Delayed blood transfusion reaction is a reaction too blood transfusion occurring after 24 hours. Can be divided to immune mediated and non-immune mediated. Share about the cause, symptoms, investigations and management.

1. DELAYED BLOOD TRANSFUSION
COMPLICATIONS

2. classification
IMMUNOLOGICAL NON_IMMUNOLOGICAL
Alloimmunisation (RBC Antigen)
(1:10)
Iron overload requiring chelation
therapy (>10-20 RBC units)
Alloimmunisation (HLAAntigen)
(1:100)
Iron overload with organ dysfunction
(>50-100 RBC units)
Delayed HemolyticTransfusion
reaction (1:2500-11000)
Transfusion transmissible infections
Post-trasfusion purpura
Transfusion-associated Graft vs Host
Disease (TA-GVHD)
Transfusion-related immune
modulation (TRIM)

3. Alloimmunisation
 Alloimmunisation to RBC,WBC and/or
platelets may result from prior exposure by
the recipient to blood components, tissue
transplantation or pregnancy
 Moderate amount of IgG and IgM may be
produced during first exposure.
 On second exposure, rapid production of IgG
in few days will attach to antigenic surface of
blood cells and causing ‘delayed transfusion
reaction’

4. Symptoms and Signs
 Mild to moderate fever
 Anemia due to decreased Hemoglobin
 Bleeding tendencies due to decreased platelets
Investigations
 History of transfusion, transplantations or
pregnancies
 Ab screen test to recipient plasma to detect
clinically significant HLA or RBC antibodies

5. Management
 Cannot be prevented, usually mild reaction
 If antibody is identified, transfused antigen-
negatives blood if further transfusion is
needed
 Give phenotyped blood early in long-term
chronic support (e.gThalassemia) to
minimize reaction

6. Delayed Hemolytic
Transfusion Reaction
 Might be due to alloimmunisation or
transfusion transmitted malaria
 Blood group antibodies associated with
DHTRs include those of the Kidd, Duffy, Kell
and MNS systems

7. Symptoms and Signs
 Fever and anemia after 2 – 14 days of
transfusion
 Jaundice
Investigations
 high bilirubin, high LDH, reticulocytosis,
spherocytosis, positive antibody screen and
positive Direct AntiglobulinTest (DAT)

8. Management
 Usually benign and no treatment needed
 Sometime, life-threatening anemia or renal
failure can occur
 If further transfusion is needed, transfused
antigen-negative blood

9. Post-transfusion Purpura
 Caused by alloimmunisation to platelet-
specific antigen, usually Human Platelet
Antigen (HPA 1a)
 Can also caused by HPA 1b or other type of
HPA and HLA

10. Signs and Symptoms
 Purpura and Bleeding tendencies
 Occurs 7-10 days post transfusion
 Bleeding from mucous membrane, GIT and
GUT. ICB can also occurred.
Investigations
 dramatic, sudden and self-limiting
Thrombocytopenia
 Antibody against platelet in recipient plasma

11. Management
 Self limiting, rarely causing mortality
 IV immunoglobulin at 1 g/kg as a single dose
and repeat as necessary. Platelet count is
expected to rise in the next 4 days

12. Transfusion-Associated Graft
vs Host Disease (TA-GVHD)
ViableT lymphocytes in the transfused component
engraft in the recipient and react against tissue
antigens in the recipient.
The 3 primary risk factors for developingTA-GVHD
are:
 Degree of recipient immunodeficiency
 Number of viableT lymphocytes transfused
 Genetic diversity in HLA expression between
donor and recipient

13. Signs and Symptoms
 Fever, rash and diarrhea 1-2 weeks post
transfusion
 Mortality rate >90%, 1-3 weeks after first
symptoms
 Can occur in patient with intact immune system
or donor from family member
Investigations
 Skin biopsy and HLA-typing
 Demonstrate donor leukocyte engraftment

14. Management
 supportive care
 corticosteroids and cytotoxic agents (largely
ineffective)
 For patients at risk, it is critical to gamma
irradiate cellular blood components

15. Transfusion-related immune
modalities (TRIM)
 Donor white cells releasing cytokines, which
leads to immune modulation.
Signs and Symptoms
 transient immunosuppression in recipients
 No specific signs and symptoms
 Incidence: not known
Management
 Leucodepletion to decrease risk ofTRIM

16. Iron overload
 Each unit of red cells contains 250mg of iron,
while body excreting 1mg/day
 In chronically transfused patient, body cannot
excrete iron quickly
 Hence, iron accumulated in
reticuloendothelial system, liver, heart,
spleen and endocrine organs

17. Signs and Symptoms
 Thalassemia or red cell aplasia patient who
needed chronic transfusion
 Muscle weakness, fatigue, weight loss
 Later: skin pigmentation, arthropathy,
diabetes and hepatic dysfunction may occur

18. Investigations
 Serum ferritin
 Organ specific marker (RFT, LFT)
 Iron quantification by MRI
Management
 Iron chelating agent can be prescribed for
prevention and management
 Deferoxamine, deferasirox, deferiprone

19. Transfusion Transmissible
Infection
Capable Infection Agents
 Bacteria (TTBI)
 HIV, Hepatitis,West NileVirus,
Cytomegalovirus etc
 Plasmodium genus causing Malaria
 Prions: Creutzfeldt-Jakob disease

20. Transfusion-Transmitted
Bacterial Infection (TTBI)
 Bacteria is most common infective agent.
(1:5000 in platelet transfusion, 1:30,000 in red
cell transfusion)
 Caused by aseptic technique (via skin or
contaminated environment) and/or blood
preparations/storage.
 High grade fever with rigors, tachycardia or
systolic hypotension. May also present with
backache, abdominal pain, vomiting and
hypothermia

21. Investigations
 Blood culture and sensitivity from blood
donor and recipient
 Branula or Catheter culture and sensitivity
 IncreasedWBC, or CRP

22. Management
 Stop the transfusion
 Hydrate and resuscitate patient
 Rule out other immunological causes
(missmatch, clerical errors)
 Repeat cross-match
 Start empirical antibiotic until specific
organism narrowed down or isolated

23. References
1. Roback JD (ed). Non-infectious complications of blood
transfusion. Chapter 27, AABBTechnical Manual, 17th
edition. AABB, Bethesda, 2011.
2. Callum JL, LinY, Pinkerton PH, Karkouti K, Pendergrast
JM, Robitaile N et al. Chapter 5,Transfusion
Reactions. Bloody Easy 3: BloodTransfusions, Blood
Alternatives andTransfusion Reactions:A Guide to
Transfusion Medicine, 3rd edition. Canada: Ontario
Regional Blood Coordinating Network, 2011. [cited 2012
Sep 13
3. Transfusion reactions, 3rd edition. AABB Press, Bethesda,
2007.
4. Brohi K. Shock and BloodTransfusion.Chapter 2. Bailey
and Love’s Short Practice of Surgery, 25th edition. Hodder
Arnold, London, 2008