Disampaikan Oleh :

dr. Ong Tjandra, MMPd., SpOG(K)

Seminar Nasional
“Selamatkan Ibu dan Buah Hati dengan Kualitas Gizi yang Baik untuk
Menghadapi Masa depan”
Program Pendidikan D4 Kebidanan STIKes Bina Permata Medika, Tangerang
• Micronutrient deficiencies during
pregnancy results in spontaneous
abortions, Pre term labour, IUGR, LBW
babies and maternal deaths.
• The cost implications include:
– Increased length of hospital stay
– Expenses related to referral, transport
of cases to hospitals with pediatric care
facilities
– Cost of incubators and Intensive care
– Cost of post maternity care
These all result in burden on State
Health Budget
Source: World Bank, 2011
http://data.worldbank.org/indicator/SH.PRG.ANEM
Definition: By WHO
Hb. < 11 gm /dl
(or haematocrit <32%).
Mild anaemia -------- 9 -10.9 gm /dl
Moderate anaemia--- 7-8.9 gm /dl
Sever anaemia-------- < 7gm /dl
Very sever anaemia-- < 4gm/dl
 During pregnancy there is a disproportionate increase in
plasma volume, RBC volume and haemoglobin mass. As
plasma volume increase more than the RBC mass
hemodilution occurs called as physiological anemia of
pregnancy.
 Criteria are:
 RBC 3.2 million/cumm
 Hemoglobin 10 gm%
 RBC morphology on peripheral smear is normal i.e.
normocytic,
 normochromic.
 PCV 30%
Source: Cunningham in Queenan et al (2010)
• Plasama volume 50% (by 34weeks)
• But RBC mass only 25%
• Results in haemodilution :
• Hb
Haematocrit
RBC count
• No change in MCV or MCH
• 2-3 fold increase in Fe requierment.
• 10-20 Fold increase in folate requirement
Common types: Rare types:
 Nutritional deficiency • Aplastic
anaemias • Autoimmune hemolytic
- Iron deficiency • Leukemia
- Folate deficiency • Hodgkin’s disease
- Vit. B12 deficiency • Paroxysmal nocturnal
haemoglobinurea
 Haemoglobinopathies:
- Thallassemias
- SCD
 Iron required for fetus and placenta ------- 500mg.
 Iron required for red cell increment ------- 500mg
 Post partum loss --------- 180mg.
 Lactation for 6 months - 180mg.
 Total requirement -------1360mg
 350mg subtracted (saved as a result of
amennorrhoea)
 So actual extra demand ----------------------1000mg
 Full iron stores --------------------------------1000mg
Depleted iron stores – dietary lack, chronic renal failure,
worm infestation, chronic menorrhagia
Chronic infections: ( like malaria)
Repeated pregnancies :
- with interval < 1 year
- blood loss at time of delivery
- multiple pregnancy.
CLINICAL FEATURES
Symptoms usually in severe anaemia
- Fatigue
- Giddiness
- Breathlessness
Mother Fetus
•High output Cardiac failure •IUGR
(more likely if precelampsia •Preterm birth
present. inadequate tissue •LBW
oxygenation increase
•Depleted Fe store
requirments for excessive
blood flow ) •Delayed Cognitive
•PPH function
•Predisposes to infection
• Risk of thromboembolism
•Delayed general physical
recovery esp after c. section
 Hb
 Haematocrit
 RBC Indices:
- Low MCV
- Low MCH
- Low MCHC
- Low PCV
 Peripheral blood picture :
Microcytic Hypochromic anaemia .
 INVESTIGATIONS

 Serum iron decreased (<12 micro mol / l)

 Total iron binding capacity :TIBC in non-pregnant
state is 33% saturated with iron .when serum iron
level fall ,<15% ofTIBC saturated.by fall in
saturation,the TIBC INCREASED.
 S.ferritin :In healthy adults ferritin circulate in
plasma in range of 15_300 pg/l. in iron deficiency
anemia it is the first test to become abnormal.
 Serum transferrin receptor(TfR) : present
on all cells as transmembrane protien that
binds transferrin iron and transfer it to cell
interior. Increased in iron def. anemia.
 Bone marrow examination.
 RFTS/LFTS.
 Urine for haemturia.
 Stool examination for ova ,cyst and occult
blood.
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
 Objectives:
1- To achieve a normal Hb by end of pregnancy
2- To replenish iron stores
 Two ways to correct anaemia:
I- Iron supplementation : Oral Fe / Parenteral Fe
II- Blood transfurion
 Choice of method:
It depends on three main factors:
Severity of the anaemia
Gestational Age.
Presence of additional risk factor
 Recommended supplementation for non-
anaemiac 30 - 60mg /day of elemental iron
 Anaemic gravidas 120 –240mg / per day
 In tolerance to iron tablets – enteric coated tablet /
liquid suspension
 Supplementation with folic acid + Vit C.
 Therapeutic results after 3 weeks – rise in Hb %
level of 0.8gm/dl/ week with good compliance.
 Treatment continued in the postpartum period to
fill the stores
 Severe anaemia: (Hb < 8gm/dl)- preferably
parenteral theraphy in the form of I/M or I/V iron
- I/M : ( Iron sorbitol) with “Z” technique
- I/V : (iron sucrose)
 Iron neede =
(Normal Hb – Pt. Hb)* Wt in Kg*2.21+1000)
Dose given I/M or I/V by slow push 100mg / day or the
entire dose given in 500 ml N/S slow I/V infusion over
1-6 hours
 Marked increase in reticulocyte count expecred in 7-14 d
Blood transfusion:
 may be required to treat severe anaemia near term or when
some other complication such as placenta praevia present.
 Gross anaemia

