TRANSFUSION Dr OT Ojo Introduction • Blood transfusion is a life saving procedure but potentially hazardous. • In spite of measures designed to remove adverse effects of blood transfusion, complications remain a source of concern. • The type and frequency of complication however depend on the amount of care exercised in the preparation for, and the supervision of the transfusion procedure. • Blood transfusion should be considered only when there is no alternative means of treatment. Complications of transfusion Immediate Delayed • Immunological • Immunological Febrile non haemolytic Haemolytic transfusion transfusion reaction reaction Haemolytic transfusion Post transfusion purpura reaction Allergic reaction GVHD Anaphylaxis • Non immunological Transfusion-associated lung Transfusion of infectious injury agents • Non immunological Iron overload Circulatory overload Bacterial contamination of donor blood unit Air embolism FNHTR • Due to reaction of alloantibodies in the recipient against transfused leucocyte antigen. • Also due to release of cytokines from leucocytes in the stored blood. • Common in previously sensitized individual- previous transfusions or multiple pregnancies. • Present with fever, occasional chills, rigors, headache, anxiety. • Occur within 30-60mins of transfusion. • R/O HTR,TRALI, bacterial contamination of donor unit. • Management- Stop transfusion, give antipyretics/ antihistamine, slow speed of transfusion. • Prevention- Leucocyte-depleted packed cells. HTR • Haemolytic complication results from premature destruction of donor cells as a result of immune antibodies in the recipient. • Classification- immediate (acute) haemolytic and delayed haemolytic. • Immediate: Often result from ABO incompatibility mediated by by IgM or sometimes IgG Anti-A or Anti-B. Usually due to Clerical error- incorrect identification of recipient and incorrect labelling of sample bottle or filling of request form HTR… • Pathogenesis: Antibodies in patient plasma bind to donor red cells→ full complement activation (C5-C9)→ Acute intravascular haemolysis→ Hbinaemia, Hbinuria, methaemoglobin C3a & C5a cause vasodilation →hypotension, ARF. Release of procoagulant from destroyed RBC stroma →activation of coagulation →DIC HTR… • Clinical features: Occurs within mins of starting transfusion Heat or pain at the infusion site, loin or low back pain, chest tightness, breathlessness,tachycardia throbbing headache, nausea/ vomiting, Pyrexia, rigor, Hypotension and vascular collapse. Others include Haemoglobinuria, DIC, Acute renal failure with Oliguria, and death. Anaesthetized patient- hypotension, excess bleeding. Management • Stop blood transfusion • restore blood volume and blood pressure with normal saline. • Investigate • Investigations Confirm that recipient identity is the same as that on compatibility label and donor unit • Repeat grouping on pre-and post-transfusion sample of recipient , as well as donor sample. • Repeat the crossmatch on donor cell against recipient pre and post-transfusion sample. • DAT on recipient pre and post-transfusion sample • Check plasma for haemoglobinaemia (pink colouration) • urine for Haemogloninuria • LFT - ↑ unconjugated bilirubin • Test for DIC- PLT, PT/APTT, FDPs • E/u/Cr • Bacteria contamination- black/ purple discolouration of RC with evidence of haemolysis Blood culture of donor unit Delayed HTR • Occurs in a patient who was previously sensitized to certain RBC antigens. • Secondary immune response. • It occurs within 5 to 10 days. • Cf- Fever, anaemia and jaundice • Usually caused by Rh (anti-c) and Kidd. • DAT is +ve Post-transfusion purpura • This is characterised by a sudden onset of severe thrombocytopaenia 7 -10 days post-transfusion. • It follows a history of previous transfusion or pregnancy and is far commoner in women. • It is due to Anti-HPA -1a, both transfused and recipient PLT are destroyed. • Usu. self-limiting. • Otherwise,IV Immunoglobulin and plasma exchange may be needed. Anaphylactic reaction • It is caused by Anti-IgA in an IgA deficient person. • Prior sensitization or without stimulation • Anti-IgA-IgA complex activate complement → C3a &C5a generation. • Features : Nausea, abdominal cramps, vomitting, diarrhoea, hypotension, breathlessness, facial edema Shock may occur rarely and can be potentially fatal. • Stop transfusion immediately. • Treat with antihistamine, hydrocortisone, adrenaline. Allergic Reactions • Due to reaction between plasma proteins and IgE antibodies in recipient’s plasma→release of histamine. • Cf- Urticaria, rash and pruritus. • Treatment-antihistamine & hydrocortisone Transfusion-related acute lung Injury (TRALI) • Leucoagglutinins from donor+ leucocytes in recipient= leucocyte aggregate, lodgement in pulmonary microcirculation causes increase in vascular permeability. • Occurs within 1-4hrs of starting transfusion • Cf- fever, chills, respiratory distress, dry cough • CXR- Diffuse pulmonary infiltrates • Donors usu. Multiparous women. • Treatment-supportive Graft-versus-host disease(GvHD) • occurs when live lymphocyte are transfused to an immunocompromised patient. • Cf-fever, skin rash, vomiting, diarrhoea, hepatitis, pancytopaenia. • Prevention- Irradiation of blood. • NON-IMMUNOLOGICAL COMPLICATIONS Transfusion of infectious agents • These include Hepatitis B virus (HBV), Hepatitis C virus (HCV), Human Immunodeficiency virus (HIV), Cytomegalovirus (CMV), Filaria, Syphilis, toxoplasma and Malaria. • Reaction to bacteria and or its pyrogen: This is rare because of sterilization of fluid and disposable equipment. Can present with circulatory collapse. Prevention is by strigent donor selection, the use of aseptic techniques in blood donation, proper screening and the storage of blood at a temperature of 2-80C. Circulation Overload • Due to rapid transfusion of large volumes of blood without equivalent blood loss. • Can also occur after transfusion of small amt of blood to a patient with abnormal cardiac or renal function. • Treatment: Prop up in bed,O2, diuretic • Prevention: give packed cells use diuretics. Others • Thrombophlebitis: This is due to indwelling venous canula. • Air embolism: This has been eliminated by the use of plastic bags and a closed system. • Post-transfusion iron overload occurs in multiply transfused individuals. Complication of massive blood transfusion • Replacement of a patient’s total blood volume with stored blood within 24hrs. Dilution of Platelets, Reduction of coagulation factors, especially factors Va and VIIIa Hypocalcaemia and Hyperkaleamia, hypothermia Acidosis Hypothermia causing cardiac irregularities •HAEMOLYTIC DISEASE OF THE FOETUS AND NEWBORN (HDN) Introduction • It is a disease in which there is destruction of RBCs of the fetus or newborn by maternal alloantibodies against paternal antigens on the child’s RBCs. • Maternal antibodies is stimulated due to blood group incompatibility between mother and fetus. • Causal Red cell antigens-Rh-D, Rh-c, kell, A and B. • Rh-D, Rh-c, kell- can cause severe HDN while ABO incompatibility cause mild disease. • Others- Duffy, Kidd , MNS •Rh HDN Introduction • RhD negative mother pregnant with RhD +ve baby. • RhD +ve fetal RBC cross into maternal circulation at parturition/ 3rd trimester and sensitize the mother to produce anti-D. • Sensitization could also be due to Amniocentesis, External cephalic version, threatened abortion,abortion and chorion villus sampling or trauma to placenta. Pathogenesis • Fetomaternal haemorrhage→10 Immune response with production of IgM abs in the 1st pregnancy, baby is not affected • FMH in 2nd pregnancy→ 20 Immune response with production of IgG abs which cross placenta to coat fetal RhD +ve RBC. • IgG coated fetal RBCs are destroyed in the spleen→ anaemia →erythroid hyperplasia in the BM →extramedulary erythropoesis in the spleen and liver. • uncojugated bilirubin in fetus cross into maternal circulation and metabolised • ↑uncojugated bilirubin in neonate due to immaturity of glucoronyl transferase, this may cross the BBB and damage basal ganglia → kernicterus. Clinical features • Variable • Mild anaemia & jaundice • Kernicterus-neurological deficit resulting in deafness, mental retardation, spasticity, and epilepsy • Still birth (Hydop fetalis)-severe anaemia, hepatosplenomegaly, ascites and anarsarca Laboratory investigations ANC: • mother History of sensitization Blood group-ABO and Rh Antibody screening, identification, titer • Blood group of the father • Fetal Amniocentesis- assess conc. of bilirubin, done between 28-32wks GA, but if bad obstetric Hx done 10wks prior to the date of previous fetal or neonatal death. Laboratory investigations… Indicated when maternal anti-D titer is 1:32, rising anti-D titer on ff up visit, bad obstetric hx (previously severely affected offspring). Liley’s chart- Zone 1 (low), II (middle), III (high) Zone III indicate severely affected fetus with imminent death: GA<34wks- intrauterine transfusion, GA >34wks- delivery Zone II- repeat and do as in I or II Zone I-proceed to term • Cordocentesis- estimate Hb and bilirubin, blood group, DAT • Velocimetry of fetal middle cerebral artery by doppler USS- ↑vel correlate with fetal anaemia (IUFT), replacing amniotic fluid spectrophotometry for fetal monitoring. Laboratory investigations… • Newborn Blood group PBF- numerous NRBCs (erythroblastosis), polychromasia DAT-+ve Hb and bilirubin conc.-do urgent EBT if Hb> 12g/dL or unconjugated bilirubin> 5mg/dL • Maternal post delivery-Betke-Kleihauer test/ flow cytometry for FMH vol. estimation Rh HDN Blood film from a baby with Rh HDN due to anti-D showing polychromasia and large numbers of NRCs, but relatively few spherocytes. Treatment • Fetus- IUFT or delivery depending on fetal lung maturity • Neonate- EBT if bilirubin is rising rapidly Phototherapy Albumin infusion Prevention of Rh isoimmunisation • During antenatal- anti-D IgG given to RhD-ve mother with potentially sensitizing episode, 250iu given before 20wks GA and 500iu thereafter. • Post delivery- administer anti-D IgG to RhD –ve mother within 72hrs of delivery of Rh D +ve neonate. Dose-500iu of anti-D IgG to neutralize 4mls of fetal red cell. Increase anti-D dose if there is FMH> 4mls, at 125iu/ mL of FMH > 4mL ABO HDN • Commoner than Rh HDN. • Usually mild • Usually cause by immune IgG abs in group O mothers carry group A or B fetus. • Ist pregnancy may be affected. • DAT may be –ve or weakly +ve. • PBF- spherocytosis, polychromasia • Treatment-phototherapy, EBT in severe hyperbilirubinaemia. ABO HDN Blood film from a neonate with ABO HDN due to anti-A, showing very large numbers of spherocytes, polychromasia and no nucleated red cells.