anemia in pregnancy

1. ANAEMIA IN PREGNANCYANAEMIA IN PREGNANCY
Commonest medical disorder.
High incidence in underdeveloped
countries
 Increased Maternal morbidity &
mortality ,20% directly and indirectly to
further 20%.
Increased perinatal mortality

2. PREVALENCE:PREVALENCE:
In india nearly 40 to 90%
pregnant women are considered
anaemic

3. DEFINITIONDEFINITION
A) By WHO ------------
1- Hb. < 11 gm /dl
2- Haematocrit <32%
B) By CDC
(Centre for disease control & prevention)
1- <11gm% in first and third trimester
2- <10.5gm% in second teimester

4. SEVERITY OF ANEMIA
 According to ICMR –
Mild - 10 – 10.9 gm%
Moderate - 7 – 10 gm%
Severe - < 7 gm%
Very severe - < 4 gm%

5. ETIOLOGY
(A)Physiological Anemia
(B)Pathological Anemia
Criteria for Physiological anemiaCriteria for Physiological anemia
 Hb = 10 gm%
 RBC = 3.2 million/mm3
 PCV = 30%
 Peripheral smear showing normal morphology of RBC
with central pallor.

6. Physiological changes inPhysiological changes in
pregnancypregnancy
• Plasma volume 50% (by 34weeks)
• But RBC mass only 25%
• Results in haemodilution :decrese Hb
Haematocrit
RBC count
 No change in MCV or MCH
2-3 fold increase in Fe requierment.
10-20 Fold increase in folate requirement

7. PATHOLOGICAL ANEMIA :PATHOLOGICAL ANEMIA :
Nutritional Anemia -
(i) Iron Deficiency anemia
(ii) Folate deficiency anemia
(iiii) Vit ‘B12’ deficiency anemia

8. (b) Anemia of chronic disease :
(i) Chronic malaria (ii) Tuberculosis
(iii) Renal disease
(c) Bone marrow insufficiency -
hypoplasia or aplasia due to radiation, drugs
(aspirin, indomethacin).
(d) Chronic blood loss
(i) Bleeding piles (ii) Hookworm infestation
(e) Hereditary –
(i) Thalassemia (ii) Sickle cell disease
(iii) other hemoglobinopathy
(iv ) Hereditary hemolytic anemia

9. COMPLICATIONS OF SEVERECOMPLICATIONS OF SEVERE
ANAEMIAANAEMIA
During Pregnancy
– Poor weight gain
– Decrease work capacity
– Decrease immune response
– Preterm Labour
– CHF at 30 – 32 Wk of pregnancy

10. DURING LABOUR
–Postpartum haemorrhage
–Cardiac failure
–Shock

11. PUERPERIUMPUERPERIUM
There is increased chance of
– Puerperal sepsis
– Subinvolution
– Failing lactation
– Puerperal venous throbosis
– pulmonary embolism

12. RISK PERIODSRISK PERIODS
The risk periods when the patient may even die
suddenly are
– At about 30-32 weeks of pregnancy
– During labour
– Immediately following delivery
– Any time in puerperium specially 7-10 days
following delivery due to pulmonary
embolism

13. EFFECTS ON BABYEFFECTS ON BABY
 Amount of iron transferred to the fetus is unaffected
even if the mother suffers from iron dificiency
anaemia.
 So the neonate does not suffer form anaemia at birth
 There is increased incidence of low birth weight
babies with its incidental hazards.
 Intrauterine death-due to severe maternal anoxaemia
 The sum effects is increased perinatal loss

14. WORK UP OF A PATIENTWORK UP OF A PATIENT
A DIAGNOSIS - ------
1- ON THE BASIS OF HISTORY.
2- ON THE BASIS OF SYMPTOMS.
3- ON THE BASIS OF CLINICAL
EXAMINATION.
4- ON THE BASIS OF INVESTIGATION.
B – MANAGEMENT
1- OBSTETRIC
2- SPECIFIC TO THE CAUSE

15. A- DIAGNOSIS.
ON THE BASIS OF HISTORY =
most often is enough to point out a
cause for anaemic state.
1.Age=at either end of the reproductive
age.
2.Menstrual history= prepregnant level
of anaemia,

