Anaemia in

pregnancy

Dr. anuja rajurkar

Jr I
A 28 year old female, referred from BGWH Gondia as G2P1L1 with
7 months amenorrhea with severe anemia.
c/o oedema feet since one month
Cold and cough since 3 days.
c/o easy fatigability and weakness.

Patient was apparently alright 1 month ago when she developed

edema over her feet, which was insidious in onset and gradually
increased over time.
Patient also developed cough and cold three days prior to
admission, acute in onset and gradually progressive. Cough was
non productive and not associated with chest pain or
breathlessness. There was no diurnal variation of cough.
No h/o breathlessness, night sweats.
There is no h/o fever, loss of weight, loss of appetite.
No h/o any orifical bleeding. No h/o blood in stools.

Obstetric history-
Patient has been married since 9 years, non consanguinous
marriage.
She has conceived spontaneously.
Patient is G2P1L1
G1-female child, 5 years of age, born of term normal delivery.
Patient received one blood transfusion during this pregnancy.
G2-present pregnancy.
History of present pregnancy-
Patient had 2 ANC visits in PHC Brahmni, both during second
trimester.
Patient received Iron and calcium supplementation but was not
consuming the medications on a regular basis.
She also received 2 doses of Inj T.T at the PHC during those
visits.

Menstrual history-
Patient had a cycle of 3-4days/ 30 days, regular cycles with
average flow.
LMP- 9/5/16
EDD- 16/2/17
Past history-
Patient has history of blood transfusion during previous
pregnancy. No history of any adverse reaction to transfusion.
Patient has no history of any medical or surgical illnesses.

Socioeconomic history-
Patient has been educated till 5 th standard and was working as a
daily wage labourer until 7 months ago.
Her husband is also a daily wage labourer.
She belongs to lower middle class as per modified kuppuswamy
scale.
Dietary history-
Patient was consuming a diet deficient in proteins and vitamins.
Decreased intake of green leafy vegetables, meat and pulses.
On examination-
General condition was moderate, pt was conscious and oriented.
She had facial and conjunctival pallor.
Patient had edema feet, pitting type extending to her ankles.
No cyanosis, icterus, clubbing, lymphadenopathy.
JVP not raised.
Pulse rate of 110/min. BP- 130/80mmhg.

Systemic examination-
CVS S1,S2 heard, no murmurs, HR 110/min, regular.
RS- AEBE, no adventitious sounds.
CNS- conscious, oriented.
P/A findings-
Ut- 30 weeks
Cephalic presentation.
 INVESTIGATIONS
DATE 30/12/16 1/1/17 04/01/17

HB 3GM% 6.6GM% 8.7GM%

RBC 91X10^6 1.91X10^6 2.74X10^6

PCV 8.4 18.8 25.4

MCV 92.3FL 98.7FL 93FL

MCH 32.9PG 34.5PG 31.7PG

MCHC 35.7GM/DL 35.1GM/DL 34.2GM/DL

RDW 15.1% 16.4% 20.6%

WBC 6.6X10^3 10X10^3 12.4X10^3

PLT 167X10^3 111X10^3 102X10^3

 LFT KFT
• TOTAL PROTEIN- 3GM/DL • SR. UREA- 14 MG%
• TOTAL BILI- 0.2MG% • SR. CREATININE-0.3MG%
• ALP-210
• SGOT- 15
• SGPT- 05 • SICKLING TEST WAS NEGATIVE.
 USG

DATE 3/1/17

BPD 33WKS

HC 33WK/3D

AC 28WKS/2D

FL 33WK/2D

EFW 1.6KG

LIQUOR ADEQUATE, AFI 11.8CM

PLACENTA FUNDAL
 INCIDENCE AND DEFINITION
 ANEMIA IN PREGNANCY IS PRESENT WHEN THE TOTAL
HEMOGLOBIN CONCENTRATION IN BLOOD IS 11GM% OR
LESS.
HEMOGLOBIN BELOW 10GM% AT ANY TIME DURING
PREGNANCY IS CONSIDERED TO BE ANEMIA.
INCIDENCE OF ANEMIA IN PREGNANCY VARIES WIDELY
FROM 40-80% IN TROPICS AS COMPARED TO 10-20% IN THE
DEVELOPED COUNTRIES.
 CAUSES OF ANAEMIA IN PREGNANCY

