Module 5 Flashcards

1
Q

What are the criteria for critical bleeding or massive transfusion? (6)

A
  • Blood loss >150ml/min
  • Loss of 1.5ml/kg/min over 20 minutes
  • > 3 x RC in any 1 hour period
  • 50% TBV replaced over 3 hours
  • > 4 x RC in any 4 hour period
  • 1 TBV or 10 RC replaced over 24 hours
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2
Q

What are some of the principles of massive transfusion?

A
  • use BALANCED products
  • treat early and adequately
  • plasma alone is insufficient to correct hypofibrinogenaemia
  • 1:1:1 FFP, plt, RC
  • TEG/ROTEM to individualise therapy
  • goal-directed therapy
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3
Q

What are the goals of MTP?

A
  • rapid control of bleeding
  • prevent and minimise coagulopathy
  • void unnecessary transfusion
  • minimise end organ dysfunction
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4
Q

What is the expected incrementation after 1 unit of platelets?

A

20-40 x 10^9

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5
Q

In which conditions are platelet transfusio`ns contraindicated?

A

ITP
TTP
HIT unless life-threatening haemorrhage

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6
Q

What is in FFP? What are some of the indications?

A

whole blood or apheresis split into 2-3 units, contains all coagulation factors (200 IU VII and V)

  • coagulopathy
  • MTP
  • CPB
  • DIC
  • warfarin overdise
  • TTP
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7
Q

How is cryoprecipitate formed? What are the components?

A

Cold-insoluble precipitate at 1-6 degrees

FVIII, vWF, fibrinogen, FXIII, and fibronectin

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8
Q

Who gets CMV seronegative components?

A

Pregnant women
Intra-uterine infusions
Neonates
Granulocyte transfusions for CMV negative patients

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9
Q

Who gets leucodepleted prducts?

A
  • solid organ transplants
  • haematopoetic stem cell transplants
  • haem onc patients
  • immunodeficient patients
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10
Q

What are the 4 broad causes of transfusion complications?

A

Immunological (alloantibodies on recipient or donor side)

Infection (viral, bacterial, prion)

Administrative (ID, lab errors, transport)

Storage (degeneration, temperature)

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11
Q

Differentiate between acute and delayed presentations of immune transfusion reactions

A

ACUTE

  • febrile non-haemolytic
  • allergic
  • haemolytic
  • TRALI

DELAYED

  • delayed haemolysis
  • alloimmunisation
  • GVHD
  • post-transfusion purpura
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12
Q

What are the presenting features and mechanism of an ACUTE haemolytic transfusion reaction?

A
fevers/chills/rigors
chest/flank pain
shock
Haemoglobinuria
Bleeding 

MECHANISM

  • ABO incompatibility or other red cell antibodies
  • Ab binds to RBC, activates complement leading to lysis or FBC
  • Cytokines, activation of coagulation, fibrinolysis leading to shock, renal failure, coagulopathy and MOF
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13
Q

What are the presenting features and mechanism of a DELAYED haemolytic transfusion reaction?

A

Inadequate rise/fall in Hb 2-14 days post transfusion
Fever/Jaundice
Positive DAT

Previously formed RBC Ab not detected on pre-transfusion testing, transfused RBCs removed/destroyed

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14
Q

Differentiate between TACO and TRALI

What is the mechanism of TRALI?

A

BOTH: dyspnoea, hypoxia, white out XR
TRALI: Hypotension, no features of overload
TACO: hypertension, pleural effusions

  1. Neutrophils become primed/susceptible due to pre-existing conditions (trauma, ventilation)
  2. Plasma with leukocyte antibodies/biologic agents
  3. Transfusion leads to damage to endothelium, capillary leak and pulmonary oedema
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15
Q

What are the signs/symptoms of transfusion-associated GVHD and what is the mechanism?

A
1-2 weeks post transfusion
Fever
Rash
Diarrhoea
Hepatic dysfunction
Progressive pancytopenia

Immunodeficient patient unable to recognise t lymphocytes in transfused product, lymphocytes engraft and destroy patient’s own cells

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16
Q

What are the laboratory findings of trauma induced coagulopathy?

A

Prolonged APTT/PT or INR >1.5x upper limit of normal with low fibrinogen in association with trauma

17
Q

What are the 2 major driving factors of trauma-induced coagulopathy?

A

Hypocoagulable state driven by upregulation of thrombomodulin and APC
○ Decreased availability of Va and VIIIa
○ Decrease in PAI1 (regulator of fibrinolysis)
Hypoperfusion results in massive thrombin release, fibrin deposition, tPA locally and globally driving fibrinolysis