BLOOD COMPONENT TRANSFUSION REACTION Flashcards

1
Q

TYPES OF TRANSFUSION REACTIONS

A

• Acute TR- occurs within 24 hours post transfusion.
• Delayed TR- develops after 24 hours post transfusion.

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2
Q

most severe type of transfusion reactions

A

Hemolytic Transfusion Reaction

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3
Q

Two types of Hemolytic Transfusion Reaction

A

• Immediate HTR/ Intravascular HTR
• Delayed HTR/ Extravascular HTR

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4
Q

• Reaction takes place within the circulatory system.
• Hemolysis occur within few min after starting transfusion (<24 hrs)
• Due to IgM Abs, mediated by the rapid activation of complement and is usually associated with the transfusion of ABO in incompatible blood.

A

IHTR or Intravascular HTR

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5
Q

MANAGEMENT and THERAPY for IHTR or Intravascular HTR

A

• Stop transfusion immediately.
• Mannitol is the agent used to prevent the renal failure.
• Hypotension: intravenous fluid and vasoactive drugs .e.g. dopamine

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6
Q

• 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.
• Hemolysis occur after few hours or after about 3-7 days of transfusion.

A

Delayed HTR/ Extravascular HTR

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7
Q

Delayed HTR/ Extravascular HTR Could be due to

A

ALLO-IMMUNIZATION or ANAMNESTIC RESPONSE

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8
Q

• an immune response to foreign antigens from another human, most commonly occurring after pregnancy or blood transfusions.
• In chronically transfused patients, the risk for them developing antibodies against the red cell antigens (RBC alloimmunization) increases by 2% to 8%.

A

ALLOIMUNIZATION

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9
Q

Any immunological response in which a second or subsequent exposure to an antigen causes a greater and more rapid reaction than that elicited by the initial exposure. It is a manifestation of immunological memory.

A

ANAMNESTIC RESPONSE

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10
Q

SIGNS and SYMPTOMS of Delayed HTR/ Extravascular HTR

A

• Fall in Hgb
• Rise in bilirubin
• Mild jaundice within 5-7 days post transfusion
• Renal failure (rare)

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11
Q

NON HEMOLYTIC TRANSFUSION REACTIONS

A

• Febrile Non Hemolytic TR (FNHTR)
• Urticarial TR (allergic)
• Anaphylactic TR
• Transfusion- Related Acute Lung Injury (TRALI)
• Transfusion Associated Circulatory Overload (TACO)
• Graft Versus Host Disease (GVHD)

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12
Q

• These reactions are the most common and account for over 90 % of TR.
• ↑ temperature, >1 Cͦ
• 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.
• These occur within minutes of starting the transfusion

A

Febrile Non Hemolytic TR (FNHTR)

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13
Q

SIGNS and SYMPTOMS of Febrile Non Hemolytic TR (FNHTR)

A

• Fever
• Chills
• Malaise

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14
Q

THERAPY and PREVENTION for FNHTR

A

• 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.

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15
Q

LABORATORY INVESTIGATIONS for FNHTR

A

• No red/pink plasma
• DCT negative
• No increase in bilirubin
• No hemoglobinuria

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16
Q

• A type of immediate hypersensitivity reaction.
• Allergic signs and symptoms appear within few minutes of exposure.

A

URTICARIAL (ALLERGIC) TR

17
Q

• The donor’s plasma contain allergens which react with reagin present in patient’s plasma.
• The donor’s plasma contains reagin that combines with allergens in the patient plasma.

A

URTICARIAL (ALLERGIC) TR

18
Q

Pathophysiology of URTICARIAL (ALLERGIC) TR

A

Allergin- Reagin complex ➡️ Attachment to mast cell surface ➡️ Release of HISTAMINE

19
Q

THERAPY and PREVENTION for URTICARIAL TR

A

Antihistamine

20
Q

• This is a severe, life-threatening reaction, which occur in rare patients who are IgA deficient and have developed anti-IgA ab’s.
• These reaction developed quickly- within minutes of starting the transfusion.

