25B06: Exam Report

Outline the potential adverse consequences of blood product transfusion including the underlying mechanisms

16% of candidates passed this question.

This question required a structured approach to cover the breadth.

A common structure in most of the recommended resources includes classification of adverse reactions into:

  1. Immune mediated
    1. haemolytic vs non-haemolytic OR
    2. immediate and delayed
  2. Non-immune mediated
    1. acute reactions OR
    2. delayed reactions

Not using a structured approach often resulted in the omission of whole sections.

Other common omissions were in not briefly describing the mechanism of each reaction which was required to score well.

Information on adverse effects related to storage lesions and massive transfusion also attracted marks.

Q4ii / 25B06: Outline the potential adverse consequences of blood product transfusion

Blood Transfusion

  • Infusion of safe and compatible blood (or its components) from donor to recipient
  • Compatibility between donor RBC antigens and plasma antibodies of recipient MUST be ensured to avoid fatal haemolytic reactions

Complications of Blood Transfusion

  • Immunological:
    • Acute (<24H)
    • Delayed (>24H)
  • Non-Immunological:
    • Acute
    • Delayed

Acute Immunological

  • Acute haemolytic transfusion reaction
    • Incompatibility of donor and recipient blood leading to widespread haemolysis, DIC and circulatory collapse
    • Ab in recipient blood attacks Ag on donor RBC
      • ABO incompatibility
  • Anaphylaxis to plasma proteins
    • IgE mediated reaction to foreign proteins in donor plasma 
  • TRALI
    • Transfusion related acute lung injury
    • Acute respiratory, non-cardiogenic pulmonary oedema
    • Like ARDS with severe hypoxaemia
    • Caused by leukocyte Ab in DONOR blood directed against HLA Ag and human neutrophil Ag of recipient
  • Febrile non-haemolytic transfusion reactions
    • Due to stored cytokines in donor blood

Delayed Immunological

  • Delayed haemolytic transfusion reaction
    • Caused by very low levels of Abs present in recipient NOT detected in cross match
    • Usually Kidd, Duffy, Kell blood group antigen antibodies 
  • Graft vs Host disease
    • Rare with very high mortality
    • Donor T cells deposit and mount an immune response against host tissue
      • Can cause destruction of host bone marrow.
  • Alloimmunisation
    • Development of antibodies during exposure to blood products
    • Hence need crossmatch ever 72H
    • e. Rhesus Alloimmunisation (Rh -ve mother exposed to Rh +ve baby blood)
  • Post-transfusion purpura
    • Consumptive thrombocytopaenia occurring 7-10D post transfusion
    • Self-limiting, lasting 2-6 weeks.

Acute non-immunological

  • Septicaemia
    • Contamination of blood products with GNB (i.e. pseudomonas)
    • Increased risk in platelets as they are stored at 20-24 degrees Celsius
  • TACO
    • Transfusion associated circulatory overload
    • Akin to APO (acute dyspnoea, tachypnoea, HTN, tachycardia)
    • Especially with FFP
    • Volume overload due to rapid or massive transfusion more than what the patient’s cardiac state can handle.
  • Air Embolism
    • Venous gas embolism from external environment → RHF → circulatory collapse
  • Storage Lesions (see below)

Delayed non-immunological

  • Iron Overload
    • Repeated RBC transfusions → Deposition of iron in reticuloendothelial tissues (seen in thalassaemia major)
  • Disease Transmission
    • Generally, HBV, HCV, HTLV, HIV (rare in Australia)
    • Can also transmit malaria and toxoplasmosis

Complications of Massive Blood Transfusion

  • Above complications PLUS complications caused by storage of blood components (storage lesions)
  • Massive transfusion – transfusion of stored blood greater than recipient’s blood volume in less than 24H

Storage Lesions

  1. Citrate toxicity and HypoCa++
    1. Citrate in PRBC as anticoagulant chelates Ca2+
    2. Occurs with RAPID infusion
  2. HyperK+
    1. K+ leaks from RBCs during storage (30mmol/L at D30 of PRBC storage)
    2. Due to inactivation of Na+/K+ ATPAse
  3. Acidosis
    1. Stored blood becomes progressively acidotic to pH 6.5-6.8 following 2 weeks
    2. Due to hyperlactataemia from RBC anaerobic metabolism in stored PRBC
    3. Citrate toxicity can contribute (but usually rapidly converted to HCO3– in liver)
  4. Hypothermia
    1. Transfusion of cold PRBCs (stored at 4 degrees Celsius)
    2. Causes left shift in ODC, decreasing O2 delivery to tissues
  5. 2,3-DPG deficiency
    1. Levels drop during storage causing left shift of ODC decreasing O2 delivery
    2. Use of CPD adenine slows 2,3-DPG depletion
  6. Dilutional Coagulopathy
    1. Stored PRBC has low clotting factors
    2. Especially if TBV replaced more than twice in 24H
    3. Also leads to dilutional thrombocytopaenia, also leading to coagulopathy
  7. Microaggregates
    1. Clumps of fibrin, platelets and leukocytes 20µm in diameter form in stored blood
    2. Traps in pulmonary vessels. Can lead to ARDS
  8. Renal Impairment
    1. Increased free Hb in stored PRBC due to RBC lysis
    2. Free Hb is nephrotoxic
  1.  

Sources:

  1. Kam and Power, 4th Edition

Author: Alex Fagarasan