Dr.

RAMYA

MODERATOR : Dr.PALLAVEE
HAEMOTOLOGICAL DISORDERS IN
PREGNANCY

ANAEMIA

PLATELET DISORDERS

HAEMOGLOBINOPATHIES

INHERITED COAGULATION DEFECTS

 ANAEMIA
Commonest haematological disorder occur
in preg.
Prevalance in pregnant women –
14 % - Developed
51% - Developing countries
65-75% - India
80 % leading to maternal deaths
 DEFINITION
Reduction in circulating Hb mass
< 12g/dl in non-pregnant women
<10 g/dl in pregnant women
CDC
Anaemia in iron supplemented preg.
Woman
Hct 33% & Hb 11g/dl – 1st & 3rd trimester
Hct 32% & Hb 10.5 g / dl - 2nd trimester
WHO grading of anemia

Mild 10g/dl
Moderate 7- 10 g/dl
Severe < 7 g/dl
ICMR GRADING
Range in g/dl

MILD 10 – 10.9

MODERATE 7 – 9.9

SEVERE <7

VERY SEVERE <4

Hemotological Changes in preg.
Physiological Anemia of pregnancy
Plasma volume s 40-50%
RBC mass s 30 %
As a result Hb concentration decreases by 2g/dl
Decreased Hb concn. Is due to haemodilution

Criteria of Physiological Anemia

1) Hb 10 gm %
2)RBC 3.2 million cells / cu mm
3)PCV 32%
4)Peripheral Smear – Normal morphology
Classification of Anaemia
Classification …….
Classification …….
Classification …….
Classification …….
ERYTHROPOISES
IRON METABOLISM
IRON Requirements during Pregnancy

Maternal req. Of total Iron -1000mg

500 mg  Mat. Hb. Mass expansion

300 mg  Fetus & Placenta

200mg  Shed through gut urine, skin

 DEVELOPMENT OF Iron def. anemia
Iron Deficiency Anemia – 3 stages
a)Depletion of Iron stores
b)Iron deficient erythropoiesis
c)Frank Iron deficiency Anemia
Symptoms of IRON DEFICIENCY ANEMIA
Fatigue
Weakness
Headache
Loss of appetite
Dysphagia
Palpitations
Dyspnea on exertion
Ankle swelling
Paresthesias
Leukoplakia
Physical examination
Pallor of varying degrees (Mucous membranes , nail
beds – Koilonychia or Platynychia
Glossitis
Stomatitis
Heart murmurs
Increased JVP
Tachycardia
Tachypnea
Postural hypotension
Crepitations- due to lung congestion
Depletion of Iron stores
Ferritin <20 ng/ml
Hb / Hct. Normal
RBC INDICES normal

Iron deficient erythropoiesis

Ferritin <20 ng/ml
Transferrin saturation<25%
Hb –Normal
Serum Iron < 60mg/dl
c)Frank Iron deficiency Anemia
ferritin <20 ng/ml
Transferrin saturation<25 %
Serum iron <60 mg/dl
Hb <10g/dl, Hct.<28%
Microcytic Hypochromic
PROPHYLAXIX
WHO - 60 mg Elemental iron + 400
micro gram Folic acid / day * 6 months
& 3 months postpartum
National Nutritional Anemia Control
Programme of India
- 60 mg elemental Iron + 500 mcg Folic
acid & Prophylactic supplementation *
100 days in 2nd trimester
Iron Supplements
Ferrous sulphate 300mg Tid orally daily after meals

To be contd for 12 months after anemia is corrected

Indicators of iron therapy response

1. Increase in Reticulocyte count (Increases 3-5 days after
initiation of therapy )
2. Increase in Hb levels. Hb increases 0.3 to 1 g/ week

3 .Epithelial changes (esp tongue & nail ) revert to normal

Hb concn. Is normal after 6 wks of therapy

PARENTERAL ADMINISTRATION
INDICATIONS
1. Intolerance to oral iron
2. Non compliance pt.
3. Inflammatory bowel disease
4. Pt. unable to absorb iron orally
5. Patients near term
TDI – Total Dose Infusion
Amount of iron needed to restore Hb conc to
normal & additional allowance to provide adequate
replenishment of iron stores

Formulae
1 Total Dose ( mg )
= ( normal Hb – Pts Hb ) * (body wt. in

kg ) * 2.21
2 Total Iron Dose (mg )
= 2.3 * wt. kg before preg * D (Target
Hb) + 500 mg for body store
MEGALOBLASTIC ANAEMIA

Incidence – 0.2 – 5 %

Caused by folic acid deficiency &

Vit B12 deficiency
Folic Acid Defciency
Pathophysiology
Preg. Causes 20 -30 fold increase in Folate
requirement (150-450 microgram / day ) to meet
needs of fetus & placenta.

