Welcome

PREPARED BY
BIPASHA DAS
M.SC (N)3rd SEMESTER
ROLL NO : 01
TRIPURACOLLEGE OF
 INTRODUCTION
Haematological disorder is the most commonly occurring
disorder during pregnancy. Haemoglobin level below
10gm/dl at any time during pregnancy. Haematological
disorder is responsible for 20% of maternal deaths in the
third world countries.
 SEMINAR
ON
“ HEMATOLOGICAL
DISORDERS IN PREGNANCY
”
 PHYSIOLOGICAL
HEMATOLOGY CHANGES
1)RED BLOOD CELLS.
2)WHITE BLOOD CELLS.
3)PLATELETS BLOOD CELLS.
4)COAGULATION FACTORS.
 WHITE BLOOD CELLS:
i. Increased neutrophils.
ii. Shift in granulocytes and toxic granulation.
iii.Lymphocyte count increased slightly in 3rd
trimester only.
iv. Monocyte increases in 1st trimester.
v. Eosinophil & basophil no change.
 PLATELETS BLOOD
CELLS:
i. Decreased by 10%.
ii. Shift of whole distribution of PLT count at
term.
iii.Haemodilution.
iv. Increased PLT consumption driver by
increased levels of thromboxane A2.
v. In multiple pregnancy owing to increased
thrombin generation.
vi.Thrombocytopenia 2nd most common
haematology after anaemia, bleeding
complications.
 COAGULATION
FACTORS:
Haemastesis: Hypercoaguable stale in
puerperium.
i. Increased clotting factors- FVIII, FVII, FX,
Fibrinogen, von-wille brand factor.
ii. Decreased coagulation inhibitors proteins,
Antithrombin, Protein C.
iii.Decreased of fibrinolysis inhibition
(hypofibrinolysis), Antiththrombotic agent
effcet:Vit-K, Low molecular weight
heparin, decreased teratogen, risk bleeding.
 DEFINITION
Anaemia is a condition in which the
number of red blood cells or their
oxygen carrying capacity is insufficient
to meet the physiological needs of the
individual, which consequently will
vary by age, sex, attitude, smoking, and
pregnancy status (WHO 2013).
 
TYPES OF ANAENIA
(SEVERITY)
Anaemia in pregnancy is defined as
haemoglobin (Hb) concentration is less than
10 g/dl (India).

 Mild : 9- 10.9 gm/dl.

 Moderate : 7.8- 9 gm/dl.
 Severe : < 7 gm/dl.
 Very severe : <4 gm/dl
 CLASSIFICATION OF
ANEMIA
1. Physiological Anaemia.
2. Pathological Anaemia.
 Iron deficiency.
 Folic acid deficiency.
 Vitamin B12 deficiency.
 Protein deficiency.
 Conti…
3.Hemorrhagic Anaemia
 Acute- bleeding in early months of pregnancy
or APH
 Chronic- hookworm infestation, bleeding piles.
4. Hereditary
 Thalassemias.
 Sickle cell haemoglobinopathies.
 Other haemoglobinopathies.
 Hereditary haemolytic anaemia.
5. Bone marrow insufficiency.
6. Anaemia of infection.
7. Chronic disease or neoplasm.
  PREVALENCE OF
ANEMIA
The global prevalence of anaemia in pregnancy
is 51%, in south-East Asia it is 74% and In
India it ranges from 68.8%-96.8%.
 PHYSIOLOGICAL ANEMIA
OF PREGNANCY
During pregnancy, maternal plasma volume gradually
expands by 50%, an increase of 1,200ml by term. Most
of the rise takes place before 32ndto 34thweek’s gestation
and thereafter there is relatively little change. The total
increase in RBCs is 25%, 300 ml that occurs later in
pregnancy. This relative hemodilution produces a fall in
haemoglobin concentration, thus presenting a picture of
iron deficiency anaemia. However, it has been found that
these changes are a physiological alteration of pregnancy
necessary for the development of fetus.
 CRITERIA OF
PHYSIOLOGICAL ANAEMIA
The lower limit of physiological anaemia during
the 2nd half of pregnancy should fulfil the following
haematological values:
i. Hb-10%.
ii. RBC-3.2 million/mm3.
iii. PVC-30%.
iv. Peripheral smear showing normal morphology
of the RBC with central pallor.
ERYTHROPOISIS
In adults, erythropoiesis is confined to the bone
marrow.
Red cells are formed through stages of
pronormoblasts normoblasts
reticulocytes nature nonnucleated
erythrocytes.
The average life- span of red cells is about 120
days after which the RBC’s degenerate and the
haemoglobin are broken into hemosiderin and
bile pigment.
 IRON REQUIREMENTS IN
PREGNANCY
During pregnancy approximately 1,500 mg iron is
needed for:-
1) Increase in maternal haemoglobin (400-500mg).
2) The fetus and placenta (300-400 mg).
3) Replacement of daily loss through urine, stool and
skin (250mg).
4) Replacement of blood lost at delivery (200mg).
5) Lactation (1mg/day).
 IRON AND FOLIC ACID
REQUIREMENT IN
PREGNANCY
 Elemental iron- 30 mg to 60 mg.
 Folic acid- 400µg (0.4 mg).
 IRON DEFICIENCY