16. 3.Obstetric history=
a)Multiparity
b)Too frequent child birth <1year interval
c) Multiple gestation and abortions
d) History of LBW baby
e) History of PPH, preeclampsia, lactational
failure
f) Puerperal sepsis
g) Prior use of IUCD,
h) Present obstetric history=of APH

17. 4.Past history=
A) Persisting anaemia
B) Chronic illness like TB, rheumatoid
arthritis, fever
C) hookworm infestation
D) bleeding piles,haemetemesis,malaria
E) any surgical history
F) history of blood transfusion

18. 5.Family history -
A- sickle cell anaemia B- thalassemia
6.Drug history-
A- intake of iron
B- intolerance to oral iron,
C- allergy to systemic iron.
D- intake of antiepileptics.

19. 7. Personal history
Recurrent UTI,
loss of appetite,
Diarrhoea constipation,
Decrese in weight gain,
Travel to endemic area of malaria.

20. 8. Geographical area, race and
socioeconomic =
9.Dietary history=
lack of iron rich foodstuff,wrong
habits,cooking habits,vegetarianism

21. ON THE BASIS OF SYMPTOMSON THE BASIS OF SYMPTOMS
Patient usually complaints =
1- Easy Fatiguability
2-decresed work or exercise tolerance
3-anorexia
4 – Giddiness or fainting attack
5- Breathlessness
6-palpitation on exertion

22. 7-some patient may complain of
pica(ice,clay)
8-in advanced stage may have
anasarca,anginal pain
9-poor weight gain
10-frontal headache
11-bony pain-in sickle cell anaemia

23. ON THE BASIS OF CLINICALON THE BASIS OF CLINICAL
EXAMINATIONEXAMINATION
1.General1.General
2.obstetric2.obstetric

24. GENERAL EXAMINATION =
from
top to bottom
1.Level of conciousness and orientation-
altered sensorium/irritablity
2.Built ,nutrition and gait
3.hair-
4-facies
5-pallor-
6-icterus

25. 7- angular stomatitis, glossitis, cheilosis,,
painful ulcer on tongue
8-neck veins and glands
9.Sternal tenderness;acute leukemia
9-breast examination
10-nail changes

26. 11- CVS –
Tachycardia,
strong peripheral pulses with wide
pulse pressure.
 Functional cardiac murmur (Ejection
murmur).
 Evidence of cardiomegaly, CHF.
-

27. 12-RS examination-for basal crepts in
CHF with anaemia
13-purpura and petechiae
14.Per abdominal-look for
hepatosplenomegaly, hernial sites.

28. 18- Edema (Renal failure).
19- Lower leg ulcers (Sickle cell
Anemia).
OBSTETRIC EXAMINATION;;
Fundal height, SFH ,abdominal
girth, to detect IUGR
On auscultation-FHS

29. INVESTIGATIONSINVESTIGATIONS
1.ROUTINE = a) Hb to be done at 1st
visit,28,32,&36 weeks
B)blood grouping & Rh typing
C)urine routine & microscopy
D)HIV,HBsAg,VDRL
E)obstetric USG
F)glucose challenge test at first visit

30. 2.INVESTIGATION TO FIND OUT
THE CAUSE OF ANAEMIA=
 if Hb <11gm% ,further investigation
A)- Complete blood count: Hb, MCV, MCH,
MCHC, reticulocyte count, TLC,& platelate
count
B) Peripheral Smear:to See – morphology
of RBC, hypersegmentation of neutrophils,
hemoparasite, evidence of hemolysis,
C) NESTROF TEST - screening test for
thalassemia;

31. D) Urine examination; WBC(infection),
casts(chronic renal disease)
E)Stool examination; parasites (ova of
hookworm),occult blood or steatorrhoea
(malabsorption).
F) Iron studies
S. ferritin,
S.iron,
Transferrin saturation,
Total iron binding capacity,
RBC protoporphyrin.

32. F) Blood urea nitrogen; for renal
disease
G) Mantoux test & sputum ; for
TB
H)Bone marrow examination;
only in refractory or atypical
anaemia.