Placenta transports folate actively to fetus even if

the mother is deficient.

This cause decreased plasma folate levels.

Causes of Folic acid deficiency

1.Diet- Poor intake, prolonged cooking.

2. Malabsorption – Coeliac disease.
3.Increased demand – Pregnancy, cell proliferation
(hemolysis )
4.Drugs – anticonvulsants, contraceptive pill,
cytotoxic drugs (Methotrexate )
5.Diminished storage – Hepatic disorders & Vit C
deficiency
Diagnostic features of Folic acid deficiency
1.Serum Folate levels – Low <3 ng/ml
2.Erythrocyte Folate levels - <20 ng/ml
3.Peripheral smear – Hypersegmented
neutrophils,Oval macrocytes,Pancytopenia
Treatment
 Pregnancy induced megaloblastic anaemia-
Folic acid, nutritious diet & Iron .
Supplementation of 1mg of folic acid daily can improve
MA by 7 to 10 days
Folic acid should be given with iron
Ascorbic acid 100mg Tid enhances action
In other conditions
Recommended folic acid dose – 5mg /day orally daily
Prophylaxis
WHO – 400 micrograms folic acid daily to prevent
neural tube defects
Vit – B12 Deficiency
Pathophysiology
Vit B12 absorption is unaltered during pregnancy
Tissue uptake is increased  Decreased serum B12
Recommended B12 intake – 3 microgram /day.

CAUSES of Vit B12 def.

Strict Veg. diet
Use of proton pump inhibitors
Metformin.
Gastritis
Gastrectomy
Ileal bypass
Crohn’s
H. Pylori infection
Pathogenisis
of
PERNICIOUS Gastric juice IF
Antibody
ANEMIA 
Clinical manifestations

Macrocytic Megaloblastic Anemia

Glossitis
Peripheral neuropathy
Subacute combined degeneration of the Spinal cord
DIAGNOSIS
Ser.Vit B12 levels ,100 pg /ml
Radio active Vit B12 absorption test . ( Schilling
Test )
Treatment
1000 microgram parenteral cyanocobalamin every
wk * 6 weeks
Pernicious Anaemia – Oral Vit B12
Total Gastrectomy – 1000 microgram Vit B12 im
every month.
Partial gastrectomy – Ser. Vit B12 levels measured.
ANAEMIA ASSOC. WITH CHRONIC INFECTIONS / DISEASE

Common in developing countries

Poor response to Haematinics unless primary cause is
treated
Worm infestations is common ( Diagnosed by stool
examination )
Urinary tract inf, & asymptomatic bacteriuria in preg.
Is assoc. with refractory anaemia
Chronic renal disorders = due to erythropoietin def.
Treated with recombinant Erythropoitin
Anaemia from acute blood loss
In preg. Abortion , ectopic preg, hydatidform mole,
PPH

Treatment.
Blood transfusion
• Indicated patient – symptomatic
• Not indicated – If hemodynamically stable, Hb < 7
g/dl, able to ambulate without adverse symptoms &
not septic.
Acquired hemolytic anemia
AUTOIMMUNE HEMOLYTIC ANEMIA
AUTOANTI-BODIES OF iGg OR WARM
ANTIBODIES AGAINST Red cell antigens, causes
premature destruction of RBC”s

ETIOLOGY
Lymphomas,Leukemias , Connective tissue diseases,
Infections , Chronic. Inflammatory diseases & drug
induced antibodies
Diagnosis
Direct Coomb’s Test
Blood smear – Spherocytosis & Reticulocytosis

