The document reviews massive transfusion protocols (MTPs) focusing on the management of hemorrhagic shock and the associated risks and complications. It outlines the goals of MTPs, which include aggressive coagulation factor therapy, minimizing crystalloid infusion, and preventing coagulopathy, hypothermia, and acidosis during treatment. Additionally, it discusses blood type compatibility for transfusions and potential adverse reactions, emphasizing the importance of monitoring and reassessment during massive transfusions.

1. MASSIVE TRANSFUSION
PROTOCOLA brief clinical review

2. OBJECTIVES
 HEMORRHGIC SHOCK
 MASSIVE TRANSFUSION
 TRANSFUSION COMPLICATIONS
 CONCLUSION

3. HEMORRHGIC SHOCK
 Tachycardia (early)
 Decreased urine output
(intermediate)
 Hypotension (late)
 Increased Mortality:
• Comorbidities
• Age
• Medications (ASA, Plavix,
Warfarin, beta blockers)
 Clinical presentation of
hemorrhagic can vary with age
(young vs old) and pregnancy

4. HEMORRHGIC SHOCK
Small Blood Volume:
tolerates blood loss
poorly
Physiological
Compromise:
unable to
compensate for
blood loss
Physiological
Reserve: may
mask blood
loss
Larger Blood
Volume:
increased
blood volume
may mask
blood loss

5. HEMORRHGIC SHOCK
The goal of care is to control bleeding and
resuscitation (minimize IV fluids, blood
products, avoid hypothermia and
acidosis).
 Hypothermia (below 35c) → Inhibits
intrinsic & extrinsic coagulation
pathways
 Excessive IV Fluids → coagulopathy
 Hypoperfusion + IV fluids (NS pH is 6.1)
→ Acidosis (inhibits coagulation and
depresses cardiac function)

6. MASSIVE TRANSFUSION PROTOCOL
 “Implementation of a Massive
Transfusion Protocol (MTP) promotes early
and aggressive coagulation factor therapy
as well as the limitation of crystalloid
infusion, the prevention of coagulopathy,
hypothermia and acidosis” (the ‘Lethal
Triad’)
 Indications & Goals?

7. MASSIVE TRANSFUSION PROTOCOL
INDICATIONS GOALS

8. MASSIVE TRANSFUSION PROTOCOL
Correct Anticoagulation
• LWMH  Protamine
• Vitamin K+ Antagonist  Vitamin K or PCC
• Direct Thrombin Inhibitors  No antidote
• Antiplatelet Agents  PLT

9. MASSIVE TRANSFUSION PROTOCOL
Control the source of the bleeding
and replace lost blood volume.
Blood products should
approximate whole blood.
Correct coagulation
abnormalities.
NURSING CARE:
• VS Q1H + PRN
• Double check all blood
products
• Monitor for transfusion
reactions
• Reassessment (meeting goals?)
• Labs

10. MASSIVE TRANSFUSION PROTOCOL
PRBC:
 ABO Rh specific
 Improve oxygen delivery (VO2)
 Replace lost volume (↑ Hgb & HCT)
 Cold (4C)
 Leukocyte reduced (reduces transfusion
reactions)
 Contains citrate
 Storage: 35 days
 K+↑ and 2,3 DGP ↓ with age
 Limited ATP stores
 Shape changes during storage (oval
shaped)

11. MASSIVE TRANSFUSION PROTOCOL
FFP:
 Correction of coagulation
disorders
 FFP contains all
coagulation factors in
normal concentrations
 No indicated for volume
expansion

12. MASSIVE TRANSFUSION PROTOCOL
PLT:
 Treatment of bleeding
 Prevention of bleeding
secondary to low platelets
 Preferred ABO Rh matching
 Administer rapidly
 Do no use an infusion
pump

13. MASSIVE TRANSFUSION PROTOCOL
Belmont Rapid Infuser
 2.5 - 750cc/min
 150 – 45,000 cc/hr
 Warms IV / blood if rate < 300cc/hr
 Bucket only required if you want to reticulate
the IV fluid / blood products
 Pressure limited: Flow will be reduced if the
pressure is excessive
 Lines:
• large bore IV (16G or 18G)
• Cordis
• RIC
• May use dual-patient line to increase the
flow rate by attaching to two access points
• Avoid micro-bore IV extensions

14. MASSIVE TRANSFUSION PROTOCOL
Small extensions will
inhibit flow.
Large bore extensions
are less problematic.
Optional: Remove
needles adaptors to
increase flow
(decreased
resistance)
Add the dual lumen
extension to the line
to increase flow.

