Blood transfusions Flashcards

1
Q

G n S and Cross match

A

GROUP and SCREEN – check ABO group and plasma antibodies in patient

Full crossmatch – checks patient’s blood against donor blood specifically

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2
Q

Grouping test

A

Use known anti-A, anti-B and anti-D reagents against the patient’s RBCs

o A positive result causes agglutination at the top
o A negative result will mean that the red cells stay suspended at the bottom of the vial

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3
Q

Antibody screen test

A

o Immune antibodies are IgG (these can cause a DELAYED transfusion reaction; extravascular haemolysis)

 (1) use 2 or 3 reagent RBCs containing all important RBC antigens between them
 (2) incubate patient’s plasma and screening cells using the Indirect Antiglobulin Technique (IAT)
• (a) Patient serum containing specific antibody added to reagent RBCs
• (b) Add Anti-Human Globulin (AHG) to promote agglutination
• (c) If +ve, reaction creates bridges between RBCs coated in IgG antibodies  visible clumps

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4
Q

Compatibility of RBC, platelets and plasma

A

RBC- ABO+D
Platelets- D
Plasma- ABO

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5
Q

What is a unit of blood

A

10 g/L increase in Hb in a 70-80 kg patient

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6
Q

When do you need to do a GnS and crossmatch

A

 For elective surgery, the patient should be group and screened before the operation
 If antibodies are not present, a crossmatch is NOT needed but the sample should be saved in the fridge
 If unexpected need for blood  provided <10 mins (by electronic issue as no antibodies are present)
 If antibodies are present, ALWAYS CROSSMATCH

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7
Q

RBC tranfusion indications

A

Major blood loss >30%
Peri-op Hb< 70
Post. hemp <80

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8
Q

Platelets tranfusion indications

A

Massive transfusion- aim for >75
Prevent bleeding (post chemo) if <10
Prevent bleeding surgery if <50
Platelets dysfunction- if active bleeding

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9
Q

1 Unit of platelets

A

Increase platelet count by 30-40 x 109/L

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10
Q

Most common acute reaction?

A

 Transfusion associated circulatory overload (TACO)

• Often pre-existing cardiac/respiratory problems

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11
Q

Types of acute reactions (<24hrs)

A
o	Acute haemolytic (ABO incompatible)
o	Allergic/anaphylaxis
o	Infection (bacterial)
o	Febrile non-haemolytic
o	Respiratory - TACO, TRALI
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12
Q

Delayed reaction (>24hrs) types

A
o	Delayed haemolytic transfusion reaction (antibodies) – Duffy and Kidd 
o	Infection (viral, malaria, vCJD)
o	TA-GvHD (week or 2 after transfusion)
o	Post transfusion purpura
o	Iron overload
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13
Q

Signs of acute reaction

A

 Increase in temperature or pulse
 Low BP

Fever, vomiting ect

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14
Q

What is Allergic transfusion reaction and treatment

A

Causes a mild urticarial or itchy rash sometimes with a wheeze – caused by allergy to donor plasma proteins

IV antihistamines

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15
Q

What is Febrile Non-haemolytic transfusion reaction

A
  • Occurs during/soon after transfusion (blood or platelets)
  • May cause a rise in temperature by around 1 degree, chills and rigors
  • Caused by the release of cytokines from white cells during storage

• Tx: transfusion stopped or slowed and may need to be treated with paracetamol

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16
Q

What is ABO incompatibility

A

• Symptoms and signs of acute intravascular haemolysis (IgM-mediated):
o General: restless, chest/loin pain, fever, vomiting, flushing, collapse, haemoglobinuria (later)
o Monitoring: Low BP, High HR, High Temperature

17
Q

Bacterial contamination

A

o General: restless, fever, vomiting, flushing, collapse
o Monitoring: Low BP, High HR, High Temperature

• Bacterial growth can cause endotoxin production which causes immediate collapse

o Platelets (stored at room temperature) > RBCs > FFP

18
Q

Anaphylaxis after transfusion

A

• Severe, life-threatening reaction soon after the start of transfusion
o Shock = Drop in BP + Rise in HR
o Very breathless with wheeze
o Often laryngeal and/or facial oedema

  • Mechanism: IgE antibodies in the patient cause mast cell degranulation
  • Most allergic reactions are NOT severe, but some can be in the case of IgA deficiency- anti IgA AB against donors IgA
19
Q

