RH Negative Pregnancy.8903883.Powerpoint

MANAGEMENT OF RHESUS
NEGATIVE PREGNANCY
DR MALLESWAR RAO K
(MBBS, MD, DGO)
FORMER CONSULTANT CSS & HOD

DEPARTMENT OF OBSTETRICS & GYNAECOLOGY
ESI HOSPITAL, SANATHNAGAR
HYDERABAD
kasinamrao@gmail.com 1
Outline
 Introduction
 Epidemiology
 Pathophysiology
 Management
 Problems in our setting
 Recommendations
 Conclusion
 References
Introduction
 The Rhesus (Rh) blood group system is one of the
35 current human blood group systems
 It's the second most important system after the ABO
system
 At present, the Rh system consists of 50 defined
blood group antigens (Ag), among which the five Ag
D, C, c, E, e are the most important
... Introduction ...
 The D Ag, also called the Rh factor is the most
immunogenic[1] of them though the others are still
clinically relevant
 The Rh factor is a red cell surface antigen named
after the rhesus monkey in which it was first
discovered.[1]
 An individual either has or does not have the D
antigen on the surface of their red blood cells
(RBCs)
 The status is usually indicated by the suffices Rh+
for those that have, or Rh- for those who lack the D
antigen
 These suffices are attached to the ABO blood type
 An Rh-negative pregnant woman is one who lacks
this antigen on the surface of their red cells.
 Historical time line
 1937: Rh blood type discovery by Karl Landsteiner &
Alexander Wiener, and noted to be distinct from ABO blood
type
 1939: The D antigen was incidentally discovered but yet
unnamed. This followed a case of haemolytic disease of the
newborn observed in a the infant of a 25 year old G2 P1 woman,
blood group O who received O type blood
 This case was subsequently published[2] by Philip Levine and
Rufus Stetson
 ... Historical time line ...
 1940: This unnamed factor was realised to be similar to the
earlier discovered blood type and a connection was made to
it[3]
 1946: Exchange transfusion created by Wiener for treatment
of Rh disease
 1960: The concept of anti-RhD for the prevention of Rh
disease was proposed by Ronald Finn
 1963: First successful intrauterine transfusion for treatment of
Rh disease was carried out by Sir William Liley
... Introduction
 ... Historical time line
 1964: First prophylactic injection for Rh disease was given
 1968: Immunoglobulin G antibody was first approved for use
in USA (as RhoGAM) and UK @300 mcg within 3 days
postpartum
 1973: Reports in the USA said 50,000 babies' lives had been
saved since approval
 1981: Rh IgG approved for routine postpartum and
antepartum administration by the US Food and Drug
Administration
Epidemiology
 Globally, the Basque population (of Spain) has the
highest incidence of Rh negativity (30-35%) [4]
 Otherwise,
 Whites: 15-16%
 African Americans: 8%
 Black Africans: 4%
 Asians and others, 2% or less
... Epidemiology
 Nigerian studies
 4.5% prevalence rate at Enugu,[5] Southeast
 0.7% incidence rate at Kaduna,[6] North
 5.5% prevalence rate at Ogbomosho,[7] Southwest
Erythroblastosis Fetalis
(Red Cell Alloimmunization)
the first description of erythroblastosis fetalis
(hemolytic disease of the newborn) dates back to
1609
until the early 1900s that the role of alloimmunization
in the pathogenesis of erythroblastosis was
established
In the past, Rh alloimmunization also has been
referred to as Rh sensitization or Rh
isoimmunization.
Pathophysiology
 Two commonest systems for blood group classification:
[8]
 ABO system
 Rhesus system
 ABO system: Groups A, B AB, O antigen (Ag)
 Rhesus system: C, c, D, E, e and G.[4]
 There's no 'd' Ag. The letter represents absence of 'D' Ag
 The D antigen is considered to be the most
immunogenic (aka Rh factor)
... Pathophysiology ...
 There are two possible alleles for each of the c or C, D
and e or E
 An individual inherits one haplotype from each parent
 Rh positive: presence of at least one of either C, D or E
antigens regardless of the combination (ie, homozygous
or heterozygous)
 Rh negative: cde/cde genotype (always homozygous)
 The D antigen
 The Rh-positive father may be homozygous (45%) or
heterozygous (55%) for D
 If homozygous for D, all children will test positive
 If heterozygous, his children will have a 50% chance of
being RhD-positive
 Thus if 'D' antigen is specifically tested, its absence will
give a negative result regardless of the presence of the
other antigens (C, E)
 The amount of foetal blood necessary to produce Rh
incompatibility varies, but as little as 0.1 mL of Rh+ cells
have been documented.[4]
 Studies have suggested that up to 30% of persons (non-
responders) with Rh- blood never develop Rh
incompatibility even when challenged with large
volumes of Rh+ blood[1]
 Rh alloimmunisation occurs by 1 of 2 mechanisms
 After incompatible blood transfusion
 After foeto-maternal haemorrhage between mother and an
incompatible foetus
 Foeto-maternal haemorrhage may occur during
pregnancy (10%) or delivery (90%)[1]
 Notwithstanding, foetal RBCs have been detected in the
maternal blood in all three (7, 16, 29%) trimesters without
an apparent predisposing factor[4]
 The initial maternal response to Rh sensitisation is low
levels of immunoglobulin (Ig) M antibodies (Ab)
 These are confined to maternal circulation being unable to
cross the placental barrier
 Within 6 weeks to 6 months, IgG Ab are formed
 These are able to cross the placenta and destroy foetal Rh-
positive cells
 Therefore, first-born infants with Rh-positive blood
type are not affected
 The short period of 1st exposure of mother to foetal RBCs is
insufficient for production of significant IgG Ab response
 Subsequent pregnancies may trigger a rapid & robust

