Adverse outcomes and the hazards of transfusion- amanda Flashcards
Does transfusions come with complications
Yes
Examples of transfusion complications
- acute transfusion reactions
- haemolytic transfusion reactions
- transfusion associated graft versus host disease
- transfusion associated acute lung injury
- transfusion associated circulatory overload
- transfusion transmitted infections
- transfusion associated necrotising enterocolitis
What does SHOT stand for?
Serious Hazards Of Transfusion
Key messages from SHOT 2022?
-deaths related to transfusion 35, although total oof 3499 incidents of incorrect practise reported
-haemolysis contributed to death in 1 case although total of haemolytic transfusion reactions were reported associated with major morbidity
-transfusion associated circulatory overload contributed to death in 8 cases out of 52 reported
-delayed transfusion contributed to death in 13 cases out of a total of 205 reported
-incorrect blood component transfusion errors reported 296 occasions
SHOT data 2015
26 deaths attributed to or related to transfusion
Major morbidity in 2015 (n=166)
ABO transfusion events- 7
Total number of errors in 2015 which didn’t result in harm (n=2555)
288 possible ABO-incompatible transfusion
What are the risks of transfusion?
Serious harm= 1:15,528
Overall risk of death where transfusion is contributory= 1:99,010 components issued
Risk of death from error= 1 in 322,581 components transfused
Complications of blood transfusion- haemolytic transfusion reaction
Immediate or delayed
Immediate- life threatening reactions frequently associated with ABO antibodies which are IgM complement activating (classical pathway) resulting in intravascular haemolysis
Delayed- reactions associated with extravascular haemolysis e.g., anti-D, anti-Jka, anti-Jkb, less severe more frequently associated with IgG antibodies
Extravascular haemolysis
Red blood cells that are coated with antibodies are specifically recognised in the reticuloendothelial system and destroyed by macrophages
What causes extravascular haemolytic reactions?
The recipients antibodies to Rh or non-ABO antigens
These patients usually have been exposed to the antigen through previous pregnancies, transplantation or transfusion
Clinical features of acute haemolytic transfusion reaction
Haemolytic shock phase:
- can occur after a few ml blood
- 1-2 hours after transfusion
Clinical features of acute haemolytic transfusion reaction
Urticaria, lumbar pain, flushing, headache, shortness of breath, vomiting, rigors, pyrexia, hypotension (low bp)
What are haemolytic transfusion reactions the result of?
Antibodies in the recipients plasma directed against antigens on the donors erythrocyts- results in rapid intravascular haemolysis of the donor red blood cells .
- ABO incompatibility due to clerical error is most frequent cause
What does ABO incompatibility in haemolytic transfusion reactions result in?
Haemoglobinemia, haemoglobinuria , disseminated intravascular coagulation (DIC), renal failure, complement-mediated cardiovascular collapse
What is urticaria?
Skin rash, pyrexia (fever)
What is haemoglobinuria
Condition in which the oxygen transport protein haemoglobin is found in abnormally high concentrations in the urine. Often associated with haemolytic anaemia in which blood cells are destroyed increasing levels of free plasma Hb
Disseminated intravascular coagulation
Leads to formation of small blood clot inside blood vessels through body- normal coagulation disrupted and abnormal bleeding occurs from the skin.
- these small clots also disrupt normal blood flow to organs such as kidneys making them malfunction
Aetiology of an acute haemolytic reaction
-incompatibility between patient antibody and donor red cell antigens
-patient antibody is usually IgM in nature and in sufficient concentration to cause red cell destruction
-IgM antibody activates classical complement cascade leading to formation of membrane attack complex on red cell surface and intravascular haemolysis of the red cell results
-anaphylatoxins C3a and C5a released due to complement activation contribute to the range of symptoms seen
Main symptoms of acute haemolytic reaction:
System: chills, fever
Vascular: hypotension, uncontrollable bleeding
Heart: increased heart rate
Chest: constricting pain
Transfused vein: heat sensation
Lumbar region: pain
Urinary: haemoglobinuria, hyperbilirubinemia
In acute haemolytic reaction why is hypotension and fever seen?
As a result of classical complement cascade activation C3a inflammatory cytokines TNF-α, IL-1 and MCP-1 are released which encourage release of histamine and serotonin from basophils and mast cells and activation of T and B lymphocytes.
Histamine can increase vascular permeability hence lowering blood pressure and can cause arteriole vasodilation as well as venous constriction dependent on receptor involved.