What is TACO and Sx and MX

A

• VERY COMMON; leads to pulmonary oedema/fluid overload – a TACO checklist exists to help alleviate
• Often caused by lack of attention to fluid balance – especially in…
o Cardiac failure, renal impairment, hypoalbuminaemia, very young/old

SoB
Low sats
High HR
High BP

• TACO responds to diuretics immediately (and has raised JVP)

20
Q

What is TRALI

A

• Looks at bit like ARDS (more common in FFP or platelet transfusion)
o Anti-WBC antibodies in donor blood
o These interact with WBCs in the patient
o Aggregates WBCs stick to pulmonary capillaries  release neutrophil proteolytic enzymes and toxic O2 metabolites  lung damage

TRALI does NOT respond to diuretics (no JVP)

20
Q

Delayed haemolytic transfusion reaction

A

Duffy and Kidd antigens

• Further transfusions with RBCs expressing same antigens  antibodies will lyse RBCs (extravascular haemolysis)
o This is IgG-mediated so takes 5-10 days

High bilirubin, reticulocytes, low Hb

21
Q

Antibody type against each RBC antigen

A

Anti-A, Anti-B = IgM antibodies

Delayed Reactions – Infections Anti-Rh, anti-Duffy, anti-Kidd = IgG antibodies

22
Q

Delayed infection in tranfusions

A

CMV
 Very immunosuppressed patients (e.g. stem cell transplant) can get fatal CMV disease
 Leucodepletion/irradiation removes CMV in WBCs

o Parvovirus
 Causes temporary red cell aplasia – so affects those with RBCs of a shortened life span
 Affects foetuses and patients with haemolytic anaemias (e.g. sickle cell, hereditary spherocytosis)

o Variant CJD

23
Q

Transfusion Associated Graft-Versus-Host Disease (TaGVHD)

A

• Rare but ALWAYS FATAL

o Donor’s blood will contain some lymphocytes that are able to divide
o Normally, the patient’s immune system will recognises these donor lymphocytes as foreign and destroy them
o In susceptible patients (very immunosuppressed), these lymphocytes are NOT destroyed
o Lymphocytes recognise patient’s tissue HLA antigens as foreign and attack

24
Q

How to prevent GvHD

A

• Prevention: irradiate blood components for very immunocompromised patients or have HLA-matched components

25
Q

Sx of GvHD

A

Diarrhoea
Liver failure
Skin desquamation
Bone marrow failure DEATH

26
Q

What is Post-Transfusion Purpura and Tx

A
  • Appears 7-10 days after transfusion of blood or platelets
  • Usually resolves in 1-4 weeks but can cause life-threatening bleeding
  • Affects Human Platelet Antigen (HPA) 1a -ve patients previously immunised via pregnancy or transfusion

• Treatment: IVIG

27
Q

What is Post-Transfusion Purpura and Tx

A
  • Appears 7-10 days after transfusion of blood or platelets
  • Usually resolves in 1-4 weeks but can cause life-threatening bleeding
  • Affects Human Platelet Antigen (HPA) 1a -ve patients previously immunised via pregnancy or transfusion

• Treatment: IVIG

28
Q

When are pregnant women scanned for RBC antigens

A

• All women have a group and screen at around 12 weeks (booking) and again at 28 weeks

29
Q

How can you treat a very anaemic baby in utero

A

• Sometimes, intrauterine transfusion may be needed if the baby is very anaemic
o The transfusion is done via the umbilical vein
o At delivery, monitor baby’s Hb and BR for several days as HDN can get worst

30
Q

Mechanism of anti-D Immunoglobulin

A

 The RhD +ve cells of the foetus will get coated by the exogenous anti-D immunoglobulin
 They will then be removed by the mother’s reticuloendothelial system (spleen) before they can sensitise the mother to produce anti-D antibodies
 For this to be effective, the anti-D injection must be given within 72 hours of the sensitising event

31
Q

Examples of sensitising events for Haemolytic disease of the newborn

A
  • Spontaneous miscarriages if surgical evacuation needed and therapeutic terminations
  • Amniocentesis and chorionic villous sampling (CVS)
  • Abdominal trauma (falls and car accidents)
  • External cephalic version (turning foetus)
  • Stillbirth or intrauterine death
32
Q

Other antibodies that can cause HDN

A

o Anti-c and anti-Kell can cause severe HDN

o IgG anti-A and anti-B antibodies from group O mothers can cause mild HDN
 This can usually be treated with phototherapy