33. I) S.Folate, RBC Folate & S.B12
level ;if peripheral smear suggestive of
megaloblastic anaemia.
J) Investigation for hemolytic
anaemia; osmotic fragility ,coomb”s
test,Hb electrophoresis,G6PD assay.
H )X-ray chest for pulmonary koch, or
patient with CHF
I) LFT & RFT

35. NORMAL VALUES OF RED CELL INDICES ANDNORMAL VALUES OF RED CELL INDICES AND
SERUM LEVELS OF ERYTHROPIETIC FACTORSSERUM LEVELS OF ERYTHROPIETIC FACTORS
RBC countRBC count 4.5 to 5.1 million/cumm4.5 to 5.1 million/cumm
HbHb 12 to 14 gm/dl12 to 14 gm/dl
PCVPCV 36 to 44%36 to 44%
MCVMCV 80 to 96 fl80 to 96 fl
MCHMCH 27 to 33 pg27 to 33 pg
MCHCMCHC 32 to 36%32 to 36%
S. IronS. Iron 60 to 150mg/dl60 to 150mg/dl
TIBCTIBC 300-350micro gm/dL300-350micro gm/dL
S.FERRITINS.FERRITIN 50-200micro gm/dL50-200micro gm/dL
Reticulocyte countReticulocyte count 0.5 to 2.5%0.5 to 2.5%

36. PERIPHERAL SMEARPERIPHERAL SMEAR
finding diagnosis
1. Microcytic Hypochromic,
anisocytosis, poikilocytosis,
Iron deficiency anemia
thalassemia.
2- Hypersegmented neutrophils,
Macrocytic
Folic Acid and Vitamin B12
deficiency
3- Polychromatophilia,
nucleated RBCs, Spherocytes,
Sickle cells, target cells,
schistocytes, neutrophilla,
thrombocytosis
Hemolytic Anemia.

37. MANAGEMENTMANAGEMENT
Objectives:
1- To achieve a normal Hb by end of pregnancy
2- To replenish iron stores
3-To prevent maternal and fetal complication
4.To improve outcome of pregnancy
Choice of method:
It depends on three main factors
1- Severity of the anaemia
2- Gestational Age.
3- Presence of additional risk factor

38. COMMON ANAEMIASCOMMON ANAEMIAS
1.IRON DEFICIENCY
2.MEGALOBLASTIC
3.THALASSEMIA
4.SICKLE CELL
5.APLASTIC

39. IRON DEFICIENCY ANAEMIAIRON DEFICIENCY ANAEMIA
1. ETIOLOGY
2. 1.INCREASED DEMAND
 Pregnancy and lactation
 Frequent &multiple pregnancies

2. Increased blood loss
 uterine cause
 Gastrointestinal causes
 Peptic ulcer
 Haemorrhoids
 Hookworn infestation,
3.malaria,TB

40. 3. Inadequate dietary intake

4. Decreased absorption
Partial or total gastrectomy
Achlorhydria
Intestinal malabsorption such as in coeliac
disease.

41. IRON REQUIRMENTIRON REQUIRMENT
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

42. TREATMENT OF IRON DEFICIENCYTREATMENT OF IRON DEFICIENCY
ANEMIAANEMIA
The response of Iron deficiency anemia to Iron
therapy is however, influenced by several factors,
1. Severity of anemia.
2. Ability of the patient to tolerate & absorb
dietary iron.
3. Presence of other complicating illnesses/ states.

43. TREATMENTTREATMENT
PROPHYLACTIC
– Avoidance of frequent child
– Supplementery iron therapy
– Daily administration of 200 mg ferrous
sulphate (containing 60 mg of element
iron) along with 1ooo microgm folic
acid
– Dietary advice

44. 
Adequate treatment should be instituted to
eradicate
1. hookworn infestation
2.malaria,
3.bleeding piles
4.urinary tract infection.

