Blood Groups and Transfusions PDF

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CharismaticMridangam

Uploaded by CharismaticMridangam

Griffith University

Wadie Rassam

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blood groups transfusions medical lectures medicine

Summary

This document covers blood groups and transfusions, including ABO and Rh blood groups, transfusion reactions, and haemolytic disease of the fetus and newborn. It also details the principles, investigations, and safety measures related to blood transfusions.

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Blood Groups and Transfusions Wadie Rassam Griffith University MD Lecturer PGY4 Doctor Learning objectives Describe the ABO and Rh blood groups and explain the basis of transfusion reactions Overview Blood groups - Genetics – antigens and antibodies Principles of transfusions - Investigations - grou...

Blood Groups and Transfusions Wadie Rassam Griffith University MD Lecturer PGY4 Doctor Learning objectives Describe the ABO and Rh blood groups and explain the basis of transfusion reactions Overview Blood groups - Genetics – antigens and antibodies Principles of transfusions - Investigations - group and hold, cross-match, emergencies - Pre-screening - Safety Transfusion products - 5 types, their constituents and indications Transfusion reactions – classify, define, aetiology, pathophysiology, clinical features, complications/prognosis à investigations and management Haemolytic disease of fetus and newborn Recap of genetics - Chromosome – structure containing DNA and protein, found in the cell nucleus - Gene – segment of DNA on a chromosome that encodes for a certain trait - Allele – alternative form of a gene Classification - There are ~250 antigens expressed on the surface of RBCs - These 250 antigens are grouped into 36 ‘blood group systems’ or ‘antigen-antibody systems’ - ABO, Rh (Rhesus), Kell, Duffy, Kidd, Diego, MNS, Lutheran, P, Lewis, I, Auberger, Junior, Xg, Scianna, Dombrock, Colton, Landsteiner-Wiener, Chido/Rodgers, Hh, Indian, Ok, Rhassociated glycoprotein (RhAG), Gerbich, Knops, Cromer, John Milton Hagen (JMH), Diego, Cartwright, Langereis, Cost, Auger, Tektin, FORS, Vel, and Wright - A bit overhwleming... Classification - For the purpose of classifying blood groups and ordering transfusions, two of these systems are most clinically relevant - ABO system – determined by a gene on chromosome 9, which comprises three potential alleles that encode for two antigens - The Rh system – determined by many genes on chromosome 1, mainly the RHD and RHCE genes, comprising two potential alleles that encode for one antigen - Someone’s overall ‘blood group’ is a combination of these blood group systems AB+ - ABO system Rhesus system ABO – genetics - antigens - The A and B alleles are codominant, meaning that if one inherits both alleles from their parents, both are expressed - The O allele is recessive. Therefore, someone’s blood type is O if they have two O alleles - Possible genotypes: ABO – genetics - antigens - The A and B antigens are based of the ‘H antigen’ - H antigen with nothing attached = blood group O - H antigen with one sugar attached at terminus = either blood group A or B differ by a single sugar ABO – genetics - antibodies - Over the course of life, we develop antibodies to the antigens within the ABO group we don’t have A cannot be given B - For example - someone who is blood type A has anti-B antibodies - This is relevant to determining blood transfusion compatibility. - When transfusing packed red blood cells (pRBCs), you are cautious about ensuring the recipient’s antibodies don’t attack the transfused RBCs’ antigens When transfusing plasma containing product (e.g. FFP), you are cautious about ensuring the plasma’s antibodies don’t attack the recipient’s RBC antigens ABO – genetics - antibodies - Extrapolating this principle: - universal recipient Blood group AB – receives AB A B O pRBCs; AB plasma Blood group A – receives A O pRBCs; A AB plasma Blood group B – receives B O pRBCs; B AB plasma Blood group O – receives O pRBCs; AB A B O plasma universal donor Remember: O is the universal dOnOr of pRBCs Rhesus – genetics - antigens - Inherited independently of the ABO system The Rh positive (Rh+) allele is dominant (D) The Rh negative (Rh-) allele is recessive (d) Possible genotypes: Rh+ Rhesus – genetics - antibodies - Unlike in the ABO system, anti-D antibodies do not naturally develop in Rh- people!! - Rather, 50% of Rh- people who are exposed to Rh+ positive blood will develop these antibodies – this occurs through inappropriate transfusion or