Due to C5a recruitment of phagocytes and neutrophils release of proinflammatory interleukins results – IL-1, IL-6, IL-8 and TNF-α occurs further contributing to hypotension and fever.
Explanation of other clinical symptoms in acute haemolytic reaction ….
Chest and lumbar pain: serotonin i a vasoconstrictor and can reduce blood flow to vital organs, constriction of the gut and bronchial smooth muscle due to C3a
Tachycardia: constriction of the blood flow to the heat-C3a, free haemoglobin can scavenge the vasodilator nitric oxide resulting in vasoconstriction to major organs
Further explanation of clinical symptoms of acute haemolytic reaction
Induction of adhesion molecules and release of tissue factor from endothelial cells-platelet activation
Hypotension provokes a neuroendocrine response including release of catecholamines which leads to vasoconstriction in alpha-adrenergic rich organs such as kidneys, lung and GIT and skin
IL-1 will lead to increase in body temp. And hypotension
Laboratory signs symptoms of acute haemolytic transfusion reactions
-haemoglobinuria
-reduced haptoglobins-binds free haemoglobin
-fall in haemoglobin following transfusion
-presence of schistocytes due to red cell haemolysis
-increased reticulocytes- physiological response to anaemia
-rise in serum LDH-released from haemolysis red cells
-pre-hepatic icterus (jaundice)-insufficient capacity to conjugate bilirubin due to rapid and sudden RBC turnover
-hyperkalaemia-potassium released from haemolysis RBCs
-Direct Antiglobulin Test positive
-disseminated intravascular haemolysis (DIC)
Causes of acute-IMMEDIATE haemolytic reactions
-sampling the wrong patient
-mislabelling the sample
-assignment of incorrect ABO group
-selecting incorrect donor group cells
-transfusing the wrong patient
Case study-bedside administration
Agency nurse looking after 2 patients on ITU- patient 1 is ORhD+, patient 2 is ABRhD+, for convince she opens patient 2’s record on bedside computer do patient 1 and leaves screen open. Patient 1’s Hb is 6.6g/dl on blood gas analyser (9.7g/dl on lab result) so transfusion is requested. Very busy so asks colleague to print blood collection lip which she does from PATIENT 2s details. Porter correctly collects red cells intended for patient 2. When red cells arrive agency nurse goes to patient 1s bedside table but can’t find wristband. Checks performed against computer screen at patient 1s bedside, still showing patient 2 details. Patient 1 is transfused blood prescribed for Patient 2. Patient 1 develops systems of ATR and transfusion stopped.
Delayed haemolytic transfusion reactions
-occur more than 24 hours following a transfusion
-Anamnestic response in a patient who has previously been sensitised to an antigen due to pregnancy or transfusion.
-symptoms usuallly mild
-unexplained post transfusion increment/anaemia in the absence of bleeding prompts investigation.
Anamnestic response
Renewed rapid production of an antibody on the second encounter with the same antigen
Causes of delayed haemolytic reactions
-misidentification of patient as indicated for acute haemolytic transfusion reactions but without patient and donor being ABO incompatible
-causative antibody is undetected in pre-transfusion tests: antibody is too weak to detect by standard technique, error in testing, historical antibody status inaccurate or unchecked
DHTR laboratory findings
-failure to achieve the haemoglobin increment
-elevated levels of unconjugated bilirubin
-increase in lactate dehydrogenase levels (LDH)
-spherocytes on the peripheral blood film
-positive DAT
-reduced haptoglobins
-repeat antibody screen tests indicate patient vs donor incompatibility
DHTR aetiology
-extravascular haemolysis of donor red cells sensitised with patients antibody
-antibodies are usually IgG in nature and therefore not as efficient at activating complement
-if complement is activated, results in formation of degradation products i.e.C3d and not to formation of the membrane attack complex (MAC)
-antibodies of the Kidd system are frequently implicated i.e. anti-Jka and anti-Jkb
DHTR aetiology continued
Antibody sensitised donor red cells are recognised by the reticuloendothelial cels of the spleen due to an abundance of Fc surface receptors on the macrophage surface
DHTR partial phagocytosis i.e. formation of spherocytes
-sensitised red cells are removed by partial or full phagocytosis of the reticuloendothelial macrophages of the spleen and to a lesser extent the liver
-partially phagocytosed red cells results in removal of part of the RBC membrane and formation of a spherocytes
-spherocytes will have a reduced survival in circulation due to lack of flexibility hence contributing to anaemia
