2. • Anaemia came from a Greek word Anaimia, meaning lack of blood,
which means the decrease in Red Blood Cells (RBCs) or less than the
normal quantity in Haemoglobin in the blood.
Also includes decreased oxygen-binding ability of each
haemoglobin molecule due to deformity or lack in
numerical development as in some other types of
Haemoglobin deficiency
3. Prevalence of anaemia Source: WHO
Global Developed Developing India
Urban Rural
Children<5 yrs 43 12 51 60 70
Children > 5yrs 37 7 46 50 60
Men 1 3 26 35 45
Women 35 11 47 50 60
Pregnant 59 14 51 65 75
Women
About one third of the global population ( over 2 billion persons ) are anaemic
Anaemia is the most common nutritional deficiency disorder in the world
Prevalence of anaemia is higher in developing countries
Prevalence of anaemia in India is very high in all groups of the population
4. ANAEMIA IN PREGNANCY -
ASIAN COUNTRIES
WHO 1992
0
1 0
2 0
3 0
4 0
5 0
6 0
7 0
8 0
9 0
Ba ngla de sh China India Indone sia Ma la y sia My a nm a r N e pa l P a kista n P hilippine s Singa pore Srila nka Tha ila nd
B
A
N
G
L
A
D
E
S
H
C
H
I
N
A
I
N
D
I
A
I
N
D
O
N
E
S
I
A
M
A
L
A
Y
S
I
A
M
Y
A
N
M
A
R
N
E
P
A
L
P
A
K
I
S
T
A
N
P
H
I
L
I
P
P
I
N
E
S
S
P
O
R
E
S
R
I
L
A
N
K
A
T
H
A
I
L
A
N
D
Prevalence of anaemia is high in South Asia. Even
among South Asian countries prevalence of
anaemia in pregnancy is highest in India.
ANAEMIA IN PREGNANCY -
ASIAN COUNTRIES
WHO 1992
0
10
20
30
40
50
60
70
80
90
Bangladesh China India Indonesia Malay sia My anmar Nepal Pakistan Philippines Singapore Srilanka Thailand
B
A
N
G
L
A
D
E
S
H
C
H
I
N
A
I
N
D
I
A
I
N
D
O
N
E
S
I
A
M
A
L
A
Y
S
I
A
M
Y
A
N
M
A
R
N
E
P
A
L
P
A
K
I
S
T
A
N
P
H
I
L
I
P
P
I
N
E
S
S
P
O
R
E
S
R
I
L
A
N
K
A
T
H
A
I
L
A
N
D
ANAEMIA IN PREGNANCY -
ASIAN COUNTRIES
WHO 1992
0
10
20
30
40
50
60
70
80
90
Bangladesh China India Indonesia Malay sia My anmar Nepal Pakistan Philippines Singapore Srilanka Thailand
B
A
N
G
L
A
D
E
S
H
C
H
I
N
A
I
N
D
I
A
I
N
D
O
N
E
S
I
A
M
A
L
A
Y
S
I
A
M
Y
A
N
M
A
R
N
E
P
A
L
P
A
K
I
S
T
A
N
P
H
I
L
I
P
P
I
N
E
S
S
P
O
R
E
S
R
I
L
A
N
K
A
T
H
A
I
L
A
N
D
5. YEAR AUTHOR PLACE PREVALENCE %
1975 Sood et al Delhi 80
1982 Prema Hyderabad 75
1987 Agarwal et al Bihar & UP 87
1989 Christian et al Chandrapur, Panchmahal 87,88
1988-92 Agarwal et al Rural Varanasi 94
1989 ICMR 11 states 87
1994 Sheshadri Baroda 74
2000 NFHS 2 All India 52.0?
99- 2000 ICMR 11 states 84.6
2002-04 DLHS –2 All districts 90.4
2006 NNMB 8 states 70.3
2007 MFHS 3 All India 57.9?
Trends in prevalence of anaemia in pregnant women in India
Over 70 % of pregnant women in India are anaemic. There has been no decline
in anaemia in the last three decades
6. Prevalence of Anaemia (%){DLHS 2003}
0%
20%
40%
60%
80%
100%
preschool
children
adolescent girls pregnant w omen
Group
Percentage
severe moderate mild no anaemia
Anaemia begins in childhood, worsens during
adolescence in girls and gets aggravated during
pregnancy
7. Source: NNMB 2003
Among the southern states, prevalence of anaemia in pregnancy is lower in
Kerala and Tamil Nadu -?due to better access to health care
9. INDIA
India’s share in global maternal deaths
It is estimated that globally there are over 5 lakh maternal deaths every year.
There are about 1 to 1.2 lakh maternal deaths in India every year
India with 16% global population accounts for 20-25 % of all maternal deaths
in the world
10. Prevalence of Iron deficiency anemia in South Asia%
Country Children
< 5 years
Women
15-49 years
Pregnant
women
Maternal deaths
from anemia
Afghanistan 65 61 - -
Bangladesh 55 36 74 2600
Bhutan 81 55 68 <100
India 75 51 87 22000
Nepal 65 62 63 760
South Asia
Region Total
25,560
World Total 50,000
About half the deaths from anaemia in the world
occur in South Asian countries. India accounts for
over 80% of deaths due to anaemia in South Asia
12. Magnitude of Problem
Incidence Globally 30 %
In developing countries & India - 40 – 90%.
