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MASSIVE TRANSFUSION PROTOCOL
A brief clinical review
OBJECTIVES
HEMORRHGIC SHOCK
MASSIVE TRANSFUSION
TRANSFUSION COMPLICATIONS
CONCLUSION
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
HEMORRHGIC SHOCKSmall 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
HEMORRHGIC SHOCKThe 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)
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?
MASSIVE TRANSFUSION PROTOCOL
INDICATIONS GOALS
MASSIVE TRANSFUSION PROTOCOL
Correct Anticoagulation• LWMH Protamine• Vitamin K+ Antagonist Vitamin K or PCC• Direct Thrombin Inhibitors No antidote • Antiplatelet Agents PLT
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
MASSIVE TRANSFUSION PROTOCOLPRBC:
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)
MASSIVE TRANSFUSION PROTOCOL
FFP: Correction of coagulation
disorders FFP contains all
coagulation factors in normal concentrations
No indicated for volume expansion
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
MASSIVE TRANSFUSION PROTOCOLBelmont 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
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.
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!
BLOOD
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
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
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.
ABO +/-TYPE ANTIGEN ANTIBODIESA + 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
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
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 !!
TRANSUSION REACTIONSAcute Hemolytic Transfusion
Reaction:
• ABO incompatibility (40% lab error / 60% bedside error)
• Fever, chills, chest pain, shock, bleeding, death
• Rapid onset (antibody mediated)
TRANSUSION REACTIONS
Delayed Hemolytic Transfusion Reaction:
• Seen in patients with previous transfusion or pregnancy
• Antibodies develop
• Develops days to weeks after the transfusion
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
TRANSUSION REACTIONSTransfusion Related Acute Lung Injury:
• Transfusion of inflammatory cytokines, active lipids, and/or antibodies.
• Respiratory distress (secondary ARDS)
• Sick patient + transfusion = TRALI
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