Iron deficiency anemia (IDA) is the most

common type of anemia in pregnancy. About 95%
of pregnant women with anaemia have iron
deficiency type. A pregnant woman is said to be
anaemic if her haemoglobin is less than 10 gm/dl.
  CAUSES OF ANEMIA
i. Dietary habits.
ii. Defective absorption of iron.
iii.Low iron stores and iron loss.
iv. Vitamin A deficiency.
v. Excess demand such as multiple
pregnancy.
vi. Blood loss.
 SIGNS & SYMPTOMS
 EFFECTS OF ANEMIA ON
THE MOTHER
1. Preterm labour (28%).
2. Pre-eclampsia.
3. Inter-current infection.
4. Cardiac failure, PPH.
5. Hemorrhagic shock.
6. Subinvolution, Puerperal sepsis.
7. Puerperal venous thrombosis.
8. Pulmonary embolism.
9. Failure of lactation.
10.Potential threat to life.
  EFFECTS OF ANEMIA ON
FETUS/ BABY
1) Intrauterine hypoxia.
2) Intrauterine growth retardation.
3) Intrauterine death.
4) Prematurity, LBW.
5) Cognitive &affective dysfunction in the neonate.
6) Anaemia after birth.
7) Increased risk of perinatal morbidity &mortality.
 DIAGNOSIS OF ANEMIA
i. Hemoglobin measurement.
ii. Peripheral blood film.
iii. Reticulocyte count.
iv. Hematocrit.
v. Blood indices.
vi. Serum iron.
vii. Total iron binding.
viii. Serum ferritin.
ix. Transferrin saturation.
x. Bone marrow examination.
  PREVENTION OF IRON
DEFICIENCY ANEMIA
The management start from childhood to prevent
iron deficiency anemia in adolescent females.
Prenatal check-up is necessary to cure anemia
before trying for pregnancy.
 
 MANAGEMENT
 Avoidance of frequent childbirths.
 Supplementary iron therapy.
 Dietary advice.
 Adequate treatments.
 Early detection.
  TREATMENT
1) Oral Iron Therapy:-
 Government of India, Ministry of Health
recommends 200mg elemental iron with 1mg folic
acid per day for treatment until Hb levels come back
to normal followed by 100mg/day upto the 3
months after the delivery.

2) Parenteral Iron Therapy:-

 Dosages- IM/100mg/day/,
 IV/1000mg/slowly every alternate day for 5-10
injections.

3) Blood Transfusion.
 CURATIVE MANAGEMENT
Women having haemoglobin level of 7.5 mg% and those
associated with obstetrical medical complications must be
hospitalized. Following therapeutic measures are to be
instituted:
i. Diet: A realistic balance diet rich in proteins, iron and
vitamins and which is easily assimilable is prescribed.
ii. Antibiotic therapy.
iii. Blood transfusion.
iv. Iron therapy which may be oral/ parental.
v. Oral iron: daily dose 120-180 gm is given.
 MANAGEMENT DURING LABOR
 1st stage:
1. Special precautions.
2. Comfortable position on bed.
3. Light analgesia.
4. Oxygenation to increase oxygenation of
maternal blood and prevent fetal hypoxia.
5. Strict asepsis.
 2nd stage:
1. Usually no problem.
2. IV Methergin 0.2mg or 20 units oxytocin in
500ml RL IV and 10units of IM given.
 3rd stage:
1) Intensive observation.
2) blood loss must be replaced by fresh pack
cell and amount must not exceed loss amount
 Puerperium
1) Diet, Bed rest.
2) Sign of infection detected and treated.
3) Pre delivery iron therapy must be continued
until patient restores.
4) Patient and family members must be
counselled for help at home regarding baby
care and household chores.
 FOLIC ACID DEFICIENCY
ANEMIA
Folic acid deficiency anaemia happens when
body does not have enough folic acid. Folic acid
is one of the B vitamins, and it helps body make
new cells, including new red blood cells.
 CAUSES:-
i. Dietary deficiency, Hyperemeis gravidraum.
ii. Malabsorption syndromes, Drugs eg- Antiepileptic.
iii. Pregnancy & Lactation.
iv. Hemolytic anemias, malignancies.
v. Tuberculosis, Crohn’s disease, rheumatoid arthritis,
Psoriasis, exfoliative dermatitis.
vi. Peptic ulcer, hookworm infestation, haemorrhoids.
vii. Chronic malaria, sickle cell anemia & thalassemia.
viii.Excess urine folate loss active liver disease,
congestive heart failure.
 CLINICAL FEATURES
1) May be asymptomatic.
2) Loss of appetite.
3) Vomiting, diarrhoea, fever.
4) Pallor with glossitis.
5) Hemorrhagic patches under skin & conjuctive.
6) Hepatosplenomegaly and polyneuropathy.
 EFFECTS ON PREGNANCY
1) Increased incidence of abortion.
2) Growth restriction.
3) Abruptio placentae.
4) Preeclampsia.
 

