2. Definition
• Any unfavorable and harmful transfusion
related events occurring in the patient during
or after transfusion of blood or components is
called transfusion reaction.”
7. Hemolytic TR
• Haemolytic TR are most severe type of
transfusion reactions and can be categorized
into two types.
1. Immediate HTR / Intravascular HTR
2. Delayed HTR / Extra vascular HTR
8. IHTR or Intravascular HTR
• In intravascular transfusion reaction the
haemolysis of red cells takes place within the
circulatory system.
• Haemolysis occur within few min after starting
transfusion ( <24 hrs ).
9. • This type of reaction is mainly due to IgM ab’s
(ant-A, & anti-B), mediated by the rapid
activation of complement and is usually
associated with the transfusion of ABO in
compatible blood.
• They occur with the transfusion of incompatible
blood products when antibodies in recipient
plasma complex with donor cellular antigens
causing compliment activation and subsequent
hemolysis.
10. SIGNS AND SYMPTOMS
Fever
• Chills
• Hypotension
• Chest and back pain
• Nausea
• Dyspnea
• Vomiting
• Haemoglobinuria
• Acute renal failure
• Pain at transfusion site
• Shock & DIC
11. MANAGEMENT AND THERAPY
• The diagnosis of hemolytic reactions is confirmed with
laboratory analysis of free hemoglobin levels, low
haptoglobin, bilirubin increases, direct antiglobulin
(Coombs) test, and evidence of hematuria.
• Stop transfusion immediately.
• Mannitol is the agent used to prevent the renal failure.
• Hypotension: intravenous fluid and vasoactive drugs
.e.g. dopamine
12. Delayed HTR / Extra vascular HTR
• Extravascular TR are rarely severe and mainly
due to IgG antibodies, e.g. Rh, kell or Duffy
system.
• These ab’s bring about the destruction of red
cells by the macrophages in the spleen or liver.
• They generally present 3 to 10 days after
transfusion.
13. SIGNS & SYMPTOMS
• Symptoms are much milder than AHTRs and
rarely result in major morbidity or mortality.
• mild fever
• Fall in Hb
• Rise in bilirubin and mild jaundice with in 5-7
days of transfusion
14. Febrile non-hemolytic TR
• the most common types of complications of
transfused blood products.
• classically present within 4 hours of
transfusion with an increase in temperature of
1°C and may be associated with chills, rigors,
anxiety, and headache.
15. • These are benign, self limiting reaction due to
the presence of ab’s to WBC or PLT antigens
and are usually seen in multi transfused
patients.
• SIGNS AND SYMPTIMS: Fever, Chills , Malaise
16. pathophysiology
• Due to the presence of anti leukocyte antibody and
antibodies to platelet in the patients serum. It may
be due to past transfusion or pregnancy.
• Ab react with donors WBCs, Ag – Ab complex
activate complement system.
• Release of pyrogens from WBCs result in rise
of temp.
17. THERAPY AND PREVENTION
• Give leukocyte poor red cells.
• Anti pyretic can be given before starting
transfusion, but they must be avoided as
much as possible as they mask IHTR.
18. Minnor allergic reaction
• Minor allergic reactions, a relatively common
type of transfusion reaction, occur in about
1% to 3% of transfusions.
• Symptoms are most commonly described as
urticaria, hives with or without pruritis.
• an immune response to recipient leukocyte
antigens or transfused plasma proteins.
• Tratment: anti-histamine.
19. Anaphylactic reaction
• These reactions are rare, but can be fatal if
unrecognized.
• These reaction developed quickly- within
minutes of starting the transfusion.
22. Transfusion related acute lung injury
[ TRALI]
• Transfusion-related lung injury was first
described in the 1950s.
• known as non cardiac pulmonary edema.
• TRALI is defined as an acute lung injury that is
temporally related to a blood transfusion;
specifically, it occurs within the first six hours
following a transfusion.
23. • It is typically associated with plasma
components such as platelets and Fresh
Frozen Plasma.
• though cases have been reported with packed
red blood cells since there is some residual
plasma in the packed cells.
24. Diagnostic criteria
• Acute onset hypoxemia.
• Ratio of Pao2/FiO2 <300 or SpO2 <90% at
room temperature.
• Occur during or within 6 hours before
transfusion.
• B/L diffuse pulmonary infiltrates.
• No evidence of left atrial hypertension(i.e.
circulatory overload.
25. Etiology and Risk factor
• The etiology of TRALI is currently not fully understood.
TRALI is thought to be immune mediated.
• Antibodies directed toward Human Leukocyte
Antigens (HLA) or Human Neutrophil Antigens (HNA)
have been implicated.
• 1. Multiparous donor- Antibodies develop through
exposure to fetal blood.
• 2. Blood component – platelet concentration
>FFP>packed red cell>granulocytes>cryoprecipitate>iv
immunoglobulin.
