Transfusion reaction: Difference between revisions
(Created page with "'''Transfusion reactions''' may occur during blood transfusion. Most commonly caused by clerical errors, like giving the blood to the wrong patient, drawing the wrong blood specimen, failing proper patient identification, wrong labelling, performing the ABO test wrong, etc. Some are mild, some are life-threatening. == Classification of reactions == According to pathomechanism: * Immune-related complications ** Antigen-antibody-mediated reactions *** Acute haemolyt...") |
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=== Treatment === | === Treatment === | ||
Iron chelation, phlebotomy. | Iron chelation, phlebotomy. | ||
<noinclude>[[Category:Transfusion medicine]]</noinclude> |
Latest revision as of 22:11, 5 November 2023
Transfusion reactions may occur during blood transfusion. Most commonly caused by clerical errors, like giving the blood to the wrong patient, drawing the wrong blood specimen, failing proper patient identification, wrong labelling, performing the ABO test wrong, etc. Some are mild, some are life-threatening.
Classification of reactions
According to pathomechanism:
- Immune-related complications
- Antigen-antibody-mediated reactions
- Acute haemolytic transfusion reaction
- Delayed haemolytic transfusion reaction
- Post-transfusion purpura
- Transfusion-related acute lung injury (TRALI)
- Anaphylaxis
- Immune cell-mediated reactions
- Transfusion-associated graft-versus-host disease (TA-GVHD)
- Transfusion-related immunomodulation (TRIM)
- Antigen-antibody-mediated reactions
- Non-immune-related complications
- Transfusion-related circulatory overload (TACO)
- Transfusion of infected blood – sepsis
- Hypothermia due to cold blood transfusion
- Massive transfusion syndrome
- Transfusion of haemolytic blood
- Air embolism
- Citrate intoxication – hypocalcaemia
- Transfusion of hyperkalaemic blood
- Haemosiderosis
- Thromboembolism
According to timeline:
- Immediate complications (0 – 15 minutes)
- Acute haemolytic transfusion reaction
- Anaphylaxis
- Air embolism
- Early complications (15 minutes – 24 hours)
- Transfusion-related circulatory overload (TACO)
- Citrate intoxication – hypocalcaemia
- Transfusion of infected blood – sepsis
- Hypothermia due to cold blood transfusion
- Thromboembolism
- Late complications (1 – 7 days after transfusion)
- Transfusion-associated graft-versus-host disease (TA-GVHD)
- Delayed haemolytic transfusion reaction
- Very late complications (weeks, months, years after transfusion)
- Haemosiderosis
- Transmission of pathogens
- Hepatitis
- Herpes viruses
- HIV
- Syphilis
- Malaria
WBCs and transfusion reactions
WBCs in blood products can cause many complications:
- Non-haemolytic febrile transfusion reactions
- Transfusion-associated graft versus host disease
- Virus transmission (CMV, EBV, …)
- HLA alloimmunization – formation of antibodies against HLA
Methods of leucodepletion/leucoreduction (removing WBCs):
- Buffy coat removal (removal of the layer containing WBCs and platelets after centrifugating blood) – removes only 80% of WBCs
- Washing – removing the noncellular fluid in RBC and platelet products and replacing it with saline – removes 70 – 90% of WBCs
- Filtration – removes 99,995% of all WBCs
Irradiation – kills all WBCs but doesn’t remove them. Useful if the function of WBCs is the problem and not the presence (i.e., antigens on them) is the problem, like in transfusion-associated graft-versus-host disease.
Acute haemolytic transfusion reaction
Etiology
- ABO incompatibility (most common)
- Incompatibility of other blood groups (rare)
- Kidd incompatibility
- Rh incompatibility
- Kell incompatibility
- etc.
Pathophysiology
- Recipient antibodies binding to A or B antigens on donor RBCs -> complement activation, phagocyte activation -> haemolysis of donor RBCs
- Activation of bradykinin (kallikrein-kinin system) -> vasodilation, hypotension, increased capillary permeability
- Hypotension -> release of catecholamines (neuroendocrine response) -> vasoconstriction in organs rich in vascular alpha-adrenergic receptors, such as kidneys, lung, gastrointestinal tract, and skin -> tissue hypoxia, kidney damage
- Complement activation -> cytokine release, granulocyte degranulation -> fever, hypotension, bronchospasm
- Activation of factor XII -> DIC
Clinical features
- Rapid onset after transfusion
- Fever
- Chills
- Suffocation
- Burning pain at IV site
- Back pain, chest pain
- Patients in coma or general anaesthesia
- Bleeding in surgical area (wounds, punctures)
- Hypotension
Complications
Treatment
- Stop transfusion immediately if any suspicion -> confirm diagnosis with direct Coombs test and re-do compatibility testing
- Supportive treatment
- Fluids
- Electrolyte correction
- etc
Delayed haemolytic transfusion reaction
Etiology
Patients who were previously sensitized to (and therefore have antibodies against) certain RBC antigens like KIDD or D antigens. Sensitization can occur during transfusion, pregnancy or transplantation.
