfusion role is FFP
and PRBCs ratio 1:1 ,
3.Surgical consultation and early indicated
intervention .

11. 1. Replacement of hemorrhage with blood
only or less than the required ratio of
crystalloid to blood loss results in persistent
hypoperfusion and acidosis and increase
mortality.
2. Fluid resuscitation of the interstitial space is
obligatory in HS.
Note
The interstitial space volume in 70 –Kg male is
approximately 10 L
The resultant edema and fluid retention is the
expected result not a harmful side effect

12. Rapid response
I. Become hemodynamically stable after initial
fluid bolus
II. Early surgical consultation is necessary

13. Transient response
I. Pts respond to initial fluid bolus but again
become hemodynamically unstable or
shown signs of hypoperfusion.
II. Cont` with fluid & blood transfusion
maintain normal hemodynamics
III. These Pts most often require rapid surgical
intervention

14. No response
I. Pt who show no response to fluid boluses
and blood transfusion have continued
hemorrhage and require Immediate
surgical intervention to stop bleeding.
II. Must keep in mind non hemorrhagic
causes of shock .
A. Tension pneumothorax.
B. Cardiac tamponade.
C. Spinal cord injury.
D. Cardiogenic shock..
E. Septic shock

15.  The goal of HS resuscitation is restoration of end-
organ perfusion
 Traditional endpoints (normalization of BP- heart
rate- urine output- capillary refill).
Tricks
BP does not equal cardiac output
Increase systemic vascular resistance (SVR) may raise
BP
Pt with shock but normal BP are referred to as being
“compansated shock” despite bleeding and
hypoperfusion.

16.  Even experienced practitioners can be
fooled by patient in compensated shock.
 Normalization of acidosis and oxygen
consumption are the best current indicators
of adequate resuscitation
 Base deficit and lactate level are good
indications of tissue perfusion.

17. 1- not realizing the need of
massive transfusion and need
to start FFP and PRBCs 1:1
and avoid massive use of
crystaloids.

18. 2-Albumin
 Albumin shown to decrease glomerular
filtration and urine output
 increase sodium retention
 worsen oxygenation
 Increase coagulopathy when used in HS

19. 3. Inotropes and vasopressors
 Increase SVR and rise BP according to
formula BP = CO X SVR
 Increase BP not mean PERFUSION
 NORMAL tissue perfusion is the GOAL of
shock resuscitation.
 VASOPRESSORS may have opposite effect
of worsening perfusion through
vasoconfusion

20. 4. Diuretics
 Well resuscitated Pts mobilize 3th space
fluid naturally 3 to 5 days after resuscitation
 Induced diuresis (eg. Furosemide ) is
unnecessary and may be harmful if it
reduces intravascular volume and perfusion
 Since normal edema resulting from proper
shock resuscitation is the result of an
inflammatory response (not cardiogenic
failure) and is obligatory it is not reversible
in the early stages of shock.

21.  Intravascular volume status should be
estimated by measurements of
 central venous pressure .

22. 5. Bicarbonate
 HCO3 combined with hydrogen ion to form
water and carbon dioxide
 CO2 diffuses into cells and worsens
intracellular acidosis
 It is not indicated for lactic acidosis from HS
 Best treatment of acidosis from HS is
restoring perfusion to ischemic tissue.

23. complications

24. MOF
Multiple organ
failure
Coagulopathy

25. Multiple organ failure
 pt who survive HS but die in the hospital later
usually die of MOF or sepsis
 MOF results from systemic inflammatory
response
 Duration and severity of HS correlate with
incidence of MOF
 Patients who get > 6 units of packed RBCs in
the first 12 hours of HS resusitation have higher
risk of MOF

26. Coagulopathy
1-Hypothermia
 Most common cause of coagulopathy in HS
 Significant coagulopathy begins at 34o c
 Undetectable on lab tests of coagulation
,blood warmed to 37 c before testing
Note that
Treate with warmed fluids and external
rewarming

27. 2-Platelet dysfunction and deficiency
 Second most common cause
 Hypothermia cause plt dysfunction
 Thrombocytopenia is common is massive
HS
 Degree of thrombocytopenia not correlated
directly with volume of blood loss
 Platelets transfusion