26. • 3. Massive transfusion
• 4. Stored blood products- inflammatory
mediators like cytokines and lipid soluble
substance accumulate during storage of blood
product.
• 5. Underlying clinical condition- factors such
as trauma, major surgery, sepsis
27. Clinical finding
• Dyspnoea/ respiratory distress requiring o2 support-
virtually all.
• Requiring mechanical ventilation-70%
• Documented hypoxemia
• Cyanosis-very common.
• Hypotension- majority.
• Fever-very common
• Clinical exam reveals respiratory distress and pulmonary
crackles may be present with no signs of congestive heart
failure or volume overload.
• CXR shows evidence of bilateral pulmonary edema
unassociated with heart failure.
28. Immediate management of TRALI
• Stop the transfusion immediately
• Support the patient.
• For mild TRALI cases Supplimental o2 and
supportive care may be sufficient.
• For the most severe case- IV fluid, mechanical
or non invasive ventilation and invasive
cardiovascular monitoring may be required.
29. Prevention of TRALI
• Avoiding blood from multiparous women
• Not using whole blood.
• Leukoreduction can be done
• avoid Blood which has been stored for long
duration
30. Transfusion-associated Graft-Versus-
Host Disease
• rare but fulminant and fatal complication of
blood products containing cellular
components (platelets and packed RBCs).
• It occurs when donor lymphocytes engraft in
the recipient and attack host cells they
recognize as foreign.
31. • Patients at risk for TA-GVHD include those
1. immunocompromised from stem cell
transplants,
2. B-cell malignancies such as multiple
myeloma, non-Hodgkin lymphoma, or acute
lymphocytic leukemia, Hodgkin’s disease,
3. congenital immunodeiciency syndromes.
4. New born infants receiving exchange
transfusion.
32. • TA-GVHD classically present 4 to 21 days after
transfusion but clinical suspicion should exist
for up to 6 weeks.
• Symptoms progress rapidly and generally
affect the skin, hepatic, digestive, and
hematopoietic organ systems causing fever,
rash, liver dysfunction, diarrhea, and
pancytopenia.
33. management
• Poor prognosis with mortality >90%.
• High dose steroid 1st line therapy
• Methotrexate and cyclosporin-A, used for
prevention.
34. Post transfusion purpura
• Defined as severe thrombocytopenia with
purpura occurring 5 to 10 days
posttransfusion.
• a very rare complication of transfusion.
• associated with high morbidity and mortality.
• Usually in multiparous female.
• Therapy: corticosteroids
35. Non-immune reaction
Transfusion associated cardiovascular overload
[TACO]
1. the occurrence of hydrostatic pulmonary edema
after transfusion of blood component therapy
2. The overall incidence of TACO ranges from 1% to
8% of transfused patients and is more prevalent
in critically ill patients with a history of
cardiovascular disease and left ventricular
dysfunction.
36. • Other risk factors that predict TACO include
the volume and rate of transfusion, especially
plasma products, and overall fluid balance.
• it responds rapidly to diuretic therapy and
afterload reduction.
37. Transfusion-Associated Hyperkalemia
• Hyperkalemia is a recognized (but inconsistent)
complication of massive blood transfusion.
• After 18 days of storage (the average time that
blood is stored), the potassium load in one unit of
packed red blood cells is 2 to 3 mEq .
• The K+ load in transfused blood is normally
cleared by the kidneys, but when systemic blood
flow is compromised (which applies to most
patients who need massive blood transfusions),
renal K+ excretion is impaired, and the K+ infused
in blood transfusions will accumulate
38. Citrate toxicity
• Citrate is a common anticoagulant used in stored
blood products and is generally metabolized by
the liver and quickly eliminated. However, with
rapid infusion rates, massive transfusion, or in
patients with liver dysfunction, citrate
accumulates in the plasma and chelates calcium
resulting in hypocalcemia. Severe hypocalcemia
leads to muscle weakness, tetany, arrhythmias,
myocardial dysfunction, and acquired
coagulopathy.
39. Iron Overload
• Packed RBCs contain approximately 250 mg of
iron per unit which can accumulate in patients
who require frequent transfusions for chronic
anemia or hemoglobinopathies.
• Iron overload occurs when deposits in the
liver, heart, and endocrine systems result in
organ dysfunction.
• Chelation therapy is the irst line of treatment.
40. Hypothermia
• The infusion of 1 unit of RBCs at 4°C can
decrease the core body temperature by
0.25°C.
• hypothermia is commonly associated with
massive transfusion and can result in platelet
and coagulation factor dysfunction,
arrhythmias, and myocardial depression.
42. • Platelet concentrates carry the highest risk of
bacterial contamination since they are stored
at 20 to 24°C, which provides a more suitable
environment for bacterial replication, as
opposed to red cell concentrates stored at 4°C
or plasma which is frozen.