 EFFECTS ON FETUS:-
1) Neural tube defects.
2) Abortion.
3) Premature babies.
4) IUGR.
5) Neonatal folate deficiency.
 INVESTIGATION
i. Fall in Hb concentration to <10g/dl.
ii. MCV>96fl, MCH>33pg and normal MCHC.
iii. Peripheral blood film.
iv. Anisocytosis.
v. A combination of low serum folate(<3ng/mL) &
red cell folate(<150ng/ml).
vi. Serum iron is usually normal or high.
vii. Bone marrow shows a megaloblastic picture, but
is rarely required.
 PROPHYLAXIS:-
The WHO recommends a daily folate intake of 800µg in
antenatal period and 600 µg during lactation.

 TREATMENT:-
 5 mg oral folate per day which should be continued for
at least 4 week in puerperium.
 Parenteral folate is only indicated in gastric intolerance
or for severe dificiency late in pregnancy.
 Vitamin C is useful.
 Associated iron deficiency should be corrected by iron
therapy.
 Blood transfusion is rarely required in severe anemia.
 VITAMIN B12 DEFICIENCY
Vitamin B12 deficiency, also known as
hypocobalaminemia, refers to low blood levels of
vitaminB12. Deficiency of vitaminB12 can also produce
megaloblastic anemia. Deficiency is most likely in
vegetarians who eat no animal product. VitaminB12 is
found in meat, fish, eggs and milk. The average daily
diet contains 5-30µg of vitaminB12 of which 1-5 µg is
absorbed.
  CAUSES
i. Inadequate diet-Strict vegetarians.
ii. Malabsorption.
iii. Defective release of cobalamin from food.
Inadequate production of intrinsic factor.
iv. Disorders of terminal ileum.
v. Fish tapewormdisease
vi. Blind loop syndrome.
  CLINICAL FEATURES
i. Hematological manifestrations are a result of
anemia and sometimes purpura results due to
thrombocytopenia.

ii. Gestrointestinal manifestations include sore tongue,

anorexia, diarrhoea.

iii. Neurological manifestations begin with

demyelination followed by axonal degeneration and
finally neuronal death. There is numbness,
paresthesia, weakness, ataxia etc.
 INVESTIGATION
i. Vitamin B12 levels are lower in blood (<90µg/I).
ii. Serum methylmalonic acid is elevated in Vitamin
B12 deficiency.
iii. Serum homocysteine is elevated in both folate and
Vitamin B12 deficiency.
iv. The deoxyuridine suppression test can differentiate
between Vitamin B12 & folate deficiency.
v. Schilling test used to diagnose pernicious anemia is
not done during pregnancy as it uses contrast.
 TREATMENT:-
i. Parenteral cyanocobalamin(250 µg) is given IM
every month.
DIMORPHIC ANEMIA:-
Deficiency of both iron and folat with finding of both
anemias but dominance of one is often seen in tropical
countries. Blood film may show macrocytic or
normocytic, normochromic or hypochromic pictures.
Bone marrow is usually megaloblastic. Treatment is
prescription of both folic acid and iron in therapeutic
doses. Pregnant women should eat more green
vegetables and fruits & should avoid over cooking of
food.
 
 SICKLE CELL ANEMIA
Sickle cell anaemia is a disease in which body produces
abnormally shaped red blood cells. The cells are shaped
like a crescent or sickle. The sickle cells also get stuck in
blood vessels, blocking blood flow. This can cause pain
and organ damage.
 PATHOPHYSIOLOGY:
It is autosomal recessive disorder. In deoxygenated state,
Hbs distorts the red cells to sickle. Being rigid in
structure, these cells block micro-vasculature. The cells
have shorter lifespan and are haemolysed resulting
anaemia and Jaundice.
 