Pathophysiology
Antibodies bind to donor RBCs -> complement and phagocyte-mediated haemolysis.
Clinical features
- Weeks after transfusion
- Similar as acute haemolytic transfusion reaction but less severe
- Can even be asymptomatic
Diagnosis
Positive direct Coombs.
Treatment
Not necessary unless there is renal impairment, just monitoring. Rarely fatal.
Non-haemolytic febrile transfusion reactions
Common complication! 0,5 – 6% of cases.
Etiology
Cytokines (pyrogens) produced by WBCs and released from RBCs during storage cause fever. Or, the recipient has antibodies against granulocytes or platelets, lysing them and releasing cytokines.
Clinical features
- Fever
- Flushing
- Chills
Treatment
Stop transfusion. Give paracetamol.
Prevention
Leukoreduction.
Post-transfusion purpura
Etiology
The recipient has anti-platelet antibodies, mostly anti-HPA-1a (human platelet antigen 1a), which will destroy both recipient and donor platelets upon transfusion.
Clinical features
- 5 – 10 days after transfusion
- Thrombocytopaenia
- Purpura
- Fever
Treatment
- IVIG (intravenous immunoglobulin)
- Highly purified immunoglobulins from a donor
- Regulates immune system
- Plasmapheresis
- Corticosteroid
Etiology
Anti-HLA or anti-HNA antibodies in donor product activates the recipient’s granulocytes.
Clinical features
- Within 6 hours
- Dyspnoea
- Hypoxia
- Cyanosis
- Hypotension
- Bilateral pulmonary oedema
Treatment
- Mechanical ventilation
- Steroids
Anaphylaxis, allergy
Etiology
- People with IgA deficiency
- Allergens inside transfused product (drugs etc)
- IgE inside transfused product
Pathophysiology
People with congenital IgA deficiency can have anti-IgA antibodies. These antibodies bind to IgA in the donor plasma and initiate allergic reaction.
Clinical features
- Allergy (mild reaction)
- Malaise
- Itching
- Urticaria
- Fever
- Anaphylaxis
- Laryngeal oedema
- Anaphylactic shock
Treatment
- Fluid replacement
- Antihistamines
- Steroids
- Epinephrine
- Airway stabilization
Prophylaxis
- IgA-free blood (washed blood) to IgA deficient patients and patients who previously had allergic reaction to transfusion
Transfusion-associated graft versus host disease (TA-GVHD)
Etiology
- Blood transfusion from relatives
- Severely impaired immunity
Pathophysiology
Donor lymphocytes are usually identified as foreign and destroyed by the recipient’s immune system, but when the donor and recipient HLA type is similar (relatives) the recipient’s immune system cannot recognize and destroy the donor lymphocytes. Immunodeficient persons also cannot destroy the donor lymphocytes. Donor T cells engraft in the recipient and recognize the recipient’s cells as foreign and mounts an immune response against recipient tissues.
Clinical features
- Days or weeks after transfusion
- Fever
- Rash
- Liver dysfunction
- Pancytopaenia
Mortality > 90%
Treatment
Largely ineffective. Immunosuppressive therapy?
Prevention
Giving irradiated blood products to patients at risk for TA-GVHD.
Etiology
Not well known.
Clinical features
- Transient immunosuppression occurring after allogenic blood transfusion
Prophylaxis
Leukodepletion of blood products.
Etiology
Large transfusion volume, too fast infusion, cardiovascular or renal disease.
Clinical features
- Hypervolaemia
- Dyspnoea
- Headache
- Hypertension
- Pulmonary oedema
Therapy
Stop transfusion. Upright position, diuretics, oxygen.
Prevention
Slow infusion.
Massive transfusion
Massive transfusion is the treatment of patient with severe shock. It can be lifesaving but can cause problems.
Clinical features
DIC, tissue hypoxia, bleeding.
Treatment
Fluid replacement, blood transfusion, cardiac support.
Cold blood transfusion
Etiology
Transfusion of too much unheated blood.
Clinical features
- Decrease in tissue oxygenation
- Bleeding
- Arrhythmias
- Exacerbates symptoms of hypokalaemia and hyperkalaemia
Prevention
Use of blood warmer.
Transfusion of infected blood
Etiology
Infection source
- Poor venepuncture technique
- Inappropriate blood storage
- Incorrect handling
Clinical features
- Severe shock
- Intravascular haemolysis
Treatment
Stop transfusion. Supportive therapy for shock. IV broad spectrum antibiotics.
Haemosiderosis
Etiology
50 – 100 units of RBC transfusion.
Clinical features
Bronze skin, cirrhosis, heart failure.
Treatment
Iron chelation, phlebotomy.