fetomaternal haemorrhage Blood groups - Being blood type O and being rhesus negative are most common O = 45%, A = 30%, B = 20%, AB = 5% (approximate) Rh+ = 85%; Rh- = 15% O+ Most common blood type is O- Combining all this… Overview Blood groups - Genetics – antigens and antibodies Principles of transfusions - Investigations - group and hold, cross-match, emergencies - Pre-screening - Safety Transfusion products - 5 types, their constituents and indications Transfusion reactions – classify, define, aetiology, pathophysiology, clinical features, complications/prognosis à investigations and management Haemolytic disease of fetus and newborn Investigations Prior to ordering a blood transfusion, you need to: - Order a group and hold AKA type and screen AKA group and save - Group = 1) define pt’s blood group 2) Screen recipient plasma for alloantibodies against the most clinically significant antigens (not only ABO and Rh) Hold = hold pt’s blood in lab incase transfusion needed - If blood is needed, order a cross match - The pt’s blood is matched to an appropriate donor The pt’s blood and donor’s blood are tested in the lab (electronic and/or serologic) prior to releease from blood bank Investigations In some instances, using cross matched blood isn’t possible e.g. catastrophic haemorrhage. This may be done following a massive transfusion protocol – blood bank releases large amounts of blood to be readily available whilst awaiting group+hold/cross match If urgent pRBCs, what type of blood would you use? O- If urgent FFP or platelets, what type of blood would you use? AB+ Pre-screening All blood from the bank is subject to rigorous screening - Questionnaire – important for prion prevention as cannot be tested for in blood - Blood test – FBC, blood type, infectious screening +/- other depending on individual pt e.g. malaria testing if recent travel - For specific patient groups, further measures taken - Irradiation – inactivates lymphocytes for patients with GvHD Washing – replaces plasma with alternative solution for patients with previous transfusion reactions CMV- blood for immunocompromised pts Safety The most common cause of ABO incompatibility transfusions is improper labelling and patient misidentification Safety measures: - Written consent prior (unless in emergency) - Labelled specimen with 3 patient identifiers. Often this must be hand written on the specimen/a patient sticker cannot be used - Administered by 2 clinical staff - Timer started once left blood bank – must be used within 4 hours; if no longer needed ideally take back to blood bank! Overview Blood groups - Genetics – antigens and antibodies Principles of transfusions - Investigations - group and hold, cross-match, emergencies - Pre-screening - Safety Transfusion products - 5 types, their constituents and indications Transfusion reactions – classify, define, aetiology, pathophysiology, clinical features, complications/prognosis à investigations and management Haemolytic disease of fetus and newborn Types of blood products Two types of blood products: - Whole blood - Fractionated blood products most common Whole blood is rarely used as patients usually only needed a single component e.g. pRBCs for severe anaemia. Therefore, more use can be made of the patient’s blood - For example, whole blood may be used in autologous manner (transfusing the pt their own blood) e.g. big blood loss during surgery OR for Jehovah’s witnesses Types of blood products Fractionated blood products: - 1) Packed red blood cells - most common Collection of RBCs with plasma removed. For haemorrhagic shock, pre-operative planning, severe anaemia (Hb < 70) though this is a guideline and clinical scenario must be considered give more if think will lose more in transfer - 2) Platelets - Platelets in plasma or additive solution For severe thrombocytopenia ( fluid on lungs, osmosis short of breath For completion - Chronic infection - e.g. BBV – very uncommon now by virtue of rigorous screening Metabolic Reactions for completion Massive transfusion related complications - Can occur with any blood product when given at high volumes hypocalcaemia, hyperkalaemia, alkalosis, hypothermia, metabolic disturbances coagulopathy acid/base disturbances primary - HFE gene mutation Iron overload (secondary haemochromatosis) - pRBCs each contain 250mg of iron (because of haemoglobin), whilst iron excreted poorly iron is excreted at a rate 1mg/day - If a patient requires iron infusion post blood transfusion, subtract 250mg for each bag of pRBCs that the patient received subtract 250 mg iron for each bag of RBC infusion avoid iron overload Haemolytic