45. CURATIVE TREATMENTCURATIVE TREATMENT
ORAL THERAPY
FORMULATION ADVANTAGE DISADVANTA
GE
FERROUS
SULPHATE 60mg
High amount of
elemental iron,good
bioavailability
GI side
effect,staining
of teeth
FERROUS
FUMARATE 65mg
same same
FERROUS
ASCORBATE 100mg
Highest iron, prevent
iron overload,
less
IRON
POLYMALTOSE
COMPLEX
Better compliance less

46. -The initial dose is one tablet to be given thrice
daily with or after meals. If larger dose is
necessary (maximum six tablets a day), it
should be stepped up gradually in three to four
days.
-The treatment should be continued till the
blood picture becomes normal; therafter a
maintains dose of one tablet daily is to be
continued for at least 100 days following
delivery to replenish the iron stores.

47. PARENTERAL THERAPYPARENTERAL THERAPY
1- Intravenous route 2- Intramuscular route
INDICATION
1- Oral iron is not tolerated: bowel upset is too
much.
2- Failure to absorb oral iron:
3- Non-compliance to oral iron.
4- In presence of severe deficiency with chronic
bleeding.
5- Along with erythropoietin:
6 –After 32 wk of gestation,parental iron
preferred,as 100% compliance.

48. Adverse effects
- skin discolouration
- local abscess
- allergic reaction
- Fe over load.
- Chest pain, rigors, chills, fall in BP, dyspnoea,
hemolysis.
Treatment:
- Stop infusion.
- Give antihistaminics,
- Corticosteroids & epinephrine.
Oral iron should be suspended at least 24 hrs prior to
therapy to avoid reaction.

49. Intramuscular PreparationIntramuscular Preparation
Iron Sorbitol Citrate :jectofer/jectocos
 Low molecular weight
 Easily Absorbed
Dose:
• 1.5 mg(1 ampule) contains 50mg elemental iron
• Given by Z technique (2ml=100mg)
Iron Dextran:Imferon
 Maximum 2ml is given at a time (2ml=100mg)
 It is associated more systemic complication and has a erratic
abortion so not preferred now days.
Routine testing for sensitivity is necessary, 0.5 ml of injection or 25
mgm should be administered as a test dose,

50. Intravenous PreparationIntravenous Preparation
Iron Sucrose complex(venofer) :
Advantage:
 no test dose recommended
 Minimum side effect
 Not associated with anaphylactic reaction
 Most preffered in patients under going hemodialysis
Dose:
• Can be given undiluted @1ml/min. maximum dose being 100mg
that is over 5min. As 5ml content 100mg iron (1amp=
2.5ml=50mg Iron)
• Other way is to dilute 5ml of vial in 100ml normal saline
(1mg /ml ) over at least 20min.
• A maximum of 200mg dose can be given at a time not more than
thrice a week.

51. Sodium Ferric Gluconate :
 Direct IV push
 12.5mg/min
 As 5ml containing 62.5 mg of iron or 125mg that is
10ml can be diluted in 100ml of saline and infused
over 60min.
 No test dose required.
Iron Dextran:
• Test dose required.
• 100mg in 250ml saline over 30-60 min.
• Associated hypotension, utricaria, dizziness, arthalgia,
lymphadenopathy, fever.

52. Intravenous ferrous sucrose has been shown
to be safer than iron dextran ((ACOG 2013)
There are equivalent increase in haemoglobin
level in women treated with oral or parentral
Iron therapy

53. FORMULA FOR CALCULATIONFORMULA FOR CALCULATION
Total iron deficit = 2.3 X B.W(KG)XHb
deficit+1000 mg
Weight in pounds x Hb deficit x 0.3,+50%
Takes 200mg of elemental iron to raise the
Hb by 1gm%+500mg

54. 3. BLOOD TRANSFUSION –

Patient factors Type of surgery
Preg Preg Elective Emergency
<36wks > 36wks C/S C/S
-Hb ≤ 5gm% - Hb ≤ 6gm% - with H/O -Always
Without CHF without CHF APH,PPH, arrange
-Hb 5-7gm%,if -Hb 6-8gm%,if previous blood.
CHF,hypoxia, CHF,hypoxia, LSCS.
Infections. Infections.
Hb <8gm%,2 units blood should be arranged.