▪ Packed red cells transfusion (Under cover of loop

diuretic)
▪ Exchange transfusion (Under cover of loop diuretic)
Side effect of Fe Oral therapy:
. G. I upset.
. Constipation.
. Diarrhoea.
Parentral:
- skin discolouration
- local abscess
- allergic reaction
- Fe over load.
 Complicates upto 1% of pregnancies
 Characterized by :
- RBC with high MCV
- White blood cells with altered morphology
(hypersegmented neutrophils).
 Usuallycaused by :
- Folate deficiency may occur after exposure
to sulfa drugs or hydroxyurea
- Vitamin B12 deficiency
At cellular level
Folic acid reduced to Dihydrofolicacid then
Tetrahydro-folicacid . (THF) e is required for cell
growth & division.
So more active tissue reproduction & growth more
dependant on supply of folic acid.
So bone marrow and epithelial lining are therefore
at particular risk.
Folic acid deficiency more likely if
. Woman taking anticonvulsants.
. Multiple pregnancy.
. Hemolytic anemia; thalasemia H.spherocytosis
Maternal risk:
Megaloblastic anemia
Fetal risk:
Pre-conception deficiency cause neural
tube defect and cleft palate etc.
Diagnosis: Increased MCV ( > 100 fl)
Peripheral smear: - Macrocytosis, hypochromia
- Hypersegmented neutrophils
(> 5 lobes)
- Neutropenia
- Thrombocytopenia

Low Serum folate level.

Low RBC folate.`
 Daily folate requirement for :
 Non pregnant women -- 50 -100 microgram
 Pregnant woman –-------- 300-400 microgram
 Usually folic acid present in diets like fresh fruits
and vegetables and destroyed by cooking.
Folate deficiency:
- 0.5-1.0mg folic acid/day
If F/Hx. of neural tube defect
- 4mg folic acid/day.
 Itis rare
Occurs in patients with gastrectomy , ileitis, illeal
resection, pernicious anaemia, intestinal
parasites.

 Diagnosis:

▪ Peripheral smear
▪ Vitamin B12 level < 80 pico g/ml
 Treatment of B12 Deficiency:
 Vit B12 1mg I/M weekly for 6 weeks.
 Normal adult Hb. after age of 6 month,
 HbA---97%, HbA2---(1.5-3.5%), HbF2--<1%.
 4 Globin chains associated with haem complex.
 Hb. A = 2 alpha +2 beta globin chains.
 Hb.A2= 2alpha+2 delta globin chains.
 Hb.F = 2 alpha+ 2 gamma globin chains.
 Hb. synthesis is controlled by genes.
 Alpha chains by 4 gene,2 from each parent.
 Beta chains by 2 genes ,1 from each parent.
DEFINITION:
 Inherited disorders of haemoglobin.
 Defect may be in:
- Globin chain synthesis------thallassemia.
- Structure of globin chains-sickle cell disease.
 Hb.abnormalities may be:
- Homozygous = inherited from both parents.
(Sufferer of disease)
- Hetrozygous = inherited from one parent.
(Carrier/trait of disease)
 The synthesis of globin chain is partially or
completely suppressed resulting in reduced Hb.
content in red cells,which then have shortened life
span.
 TYPES:
- Alpha thalassaemia.
- Beta thalassaemia:
. Major
. minor
 Beta Thallassemia trait
 Heterozygous inheritance from one parent.
 Most frequent encountered variety.
 Partial suppression of the Hb. synthesis.
 Mild anaemia.
Investigations: Hb----around 10 g/dl.
 Red cell indices: low MCV.
low MCH.
normal MCHC.
 Diagnostic test: Hb. Electrophoresis.
 Management:
 Same as normal woman in pregnancy.
 Frequent Hb. Testing.
 Iron & folate supplements in usual dose.
 Parenteral iron should be avoided. because of
iron overload.
 If not responded ---I/M folic acid.
 blood transfusion close to time of delivery.
 Homozygous inheritance from both parents.
 Sever anaemia.
 Diagnosed in paediatric era.
 T/m: is blood transfusion.

ALPHA THALASSAEMIA:
 Both heterozygous & homozygous forms exist.
 Alpha thallassaemia trait.
 HbH disease.
 Alpha thallassaemia major.
 Autosomally inherited .
 Structural abnormality.
 HbS - susceptible to hypoxia, when oxygen
supply is reduced.
 Hb precipitates & makes the RBCs rigid &
sickle shaped.
 Heterozygous----HbAS.
 Homozygous-----HbSS.
 Compound heterozygous---HbSC etc.
 Sickeling crises frequently occurs in pregnancy,
puerperium &in state of hypoxia like G/A and
Hag.
 Increased incidance of abortion and still birth
growth restriction, premature birth and
intrapartum fetal distress with increased perinatal
mortality.
 Sickle cell trait:(carrier state)
Does not pose any significance clinical problems
 Diagnosis:
- Hb. Electrophoresis
- Sickledext test is screening test
 Management:
- No curative Tx.
- only symptomatic
- Well hydration, effective analgesia, prophylactic
antibiotics, O2 inhalation, folic acid, oral iron
supplement (I/V iron is C/I), blood transfusion
 Comfortable Position
 Adequate analgesia
 O2 inhalation
 Low threshold of assisted delivery
 Avoid ergometrine
 Prophylactic antibiotics
 Continue iron &folate therapy for 3 mo after
delivery
 Appropriate contraceptive advice
The End…..