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Haemolytic Anaemia

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Sonam Rawat
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8 views22 pages

Haemolytic Anaemia

Uploaded by

Sonam Rawat
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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HAEMOLYTIC ANAEMIA

MADE BY
DR.SUNIL KUMAR
GOOD MORNING

STAY HOME STAY SAFE


INTRODUCTION

Haemolysis is said to occur when the mean


RBC survival is less than 120 days . If the
bone marrow does not compensate
sufficiently , a haemolytic anaemia results .
ETIOLOGY ( CONGENITAL )
• Membrane abnormalities( hereditary spherocytosis,
hereditary elliptocytosis , acanthocytosis ,
stomatocytosis ) .

• Haemoglobin abnormalities ( thalassaemia)

• Red cell enzyme defects [ glucose – 6 – phosphate


dehydrogenase ( G-6-PD) ] .
ETIOLOGY (ACQUIRED)
A. IMMUNE
a) Isoimmune
b) Autoimmune
• WARM ANTIBODY TYPE ( IgG ) – SLE ,
lymphoma .
• COLD ANTIBODY TYPE ( IgM ) – Cold
haemagglutinin disease , paroxysmal cold
haemoglobinuria ( PCH ) , mycoplasma
pneumonia.
• DRUG RELATED – Drug absorbed
onto RBC surface : penicillin ,
cephalosporins .

• IMMUNE COMPLEX MEDIATED


– Sulphonamides , quinidine .
DIFFERENCES BETWEEN
WARM AND COLD ANTIBODY
WARM ANTIBODY COLD ANTIBODY
• Agglutinates red cells at 37 • Agglutinates at lower
degree Centigrade . temperatures
• Antibodies generally
belongs to IgG class . • Antibodies are IgM class .
• Haemolysis takes place • Haemolysis occurs
extravascularly in spleen . intravascularly or in liver .
B. NON IMMUNE
• Mechanical ( artificial valves , burns )
.
• Infection ( malaria )
• Drugs ( sulphonamide )
CLINICAL FEATURES
• General symptoms of anaemia are seen in the
patients of haemolytic anaemia . Haemolysis leads
to distinctive features in acute and chronic forms . In
acute haemolytic episodes , sharp rise in
temperature , haemoglobinuria , acute renal
failure,disseminated intrvascular coagulation and
shock are present . In chronic cases of haemolysis
facies , splenomegaly , cholethiasis , pigmentation
and iron overload states are seen .
INVESTIGATIONS
A . Tests to detect the presence of
haemolysis
1. Life span of RBC – This is determined by chromium
labelling and the major site of RBC breakdown may
also be identified .
2. The presence of haemolysis can be inferred by
demonstrating .
• Reticulocytosis – Increase in reticulocyte count above
1.5% suggests increased erythropoiesis .
• Bilirubin – Presence of unconjugated
• Bone Marrow – The bone marrow shows erythroid
hyperplasia .
B. Tests to detect the cause –
1. Blood film shows polychromasia , macrocytes ,
spherocytes , elliptocytes or sickle cells ( sickle
cell anaemia ) .
2. DIRECT COOMBS TEST – This test identifies red
cells coated with antibody and/or complement and
a positive result usually indicates an immune cause
for the haemolysis .
MANAGEMENT
A. GENERAL MEASURES –
When the drop in Hb is severe , it has to be
restored by tranfusion of packed
erythrocytes . In acute intravascular
haemolysis emergency transfusion is needed
to avoid cardiorespiratory failure .
B. THE SPECIFIC TREATMENT –
Immune haemolytic anaemias involve the
administration of corticosteroids and
immunosuppressants . Splenectomy is the treatment
of choice in hereditary spherocytosis . In enzyme
deficiencies and haemoglobinopathies ,
splenectomy is not generally indicated .

C. INTRAVENOUS IMMUNOGLOBULIN –
Given in the dose of 0.4g/kg b.w daily for3-4 days
is effective in acute haemolytic episodes .
HAEMOLYTIC DISEASE OF
NEWBORN
• Rh incompatibilty accounts for the vast
majority of isoimmune haemolytic
anaemias of the newborn .
ETIOLOGY
• The newborn may suffer from the Rh
incompatibility or ABO incompatibility if there is
Rh or ABO incompatibility between the parents . If
the father is Rh positive the foetus may also
sometimes be Rh positive and entry of foetal
eyrthrocytes into the Rh negative , mother leads to
production of anti negative-Rh antibodies which
reach the foetus and destroy its erythrocytes . A
similar phenomenon may occur in ABO
incompatibility as well .
Rh Incompatibility
• It occurs due to ‘D’ antigen present on
erythrocytes. About 17 % of Rh
negative women get immunised
during pregnancy if the foetus is Rh
positive .
CLINICAL PRESENTATION
• The mild form manifests as moderate haemolytic
anaemia in the first days of life.
• Hepatosplenomegaly may be just detectable . The
moderately severe form presents as Icterus gravis
neonatorum . This leads to jaundice within 24 hours
of birth and this feature distinguishes it from
physiological jaundice . Anaemia may progress and
lead to cardiac failure .
INVESTIGATIONS
A. SUSPECTED CASE OF Rh ISOIMMUNISATION
–
The mother’s blood shows the presence of
antibodies by the Indirect Coomb’s test .

B. POSTNATAL DIAGNOSIS –
The baby’s blood shows positive direct Coomb’s
test, elevated serum bilirubin , reticulocytosis .
MANAGEMENT
• Rh immunisation is a preventable disease by proper
Rh typing during the prenatal check up .

A. PRENATAL MANAGEMENT –
• When the mother is not immunised or the Rh
antibody titre is low and static the pregnancy is
allowed to continue .
• If the risk of hydrops foetalis or stillbirth is high ,
induction of labour between 34 weeks and 38
weeks is indicated .
B. POSTNATAL MANAGEMENT –
• The principles of management include the
correction of anaemia , hypoglycaemia
and hyperbilirubinaemia .
• Exchange transfusion with Rh negative
group O is indicated .
PREVENTION
• Rh negative mothers who are at risk are
protected from getting immunised by the
administration of 300 microgram of anti- D
gammaglobulin (RhoGam) within 72 hours of
delivery or abortion .

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