 SICKLE-CELL CRISIS:
Repeated painful crisis occurs due to obstruction of
vessels causing ischaemic pain in bones and joints.
Haemolytic crisis occurs due to haemolysis resulting in
developing anaemia quickly.
 
 DIAGNOSIS:
1) Refractory hypochromic anaemia not responding to
iron.
2) Screening test for sickle cell Hb by sickling.
3) Electrophoresis to identify the type of
haemoglobinnopathies.
 CLINICAL FEATURES:-
1) Painful crisis.
2) Chronic haemolytic anemia.
3) Chest syndrome.
4) Higher infection rate.
5) Increased risk of cerebrovascular accidents.
6) Hyposplenism.
7) Avascular bone necrosis.
 EFFECTS OF SICKLE-
CELL DISEASE
i. Miscarriage.
ii. Infection.
iii. Preeclamsia.
iv. Prematurity.
v. Fetal growth restriction.
vi. Thromboembolic events.
vii. Maternal morbidity.
viii.Stillbirth.
ix. perinatal mortality.
  MANAGEMENT DURING
PREGNANCY
Pregnancies with sickle cell disease are high-risk
pregnancies

 TREATMENT:
1) Adequate oxygenation.
2) Partial exchange transfusion of Hb% blood.
3) Folic acid supplementation.
4) Monitoring fetal growth.
5) Prepare for preterm labour.
6) Labour is managed as woman suffering from
anaemia.
 
 LABOR MANAGEMENT:-

1) Labor should be managed in the same way as for

heart disease patients.
2) Over sedation is avoided.
3) Epidural analgesia is suited for labor and delivery.
4) Vaginal delivery is ideal but also elective CS at
36weeks after partial exchange transfusion.
5) Avoidance of dehydration and acidosis.
6) Compatible blood should be kept available.
7) Circulatory overload should be avoided.
 MTP:
Identifying fetus with SS homozygous by DNA
analysis, by cordocentesis or chorionic villus
biopsy. MTP may be considered after counselling.

 CONTRACEPTION:
Barrier method is the best, sterilisation after one
child is advisable.
THALESEMIA SYNDROMES
Thalesemia syndrome are commonly found
genetic disorders of the blood. The basic defect is
reduced rate of haemoglobin chain synthesis. This
leads to ineffective erythropoisis and increased
hemolysis with resultant inadequate haemoglobin
content. 1in 400 of all pregnancies.
  TYPES:-
 α- Thalassemia: Due to defect in synthesis
of α- chain of globin in haemoglobin. α- chain
is controlled by four genes.

 β- Thalassemia: Here β-chain synthesis is

decreased and excess α-chains cause damage to
red cell membrane.
 
 DIAGNOSIS OF THALASSAEMIA
i. Family history of thalassaemia.
ii. History of birth of thalassaemic baby in previous
pregnancy.
iii. Persistent mild variety of anaemia not responding to
iron therapy.
iv. Splenomegaly.
v. Low MCV, Low MCH, but normal MCHC.
vi. Serum iron or TIBC is normal or elevated.
vii. Hb electrophoresis- HBA2 is raised to 5% , HbF normal
or raised.
  TREATMENT DURING
PREGNANCY
1) Regarded as high risk pregnancy.
2) Oral folic acid is given.
3) Iron supplementation is given only if iron
deficiency is present. Parenteral iron should
never be given.
4) Blood transfusion may be needed.
  THALASSAEMIA &
GENETIC COUNSELLING
i. Autosomal recessive disease.
ii. If one partner is minor(carrier), the fetus can be thalassaemia
minor.
iii. If both partners are thalassemia minor (carrier), the fetus has 1
in 4 chance of thalassaemia major.
iv. When women is β- thalassaemia major & husband normal, the
fetus has 25% chance of normal haemoglobin & 50% chance of
β- thalassaemia minor.
v. If woman is β- thalassaemia major and husband minor, there is
50% chance of the fetus to be β- thalassaemia major.
vi. Antenatal diagnosis can be made by CVS and amniocentesis.
vii. Preimplantation genetic diagnosis for blastomere is possible to
select unaffected embryo in ART programme.
 PLATELET DISORDERS
Thrombocytopenia is considered when platelet
count is less than 1,50,000/uL/mm3. Platelet count
of 97,000/ml to 1,50,000/ μl during pregnancy is
not associated with any increase in maternal or
fetal morbidity.
  CAUSES OF
THROMBOCYTOPENIA
Thrombocytopenia in pregnancy may be due to:
i. Defective production.
ii. Sequestration (enlarged spleen).
iii. Non-immunological: Preeclampsia, HELLP
syndrome, Abruptio placenta, DIC.
iv. Immunological: Thrombocytopenic purpura,
anti-phospholipid antibody, SLE, lupus
anticoagulant.
v. Others: HIV, folic acid deficiency.
  TYPES OF
THROMBOCYTOPENIA
i. Gestational thrombocytopenia.
ii. Immune (idiopathic) thrombocytopenic
Purpura.
  MANAGEMENT:
Maintain platelet count more than 50,000/uL.

