9. Preterm- RDS/ SGA(2.28kgs) / severe
HDN
� 35+4 weeks preterm/ fmh delivered on 4/5/2015 at 1: 46pm, had distress
after birth CPAP X 2 d
� This infant developed jaundice in few hours of life (SBR : 10.4) , on
examination severe pallor , liver 3cm and spleen 1.5 cm .
� SBR : 10.4 (indirect), rh incompatibility, DCT : + ve , reti- count : 20% , Hb:
12.6
� Over the next 10 hours , SBR raised . Hence double volume exchange
transfusion with compatible O-ve blood carried out .
� Albumin (1gm/kg) primed exchanged transfusion
� IVIG given
� Post –transfusion SBR values were below exchange range hence started
on intensive phototherapy x 7-9 days , SBR monitored regularly
� On D8 , baby had severe anr=emia( Hb : 8.9g/dl) , 15ml/kg of PRBCs
transfused and started on erhthropoietin . Repeat values normalized.
12. HISTORY
� The first description of HDN is thought to be in 1609 by a French
midwife who delivered twins—one baby was swollen and died
soon after birth, the other baby developed jaundice and died
several days later. For the next 300 years, many similar cases were
described in which newborns failed to survive.
� It was not until the 1950s that the underlying cause of HDN was
clarified; namely, the newborn's red blood cells (RBCs) are being
attacked by antibodies from the mother. The attack begins while
the baby is still in the womb and is caused by an incompatibility
between the mother's and baby's blood.
13. INTRODUCTION
� Due to incompatibility in the Rh, ABO and minor blood group
systems between mother and baby .
� Erythroblastosis : rhesus incompatibility between mother and
fetus
� Important cause of hyperbilirubinemia requiring exchange
transfusion
� This is an alloimmune condition that develops in a fetus, when
the IgG molecules produced by the mother pass through the
placenta
� No inborn antibodies in the rhesus blood group system
14.
15. CLINICAL MANIFESTATION
� Wide spectrum : normal to still baby with hydrops fetalis
� Hemolysis leads to elevated bilirubin levels . Jaundice develops
within 24 hours and rapidly increases in intensity. Unconjugated
component is high
� the possibility of acute or chronic kernicterus
� Profound anemia can cause: high-output heart failure, with pallor,
enlarged liver and/or spleen,
generalized swelling, and
respiratory distress.
16. � Post –natal problems : asphyxia, pulmonary hypertension , pallor,
odema respiratory distress, coagulopathies (reduced platelets and
clotting factors) , jaundice and hypoglycemia ( hyperinsulinemnia
from islet cell hyperplasia)
� The prenatal manifestations are known as:
hydrops fetalis;
in severe forms this can include petechiae and purpura.
The infant may be stillborn or die shortly after birth.
17. DIAGNOSIS
� Blood tests done on the mother : Positive indirect Coombs test
� Blood tests done on the newborn baby : blood grouping and typing ,
DCT, Hb , reticulocyte count, peripheral smear and serum bilirubin
� Lab findings:
Anaemia
hyperbilirubinemia
reticulocytosis (6-40%)
thrombocytopenia
leukopenia
positive DCT
hypoalbuminemia
smear : polychromasia , anisocytosis, no spherocytes
18.
19. MANAGEMENT
Before birth : Intrauterine transfusion :
� given to fetus to prevent hydrops fetalis and fetal death
� Level of anti –D antibodies and optic density of amniotic fluid are
calculated from 24 weeks onwards every forthnightly
� Modified liley’s chart for antenatal detection of severity of fetal
disease in rhesus iso-immunisation is used.
� O.D.D > 0.1 or a rising titre indicates
severely affected baby severe anemia
20. Condt..
� Severe anemia 50ml of O –ve PRBCs are infused intrauterine into
fetus by cordocentesis .
