Symposium "Transfusion Medicine--ll

Haemolytic Disease of Newborn

Anil Narang and Naveen Jain

Neonatal Division, Department of Pediatrics, Postgraduate Institute of Medical Education and Research
(PGIMER), Sector 12, Chandigarh

Abstract : Hemolytic disease of the newborn (HDN) occurs due to maternal IgG antibodies crossing the placenta
thereby producing hemolysis mainly due to Rh, ABO and Kell groups. A systematic approach to the Rh HDN involves
an obstetric history of previous isoimmunised baby, timing and regular monitoring of maternal Rh antibodies and
pigment assay of amniotic fluid. Timely decision regarding in utero transfusion and early termination of pregnancy
based on the maternal monitoring has radically improved the outcome of these babaies. Antenatal prophylaxis with
anti D has resulted in great reduction in the magnitude of Rh problem. The fetal blood sampling and in-utero intravenous
transfusions has made it possible for almost 100% survival of isoimmunised pregnancies without hydrops. Alternative
methods - IVIG and plasma exchange are still of limited application. ABO HDN though common is not a serious form
of disease and dose not warrants invasive antenatal monitoring. Anti-Kell is found in patients having received multiple
transfusions and the rapid progress of hemolysis in them may not allow such systematic follow up as in Rh HDN.
[Indian J Pediatr 2001; 68 (2) : 167-172]

Key words: Rh hemolytic disease; Neonate;Antenatal approach; ManagementProphylaxis.

Hemolytic disease of the newborn results from the blood
group incompatibility between mother and fetus ~.
Maternal IgG antibodies produced in response to the
antigens derived from fetal red cells, cross the placenta,
and are responsible for hemolysis and anaemia. The
most important one in terms of severity is due to anti-
D antibodies of Rh-negative mothers. The others are
ABO incompatibility, Kell group, anti-C and other rare
g r o u p incompatibilities. With the control of Rh
isoimmunisation due to prophylaxis, and in-utero
transfusion, the rare groups causing hemolytic disease
are becoming increasingly important.
Historical Aspect : A New Blood Group System 2
Levine and Stetson (1939) proposed a new blood group
system when they described a severe blood transfusion
reaction in a woman with post partum hemmorhage, her
blood causing agglutination with her husbands cells as
well as with 80% of the other blood group 'O' samples
(both patient and her h u s b a n d w e r e group 'O').
Landsteiner and Weiner (1940) discovered ('Rhesus
antibodies' from Rabbits injected with Rhesus monkey
RBC's. Levine, Kalrin and Burnham (1941) discovered
Rh antibodies and proposed that Erythroblastosis fetalis
was an isoimmune disorder caused by them. Fisher
made a major contribution to genetics of Rh antigens;
Reprint request 9Dr. Anil Narang; Neonatal Division, Dept.
of Pediatrics, PGIMER, Sector 12, Chandigarh.
E-mail : anilnarang@yahoo.com
Bevis (1950) introduced the concept of analysing blood
pigments in amniotic fluid to assess the severity of
hemolytic disease and Liley extended this work for the
management of affected pregnancies.
Magnitude of the Problem
The incidence of hemolytic disease of the newborn
depends on prevalence of Rh-negative women. 8% of
Indian women are Rh negative as compared to 14.4% of
Americans, and 11-21% of Europeans whereas none of
the Chinese and Japanese 3 is Rh negative. At PGI, 6.9%
women were found as Rh negative as compared to 5.7%
of the women in Mumbai 4-5. Even amongst them, only
6-8% of them are isoimmunized with varying degree of
severity. ~6
Clinicians Approach to the Rh Problem
Once a mother is known to be Rh negative, the fol-
lowing sequence should be followed-
(a) Husband's Blood Group and Zygosity
If the husband is Rh positive, and homozygous (DD), all
fetuses are likely to be affected. If he is heterozygous,
(Dd), 50% case may be unaffected. There is no recog-
nised anti-d serum, so zygosity can be predicted only by
indirect means. The other antigens are identified by
Anti-D, anti-c, anti-C, anti-E, and anti-e sera.
Recently prenatal diagnosis by fetal DNA studies has
been attemped 46but genetic diversity make it difficult