Responsible for 40% of maternal deaths in third world
countries.
Important cause of direct and
indirect maternal deaths (20% each)
- Vitere FE Adv Exp Med Biol 1994;352:127
13. Definition
Anemia - insufficient Hb to carry out O2
requirement to the tissues.
WHO definition : Hb conc. 11 gm %
CDC definition : Hb conc. < 11gm % in 1st and 3rd
trimesters and < 10.5 gm% in 2nd trimester
For developing countries : cut off level suggested is
10 gm %
- WHO technical report Series no. 405, Geneva 1968
Centre for disease control, MMWR 1989;38:400-4
14. ANAEMIA IN PREGNANCY
Definition: By WHO
Hb. < 11 gm /dl
(or haematocrit <32%).
Mild anaemia -------- 9 - 10.9 gm /dl
Moderate anaemia--- 7 - 8.9 gm /dl
Severe anaemia-------- 4 - 6.9 gm /dl
Very severe anaemia-- < 4gm/dl
15. Predisposing Factors During
Pregnancy
Increased demands of Iron, Folic acid, B12.
Diminished intake (poor diet, morning sickness.)
Distributed metabolism (pregnancy induced depression of the
bone marrow).
Infection ( Malaria, Asymptomatic bactoriuria, Piles Worm
infestation.)
Pre pregnant state of iron reserves.
Twin gestation.
16. Major causes of anemia
low vegetable consumption and perhaps low B12
intake
Poor bioavailability of dietary iron from the fibre,
phytate tannates, polyphenols rich diets
Chronic blood loss
Increased requirement of iron during pregnancy
Mal absorption
Poor pre-regnancy iron balance due to –
untreated systemic diseases , closely spaced
pregnancies & menstrual disorders
17. Reason For Increased Incidence Of Anemia
Low socioeconomic status and poor hygiene
Chronic malnutrition
Poor availability of iron due to
predominantly veg diet,
diet low in calories but rich in phytates.
Food and religious taboos
GI infections and infestations (e.g. Kala azar, worm infestations)
Chronic infections: ( like malaria)
Repeated pregnancies :
- with interval < 1 year
- blood loss at time of delivery
- multiple pregnancy
20. Physiological Anemia Of
Pregnancy
During pregnancy there is a dispropotionate increase in
plasma volume , RBC volume and hemoglobin mass.
There is all time a physiological iron deficiency state
during pregnancy.
The above two factors result in less hemoglobin
concentration in pregnancy which is called Physiological
Anemia Of Pregnancy.
24. Anemias Characterized by Mechanism
Decreased red blood cell production
• Iron deficiency anemia
• Anemia associated with vitamin B12 deficiency
• Folic acid deficiency anemia
• Anemia associated with bone marrow disorders
• Anemia associated with bone marrow suppression
• Anemia associated with low levels of erythropoietin
• Anemia associated with hypothyroidism
26. Anemias Classified by Mean Corpuscular
Volume
Microcytic (MCV less than 80 fL)
• Iron deficiency anemia
• Thalassemias
• Anemia of chronic disease
• Sideroblastic anemia
• Anemia associated with copper deficiency
• Anemia associated with lead poisoning poisoning
27. Normocytic (MCV 80–100 fL)
• Hemorrhagic anemia
• Early iron deficiency anemia
• Anemia of chronic disease
• Anemia associated with bone marrow suppression
• Anemia associated with chronic renal insufficiency
• Anemia associated with endocrine dysfunction
• Autoimmune hemolytic anemia
• Anemia associated with hypothyroidism or
hypopituitarism
• Hereditary spherocytosis
• Hemolytic anemia associated with paroxysmal
nocturnal hemoglobinuria
28. Macrocytic (MCV greater than 100 fL)
• Folic acid deficiency anaemia
• vitamin B12 deficiency
• Drug-induced haemolytic anaemia (eg, zidovudin
Acyclovir, Mtx, NO inhalation)
• Anaemia associated with reticulocytosis
• Anaemia associated with liver disease
• Anaemia associated with ethanol abuse
• Anaemia associated with acute myelodysplastic
syndrome
29. Abnormalities Of RBC Morphology
Anisocytosis : Variation in cell size
Poikilocytosis: Variation in cell shape.