TREATMENT
 Prednisone 1mg / kg / day orally
 Azathioprine
 Splenectomy
2)Preg. Induced hemolytic anemia
Unexplained hemolytic anemia uring pregnancy is rare
Severe hemolysis occurs early in pregnancy & resolves
within months after delivery
No evidence of immune mechanism or defects in RBCs
Prednisone given untill delivery

3) Paroxysmal Nocturnal Hemoglobinuria

Acquired hemolytic anemia
Arises from one abnormal clone of cells like neoplasm
Anemia is insiduous in onset & hemoglobinuria
develoes at irregular intervals
Hemolysis may be initiated by transfusion ,
infections or surgery
40% suffer venous thrombosis, renal failure , HTN &
Budd Chiari syndrome.
Prophylactic anticoagulation is required
Bone marrow transplantation – Definitive treatment

Effect on pregnancy
Serious & unpredictable
Maternal mortality 10 – 20%
Venous thrombosis occurs during post partum
APLASTIC ANAEMIA
Rarely seen in preg.
Marked decrease in marrow stem cels

ETIOLOGY
Infections
Irradiation
Leukemia
Immunological disorders
May be Immunological mediated or
autosomal recessive inheritance
30% cases Anaemia improves once
pregnancy is terminated.

Complications
Infection
Haemorrhage
Diagnosis
Blood Values –
 Anemia
 Leucopenia
 Thrombocytopenia

Bone Marrow - Hypocellular

Management
Supportive care – Cont. Infection surveillance & anti
microbial therapy
Red cell transfusions to maintain Hct. > 20
Granulocyte transfusion given only during Infections
Platelet transfusion to control haemorrhage.
Glucocorticoid therapy may be helpful

IN SEVERE cases
Bone marrow or Stem Cell Transplantation
Vaginal delivery is preferred
Effect of anaemia in preg.
In MOTHER
During preg.
 Pre eclampsia
 Infectuion
 Heart failure
 Pretem labour

Labour
 Uterine inertia
 Postpartum Haemorrhage
 Cardiac failure
 Shock

Puerperium
 Puerperal sepsis
 Subinovulation
 Failure of lactation
 Puerperal venous thrombosis
 Pulmonary embolism
Fetus
Amount of iron transferred to fetus is unaffected
even if mother is in iron deficient state
Prematurity
Low birth weight babies
Intra uterine deaths due to severe maternal
anoxemia
Effect of pregnancy in anaemia

Pt. Mildly anemic progresses to marked

Anaemia

Pt. Who is severely anemic becomes

symptomatic by the end of 2nd trimester
DIAGNOSIS OF
ANEMIA
DURING
PREGNANCY
PLATELET DISORDERS
Thrombocytopenia - Gestational
- Immune mediated
Mild – 1,50,000 – 1,00,000
Moderate – 1,00,000 – 50,000
Severe - < 50,000
Abnormalities of Platelet function
Causes of Thrombocytopenia during Pregnancy
COMMON CAUSES
1. Gestational Thrombocytopenia
2. Severe Pre-eclampsia
3. HELLP syndrome
4. Immune thrombocytopenic Purpura
5. Disseminated Intravascular coagulation

RARE CAUSES
1. Lupus anticoagulant/APA syndrome
2. SLE
3. Hemolytic Uremic Syndrome
4. Type 2b Von- Willebrand’s syndrome
5. Folic acid def.
6. HIV infections
7. Hemotoligical malignancies
8. May – Hegglin syndrome – Congenital Thrombocytopenia
Gestational Thrombocytopenia
Benign Common disorder
Appears in 8% of all preg.
Unknown cause
Rarely drops < 70,000 /mm3

FEATURES
Diagnosis of Exclusion – No specific test available
Mild Thrombocytopenia , Count > 70,000 – 1 lakh
No maternal bleeding
No past history of thrombocytopenia
Occurs in 3rd trimester
 No assoc. fetal thrombocytopenia
Spont. Resolution after delivery
May reccur in subsequent pregnancies
Management
Majority cases treated as normal
In mod. To severe cases – Reluctance of
Anaesthesiologists to give spinal or epidural if
Platelets = < 80,000 /cu mm
Treatment with steroids & IgG or platelet transfusion
before delivery
Cord sample should be taken
Samples taken on day 1 & 4
CS reseved for obstetric indications
Immune Thrombocytopenia
Chronic condition , Incidence 1 in 1000 to 1 in 10000
pregnancies
Charecterised by autoantibody mediated destruction
of maternal platelets