Indian Journal of Pediatrics, 2001; 68 (2) : 167

 Anil Narang and Naveen Jain
and the major silent RHD allele (named RHD2) is found
with no expression to add to the confusion.
(b) Past Obstetric History
If the mother has history of fetal/neonatal death, or af-
fected child requiring treatment, then the severity in the
present pregnancy is likely to be more with similar time
of affection.
(c) Assessment of Maternal Antibody
It may be several weeks, before the mother actually pro-
duces antibodies after exposure and sensitisation to
Rh+(ve) fetus. Hence first sample tested may be nega-
tive for antibodies thereby requiring repetition at least
2-3 times, the last time in the third trimester. The tim-
ing of detection of antibody has a bearing on the like-
ly outcome of the pregnancy. A maternal antibody ti-
tre of greater than 1:4 indicates sensitisation and a titre
of 1:16 is considered critical (may very from lab to lab)
i.e., below this titre no severe affection/fetal loss occurs.
If there is no previous history of affected pregnancy,
monthly assessment is sufficient starting at 16-18 weeks
till critical titre is reached. Incase of previous history,
start assessment similarly, with more aggressive mon-
itoring (using amniocenteses) from the gestation at
which previous sibling was affected. In PGIMER, Chan-
digarh, two weekly assessment is done till 30 weeks and
then weekly till term in isoimmunised cases. Actual
antibody level assay is 8less tedious, more accurate
method, critical level being 4iu/ml, 4-8 being moder-
ately severe and more than 10-severe disease.
(d) Spectrophotometric Analysis of Amniotic Fluid
It should be performed (i) when maternal antibody level
reaches critical level or (ii) at least 10 weaks before the
previous fetal/neonatal death, intrauterine transfusion,
but not before 17-18 weeks because fetal RES is not well
developed by then, and cannot destroy RBC. Repeat
tests should be done twice on weekly basis depending
upon the severity a n d the previous result.
The fluid is centrifuged and optical density at differ-
ent wavelengths between 300 and 700 m m plotted. If
bilirubin is present, a peak is observed between 425-450
ram. The amniotic fluid obtained under USG guidance
is clear in a normal pregnancy. But in Rh isoimmunisa-
tion it is bright yellow because of the bilirubin. The fluid
is photosensitive and should not be exposed to light. The
levels of deviation from expected slope (ODD at 450) are
classified by Liley 14 into 3 zones. Zone I-Mild/safe,
Zone II-Moderately severe, repeat after few days, Zone
III-indication for IUT (Intrauterine transfusion) or ter-
mination if gestation sufficient. This method is reliable
beyond 27-wks although extended 19-26 week charts
are available. (Bowman).
168
This method does not correlate well with PCV of fetus
but prognosticates outcome fairly accurately. A high
zone indicates cardiac failure resulting in inability of
fetus to deliver the break d o w n products to placenta, is
This predicts hydrops / neonatal death. So IUT / delivery
is indicated. Mid zone indicates that fetus is definitely
affected but is not in immediate jeopardy. Meconium
can produce similar ODD 450 tracing. But marked ab-
sorption and steep slope may help to differentiate. It
dears up in 2-3 weeks however, if noted after 35 weeks
it itself may be an indication to terminate the pregnancy.
Fetal blood may give false positive tracing due to high
level of bilirubin in it. Repeated amniocentesis is asso-
ciated with a hazard of increased feto-maternal hem-
morhage and increased antibody titre in mother. 16An
action line method was developed28 and tested to fore-
cast presence, severity, rate of increase of fetal hemol-
ysis and optimal time for intervention.
Alternative methods of spectrophotometry include
extraction on chloroform and their assays. This elimi-
nated false positives, heme pigments, meconium etc. 19
Imaging in Rh Isoimmunisation
Ultrasonography can be utilised for evaluating hepat-
osplenomegaly.2~Umbilical vein and Intrahepatic Portal
vein flow velocities, fluid in serious cavities and pres-
ence or absence of polyhydramnios. Evaluation of pla-
centa is also a useful modality in monitoring pregnancy
affected by hemolytic disease of the newborn. Ultra-
sound is necessary to guide in intrauterine transfusion
and continuous non-invasive monitoring of the fetus.
Recently with increasing safety of fetal blood sampling,
the reliability of ultrasound alone for monitoring for hy-
drops is decreasing.
FETAL BLOOD SAMPLING
Fetal blood sampling is advantageous for identification
of fetal blood group and need to follow up in case it is
positive, direct assessment of fetal PCV and need to
treat. It carries risks of procedure related unexplained
mortalities, bleeding, fetomaternal hemmorhage and
sensitisation. Hence it requires expertise to perform the
procedure otherwise it could result in failure of the
procedure and unacceptably higher complications.
Intrauterine Transfusion
Intrauterine intravascular transfusion (IVT), with in-
creasing experienceY ,28is becoming more popular than
intraperitoneal approach. The amount of blood to be
transfused, 27depends on pretransfusion PCV estimat-
ed fetal weight and planned post transfusion PCV. Sev-
eral formulas have been designed. Repeat transfusion
is not later than 2 weeks after the first, because the se-
Indian Journal of Pediatrics, 2001;68 (2)
 Haemolytic Disease of Newborn