A

ANAPHYLACTIC TR

21
Q

THERAPY and MANAGEMENT for ANAPHYLACTIC TR

A

• Keep IV line open with normal saline.
• Inject epinephrine
• Inject antihistaminic
• In cases of Hypoxia- give oxygen by mask

22
Q

Also known as non cardiac pulmonary edema

A

TRANSFUSION RELATED ACUTE LUNG INJURY
(TRALI)

23
Q

• Altered permeability of the pulmonary capillary bed by activation of complement, histamine mediated events, or prostaglandins which leads to fluid accumulation, inadequate oxygenation, and reduced cardiac return.
• Happens within 6 hours during transfusion
• Pathophysiology is not well established

A

TRANSFUSION RELATED ACUTE LUNG INJURY
(TRALI)

24
Q

Both the immune and nonimmune of this lead to damaged endothelium, leading to pulmonary capillary permeability and resulting in noncardiogenic pulmonary edema.

A

TRANSFUSION RELATED ACUTE LUNG INJURY
(TRALI)

25
Q

Types of TRALI

A

Immune TRALI
Nonimmune TRALI

26
Q

antibody mediated, one-hit event. Antibody against Human Leukocyte Antigen (HLA) or Human Neutrophil Antigen (HNA) react with recipient’s leukocytes, causing aggregates that occlude the pulmonary circulation.

A

Immune TRALI

27
Q

consists of a two-hit event. The first hit (i.e., lung trauma or an infectious or inflammatory disease in the patient) may result in priming of the patient’s neutrophils. Therefore, a proinflammatory priming event of the patient’s endothelium, which primes the patient’s neutrophils. The second hit (i.e., transfused biologically active substances accumulated during storage or antileukocyte antibodies) causes the activation of the primed neutrophils.

A

Nonimmune TRALI

28
Q

SIGNS and SYMPTOMS of TRALI

A

• Acute onset of respiratory distress
• Dyspnea
• Cyanosis
• Fever
• Chill

29
Q

THERAPY and MANAGEMENT for TRALI

A

• Oxygen therapy
• Intubation
• Intravenous steroids
• Leukocyte poor component is used

30
Q

• Occur with platelet concentrate transfusion.
• Rapid onset of thrombocytopenia due to production of platelet alloantibodies.
• Usually in multiparous female.
• Duration: 7-14 days from transfusion.

A

POST TRANSFUSION PURPURA (PTP)

31
Q

Therapy for POST TRANSFUSION PURPURA (PTP)

A

corticosteroids

32
Q

Complication of blood component therapy or bone marrow transplantation.

A

GRAFT versus HOST DISEASE (GVHD)

33
Q

Patients at risk for GRAFT versus HOST DISEASE (GVHD)

A

• Lymphopenic patients
• Bone marrow suppressed cases
• Fetus receiving intrauterine transfusion
• Newborn infants receiving exchange transfusion
• Congenital immunodeficiency syndrome

34
Q

THERAPY for GVHD

A

corticosteroids , prevention.

35
Q

Give the 2 NON IMMUNE, NON HEMOLYTIC TR

A

• IMMEDIATE: Bacterial overload, Circulatory overload
• DELAYED : Iron overload

36
Q

• an acute nonimmune transfusion reaction presenting with body temperatures usually 2°C or more above normal and rigors that can be accompanied by hypotension.
• occurs when a bacteria-contaminated blood component is transfused.
• Abruptness of presentation may be similar to AHTR

A

TRANSFUSION- ASSOCIATED SEPSIS (TAS)

37
Q

• More volume of blood transfused
• Cause : fast rate
• Leads to congenital heart failure , pulmonary edema
• Signs: chest pain, cough, hypertension

A

TRANSFUSION ASSOCIATED CIRCULATORY
OVERLOAD (TACO)

38
Q

• Long term complication of RBC transfusion
• Also known as transfusion haemosiderosis.

A

IRON OVERLOAD

39
Q

Therapy for IRON OVERLOAD

A

iron chelating agent.