MECHANISM
Autoanti bodies react with platelet Glycoprotein
complex & antibody coated platelets are
phagocytosed by Macrophages
SYMPTOMS
Usually asymptomatic , sometimes
Bleeding , Petechiae

DIAGNOSIS
Plat count < 50,000 / cu mm with past h/o
bleeding disorders
No specific diagnostic test
Prepregnancy counselling for ITP ( RCOG 2009 )
May relapse or worsen
If treatment reqd, it will carry for both maternal &
fetal risks
Increased risk of Hemorrhage at delivery
Epidural Anaesthesia is not possible
Risk prediction in neonate is not possible. High
risk if sibling has thrombocytopenia or mother has
undergone splenectomy
Maternal deaths / serious outcome – RARE
Risk of Intracranial Haemorrhage in fetus is very
low.
Management
Adequate Plat. Count should be maintained
Counts monitored throughout pregnancy
If > 30,000 – No treatment
If< 30,000 - 1 ) Prednisolone 1 -2 mg / kg oral daily,
2) IV IG – 2g/kg over 2 to 5 days , If no
response then
3) Splenectomy
4) Immunosuppressive drugs like
a) azathioprine
b) Cyclophosphamide , Cyclosporine
Management Of delivery
Platelet > 50,000 / cu mm – Vaginal or operative
delivery
Platelet 50,000  Platelets standby
CS not routinely recommende
Measures should be taken to avoid trauma to baby
head
Cord sample taken, If low  confirmed by capillary
sample
If count low, further day 1 & 4 is collected
Inj im Vit K avoided till count is known
Fetal & Neonatal Effects
PA IgG antibodies crosss placenta  causes fetal &
neonatal Thrombocytopenia
Maternal treatment do not have effect o fetal count
Role of Intracaranial hemorrhage < 1 %
MICROANGIOPATHIES
Thrombotic thrombocytopenic purpura
Rare – life threatening
Signs & symptoms ( PENTAD )
1. Microangiopathic hemolytic anemia
2. Thrombocytopenia
3. Neurological symptoms
4. Renal dysfunction
5. Fever
ETIOLOGY
Severe def. of VON WILLIBRAND FACTOR
( cleaving protein ( ADAM TS13)
Acqd  autoantibody
Congenital  Genetic defect

Incidence
1 in 25000 pregnancies
Time of onset of TTP is variable
1st trimester to several wks post partum
Maternal mortality is high
MANAGEMENT
ACQUIRED
Plasma Exchange
Fresh frozen Plasma infused daily until Platelets turn
to Normal
Rituximab, Monoclonal antibodies against CD20

CONGENITAL
FFP
Platelet transfusion contraindicated
HEMOLYTIC UREMIC SYNDROME
Microangiopathic hemolytic anaemia &
thrombocytopenia with predominant Renal
involvement

Due to endothelial damage by bacterial or viral

infections

In Preg. Response is poor for plasma exchange

THROMBOCYTOSIS
Defined as persistant Platelet count >4.5 lakhs / cumm
CAUSES
1 )Secondary or Reactive ( > 80000)
a)Iron def.
b) Infections
c) Splenectomy
d) Surgery & Trauma ( bone fractures )
e) Malignancy
 2) Essential Thrombocytosis > I million
a) Idiopathic
b) Myelodysplastic syndromes
SIGNS & SYMPTOMS
Usually asymptomatic
Arterial & venous Thrombosis
Hepatomegaly
Bone marrow – Hyperplastic with gross increase in
megakaryocytes
Blood picture ->1 million
Leucocytosis
Anemia or mild polycythemia
Anisocytosis & Poikilocytosis
In Pregnancy – Spont. Abortion , fetal demise &
preeclampsia.

TREATMENT
Aspirin , Dipyramidole, Heparin, Plateletpheresis

PROGNOSIS depends on underlying disease

Death due to either thrombosis / hemorrhage /
comp of Myeloproliferative disorders/ marrow
failure.