55. Guidelines for transfusion:
 Prefer fresh Packed cells.
 Do not repeat tranfusion within 24 hrs.
Effects of Transfusion:
 ↑ O2 carrying capacity of blood.
 Viscosity increases by 33%.
 Hb increases by 1gm/unit.
 Heart rate decreases by 7%.
 Supplies natural constituents of blood.
 Improvement with in 3 days.
Drawbacks:
 Premature labour (blood reaction).
 CHF
 Transfusion rexn.
 Infections: HIV, Hep B etc.

56. Pregnancy
<30wks
Pregnancy
30-36wks
Pregnancy
>36wks
IDA FA
def.
Oral iron Oral FA
Intolerance or
Non-compliance
I/M iron I/V
iron
IDA FA def.
Parenteral Oral
FA
I/M iron I/V
iron
Blood
transfusion
PROTOCOL OF SEVERE ANEMIA IN PREGNANCY

57. RESPONSERESPONSE
Therapeutic results= after 3 weeks
Clinical improvement
A)incresed sense of well being.
B)increse in work capacity
C)increse in appetite .

58. HEAMATOLOGICAL EXAMINATION
1)- 5-7 days – increasing reticulocyte count to upto 5%
(normal 0.2- 2%)
2)- 2-3 wks – rising haemoglobin level 0.8- 1 gm/ dl/wk.
improvement in RBC indices – MCV, MCH, MCHC.
.
3)- 6-8 wks – haemoglobin level come to normal level
 Peripheral smear show normocytic normochronic RBC.
 Increasing in serum ferritin level.

59. MEGALOBLASTIC ANAEMIAMEGALOBLASTIC ANAEMIA
Complicates upto 1% of pregnancies
Usually caused by :
- Folate deficiency may occur after exposure
to sulfa drugs or hydroxyurea
- Vitamin B12 deficiency

60. FOLIC ACID DEFICIENCYFOLIC ACID DEFICIENCY
FA is cofactor in nucleic acid synthesis
and has imp. role in cell division.
Daily requirement is 300-500microg.
High incidence in multigravida, twin
pregnancy, hyperemesis gravidarum,
alcohol consumption, smoking,
malabsorption, antiepileptic drugs.

61. Maternal risk:
Megaloblastic anemia,high abortion
Fetal risk
-premature birth,
Pre-conception deficiency cause neural tube defect
and cleft palate etc.

62. Diagnosis: 1.blood inv-Increased MCV ( > 100 fl)
2.Peripheral smear: - Macrocytosis, hypochromia
- Hypersegmented neutrophils
(> 5 lobes)
- Neutropenia
- Thrombocytopenia .
3.confirmatory
- Low Serum folate level < 2 ng/ml
- Fasting Serum folate < 6microg/l

63. MANAGEMENTMANAGEMENT
1- 0.5-1.0mg folic acid/day orally
2- For severely anaemic;1mg/day i/m for 7 days
3- If Family history of neural tube defect so for
prevention;
- 4 mg folic acid/day ,1 month
before conception upto 12 weeks of pregnancy .

64. Vitamins BVitamins B1212 DeficiencyDeficiency
It is rare
Occurs in patients with gastrectomy , ileitis, illeal
resection, pernicious anaemia, intestinal parasites.
Inadequate intake,strict vegetarianism,

Clinical features :apart from general features of
anaemia,development of neurological symptoms in
B12 deficiency anaemia.

65. Diagnosis:
 A) Hb must be below 10gm%
B) with 2 of the following in film
1-4% of White blood cells with altered
morphology(hypersegmented neutrophils)
2-macrocytes with diameter>12 micron
3-Howell-Jolly
4-nucleated RBC
C) Blood indices
a) Vitamin B12 level < 100 pico g/ml

66. Treatment of B12 Deficiency:
a)Vit B12 250micro gm I/M weekly for 6
weeks.
b)in severely anaemic; 100 micro gram/day
i/m for 1 week

67. HAEMOGLOBINOPATHIESHAEMOGLOBINOPATHIES
DEFINITION:
Inherited disorders of haemoglobin.
Defect may be in:
- Globin chain synthesis------thallassemia.
- Structure of globin chains-sickle cell
disease.