verity of hemolysis is unpredictable at that time. Need
to repeat transfusion depends of post transfusion PCV.29
Approximately 1% fall o c c u r s / d a y in non-hydropic
cases and transfusion is indicated at a PCV, 30 in less
than 26 weeks and less than 25 at >26 weeks of gesta-
tion. With repeated transfusions, most of fetal circula-
tion consists of donor RBCs that are not susceptible to
hemolysis, hence the fall in PVC and need for transfu-
sion decreases.
IVT may even reverse hydrops fetalis and has im-
proved prognosis of severely affected Rh isoimmunised
fetuses.3~Recent series with 'almost 600 transfusions have
reported 98% survival in non-hydropic fetuses more
than 24 weeks gestation and 70% in hydropic fetuses less
than 24 weeks
Intraperitoneal Transfusion
This procedure was the beginning of intrauterine trans-
fusion and increased survival of severely affected fetus-
es. It still has a role in failed IVT and also as a combina-
tion with IVT. This causes slow absorption of RBC's and
delays the need for next transfusion. In general, 20%

]
Identification of maternal antibody I
I
$
Determine paternal blood group and genotype

Rh § (or other Rh- (or other

critical Ag pos) critical Ag neg)
$ $
Perform serial maternal blood levels ] No further studies indicated
$
Critical antibody level reached
> 4 IU/ml or titre > 1:16 r
Homozygous paternal genotype
$

$
Offer amniocentesis for fetel
l
Monitor with serial zXOD4s0
blOod type if placenta easily levels and ultrasound scans
avoidable

J
Fetus Rh- Fetus Rh+ .Approaching or crossing action
line of Bowman Liley or graph

1
Monthly maternal antibody levels
$
Fetal blood sampling
for caution but no other major
studies indicated
/// ~X
Fetal Hb< SD for gestation [Fetal HB>2 SD for gestation
L

$
If placenta anterior FBS only when Intrauterine transfusion;
maternal titre > 15IU/ml see text for finding of
to avoid unnecessary sensitization delivery / further IUT

Fig. Proposed Algorithm for the management of Ailo-imune Hemolytic Disease.

