Products Flashcards
Define Massive transfusion protocol
Replacement of >1 blood volume in 24 hours
>50% of blood volume in 4 hours
In children tranfusion of >40ml/kg (blood volume in children 1 month old is approximately 80 ml/kg)
Discuss goals of MPT
Temperuture >35
Acid base status
-Ph >7.2
-Base excess < 6
lactate <4 mmol/l
Clotting -Ionised calcium >1.1mmol -PLatelets >50 Ot/APTT <1.5 of normal -INR <1.5 -Fibrinogen >1.0 g/L
Discuss risk and complications with large volume resuscitation with blood products
- Volume overload
- Over transfusion
- Hypothermia
- Dilutional coaguloapthy of clotting factors and platelts
- Transfusion related acute ung injury
- excessive citrate causing metbaolic alkalosis and hypocalcamiea
- Hyperkalaemia
- disease transmission
If using unmatched
- difficulty with cross matching future blood products
- difficulty with matching solid organs
Discuss the physioogical affect of giving PRBC
Electrolyte load NA- +15mmol K+2mool Cl- 15mmol Hco3 1mmol Lactate 0.9 mmol
Citrate load can also lower ionised calcium level
Discuss TACO
Transfusion associated circulatory overload
Defined as onset or exacerbation of three or more of the following within 12 hours of the end of a tranfusion wihtout another explanation
-respiratory distress (acute or worsening)
-Evidence of pulmonary oedema on examination or radiographs
-elevated BNP
-Other unexplained CVS changes
Treatment is similar to fluid overload from any other cause
Discuss definitions of TRALI
Type 1 - no risk factors for ARDS and all the following are met
#a)
-acute onset
-hypoxemia (pao2/fio2 <300mmHg or spo2 <90% RA)
-Clear evidence of bilateral pulmonary oedema on imaging
-no evidence of LAH or if LAH is present it judged to not be the main contribute to the hypoxemia
#b: onset during or within 6 hours of transfusion
#c: no temporal rlationship to an alternative risk factor for ARDS
Type 2: risk factors for ARDS are present or mild ARDS at baseline, but with respiratory status deterioation that is judged to be due to transfusion based on both of the followin
1) findings as describeds in categories a and b of TRALI type 1
2) stable resp status in the 12 hours before transfusion
Discuss risk factors for development of TRALI
Recipient risk factors
- liver transplantation surgery
- chronic alcohol abuse
- shock
- higher peak ariway pressure while being mechanically ventilated
- current smoker
- higher interleukin 8 levels
- positive fluid balance
Blood componenet
- Donor sex (Female and increased parity)
- high plasma volume blood products (whole blood, plasma, apheresis platelet concentrate)
Rd cell storage duration
Discuss pathogenesis of TRALI
Two hit mechanism
First hit involves neutrophil sequestration and priming in the lung microvasculature due to recipient factors such as endothelial injury. Priming refers to shifting of neutrophils to a state where they will respond to an otherwise innocuous or weak signal.
Second hit activation of recipient neutrophils by a factor in the blood product. Activation is associated with the release from neutrophils of cytokines reactive oxygen species oxidases and proteases taht damage the pulmonary capillary endothelium. This damage cause not hydrostatic pulmonary oedema.
Discuss management of TRALI
If TRALI is suspected the transfusion should be ceased and blood bank alerted to iniate and evaluation for a transfusion reaction. This is important for the protection of future recipients as well as for TRALI lab testing and work up
Otherwise treatment is the same as for ARDS
Discuss acute transfusion realted haemolytic reactions
occurs during the tranfusion or with the first 24 hours after the tranfusion.
ABO associated AHTRs often occur during the early minutes of the transfusion although they may not be immediately appreciated
Patient develop chills, fever, hypotension, haemoglobinuria, renal failure, back pain or signs of DIC
Discuss IX of acute transfusion related haemolytic reactions
Blood should be ideally drawn from the contralateral side.