Hypochromia: Amount of Central Pollar
Polychromatophilia: Amount of bluness
30. Erythropoiesis
Site: Bone marrow in adults
Av. Life Span Of RBC’s : 120 days
Requirements for Erythropoiesis:
1. Minerals : Iron (Hb synthesis),cu, cobalt
2. Vitamins : B12 and Folic acid ,vit C( reduces
ferric to ferrous form & folic A-Folinic A)
3. Proteins for synthesis of Globin
4. Erythropoietin Progesterone and HPL
increase secretion
Produced in kidneys (90%) & liver
31. CHARACTERISTICS SYMPTOMS
DYSPHAGIA ( Plummer-Vinson syndrome)
GLOSSITIS, STOMATITIS
ATROPHIC GASTRITIS DRY, PALE SKIN
SPOON SHAPED NAILS, KOILONYCHIA,
BLUE SCLERAE
HAIR LOSS
PICA (APETITE FOR NON FOOD SUBSTANCES :
ICE (pagophasia), starch(amylophasia), clay(geophasia)
37. Consequences of anaemia in pregnancy
8-11 g/dL: easy fatigue, poor work capacity
5-7.9 g/dL: impaired immune function, increased
morbidity due to infections
<5 g/dL: increased morbidity and maternal mortality
due to inability to withstand even small amount of
bleeding during pregnancy /delivery and increased
risk of infections
<5 g/dL: 1/3rd develop severe congestive failure and
many succumb either during pregnancy or during
labour
There is 8 to 10 fold increase in MMR when the
Hb is <5 g%
38. EFFECTS OF ANAEMA IN PREGNANCY
Mother
cardiac failure (more likely with excessive blood loss)
PPH
Predisposes to infection
Risk of thrombo-embolism
Delayed general physical recovery esp after c. section
42. The Objectives Of Investigation
Are:
1. Degree Of Anaemia
2. Type Of Anaemia
3. Cause Of Anaemia
43. To Note The Degree Of Anaemia
1. Haemoglobin
2. Total Red Cell Count
3. Determination Of Packed Cell Volume
All these helps to identify the physiological anaemia of
pregnancy and also to note the degree of Pathological anaemia
Arbitrary grading of pathological anaemia is done according to
the level of haemoglobin.
44. To Ascertain Type Of Anaemia : PB FILM
MICROCYTIC HYPOCHROMIC SMEAR in iron deficiency -
small pale staining cells
Macrocytic cells (>100cubic microns) in vit B 12 & folic acid
deficiency, Also in liver ds., alcohlism , reticulocytosis
Anisocytes (variation in cell size )& poikilocytes variation in
cell shape) in haemolytic anemia
Normocytic in other & in early iron deficiency
Target cells in thallassemia
Hypersegmented neutrophills in megaloblastic anemia
Platelets may be less
Parasites may be seen
45.
46. To Find Out The Causes Of Anaemia
1. Examination of stool:
It should be done regularly specially in
tropics to delete helminthic infection.
2. The urine is examined: a. For the presence of protein, sugar
and pus cell.
b. A clean catch mid stream specimen of urine is subjected to
culture and colony count
c. Chest X-ray
d. Fractional test meal analysis ( Achlorhydria).
e. Total s. proteins
f. Osmotic fragility in HS & haemoglobinopathies
47. BONE MARROW
Indications- Refractory anaemia
- Aplastic/hypoplastic anaemia
-to diagnose Kala-azar
In Iron deficiency :
Normoblastic marrow
Absence of stainable iron
B M exam should supplement (should not Replace)
PBF
48. Iron Deficiency Anemia
Iron is involved in a spectrum of biological reaction
and is therefore essential to all life.
Iron when complexed with porphyrin forms HEME.
Heme binds with globin to form Hemoglobin, which
binds to oxygen reversibly.
Heme may also bind to cytochromes and is responsible
for various oxidation-reduction reaction.
49. Physiology Of Iron
Iron Absorption:
Site: Duodenum & Upper Jejunum through Brush-boarder into blood
Dietary Iron: mainly in ferric form, ferrous form better absorbed
Increased absorption:
- gastric acidity, citrate, ascorbate. Amino acids, lactate(reduce ferric
to ferrous form)
- Iron deficiency anemia
- Exposure to hypoxia (high altitude)
Decreased absorption: teas, tannins, antacids, polyphenols phytates,
phosphates( form insoluble iron salts) & Ca
phytase in cereals destroys phytic acid
50. Pathway Of Iron Absorption
Intestinal Lumen Food Iron
Fe+2 Heme Exfoliation
Mucosa Fe Ferritin
Mucosal transport Protein
Blood Transferrin
54. The Body Content Of Iron In An Adult
Form of Iron Total
(gms)
Hemoglobin
Myogloin and Enzymes
Storage iron
2.5
0.3 (0.2 &0.1 g respectively)
1.0 - 1.5(2/3rd ferritin,1/3rd haemosidrin)
Total 4-5 grams
55. The total amount of iron in the body is determined by
intake, loss, and storage
There are approximately 2.3 g of total body iron in
women. Additional iron stores during pregnancy
(approximately 1 g) to support increased red blood cell
mass, the fetus and placenta, and the anticipated blood
loss accompanying delivery.