68. THALASSAEMIASTHALASSAEMIAS
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:
.

69. DIAGNOSISDIAGNOSIS
Clinical featuresClinical features
1.history of blood transfusion dependent
anaemia
2.anaemia not responding to oral iron
supplements
3.alpha thalassemia trait if patient with mild
anaemia with low MCV,not responding to
iron & B thalassemia excluded.

70. ThalassaemiaThalassaemia
 Quantitative abnormalities of polypeptide globin chain
synthesis.
TypeType HbHb HbHb
electropelectrop
horesishoresis
ClinicalClinical
syndromesyndrome
TreatmeTreatme
ntnt
αα--
thalassaemiathalassaemia
1.Hydrops1.Hydrops
foetalisfoetalis
(deletion of 4(deletion of 4
αα-genes)-genes)
3-3-
10g/dl10g/dl
HbHb
Barts(100%Barts(100%
))
Maternal-Maternal-
PE,polyhydramnios,PE,polyhydramnios,
Fetus-fatal in uteroFetus-fatal in utero
or in earlyor in early
infancy,survivinginfancy,surviving
infants have limbinfants have limb
reduction,hypospadireduction,hypospadi
as,urogenitalas,urogenital
abnormalitiesabnormalities
No specificNo specific

71. TypeType HbHb HbHb
electrophelectroph
oresisoresis
Clinical syndromeClinical syndrome TreatmentTreatment
2.HbH2.HbH
diseasdiseas
ee
(deleti(deleti
on of 3on of 3
αα--
genes)genes)
2-2-
12g/dl12g/dl
HbH (2%),HbH (2%),
restrest
HbA,HbAHbA,HbA2,,
HbFHbF
Hemolytic anemiaHemolytic anemia
&crisis(in&crisis(in
fever,infection),Hepatfever,infection),Hepat
osplenomegaly,choleosplenomegaly,chole
lithisis,may belithisis,may be
associated withassociated with
H.fetalis or IUDH.fetalis or IUD
-Prenatal-Prenatal
diagnosisdiagnosis
--
periconceptiopericonceptio
nal 5mg/daynal 5mg/day
-iron only if-iron only if
deficientdeficient
-blood-blood
transfusion iftransfusion if
severesevere
anaemiaanaemia
-assessd iron-assessd iron
overloadoverload

72. TypeType HbHb HbHb
electrophelectroph
oresisoresis
ClinicalClinical
syndromesyndrome
TreatmentTreatment
3.3.αα--
thalassaethalassae
mia traitmia trait
(deletion(deletion
of 2of 2 αα--
genes)genes)
10-10-
14g/dl14g/dl
normalnormal MicrocyticMicrocytic
hypochromichypochromic
bloood picturebloood picture
but no anemiabut no anemia
-Folate-Folate
supplementionsupplemention
-Iron only if-Iron only if
deficientdeficient
-parentral iron-parentral iron
contraindicatedcontraindicated
-genetic-genetic
screening-screening-
-prenatal-prenatal
diagnosis –MTPdiagnosis –MTP
if affectedif affected

73. TypeType HbHb Hb-Hb-
electrophoresiselectrophoresis
ClinicalClinical
syndromesyndrome
ß-ß-
thallassaemiasthallassaemias
1.1. ß-ß-
thallassaemiasthallassaemias
Major (Cooley’sMajor (Cooley’s
anemia)anemia)
<5g/dl<5g/dl HbA(0-50%)HbA(0-50%)
HbF(50-98)HbF(50-98)
Severe cong.Severe cong.
HemolyticHemolytic
anemia,requ BTanemia,requ BT
2.2. ß-ß-
thallassaemiasthallassaemias
IntermediaIntermedia
5-10g/dl5-10g/dl VariableVariable Severe anemiaSevere anemia
but no regularbut no regular
BTBT
3.3. ß-ß-
thallassaemiasthallassaemias
minorminor
10-12g/dl10-12g/dl HbAHbA2(4-9%)(4-9%)
HbF(1-5)HbF(1-5)
UsuallyUsually
asymptomaticasymptomatic

74. Beta thallassemia minorBeta thallassemia minor
-Heterozygous inheritance from one parent.
-Most frequent encountered variety.
Investigations:
1.Hb----around 10 g/dl.
2. Red cell indices: low MCV.
low MCH.
normal MCHC.
3.Diagnostic test: Hb. Electrophoresis.