- Repeat ABO compatibility screen
- Additional antibody studies if ABO incompatibility is excloded
- repeat Crossmatch wiht pre and post tranfusion specimens
- Direct COombs testing which may be positve in AHR but may by negative in ABO incompatilibility if haemolysis is so severe taht all RBCs with antibody on the surface have been lysed.
- Haemolysis screen -LDH, conjugated and unconjugated biliruibin, haptoglobin
test for DIC
- PT, APTT, INR all prolonged
- Low fibrinogen
- low platetlets
- Low fibrinogen
- high fibrin degradation products (FDP/D-dimer)
Monitor electrolytes
Discuss management of acute transfusion related haemolytic reaction
Stop tranfusion
establish IV
Confirm correct product for patient
Assess patient for fever, CVS status, resp status, urticaria/angiooedema
If the intiial bedside evaluation is cconsistent with intravascular haemolysis normal saline should be infused immediatly to reduce the risks of hypotension and renal injury. -infuse at rates of 100-200ml/hr aiming for 1ml/kg/hr urine output
Discuss febrile nonhaemolytic reactions
The most common of all transfusion reactions
They occur in approxaimtly 0.1-1% of all tranfusions
RIsk factors include
- age more common in children than adults
- product:-more likley with cellular products such as platelets or PRBC
- Leykoreduction rends FNHTRS much less likley
FNHTR occur wihtin 1-6 hours after initiation of a transfusion- these include
- fever
- rigors
- mild dyspnoea
DIscuss management of febrile nonhaemolytic reactions
FNHRTS are benign causing no lasting sequalae but they are uncomfortable and sometimes frightening tio the patient. Management is typicllay as follows
- stop infusion
- admin antipyretics
- evaluate for other cuases of fever inclduing more serious transfusion reactions
List other types of transfusion reactions
Urticarial transfusion reaction - urticaria with nils otehr system involvment
IgA anaphylactic transfusion reaction. Anaphylactic reation may occur in IgA defiecient individuals who produce anti-IgA antibodies that react with IgA in the transfused product leading to anaphylaxis
Discuss FFP
FFP contains all of the clotting factors, fibrinogen, plasma proteins, electrolytes, physiolgocial anticoagulants ([protein C, protein S, antithrombin, tissue factor pathway inhibitor)
Discuss prothombinex
Contains factors 2, 9 and 10
dose of 25-50 IU/Kg
Briefly discuss how ROTEM is perfromed
Sample of whole blood is placed in contact with a rotating pin. As the pin rotates a clot is formed which causes impairement to the rotation. This forces are read by the machine to output a tegogram.
Discuss clotting time and causes of prolongation
The time from when the test first started until the temogram reaches 2mm
Prolonged
- low fibrinogen- most common
- low clotting factors
- anticoagulation such as heparin
Discuss tegogram amplitude
Amplitude is the clot strength
-formed by fibrinogen or platlets if low in amplitude issue with one or the iother
Measured at different time spots
- MCF - maximal clot firmness - -30-40 minutes
- A5 - clot firmness at 5 minutes-
Discuss lysis times
Degree of loss of clot strength
can be measured at 30minute - LI30 or at maximum lysis
Discuss Extem
Basic screening test - to test overall clotting profile
1st step is clotting time if low
- low fibrinogen
- coag factors or heparin
2nd step is A5/10/MCF
- platelets
- fibrinogen
3rd step is looking at maximal fibrinolysis
Discuss Fibtem
Fibtem is Extem + antiplatelet agent
This allows evaluation of fibrinogen contribution to clot strenght – which is the most common reason for poor clotting
Amplitude at A5, A10 and MCF can be used
Low fibtem
-consumption
hyperfibrinolysis
Discuss limitations of ROTEM
Difficult to directly assess antiplatelet drugs
Von-willibrands diseasse
?NOACs and Warfarin