15. MASSIVE TRANSFUSION PROTOCOL
– The goal of the MTP is to
rapidly replace lost whole
blood volume (red blood
cells, platelets, and
fibrinogen).
– Reassess frequently to see if
goals have been achieved.
–
– Avoid acidosis, hypothermia,
and coagulopathy.
– Be familiar with the Belmont
Rapid Infuser and the
enFlow fluid warmer. Don’t
meet them for the first time
during a major bleed!

16. BLOOD

17. ABO
 Karl Landsteiner, who identified the O, A,
and B blood types in 1900.
 Alfred von Decastello and Adriano Sturli
discovered the fourth type, AB, in 1902.
 Antigen – marker expressed on the call wall
 Antibodies –used by the immune system to
neutralize pathogens
 RBC – 100 to 120 day life span / oxygen
transporters

18. ABO
 Type A blood has type A antigen
expressed on its surface
 Type B has type B antigen expressed
on its surface
 Type AB has type A & B antigen
expressed on its surface.
 Type O (sometimes referred to as type
zero outside North America) has not
antigen expressed on its surface.
 Antibodies (anti-A, anti-B, or anti-A &
anti b) antibodies will develop within

19. RHESE FACTOR
 Discovered in 1937 by Karl Landsteiner and
Alexander S. Wiener.
 Rh positive indicates that the type D antigen is
expressed.
 Rh negative indicates that the type D antigen is
expressed.
 You need to be exposed to antigen D (Rh +) to
develop antibodies (i.e. mother-fetus)
 Furthermore, many other antibodies exists and
many be tested for in unique clinical situations.

20. ABO +/-
TYPE ANTIGEN ANTIBODIES
A + A & D Anti-B antibodies
A - A Anti-B antibodies
B + B & D Anti-A antibodies
B - B Anti-A antibodies
AB + A, B & D No antibodies
AB - A & B No antibodies
O + Zero Anti-A and Anti B antibodies
O - Zero Anti-A and Anti B antibodies

21. ABO +/-
 Blood Transfusions:
• AB+ is the universal recipient
because the RBC expresses the A,
B and D antigen. Therefore, any
type of blood can be transfer
without an antibody reaction.
• O- is the universal donor. Type O
or type ‘zero’ RCB has no A, B or D
antigens expressed on its surface.
Therefore, when transfused won’t
create an antibody reaction.
• Rh (+) recipients may receive a
type specific Rh (-) transfusion.
• However, Rh (-) recipients may
not receive a Rh (+) transfusion. D
antibodies will develop causing a
transfusion reaction

22. TRANSUSION REACTIONS
 Acute Hemolytic Transfusion Reaction (AHTR)
Delayed Hemolytic Transfusion Reaction (DHTR)
 Febrile Non-hemolytic Reaction
 Allergic Reaction
 Anaphylaxis
 Transfusion Related Acute Lung Injury
!! DANGER !!

23. TRANSUSION REACTIONS
Acute Hemolytic Transfusion
Reaction:
• ABO incompatibility (40% lab
error / 60% bedside error)
• Fever, chills, chest pain,
shock, bleeding, death
• Rapid onset (antibody
mediated)

24. TRANSUSION REACTIONS
Delayed Hemolytic
Transfusion Reaction:
• Seen in patients with previous
transfusion or pregnancy
• Antibodies develop
• Develops days to weeks after the
transfusion

25. TRANSUSION REACTIONS
Allergic Reaction  Anaphylaxis:
• Allergic reactions are common in
transfusion recipients (1-3%).
• Allergic reactions are thought to be
mediated by recipient antibodies to
proteins or other soluble substances in
donor.
• Anaphylaxis (rare): severe life threating
allergic reaction

26. TRANSUSION REACTIONS
Transfusion Related Acute Lung
Injury:
• Transfusion of inflammatory
cytokines, active lipids, and/or
antibodies.
• Respiratory distress (secondary
ARDS)
• Sick patient + transfusion = TRALI

27. TRANSFUSION COMPLICATIONS
 Metabolic Effects:
• Hyperkalemia (especially in patient with acidosis
and renal failure)
• Citrate Toxicity: ↓Ca+ and metabolic alkalosis
 Hypothermia
• Associated with poor outcomes
• Warm blood when possible