75. Management:
Screening of the partner with MCV &Hb
electrophoresis
Genetic counseling if the partner is screen
positive.

Frequent Hb Testing.
Iron & high dose folate(5mg/day)
supplements .

76. Parenteral iron should be avoided. because
of iron overload.
If not responded ---I/M folic acid.
 blood transfusion close to time of delivery
if Hb<8gm%.
Erythropoitin may be given in severe
anaemia.

77. Beta Thallassaemia MajorBeta Thallassaemia Major
-Homozygous inheritance from both parents.
-Diagnosed in paediatric era
Effect on mother;
 1.anaemia with myocardial hemosiderosis- heart
failure
2.Early pregnancy loss
3.Small built-CPD-high rate of cesarean.
4.Risk of venous thrmbosis

78. Effect on fetus- teratogenic effect of iron
chelating agent like
-vertebral aplasia,
 -retardation of bone ossification
-fusion of ribs,
-IUGR
-prematurity
-perinatal morbidity & mortality
-rickets like bone

79. MANAGEMENTMANAGEMENT
A-PRECONCEPTIONAL EVALUATION
1.assessment of transfusion needs of the
patient
2.compliance with chelation therapy
3.iron load assessment
4.end organ damage
5.screening for transfusion related
infections

80. B.PRECONCEPTIONAL COUNSELLING
Partner is screened for beta thalessemia.
Prenatal diagnosis is offered if found
positive.
Chelation should be stopped as soon as
pregnancy diagnosed.
Folic acid supplementation.

81. C.ANTENATAL&C.ANTENATAL&
INTRANATAL CAREINTRANATAL CARE
1.High dose folic acid
2.stop chelation therapy and vitamin C
3.in aspleenic patients-hep B and
pneumococcal vaccine
4.Evaluation of cardiac and hepatic function
repeated in 2nd
and 3rd
trimester
5.Complete blood count every 2 weeks
6.Transfusion therapy continued to maintain
hb level at 10gm%


82. POSTPARTUM CAREPOSTPARTUM CARE
1.Lactation is not C/I
2.Chelation therapy restarted at 3wks
3.Cardiac and hepatic re-evaluation at 4-6
month
4.Any type of contraception (except OCP in
aspleenic pt due to risk of thrombosis)
5.Bone marrow transplant is only curative
procedure.

83. SICKLE CELL ANAEMIASICKLE CELL ANAEMIA
Diagnosis:
1.Hb <8gm/dl
2.blood smear-sickle cell,target cell,cigar shaped
cells
3.blood indices-high WBC,high platelet,low
ESR,high LDH,low MCV,high MCHC
4. Sickling test is screening test.
5.Hb electrophoresis-HbS

84. MANAGEMENTMANAGEMENT
ANTEPARTUM CARE-
2 weekly visit in 1st
&2nd
trimester,weekly in
3rd
.
1.should be vigilant for long term
complication like renal
failure,hypertension,liver or cardiac
involvement.
2.all routine investigation with USG for
fetal well being
.

85. 3.1mg/day folic acid
4.adequate hydration & warned to infection
5.after 24 weeks,monthly to assess fetal
growth
6.weekly Non stress test.
7.Doppler at 28 to 30 weeks for IUGR
8.blood transfusion if Hb <6
9.admission if crisis,PE,eclampsia,blood
transfusion.
 10. Prophylactic transfusions almost always prevent
vaso-occlusive episodes.

86. PRENATAL DIAGNOSISPRENATAL DIAGNOSIS
1.Screening of partner,if positive
2.chorionic villus sampling at 10 to 12
weeks
3.PCR on fetel DNA
4.if affected -MTP

87. INTRAPARTUM CAREINTRAPARTUM CARE
1.intravenous fluid to dehydration
2.oxygen supplementation
3.adequate pain relief –epidural
4.continuous fetal monitoring
5.vaginal delivery preffered
6.if cesaerean GA should be avoided.