� Severely affected fetus , transfusion done every 2-3 weeks till the
baby is mature enough for extra-uterine survival (once fetal lung
maturity achieved)
� After multiple IUTs, most of the baby’s will be D – ve donor blood
(DCT – negative ), however baby should be given exchange
transfusion to remove circulating maternal anti-D antibodies and to
correct anemia
21. Treatment
� After birth, treatment depends on the severity of the condition, but
could include:
� temperature stabilization and monitoring,
� phototherapy,
� transfusion with compatible packed red blood,
� exchange transfusion with a blood type compatible with both the
infant and the mother,
� Intravenous immunoglobins
� sodium bicarbonate for correction of acidosis and/or assisted
ventilation.
23. Early indicators of exchange tranfusion
� Cord haemoglobin of <10g/dl or hematocrit <30%
� Cord bilirubin of 5mg/dl or more
� Unconjugated serum bilirubin of 10mg/dl within 24 hours or 15mg/dl
in 48 hours or rate of rise of >0.5mg/dl/hour .
� Levels based on bilirubin nomogram
� Those with risk factors are transfused at a relatively lower bilirubin
level.
24. Goals of exchange transfusion
� Remove sensitized cells
� Reduce levels of maternal antibody
� Removes about 60% of bilirubin from plasma , resulting in a
clearence of about 30-40% of total bilirubin
� Corrects anemia
� Replacement with donor plasma restors albumin and needed
coagulation factors
� Rebound- usually 2 volume exchange is needed as bilirubin in tissues
will return to blood stream
25. Condt..
CHOICE OF BLOOD :
� O –ve blood cross- matched against maternal serum
� For subsequent exchange transfusions, irrespective of ABO group of
infant, O –ve blood cross matched against infant’s serum is used.
� HCT >80% , Screened for HIV, HbsAg , CMV etc
� Fresh citrate phosphate dextrose blood (not old than 3 days )
AMOUNT TO BE TRANSFUSED :
Double the blood volume of baby (160-180ml/kg)
PRE-TRANSFUSION :
CPD blood to be prewarmed ,Albumin primed exchange transfusion
Hb, PCV, bilirubin, glucose, potassium ,pH
26. Procedure
� Infant under servo-controlled radient warmer , monioring of HR, BP,
SPO2. iv cannula – ivf
� Assistant assigned to record blood volumes exchanged and
monitoring .
� Under aseptic precautions , exchange transfusion is carried out by
PUSH – PULL TECHNIQUE through umbilical vein.
� ISOVOLUMETRIC exchange transfusion ( simultaneous pulling
blood out of umbilical artery and pushing new blood in the
umbilical) – tolerated in sick newborns
� Transfused in small aliquots over 1 hour
� Post- exchange – started on phototherapy
� Post transfusion : Hb, PCV , bilirubin q4-6h , glucose, calcium ,
potassium and pH
29. INTRAVENOUS IMMUNOGLOBIN
� Normally FC receptor bearing cells from RES , mediates the
hemolysis of neonatal RBCs by IgG Antibodies .
� IVIG : inhibits this FC receptor mediated hemolysis and accelerates
the catabolism of anti- D antibodies
� IVIG : 0.5-1.0g/kg as a slow infusion over 2 hours
� Advantages: reduces the number of exchange transfusion and
duration of phototherapy
30. PREVENTION
� Anti –D immunoglobins (300ug) given IM , 72hours of delivery,
destroys the Rh +ve fetal RBCs , which might have seeped into the
maternal circulation (98%- protective efficacy)
� 300ug = 10ml of transplacental hmrrghe. If excessive haemorrhage,
large dose given. If in case twins : double doses given .
� Antenatally : 500ug of anti- D Ig , to all unsensitized Rh –ve women
around 28-32 weeks f GA , if delivery occurs 4 weeks later , additional
500ug of anti- D within 72 hours of delivery .
� App dose : 25ug / ml of fetal RBCs
� Prophylaxis : after abortion of Rh +ve conception, situations with
increased risk of fetomaternal haemorrhage .