HEREDITARY CAUSES ACQUIRED CAUSES

1. THALESSEMIAS 1. IRON DEFICIENCY AMAEMIA

2. SICKLE CELL 2. ANAEMIA DUE TO ACUTE
HEMOGLOBINOPATHIES BLOOD LOSS
3. OTHER 3. ANAEMIA OF CHRONIC
DISEASE
HEMOGLOBINOPATHIES
4. MEGALOBLASTIC ANAEMIA
4. HEREDITARY HEMOLYTIC
ANAEMIAS 5. ACQUIRED HEMOLYTIC
ANAEMIA
6. APLASTIC OR HYPOPLASTIC
ANAEMIA
 PHYSIOLOGICAL ANAEMIA
• THERE IS INCREASE IN THE MATERNAL PLASMA VOLUME BY ABOUT 40-
50%, BECOMING ALMOST 1.25 LITRES
• THE RED CELL MASS INCREASES BY 20%-30%, MAXIMALLY REACHING 350
ML.
• THIS DISPROPORTIONATE INCREASE IN PLASMA AND RBC VOLUME
PRODUCES A STATE OF HEMODILUTION DURING PREGNANCY.
• IRON DEMAND ALSO INCREASES IN PREGNANCY,NOT FULFILLED EVEN BY
IRON SUPPLEMENTATION, LEADING TO A STATE OF PHYSIOLOGICAL IRON
DEFICIENCY.
• THUS, HEMOGLOBIN DECLINE IS CONTRIBUTED TO BY BOTH
HEMODILUTION AND NEGATIVE IRON BALANCE.
BLOOD VALUE NON-PREGNANT STATE PREGNANT STATE
HEMOGLOBIN 14.8GM% 11-14GM%
RBC 5MIL/CU MM 4-4.5MIL/CU MM
HEMATOCRIT 39-42% 32-36%
MCV 75-100 CU MICRON 75-95 CU MICRON
MCH 27-32 PG 26-31 PG
MCHC 32-36% 30-35%
SR. IRON 60-120UG SLIGHTLY LOWERED
TOTAL IRON BINDING 300-350 UG/100ML 300-400 UG/100ML
CAPACITY
SATURATION PERCENTAGE 30% LESS THAN 16%
SR. FERRETIN 200-300UG/L 150UG/L
 CLINICAL FEATURES OF ANEMIA IN
PREGNANCY
SYMPTOMS SIGNS

LASSISITUDE AND WEAKNESS PALLOR

EASY FATIGABILITY STOMATITIS

LOSS OF APPETITE EDEMA

PALPITATIONS SOFT SYSTOLIC MURMUR AT MITRAL AREA

BREATHLESSNESS FINE CREPTS AT LUNG BASE

GIDDINESS PALE NAILS, KOILONYCHIA

SWELLING OF FACE AND EYELIDS STERNAL TENDERNESS

BLACKOUTS HEPATOSPLENOMEGALY
 IRON DEFICIENCY ANEMIA

COMMONEST CAUSE OF ANAEMIA

DURING PREGNANCY IS IRON
DEFICIENCY.
HEMATOLOGICALLY IT PRESENTS
AS MICROCYTIC HYPOCHROMIC
ANAEMIA.
 CAUSES OF IRON DEFICIENCY DURING
PREGNANCY

• INADEQUATE IRON INTAKE.