Ab response - Anamnestic response
 Anamnestic theories:
– Grandmother theory
– “Sensibilization” theory
 Maternal O blood type appears particularly protective
 Sequence of inutero events
 Maternal IgG enters foetal circulation via placenta
 Destruction of foetal red cells occur - foetal anaemia
[HCT<30%]
 Haem is formed and converted to bilirubin – foetal
hyperbilirubinaemia
 Both are neurotoxic, but effectively cleared by placenta and
metabolised by the mother
 Extramedullary erythropoeisis is stimulated
 Immature erythroblasts are produced
 When cell destruction exceeds production
 Severe anaemia occurs
 More demand on extramedullary sites to produce more red
cells – hepatosplenomegaly
 Heart failure eventually results, with ascites, oedema and
pericardial effusion – erythroblastosis foetalis
 Hydrops foetalis, occurs when the haematocrit falls below 15%.
Often results in foetal death shortly before or after birth
• Male to Female foetus = 13.1 to 1
 The risk and severity of sensitisation response increases
with each subsequent pregnancy involving an ABO-
compatible foetus with Rh-positive blood
 Without prophylaxis, this risk is 16% after two
deliveries;
– 1.5-2% occur antepartum
– 7% within 6 months of delivery
– 7% manifest early in 2nd pregnancy
 With prophylaxis, the risk drops to 0.1%
... Pathophysiology
 The aforementioned risk depends on the 3 main factors
 Volume of transplacental haemorrhage
 Extent of the maternal immune response
 Concurrent presence of ABO incompatibility (protective –
risk drops to 1.5-2%)[4]
 Rh incompatibility is only of medical concern for
females who are pregnant, or plan to get pregnant in
future
Maternal Immunologic Response:
30% of Rh-negative individuals appear to be

immunologic “nonresponders”who will not become
sensitized
ABO incompatibility diminishes the risk of
alloimmunization to about 1.5% to 2.0% after the
delivery of an Rh-positive fetus
The effect is most pronounced if the mother is type O and
the father is type A, B, or AB.
Management
 This includes history taking, clinical examination,
appropriate investigations, and treatment
 Two groups of women are catered for
– Unsensitised Rh-negative women
– Sensitised Rh-negative women
 There is usually no specific finding on the history
and clinical examination for the woman that is not
sensitised
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MANAGEMENT OF RHESUS

FORMER CONSULTANT CSS & HOD

 Subsequent pregnancies may trigger a rapid & robust

30% of Rh-negative individuals appear to be

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