Indian Journal of Pediatrics, 2001' 68 (2) 169

 Anil Narang and Naveen Jain
procedure associated complication, sudden deaths due
to increased intraperitoneal pressures and poor absorp-
tion in hydrops have made the procedure unpopular.
Alternative Methods to Prevent/treat Rh Disease
Oral Densitisation 34: Marked reduction of Rhesus
HDN has been reported following oral administration
of Rh D positive red cell stroma in enteric-coated cap-
sules. The mechanism of action is obscure. The results
of the original study must only be considered experi-
mental.
Intravascular immunoglobuin35,36: Maternal high dose
M G 400 m g / k g x 5 days has been able to control severe
hemolytic disease. Proposes mechanisms include
(1) Blocking of Fc receptor of RES of fetus thus, pre-
venting destruction of RBC's and (2) Fc blocking of ma-
ternal IgG antibodies, retarding their transplacental
transfer.
Plasma exchange to reduce maternal antibody: Regular
plasmapheresis, two or three times weekly from as eas-
ily as 10 weeks gestation, has been reported to reduce
severity of fetal HDN. 38Although anti-D levels may be
reduced initially, they rise very rapidly when the plasma
exchange is discontinued probably due to absence of
inhibiting effect on feed back loop in mother.
PROPHYLAXIS OF RHESUS
ISOIMMUNISATION
In 1964 multicentric trials were conducted and it was
found that 300 mcg of anti-D protected all but 0.19%
mothers. The principle behind the dose is that 95% of
total RBC's must be eliminated by 24 hours. 300 mcg is
a safe dose considering the volumes of foeto-maternal
haemorrhages. Foeto-maternal hemmorhage should be
measured by Kleihauer test and if foetal RBC leak is
more than 4 ml (> I fetal cell/500 adult cells), larger
doses of anti-D s h o u l d be given. A n t e p a r t u m
prophylaxis should be considered in threatened,
inevitable and induced abortions, ectopic pregnancy and
when ever prenatal diagnostic investigations such as
chorion villus sampling and procedures like external
cephalic version have been done.
Recommended doses : First trimester abortions or ectop-
ic pregnancy is 50 mcg, 3rd trimester abortions or ectopic
pregnancy or amniocentesis is 300 mcg and Prophylaxis
at 28 weeks is 300 mcg. APH (trauma., abruptio placen-
tae, unexplained fetal death, placenta praevia etc.)
should be quantified for feto-maternal hemmorhage for
determining the exact dose of anti-D. In threatened
abortion repeat doses may be indicated every 6 weeks
if repeat-bleeding occurs. Recommendations 32 were
revised in 1997 regarding threatened abortion before 12
weeks of gestation. No anfi-D is necessary in threatened
170
abortion with viable fetus before 12 weeks of gestation
unless repeated/large bleeding occurs nearing 12 weeks.
Management of Isoimmunised Neonate
Cord blood is taken for ABO, Rh grouping, direct
coomb's test, hemoglobin and bilirubin assessment. Se-
verely hydropic babes require immediate resuscitation
at birth, including thoracocentesis and paracentesis to
allow lungs to expand. A partial exchange with 'O'
negative red cells may be required to correct the severe
anaemia. Once the body is stable double volume ex-
change transfusion may be performed.
Less severe form may present with indications for ex-
change at birth. Hb<11 cord bilirubin >4.5 or rapidly
rising bilirubin > I mg / kg / hr or >0.5 mg / kg / hr inspite
of intense phototherapy. Albumin I gm / kg before ex-
change extracts more bilirubin and may reduce need for
repeated exchanges. For those less affected intense pho-
totherapy is initated. Babies that receive in-utero trans-
fusions may require only phototherapy and occasion-
al top up transfusions. They may also develop a late
hypo regenerative anaemia (2-3 months of life) respond-
ing well to Erythropoietin. 39
ABO Hemolytic Disease of Newborn
It is the most c o m m o n form of HDN (1:150 births)
t h o u g h severe f o r m is rate; r e q u i r i n g e x c h a n g e
transfusion in I in 3000 births, less than <5% require
phototherapy. Unlike Rh HDN even 1st pregnancy may
be affected and the disease does not get worse with
following pregnancies. Attempts have been made to
predict or diagnose ABOHDN by serological studies
with maternal and fetal blood. High Ig M and IgG fitres
more than 1:1024 is followed by severe HDN requiring
exchange transfusion. 41 But the rarity and absence of
need for intrauterine transfusion/therapy, makes these
tests less important.
Kell Blood Group System
With decreasing Rh HDN, this is now an important
cause of HDN. The antibody anti-K is usually found in
patients who have had multiple transfusions. The kell
HDN can be a very severe form of disease. It can be
rapidly fatal in utero and weekly ultrasound scans may
miss an impending hydrops / death. The main proposed
mechanism of anaemia is depression of bone marrow
and erythropoieses rather than hemolysis?3So anaemia
may be severe without rise in bilirubin and hence ODD
450 may be unreliable. 44
Other Blood Groups
Anti-C may produce rarely a HDN as severe as anti-
D and is managed in a similar fashion. Isolated anti-E
Indian Journal of Pediatrics, 2001 ; 68 (2)
 Haemolytic Disease of Newborn
is not a serious p r o b l e m ; in c o m b i n a t i o n with a n t i - C
m a y need treatment. 45
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