• INCREASED IRON DEMAND DURING
PREGNANCY.
• DIMINISHED ABSORPTION OF IRON.
• METABOLIC DISTURBANCES.
• PRE-PREGNANT HEALTH STATUS.
 INVESTIGATIONS FOR DIAGNOSIS AND TO
DETERMINE THE MANAGEMENT OF ANAEMIA

TO NOTE THE DEGREE OF TO ASCERTAIN THE TYPE OF TO DETERMINE THE CAUSE OF

ANAEMIA ANAEMIA ANAEMIA
• HEMOGLOBIN ESTIMATION • PERIPHERAL SMEAR • STOOL EXAMINATION
• TOTAL RED CELL COUNT EXAMINATION • URINE EXAMINATION
• DETERMINATION OF • BONE MARROW STUDY
HEMATOCRIT • HEMATOLOGICAL INDICES
LIKE MCH, MCV AND MCHC,
ARBITRARY GRADING OF OF WHICH MCHC IS MOST
PATHOLOGICAL ANAEMIA IS AS SENSITIVE INDEX OF IRON
FOLLOWS- DEFCIENCY ANAEMIA
MILD- HB BETWEEN 8-10GM%
MODERATE- HB BETWEEN 7-
8GM%
SEVERE- LESS THAN 7GM%
 MANAGEMENT OF IRON DEFICIENCY ANAEMIA DURING
PREGNANCY
PROPHYLAXIS CURATIVE THERAPY
SUPPLEMENTARY IRON DEPENDING UPON THE DEGREE,
THERAPY TYPE AND CAUSE OF ANAEMIA,
INTAKE OF BALANCED DIET TREATMENT IS INSTITUTED AND
IT INCLUDES-
ADEQUATE TREATMENT OF
INFECTIONS AND PARASITIC HOSPITALISATION
INFESTATIONS. GENERAL TREATMENT
SPECIFIC THERAPY
 TREATMENT MODALITIES
ORAL IRON THERAPY PARENTERAL IRON THERAPY BLOOD TRANSFUSION
 FERROUS FORM OF IRON IS  INTRAVENOUS- IRON SUCROSE, INDICATIONS-
USED MOST COMMONLY. SODIUM FERRIC GLUCONATE  CORRECTION OF ANAEMIA DUE
 OTHERS ARE FERROUS COMPLEX, IRON DEXTRAN, FERRIC TO BLOOD LOSS.
FUMARATE, GLUCONATE, CARBOXYMALTOSE.  SEVERE ANAEMIA IN LATER
ASCORBATE.  INTRAMUSCULAR- ION SUCROSE STAGES OF PREGNANCY.
(20MG/ML), FERRIC GLUCONATE  REFRACTORY ANAEMIA.
 ADVANTAGES- EASY, SAFE TO COMPLEX (12.5MG/ML), IRON  ASSOCIATED INFECTIONS.
ADMINISTER DEXTRAN (50MG/ML)
 DISADVANTAGES-  ADVANTAGES- BUILDS UP
NONCOMPLAINCE TO ORAL  ADVANTAGES- CAN BE GIVEN TO HEMOGLOBIN, SUPPLES
IRON, UNPREDICTABLE RATE THOSE INTOLERNT TO ORAL IRON, CONSTITUENTS LIKE PROTEINS,
OF ABSORPTION, EFFECTIVE REPLENISHMENT OF ANTIBODIES ETC.
INEFFECCTIVE IRON STORES.
REPLENISHMENT OF IRON  DISADVANTAGES- ADVERSE
STORES. REACTIONS (IRON DEXTRAN),
PAINFUL INJECTIONS
 COMPLICATIONS OF ANAEMIA

DURING PREGNANCY DURING LABOUR PUERPERIUM

 PRE-ECLAMPSIA  POST PARTUMM  PUERPERAL SEPSIS

 INTERCURRENT INFECTION HAEMORRHAGE
 HEART FAILURE  CARDIAC FAILURE
 PRETERM LABOUR AND LOW  SHOCK
BIRTH WEIGHT.
SICKLE CELL ANAEMIA