When there is adequate iron to meet needs, more than
70% is classified as functional iron, and the remainder as
storage iron. Of the functional iron, more than 80% is
found in the red blood cell mass as hemoglobin, with the
remainder in myoglobin and in respiratory enzymes
56. Tissue iron stores
Stored in liver; spleen ,bone-marrow, lymph-nodes
&R-E system
2 forms –
1 Ferritin- (2/3rd ) Appoferritin combined with
ferric hydrophosphate; water soluble
2 Haemosiderin-(1/3rd )
A conglomerate of ferritin molecules
Granular, water insoluble
Gives blue color(prussian blue) when
ferricyanide is added
57. Functions of tissue Iron
Myoglobin(red muscles) serves as a small tissue
oxygen reserve( binds loosely & reversibly with O2)
during vigorous exercises
Peroxidase activates H2O2 to oxidise suitable
substrates
Catalase decomposes H2O2 to form H2o & molecular
o2
Cyt & Cyt. Oxidase are concerned with oxidation
processes & electron transfer in tissues ( not like Hb
which carries molecular O2)
59. Early
Pregnancy
2.5 mg / day
32 to 40
weeks
6.8 mg / day
TOTAL
800 – 1000 mg
20 to 32
weeks
5.5 mg / day
Iron Requirement During Pregnancy
60. Iron Requirement During Pregnancy
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
61. Hb 13.5 – 14 gm %
R.B.C. 4.5 – 4.7 million/cu mm
Serum Iron 40-– 175 μg / dL
TIBC 216 – 400 μg / dL
Transferrin saturation 16- 60 %
S. Ferritin level >10μg / dl
Red Cell protoporphyrin <30 μg / dL
Erythropoietin 15.20 U / Lit
MCV 76 – 100 fL
MCH 27 – 33 pg
MCHC 33.37 gm / dL
PCV 32 – 40 %
Normal Indices In Pregnanacy
62. Normal hemoglobin by gestational age in
pregnant women taking iron supplement
12 wks 12.2 [11.0-13.4]
24wks 11.6 [10.6-12.8]
40 wks 12.6 [11.2-13.6]
63. IRON DEFICIENCY ANAEMIA
PREVALENCE IN TROPICS IS HIGH:
loss in sweat
less reserve – Closely spaced pregnancies.
Prolonged breast feeding, exessive menstrual
losses, malnutrition & malabsorption
hook worm infestation ( each worm extracts upto
0.05 ml blood/day ( Iron loss 0.5- 2mg/day)
64. ETIOLOGY OF IRON DEFICIENCY ANAEMIA
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.
65. IRON DEFICIENCY ANEMIA
ETIOLOGY CONTD.
CHRONIC BLEEDING
MENORRHAGIA
PEPTIC ULCER
STOMACH CANCER
ULCERATIVE COLITIS
Angiodysplasia of colon
INTESTINAL CANCER
HAEMORRHOIDS
DECREASED IRON INTAKE
INCREASED IRON REQUIRMENT (JUVENILE AGE,
PREGNANCY, LACTATION)
66. Iron Deficiency Anaemia
Symptoms:
1. Lassitude and a feeling of exhaustion or
weakness may be the earliest
manifestation.
2. The other features are anorexia and
indigestion, palpitation caused by ectopic
beats, dyspnoea, giddiness and swelling of
legs.
67. Iron Deficiency anaemiaHaematological Indices: Iron Deficiency
Haemoglobin: < 10gm%
RBC: < 4million/mm3
PCV: <30%
MCV: <75cubic micron
MHC:<25pg
MCHC: <30%( most dependable ,r b c count not
involved in calculating MCHC )
Haematological Indices should supplement PBF
68. Other indices: Iron deficiency
anaemia
S. iron <30 microgr/100ml
TIBC > 400 microgr/100ml
%age saturation< 10%
S.ferritin <30 microgr/L
69.
70. Laboratory Diagnosis of Anaemia
IDA Thalassemia Chronic Diseases
Serum Iron Decreased
<30microg/100ml
Normal /
Increased
Decreased
TIBC Increased>400microg/10
0ml
Normal Decreased or N
Transferrin
Saturation
Decreased 10% / less N or
Increased
N or Decreased
Serum Ferritin Decreased < 30microg/ l N or
Increased
N
Marrow Iron Decreased / absent N or
Increased
N
Therapeutic test with
oral iron
Rise in Hb No rise in Hb No rise
71. BLOOD AND
BONE MARROW SMEAR
PERIPHERAL BLOOD SMEAR
microcytosis,h ypochromia, anisocytosis
poikilocytosis
BONE MARROW
high cellularity
mild to moderate erythroid hyperplasia
polychromatic and pyknotic, cytoplasm of
erythroblasts is vacuolated and irregular in
outline (micronormoblastic erythropoiesis)
absence of stainable iron
72. Prophylaxis : Iron Deficiency
Anaemia
Avoidance Of Frequent Child-birth:
A minimum interval should be at least
two years
Supplementary Iron Therapy:
Daily administration of 200mg of
ferrous sulphate (containing 60 mg of iron) along with 1
mg folic acid is quite effective prophylactic measure.
Dietary Prescription:
A balanced diet, rich in iron and protein
should be prescribed which should be within the reach of
the patient and should be easily digestible.
73. Iron Therapy : Curative
1. Oral Therapy:
a) Fersolate tablet contains 200mg ferrous sulphate
which contain 60 mg of elemental iron, trace of
copper and manganese.
b) The initial dose is one tablet to be given thrice daily
with or after meal.
c) The treatment should be continued till the blood
picture becomes normal, thereafter a maintenance
dose of one tablet daily is to be continued for at least
100 days following delivery to replenish the iron
stores.
74. Drawbacks of oral therapy:
a) Intolerance.
b) Unpredictable absorption rate.
c) The serum iron may be restored but there is difficulty in replenishing the iron
store.