88. POSTPARTUM CAREPOSTPARTUM CARE
Early ambulation
Breast feeding
Contraception-best DMPA,OCPs & IUCD
relatively contraindicated
Neonatal screening by cord blood for sickle
cell
Babies with sickle cell-prophylactic
penicillin at 3rd
month.

89. APLASTIC ANAEMIAAPLASTIC ANAEMIA
CLINICAL FEATURES
Apart form general features of anaemia
Mucosal or gingival bleeding and rashes
 overt infections fever with chills and
sweating
Chronic skin and chest infections
h/o radiation
Family h/o aplastic anaemia

90. Examination
1.pallor
2.petechie
3.spleen is rarely palpable
4.liver is palpable in severe anemia

91. INVESTIGATIONSINVESTIGATIONS
1.PERIPHERAL SMEAR
Normocytic normochromic anaemia
Neutropenia and thrombocytopenia
Low Reticulocyte count
2.BIOCHEMICAL PROFILE
Serum bilirubin-raised
LDH level-raised
RFT-deranged

92. BONE MARROW EXAMINATION
Hypocellular bone marrow-basis of severity
of disease
1.SEVERE ----cellularity<25% with
neutrophils <0.5x10/lt
2.VERY SEVERE
----neutrophile<0.2x10/lt


93. CLINICAL COURSE
Spontaneous improvement without
treatment after delivery
Risk of relapse
COMPLICATION
Maternal-anaemia,infection,hemorrhage
Fetal-IUGR,IUD,fetal thrombocytopenia,

94. MANAGEMENTMANAGEMENT
Identification & elimination of causative
agent
Supportive care-
a)prevent infection
b)blood transfusion-Hb should be >8
c)Hematocrit >20
d)Platelet should be administered if
<20x10/l
e)Fresh blood donated <24 hours old
f)WBC transfusion only in severe anaemia
to prevent chorioamnionitis

95. Measures to accelerateMeasures to accelerate
recovery from pancytopeniarecovery from pancytopenia
1.immunosuppressive agents
a.prednisolone 10-20mg/kg
b.cyclosporine with GM-CSF
c.anti- lymphocyte globulin-under trial
2.Bone marrow transplantation-C/I during
pregnacy
3.GROWTH FACTORS –G-CSF safe in
pregnancy.

96. OBSTETRIC MANAGEMENTOBSTETRIC MANAGEMENT
Common to all types of anaemia
Aim is to safely deliver the baby without
compromising mother

97. Management During labourManagement During labour
A.FIRST STAGEA.FIRST STAGE
Comfortable Position-propped up
Adequate analgesia
O2 inhalation if required
Monitoring of vitals
Intermittent chest auscultation
Sedation & analgesic
Strict asepsis
Minimum no. of per vaginal examination
 progress of labour to be monitored.

98. 2.SECOND STAGE2.SECOND STAGE
Prophylactic ventouse or outlet forceps to
cut short 2nd
stage
Strict asepsis
Oxytocin if required should be given in
concentrated form 20 unit in 500cc.

99. 3.THIRD STAGE3.THIRD STAGE
Active management of 3rd
stage
Controlled cord traction
Look for genital trauma& control bleeding
Diuretics 40 mg after delivery of placenta in
patient with cardiac failure.

100. PUERPERIUMPUERPERIUM
Watch till 6 hours for any sign of failure
Prophylactic antibiotic for 7 days
Continue iron folic acid for atleast 3 months
Adequate rest with early ambulation to
prevent deep vein thrombosis
Exclusive breast feeding till 6 months
Puerperial exercises

101. CONTRACEPTION ADVICECONTRACEPTION ADVICE
Should not conceive for atleast 2 years
Postpartum sterlization if family completed
IUCD except in sickle cell anaemia
OCP except in splenectomised patient of
thalassemia due to risk of thrombosis
Inj DMPA after 6 weeks
Barrier contraceptives safe but high failure

102. SUMMARYSUMMARY
1.Hb,if<11
2.peripheral smear
3.meanwhile start iron
4.confirmatory test
5.treat additional risk factor
6.monitore fetal well being
7.specific treatment as per investigation
8.prophylaxsis for infection
9.carefully manage intrapartum period to
prevent mortality

103. Thank you