Caused by single beta

chain substitution of
glutamic acid by valine,
resulting in formation of
haemoglobin S.
Sickle cell syndrome
includes Sickle cell
anemia Hb-SS, Sickle cell
Hemoglobin C disease-
HbSC, Sickle cell Beta
Thalessemia and Sickle
cell haemoglobin E
disease.
• Red cells with HbS undergo sickling when they are deoxygenated,
resulting in formation of haemoglobin aggregates.
• Repetitive sickling and unsickling causes membrane damage,
causing the cell to be irreversibly sickled.
• Such red cells block the microcirculation, giving rise to
vasoocclusion, in any event that slows down the red cell transit
through the microcirculation.
• This produces severe pain, called a sickle cell crisis- which can be
aplastic, sequestration, megaloblastic, haemolytic type.
• Changes that can occur because of sickling are- osteonecrosis of
femur and humeral head, renal medullary damage,
autosplenectomy in SS patients, ventricular hypertrophy,
infarctions, leg ulcers, hepatomegaly, cerebrovascular accidents
and propensity for infections and sepsis.
 COMPLICATIONS
DURING PREGNANCY

• CARDIOMYOPATHY, PULMONARY HYPERTENSION, RENAL

FAILURE.
• COMPLICATIONS DURING PREGNANCY INCLUDE- CEREBRAL VEIN
THROMBOSIS, PNEUMONIA, PYELONEPHRITIS, DEEP VEIN
THROMBOSIS, PULMONARY EMBOLISM, SEPSIS SYNDROME.
• DELIVERY COMPLICATIONS- GESTATIONAL HYPERTENSION/PRE-
ECLAMPSIA, ECLAMPSIA, PLACENTAL ABRUPTION, PRETERM
DELIVERY, FETAL GROWTH RESTRICTION
 MANAGEMENT OF SICKLE CELL SYNDROMES
• Pre-natal folic acid supplementation to support the rapid cell
turnover.
• During sickle cell crisis, oxygen supplementation through nasal
cannula, maintenance of adequate hydration and opiods to relieve
pain.
• Prophylactic transfusions also reduce vasoocclusive crisis.
• Immunisation with polyvalent pneumococcal, haemophilus influenza
and meningococcal vaccines for those who have sickle cell disease
and asplenia.
• Epidural analgesia during labor is beneficial.
MEGALOBLASTIC
ANAEMIA
Deranagement of red cell
maturation with the production of
abnormal cells in the bone marrow
called as the megaloblasts due to
impaired DNA synthesis.
Causes of vit B12 deficiency are-
strict vegetarian diet, gastrectomy,
ileal bypass, gastritis, use of proton
pum inhibitors.
Causes of Folate deficiency-
increased demand during
pregnancy, inadequate intake,
diminished absorption, diminished
storage.
 MANAGEMENT AND COMPLICATIONS
• Complictions that may arise are- miscarriage, prematurity, fetaal
malformations including neural tube defects.
• Prophylactic folic acid in a dose of 4mg/ day should be given to all
pregnant women, and should be given in the pre-conceptional period
as well.
• For dimorphic anaemia, which is commonly seen in the tropics, both
iron and folic acid supplementation is given. Here the red cells
become macro or normocytic with normo or hypochromia.
 Aplastic anaemia
• Blood picture shows decline in all cell forms- leucopenia,
thrombocytopenia and anemia.
• Bone marrow is markedly hypocellular.
• Management consists of efforts to maintain hematocrit above 20.
• Granulocyte transfusion and platelet transfusions may be given to
combat infections and control of haemorrhage respectively.
• Bone marrow or stem cell transplantation is effective.
 THALASSEMIA
• Classified as alpha or beta thalassemia according to the globin chain
deficient.
• Alpha thalassemia has four types depending upon the number of gene
deletions- alpha thalassemia minor with deletion of two alpha chains and
alpha thalassemia major with deletion of all four alpha chains.
• Beta thalassemia also is categorised as beta thalassemia major and minor
with homogygous and heterozygous state respectively. In beta thalassemia
major, there is severe anaemia and intense hemolysis. Patients are majorly
dependent on transfusions with a high ironload in the body.
• Transfusions are given throughout pregnancy in beta thalassemia to
maintain haemoglobin levels above 10gm%
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