2. Parental Therapy:
a) The main advantage is the certainty to correct the haemoglobin deficit
and to build up the iron store.
b) The expected rise in haemoglobin conc. is 0.7 to 1 gm/100 ml per week.
c) Parental therapy are of two types:
1. Intravenous route.
2. Intramuscular route.
75. Total dose infusion
Compound used- iron Dextrose / Iron sucrose ( Safe,
effective, less side effects
Estimation Of Total Dose :
Iron Dextran = 0.3x W ( 100- Hb%) mg + 50%
( W- wt in pounds )
Iron Sucrose = 2.3 x W x D+ 500 mg
( W= wt in kg, D= (Target Hb- Actual Hb )g/dl )
Infuse 100 mg in 100 ml NS over 15 min
follow manufacturers instructions
Omit Drip in case of adverse reaction
76. Advantages of Intravenous route:
It eliminates repeated and painful intramuscular injections.
The treatment is completed in a day and the patient may be
discharged much earlier from the hospital.
It is less costly compared to the repeated intramuscular therapy.
Limitations of Intravenous route:
As the maximum haemoglobin response does not appear before
four to nine weeks, the method is unsuitable if at least four weeks
time is not available, to raise the haemoglobin to a safe level of 10
gm% before delivery.
Previous history of reaction to parental therapy is a
contraindication for its use.
77. Intramuscular Therapy
The compounds used in intramuscular therapy are:
1. Iron-dextran (Imferon)
2. Iron- sorbitol-citric acid complex in dextrin(Jectofer)
( Both contain 50mg of elemental iron in one milliliter)
Total dose is calculated as in i/v therapy . Doseof iron
sorbitol complex is to be adjusted because of its 30%
excretion in urine.
Oral iron should be suspended at least 24 hours prior to
I /M therapy to avoid reaction.
78. Intramuscular Iron Therapy
1 ml ( 50 mg ) test dose
2 ml ( 100 mg ) inj with 2 inch needle deep I/M
Z- technique
Inject air / saline before withdrawing
79. Drawbacks of Intramuscular Therapy
The injections are painful although less with Jectofer.
Chance of abscess formation and a discoloration of the
skin over the injection sites are real problems specially
with Imferon
Reactions -- pyrexia, lymphadenopathy, headache,
vomiting and allergic reactions are infrequent
80. Place Of Blood Transfusion
The indication of blood transfusion in anaemia during
pregnancy are :
To correct anaemia due to haemorrhage (APH & PPH)
Patient with severe anaemia & POG> 36weeks
The primary concern is not only to correct anaemia but also
to make the patient fit to withstand the strain of labour and
blood loss following delivery.
Refractory anaemia.
Associated Infection.
81. The Quality and quantity of Blood:
1. The blood to be transfused should be fresh, properly
typed, grouped and cross matched.
2. Only packed cells are transfused
3. Start at slow rate @ 10 d/min & increase rate gradually
4. The quantity should be 350 cc at a time.
5. Monitor vitals , look for signs of reaction, basal crepts
6. To allow time for circulatory readjustment, transfusion
should not be repeated within 24 hours.
82. Precautions
Check name, cr no. donor no., cross-match no., blood
group Rh type ,date of collection & expiry date
Check HIV, STS, HBS Ag status
Give frusemide 20 mg i/v prior to transfusion to create
negative fluid balance
Give inj Phenargan 25 mg i/m to minimise reaction
Follow strict asepsis & use Blood filter set
84. Advantages of blood Transfusion:
1 Increase oxygen carrying capacity of the blood
2 Stimulates erythropoiesis.
3 Haemoglobin from the haemolysed red cells may be
utilized for the formation of new red cells.
4 Supplies the natural constituents of blood like
proteins, clotting factors & antibodies etc.
5 Improvement is expected after 3 days.
85. Exchange Transfusion
Its Indications Are:
1. Cardiac failure due to severe anaemia
2. Cases of severe anaemia requiring surgery.
3. Severe anaemia whatever may be the type near term
as a safer alternative to simple transfusion.
The chief Drawback are:
1. Large quantity of fresh blood is required and that too
has to be collected from several donors.
2. Chance of serum hepatitis is more.
86. Management During labour
Comfortable Position / prop up position
O2 inhalation
Adequate analgesia
Strict asepsis
Prophylactic outlet forceps/ assisted delivery
Withhold inj ergometrine
Prophylactic antibiotics
87. Second Stage:
1. Asepsis is maintained.
2. Prophylactic low forceps or vacuum delivery may be done to
shorten the duration of second stage.
3. Intra venous methergin 0.2 mg shouldnt be given following
the delivery of anterior shoulder.
Third Stage:
1. One should be very vigilant during the third stage.
2. Significant amount of blood loss should be replenished by
fresh packed cell transfusion after taking the usual
precautions mentioned earlier.
3. The danger of postpartum overloading of the heart should
be avoided.
88. Remain vigilant for PPH / CCF
1. Significant amount of blood loss should be replenished
by fresh packed cell transfusion after taking the usual
precautions mentioned earlier
2. Give inj Lasix at time of BT.
3. The danger of postpartum overloading of the heart
should be avoided
Continue iron & folate therapy for 3 months after delivery
Appropriate contraceptive advice
89. Puerperium
Prophylactic antibiotics
Look for sepsis, subinvolution, failing lactation, CCF&
PE
Continue anti anaemic therapy till normal clinical &
hematological state
Even in normal state continue iron therapy for 3
months
Warn about risk of recurrence
Counsel about diet , spacing & contraception
Recheck Hb before D/S
91. FOLATE DEFICIENCY ANAEMIA
At cellular level Folic acid reduced to Dihydrofolic acid
then to Tetrahydro-folic acid (THF) which is required for
cell growth & division.