 DURING PREGNANCY:
i. Methylprednisolone (1-1.5 mg/kg), Gamma globulin
(IVIG)-only if platelet count is <20,000/mm.
ii. Platelet transfusion.
iii. Splenectomy.
iv. Thrombocytopenic purpura plasma exchange should
be done.
v. Azathioprine and cyclophosphamide have been used.

 DURING LABOR:
i. Vaginal route is the preferred method as severe
thrombocytopenia is rarely encountered.
 THROMBOPHILIAS
Thromobophilia is defined as a predisposition to
thrombosis secondary to a hypercoagulable state
and can be inherited or acquired.
 CAUSES
i. Patients history of venous thromboembolism.
ii. Deficiency of important protein inhibitors.
 Protein C.
 Protein S.
 Antithrombin III.
 Factor V Leiden.
 Prothrombin gene mutation.
iii. Hyperhomocystinemia.
iv. Elevated factor VII.
v. Antiphospholipid syndrome.
EFFECT ON PREGNANCY
There is increased risk of pregnancy
complications such as:
a)Recurrent miscarriage.
b)Fetal growth restriction.
c)Preeclampsia.
d)Abruptio placentae.
e)Intrauterine fetal death.
 MANAGEMENT
Thrombophilias can cause venous
thromboembolism during pregnancy and need
treatment with inj-Heparin/5000IU/BD/SC
along with oral low dose Aspirin-60mg. Low
molecular weight Heparin can also be given in
dose of 40-60mg/day till 34-36 weeks of
pregnancy.
CURRENT REVIEW OF LITERATURE
Sinha.A.et.al.(2011).Conducted a study to assess anaemia and its
risk factors among pregnant women attending antenatal clinic of a
rural medical college of West Bengal. Methods and Methodology
of this study were hospital-based cross-sectional descriptive study,
200 antenatal women, every fifth woman visiting antenatal clinic
within the duration of 2months on alternate days, Data were
collected using a predesigned, pretested semi-structured schedule.
Data were analyzed using Chi-square test and 'T' test of
significance. Results: prevalence of anaemia to be 90% among
pregnant women. Most of the anaemic patients (60.5%) belong to
moderate severity according to the WHO classification. Three
factors socioeconomic status, gravida and time of 1st antenatal visit
were significantly associated with prevalence of anaemia in
pregnancy. Conclusion: In this study, a high prevalence of anaemia
was found in pregnant women.
 SUMMARY:-
Anaemia is the most common hematological disorder in
pregnancy. It is a major public health concern in
developing countries. The majority of anaemia in
pregnancy is due to iron, folate or vitamin B12
deficiency. Less community, it could be a consequence
of hemoglobinopathies such as thalassemia and sickle
cell anaemia. To reduce complication proper treatment
should be given.
 CONCLUSION
Haematological disorder in pregnancy is the most
commonly occurring disorder during pregnancy, so every
mother who are pregnant must screen for anaemia and
others haematological disorder, must take treatment as
soon as possible along with foods rich in iron and also
must have family support and care throughout
pregnancy. Awareness and education programs should be
generated to make people come to know about anaemia,
its complications during pregnancy and ways to prevent
it.
 BIBLIOGRAPHY:
1) D.C Dutta’s, “ Textbook of Obstetrics”, 7th ed. 2013, New Central
Book Agency ( P) Ltd, London, page no:- 260- 268.
2) J.B Sharma,Midwifery & gynaecological nursing,1st ed , Avichal
publishing company ,new delhi.page no -275-287.
3) A.K Majhi, “ Bedside clinics in obstetrics” 3rd ed. 2015,Bimal
Kumar Dhur of Academic publishers, pvt.Ltd. Kolkata. Page no-
221-238.
4) Myles, “textbook of midwies”, 6th ed.2014, Elvester (Ltd), page
no: 273-275.
5) https://www.slideshare.net/lisachadha/anaemia-in-pregnancy-13096
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