disease of the fetus and newborn Underlying sciences – discussed earlier in slide Define - Disorder characterised by destruction of fetal/newborn RBCs by maternal antibodies due to blood group system incompatibility Classification/aetiology. - Whilst Rh incompatibility is most talked about, it can occur with numerous blood groups - - Rh incompatibility - most serious form ABO incompatibility – present in 20% of all pregnancies; however only 5-10% give anti-D prophylaxis of babies are symptomatic Other blood group systems e.g. Kell avoid sensiti Haemolytic disease of the fetus and newborn Classification/aetiology anti-D antibodies. Seen in Rh - mother and Rh + baby - This is caused by maternal exposure to fetal blood in pregnancy - Pregnancy complications e.g. placental abruption, ectopic pregnancy, miscarriage Antenatal procedures e.g. amniocentesis Sequalae of trauma - Rh incompatibility is rare and will usually only occur in pts who had poor cause mum's blood to mix with baby's amniocentesis antenatal care Pathophysiology – Rh incompatibility - First pregnancy with Rh- mother and Rh+ baby – fetomaternal haemorrhage à mum produces IgM antibdoies against Rh antigen à sensitise to future pregnancies seroconverts to IgG which can cross placenta small enough to cross - immediate response - This antibody production usually occurs at birth or with fetomaternal haemorrhage, therefore first baby is not affected Haemolytic disease of the fetus and newborn Pathophysiology – Rh incompatibility - Second pregnancy: maternal IgG antibodies against Rh antigen cross placenta à causes fetal RBC agglutination and haemolytic anaemia Clinical features - Note that ABO incompatibility is more common but usually has a mild disease course! agglutinate, destroy - These features are are far more common in HFND caused by Rh incompatibility - Prenatal – hydrops fetalis – very high mortality rate Postnatal – anaemia, jaundice, HSM if survive - significant pathophysiology Haemolytic disease of the fetus and newborn Diagnostics - Prenatal – USS for evidence hydrops fetalis (widespread oedema) - Postnatal - evidence of haemoloysis in chemistry FBC – anaemia Coombs test - confirms the incompatibility Treatment - very advanced level treatment required in a tertiary hospital. May involve blood transfusions, phototherapy for jaundice and IVIG to treat anaemia destroy unconjugated bilirubin - stop deposition in brain from crossing BBB Haemolytic disease of the fetus and newborn Prevention - Rh incompatibility is now rare due to prophylaxis. - How it works: Seems counter-intuitive – the mum is producing anti-D against the baby’s Rh antigens, why would you give more anti-D? Rh - ve - give Anti-D Preventing mother from creating antibodies - When to give – for Rh- mums only Rh + - give Anti-D again within 72 hours post-birth - 28 weeks gestation anti-D to: destroy foetal blood cells - stop sensitisation 34 weeks gestation saves reactions in future pregnancies stop anti-D antibodies produced by mother in future IF the baby is Rh+, give within 72 hours post-natally AND if fetomaternal haemorrhage has occurred, give during the pregnancy Questions 1) Why does 250mL of pRBCs have a much higher risk of causing fluid do not distribute b/w intravascular and extravascular space overload compared to 250mL of 0.9% NaCl? RBCs overload 2) Which of these CXRs belongs to someone with TACO vs TRALI? Why? TACO - simply fluid overload, pumped through lungs Questions 3) A mother who is O+ has an A+ baby and has HDFN due to ABO incompatibility. This is her first pregnancy. Unlike HDFN due to Rh incompatibility which does not occur in the first pregnancy, why could it occur in the first pregnancy if its caused by ABO incompatibility? mother has already formed A and B antibodies naturally FNHTR Clinical scenario A 72 year old male is admitted to the orthopaedic ward following a total hip replacement. He has 1.5L of intra-operative blood loss and a FBC D1 post-op shows a Hb of 69. His medical history includes HTN on hypertension Amlodipine, GORD on pantoprazole and Crohn’s disease on mesalazine. transfuse As he is symptomatic from his anaemia with SOB, he is transfused 1 unit of PRBCs. He develops a fever of 38.3C shortly after this. His blood pressure and heart rate are both normal and he feels otherwise well. He has no infective symptoms and the hip examines unremarkably with a well opposed wound. FNHTR How would you approach this? Order investigations Inflammatroy reaction UEC Venous gas status Cultures - culture blood Thank you! Email: [email protected] Good luck!!! J

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