So more active is the tissue reproduction & growth more
it is dependant on supply of folic acid( bone marrow and
epithelial lining are therefore at particular risk)
Folate requirement increases in pregnancy ( to meet the
needs of fetus, placenta, uterine hypertrophy & expanded
RBC mass)
92. Folic acid deficiency anaemia
Etiology-Lack of grean leafy vegetables, legumes& animal
products in diet& alcohlism
Intense anorexia may co-exist with intense folate
deficiency (aggravates folate def)
Daily requirement-
50-100microgram(non-pregnant)
400 microgram(pregnant)
WHO- 800microgram(pregnant) &
600 microgram(lactation)
93. Folate deficiency anaemia
Earliest biochem evidence-- low plasma folate conc
(appears after 3wk of folate deficient diet)
2 wks later- hypersegmented neutrophils appear
After 17 wks – rbc folate levels fall (<165microg/dl) &
-marrow appears megaloblastic
(Increased urinary FIGLU excretion not useful in
pregnancy((altered Histidine metabolism))
Earliest morphological change- appearance of macrocytes,
hypersegmented neutrophils megaloblastic marrow
thrombocytopenia & /leukopenia in severe anaemia
96. Treatment of folate deficiency
Oral FA tab 1mg/day once daily
By 4-7 days – improvement in Reticulocyte count
- improvement in Leukocyte &
thrombocyte count
ACOG( 2003) recommendation
all women of reproductive age should consume
atleast 400 microgram /day FA
97. Additional supplements of FA
Additional supplement s of 4 mg / day in pts with-
Multiple gestation
Alcohlism,
Haemolytic anaemia (routine oral therapy )
Crohns disease & infammatory skin disease,
Pts on anticonvulsants
Prev baby with NTD, cleft palate & cleft lip –
(Periconceptional folate reduces recurrence of NTDs)
Give parentral therapy for severe deficiency
98. Vitamin B12
Molecule of B12 consists of 2 major parts-
1 Nucleotide
2 corrin ring ( porphylin like)- but has a
cobalt atom at its centre
There are 4 different forms of B12 (different ligands
attached to the Co atom )
99. 4 forms of B12
Co-enzyme B12 (DACobalamin) :Present in liver,
animal tissues &bacteria, main dietary form ,produces
isomerization of methyl melonyl CoA
Methyl cobalamin : in plasma , methylates
homocysteine to form methionine
Hydroxy cobalamin : formed from other Cobalamins
on exposed to sun light , more firmly bound to plasma
globulins ( best B12 for tt of pernicious anaemia
Cyano cobalamin : 1st crystallised in this form, converts
to Hydroxy Cobalamin on exp to SL.
100. Sources-B12Humans are totally dependent on dietary B12
B12 is synthesized by Microorganisms in water, soil &
intestines
B12 occurs in all animal tissues, no plant source unless
contaminated with bacteria
Minimal daily requirement in an adult is 2 microgram
Daily loss of B12 is 0.1 % of the total pool of B12 (3-4mg)
When the size of the pool decreases daily loss also
decreases
Entero-hepatic circulation helps to meet demands even
with diminished stores (0.5 -5 microgram excreted in bile
daily, daily need-2.0 microgram/day)
Normal mixed diet provides 5- 30 microgr/day
101. Absorption of Vit
B12
Vit B12 is absorbed by 2 processes
1. Passive inefficient, process,
• occurs throughout the jejunum
& ileum
•Doesn’t require IF
•Quantitatively inefficient
2. Highly efficient, effective &
active process, requires IF &
occurs largely in terminal ileum
102. Vitamins B12 Deficiency
Rare
Develops over 3-4 yrs
High risk patients
Vegans
Patients with gastrectomy ,
Ileitis, ileal resection,tropical sprue, whipples disease &
gluten enteropathy
Pernicious anaemia,
Zollinger- Ellison syndrome
Intestinal parasites (D. latum – fish tapeworm)
Confirmed by response to physiological dose of b12
(1 microgram/day)
103. screening measurement of serum
B12
significant gastric resections or
a low dietary intake of cobalamin, i.e. Women on ovo-lacto, lacto-vegetarian or
vegan diets. Otherwise
patients with unexplained elevations in MCV on a complete blood count.
If reduced serum B12 levels are detected in vegetarian women, they should
be offered oral B12 supplement
, parenteral cobalamin is not essential.
some women may prefer a single intramuscular injection of 1000 g of
hydroxycobalamin , may be sufficient for the entire pregnancy.
Patients with B12 deficiency due to pernicioius anemia or gastrectomy
may be treated with 1000 g every day for 1 week, followed
by 1000 g every week for 4 weeks and then 1000 g every
month thereafter.
104. Diagnosis:
Peripheral smear Same as in Folate
deficiency
Vitamin B12 level < 80 pico g/ml
Increased urinary excretion of methyl
melonyl Co-A
Confirmed by response to physiological
dose of b12 (1 microgram/day )
Treatment of B12 Deficiency:
Vit B12 1 mg I/M weekly for 6 weeks.
