COMPLICATIONS AND DISEASES

ASSOCIATED WITH BLOOD

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 transfusion
reactions  Haemolytic transfusion
 Haemolytic transfusion reaction reaction
 Allergic reaction  Post transfusion purpura
 Anaphylaxis
 Transfusion-associated lung injury
 GVHD
• Non immunological • Non immunological
 Circulatory overload  Transfusion of infectious
 Bacterial contamination of donor
blood unit
agents
 Air embolism  Iron overload
 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
transfusion or pregnancy.
• Present with fever, occasional chills, rigors, headache.
• Occur within 30-60mins of transfusion.
• R/O HTR and 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.
 C3a & C5a cause vasodilation →hypotension,
ARF.
 Release of procoagulant from destroyed RBC
→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, throbbing
headache, nausea/ vomiting, Pyrexia, rigor,
Hypotension and vascular collapse.
 Others include Haemoglobinuria, DIC, Acute renal
failure with Oliguria, and death.
 Anaesthetized patient- hypotension, DIC
 Management
• Stop blood transfusion
• restore blood volume and blood pressure.
• 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 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
 Delayed HTR
• Due to secondary response in a patient
already previously sensitized to antigens
present on recently transfused red cells.
• It occurs within 5 to 10 days.
• Cf- Anaemia and jaundice
• Usually caused by Rh (anti-c) and Kidd (anti-
JK).
• 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, Immunoglobulin or 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.
• Cf- fever, chills, respiratory distress, dry cough
• CXR- Diffuse pulmonary infiltrate
• 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 the use of aseptic techniques in
blood donation, 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.
• 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 –
 Acidosis
 Hypothermia causing cardiac irregularities
•HAEMOLYTIC
DISEASE OF THE
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
•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, 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, ascitis 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
 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)
 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.