105. Hematologic features of B12
and folate deficiency
Oval macrocytes
Hypersegmented neutrophils
Howell-Jolly bodies
Thrombocytopenia
neutropenia
Red cell fragments and tear drop red cells
Both have same s/s & megaloblastic picture
Neuropathy occurs only in B12 deficiency
106. Interrelationship
between Cbl & Folate
metabolism
Exess of MM Co-a &
Homocysteine occurs in
B12 def
Exess of Homocysteine
alone occurs in FA def
A reduction in Hcy
levels in pregnancy (Inc
GFR) & lack of a defined
normal range for
pregnancy may
limits the utility of these
lab tests
107. HAEMOGLOBINOPATHIES
DEFINITION:
Inherited disorders of haemoglobin.
Defect may be in:
- Globin chain synthesis------thalassemia.
- Structure of globin chains-sickle cell disease.
Thalassemia is caused by mutations that lead to reduced or absent
production of structurally normal -globin chains.
Haemoglobinopathies result from mutations that
produce usually normal amounts of structurally abnormal or variant
hemoglobins
Hb abnormalities may be:
- Homozygous = inherited from both parents.
(Sufferer of disease)
- Heterozygous = inherited from one parent.
(Carrier/trait of disease)
108. Hemoglobinopathies
Hb. synthesis is controlled by genes:
Alpha chains by 4 gene,2 from each
parent.
Beta chains by 2 genes ,1 from each
parent
Disordered synthesis of the -globin
chain usually results from point
mutations of the -globin gene,
Over 200 different mutations have
been described
109. HAEMOGLOBINOPATHIES.
Normal adult Hb. after age of 6 month,
4 Globin chains associated with haem complex.
HbA---97%, = 2 alpha +2 beta globin chains
HbA2---(1.5-3.5%), = 2alpha+2 delta globin chains
HbF --<1%. = 2 alpha+ 2 gamma globin chains
4 beta chains –Hb H : mod to severe haemolytic anaemia
may worsen in pregnancy
4 gamma chains – Hb Bart : comman cause of stillbirths in SE
Asia or neonate may die) , binds more firmly to o2
110. Hb Bart
Absence of –beta globin chain leads to Hb Barts ( made by
tetramer of the gamma-globin chain )
Hb Bart has a very high oxygen affinity and does not
release oxygen to fetal tissues, leading to severe hypoxia
and fetal hydrops.
Hydrops fetalis most commonly results from inheritance
of Alpha -0 thalassemia from each parent .
111. Hb C
Hb C is caused by a single point mutation at position 6 on the beta-
chain where glutamine is replaced by lysine
variant Hb ( less soluble than Hb A and also has a lower oxygen
affinity)
Individuals heterozygous for Hb C are clinically well
Homozygotes exhibit mild, chronic hemolytic anemia.
Combinations of Hb C with –thalassemia or other variant hemoglobins,
especially Hb S, lead to clinically significant disorders.
Hb C & Beta 0-thalassemia have moderately severe anemia with
splenomegaly
Hb C and mild beta +-thalassemia have mild to moderate hemolytic
anemia.
112. Hb E
Hb E is caused by a single point mutation at position 26 on
the beta globin-chain where glutamine is replaced by
lysine, resulting in reduced synthesis of the beta-globin
chain.
Individuals who are heterozygous or even homozygous for
HbE are completely asymptomatic and its clinical relevance
stems from the consequences that occur when this very
common hemoglobin variant combines with -thalassemia
trait.
Compound heterozygotes for HbE and -thalassemia have a
wide rangeof clinical manifestations from mild anemia to
the most severe form of thalassemia major.
113. Hb Lepore
Results from fusion – delta & beta globin gene, due to
abnormal cross-over during meiosis.
leads to a thalassemia phenotype.
Heterozygous for Hb Lepore are asymptomatic with
microcytic, hypochromic red blood cell indices.
The homozygous state varies between transfusion-
dependent thalassemia major and thalassemia
intermedia.
Compound heterozygotes for Hb Lepore and
thalassemia manifest as thalassemia major.
114. THALASSAEMIAS
The synthesis of globin chain is partially or completely
suppressed resulting in reduced Hb. content in red cells, which
have shortened life span.
Result is ineffective erythropoesis, haemolysis & varying degree
of anaemia
Incidence: 1 in 300 – 500 pregnancies
TYPES:
- Alpha thalassaemia (impaired production of Alpha chain).
- Beta thalassaemia:
. Major
. Intermedia
. minor
115. Thalassemia
chains encoded by 2 pairs of genes on
chromosome 16
chains encoded by single pair of genes on
chromosome 11
thalassemia more common and presents as either
°(major) or + (minor)
116. Most severe clinical phenotypes occurs in individuals
homozygous for beta mutations - Complete absence of -globin
chain production
Presents in the first year of life ( severe
anemia,hepatosplenomegaly, bone deformities and growth
delay)
Individuals who are compound heterozygotes for beta o &beta +
mutations show variable clinical manifestations
Thalassemia major or intermedia - increased risk of
venous thromboembolism, (especially after splenectomy)
The anemia ( in beta thalassemia ) due to ineffective
erythropoiesis and hemolysis ( due to excess of alpha-chains)
117. Beta thalassemia minor
Beta Thalassemia 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.
118. Beta Thalassaemia Major
Homozygous inheritance from both parents.
Severe anaemia.
Diagnosed in paediatric age.
Hypogonadotropic hypogonadism, diabetes & thyroid
diseases
T/m: is blood transfusion.
.
121. Alpha thalassemia
Single gene deletions –usually silent
2 gene deletions – may be from a single chromosome
- or single gene deletion from each
chromosomes
Thalassemia trait is phenotypically mild with
microcytic, hypochromic red cell indices and
occasionally mild anemia
Hb H is due to loss of 3 alpha chains . Tetramer of 4
beta chain is relatively unstable forms intracellular
precipitates that ultimately shorten rbc life
124. Diagnostic Strategy for Thalassemias
Hb Electrophoresis +
CBC
Abnormal
band
Normal No action
MC
V
MC
H
Quantitative
Hb
electrophores
is
Raised Hb
A2
B
Thalassemia
Normal
se
d
Examine partners
blood
? X
Thalassemia
DNA analysis
for x gene
defects
125.
126.
127. SICKLE CELL SYNDROME.
Autosomally inherited .
single beta chain substitution of glutamic acid by valine (
A for T substitution at codon 6 of beta globin chain)
Heterozygous----HbAS.
Homozygous-----HbSS.
Compound heterozygous---HbSC etc.
HbS - susceptible to hypoxia,
when oxygen supply is reduced.Hb precipitates
(polymerizes, gels/ crystallises &
makes the RBCs rigid & sickle shaped.
Constant sickling & desickling leads to membrane damage
& cells may be irreversibly sickled
Slow rbc transit through microcirculation contributes to
vaso-occlusion
128. Sickle Cell Disease
Structural Hb variant
Exists in homo(Hb-SS) &
heterozygous forms( Hb-SC)
Under hypoxic conditions, HbS
polymerizes, gels or crystallizes.
hemolysis of cells, &
thrombosis of vessels in
various organs
In long standing cases,
multiple organ damage.
129. Sickle Cell Disease
Slow erythrocyte transit -
- endothelial cell adhesions,
- erythrocyte dehydration
- vasomotor dysregulation)
Ischaemia & infarction of various organs may cause severe pain- the
sickle –cell crisis
- osteonecrosis femoral/ humoral head
- Renal medullary necrosis
-Autosplenectomy in Hgb SS disease &splenomegaly in variants
- Hepatosplenomegaly
-Pulmonary infarction
-Pulmonary Hypertention (20 % )
Sickeling crises frequently occurs in pregnancy, puerperium & in state
of hypoxia .
130. Sickle-cell disease& Pregnancy
Abortion and still birth
Intra uterine growth restriction
Premature birth
Intrapartum fetal distress
Increased perinatal mortality
Aplastic , megaloblastic sequestration & haemolytic
crisis
Sickle cell trait:(carrier state)
Does not pose any significance clinical problems in
pregnancy
131. SCD
Diagnosis:
- Hb. Electrophoresis
Management:
- No curative Tt.
- only symptomatic
- Well hydration, effective analgesia, prophylactic
antibiotics, O2 inhalation, folic acid, oral iron
supplement (I/V iron is C/I), blood transfusion
BT reduces pain, prevents crises , not shown to improve
perinatal outcome
Some advocate exchange transfusions ( 4 times blood usages)
Esp in chest syndrome, cv events & MOD
134. Take Home Message
Anaemia although preventable is a global problem
Anaemia still is the commonest cause of maternal mortality and
morbidity in spite of easy diagnosis and treatment
Anaemia can be due to a number of causes,
including certain diseases or a shortage of iron, folic
acid or Vitamin B12.
The most common cause of anemia in pregnancy is
iron deficiency.
Iron therapy is best given orally
135. Adequate Treatment:
It should be instituted to eradicate
hookworm infestation, dysentery, malaria, bleeding piles and
urinary tract infection.
140. Testing for hemoglobinopathiesis recommended if the MCH is less than
27 pg [23]. The peripheral blood smear should be examined
for abnormal red cell morphology, such as target cells (red
blood cells characterized by a densely stained center surrounded
by a pale unstained ring that is encircled by a dark
irregular band), stippled cells (small basophilic inclusions
distributed throughout the cytoplasm), sickle cells (the characteristic
sickle-shaped cell), nucleated red cells and red cell
inclusions (round dense bodies of variable size, usually single
and staining similarly to a nucleus, also known as Howell
Jolly bodies). The Hb H inclusions of - thalassemia (globular
bodies scattered throughout the red cell cytoplasm) can
be generated in vitro by using an oxidative dye such as new
methylene blue and the peripheral blood smear reviewed to
determine their presence and the number of red cells affected.
Hemoglobin electrophoresis is routinely used to detect the
presence and quantity of normal and abnormal hemoglobins
although high- performance liquid chromatography (HPLC)
is a useful tool for this purpose. And serendipitous discovery
of variant hemoglobins is becoming more frequent as HPLC
is also used to quantify glycosylated Hb (Hb A1c) in people
with diabetes. Specific laboratory tests are used to detect
sickle cell trait and disease. A diagnostic pathway for investigation
of hemoglobinopathies
