Anemia in Pregnancy is the most common medical condition
Anemia is the most common medical disorder during pregnancy and is responsible for a significant percentage of maternal deaths, particularly in developing countries.
What isAnaemia ?
Anaemia is defined as reduction in
circulating haemoglobin mass below the critical
level.
The normal haemoglobin (Hb) is 12-14 gm%.
WHO has accepted up to 11 gm% as the
normal haemoglobin level in pregnancy.
Therefore any haemoglobin level below 11gm
in pregnancy should be considered as
anaemia
3.
Anaemia inpregnancy is present in very
high percentage of pregnant women in
India.
Exact data is not available about the prevalence
of nutritional anaemia. However according to
WHO, the prevalence of Anaemia in pregnancy
in south East Asia is around 56 %.
In India incidence of anaemia pregnancy
has been noted as high as 40-80%.
4.
Total iron requirementis 1000 mg.
Fetus and placenta -- 300 mg
↑ in red cell mass – 500 mg
Basal loss – 200 mg
Average requirement is 4-6mg/day.
2.5 mg/day in early pregnancy
5.5 mg/day from 20-32 weeks
6-8 mg/day from 32 weeks
onwards
5.
Anaemia isoften classified
as Mild degree (9-11 gm %)
Moderate (7-9 gms %)
Severe (4-7 gm %)
Very severe (<4gm %)
It is also classified according to
Haematocrit (PCV) %.
6.
Antenatal Period
-Poor weight
gain
-Pretermlabour
-PIH
-Placenta Previa
-PROM
Postnatal Period
-Postnatal
sepsis
-Sub involution
-Embolism
Intranatal Period
-Dysfunctional
Labour
-Intranatal
-Hemorrhage
-Shock
-Cardiac Failure
-Anaethesia risk
MATERNAL COMPLICATIONS
Serum Folate
RBC folate
Serum Vit B12
Serum Bilirubin
Coombs test
HB electrophoresis
NESTROF test
Red cell osmotic
fragility
12.
Routine screeningfor anaemia for
adolescent girls from school days
Encouraging iron rich foods
Fortification of widely consumed food with
iron
Providing iron supplementation from school
days
Annual screening for those with risk factors
13.
PROPHYLAXIS OFNON-PREGNANT WOMEN – 60 MG
OF ELEMENTAL IRON DAILY FOR 3 MONTHS.
Iron supplementation during pregnancy.
Routine iron supplementationis debatable in
western countries
It has to be given in non-industrialized countries
W.H.O RECOMMENDATION: Universal oral iron
supplementation for pregnant women(60 mg of
elemental iron and400 µg of folic acid) for 6 months in
pregnancy and additional of 3 months post-partum
where the prevalence is morethan 40%.
14.
MINISTRY OFHEALTH, GOVT. OF INDIA
RECOMMENDATION: [CSSM] 100 mg of elemental iron with
500 µg of folic acid in second half of pregnancy for atleast 100
days. 2 injections of iron dextran (250 mg each) given IMI at 4
weeks interval with TT injection.
Treatment of hook worm infestation
Single albendazole (400 mg)or mebendazole (100 mg x BD x
3days)
Change in defecation habits and avoidance of walking b
a
r
e
footed.
ORAL IRONTHERAPY
1. Safe,inexpensive and effective way
to administer iron
2. National nutritional anemia prophylaxis
program suggest 60 milligrams of
elemental iron and 500 micrograms of
folic acid daily
3. However it is suggested that 120 milligram
of elemental iron and 1 milligram of
folicacid are the optimum daily dose
needed
SIDE EFFECTSOF ORAL IRON
A. UPPER GI TRACT
Nausea,gastric discomfort,loss of
apetite,staining of teeth
A. LOWER GI TRACT
Constipation,diarrhoea,flatulance
21.
PARENTRAL IRONTHERAPY
Preparation
Iron sucrose-Imax S[100mg/5ml],orofer
s[50mg
/2.5ml]
Iron sorbital citric acid complex-
jectocos Iron dextran-imferon
22.
Intramuscular iron
1.0.5ml test dose should be given
2. 75/100mg/day is given daily on alternate
days
3. Given deep Im by Z-techniue to prevent
skin staining
4. Side effects-
painful,discolouration,injection abscess
23.
INTRAVENOUS IRON
1.Formula-0.66*% deficit of Hb*wt in kg=mg of
iron
2. Total dose in mg/50=ml of imferon
3. Total dose is given in normal saline
COMPLICATION
Local-thrombophlebitis at IV site
Systemic-malaise,fever,arthralgia,utricaria
lymphadenopathy
24.
BLOOD TRANFUSION
1.Indicated insevere anemia at any
GA,moderate anemia beyond 36wks and
when there is a failure of response to iron
therapy,severe hemorrhage like
APH,PPH,rupture uterus,cesarean section,first
trimester hemorrhage,thalassemiasand
sickling disorders in pregnancy
25.
ADVERSE REACTIONS
1.Tranfusion reaction
2. Infection
3. Volume overload
4. Others like hypothermia,citrate
toxicity,hyperkalemia,hypocalcemia and
rarely air embolism
26.
FIRST STAGE– COMFORTABLE POSITION
ADEQUATE ANALGESIA
Arrangement for oxygen,
Digitalization maybe required in cardiac failur
e
due to severe anaemia
Antibiotic prophylaxis
27.
SECONDSTAGE –CUT SHORTBYFORCEPS APPLICATION.
Active managementof third stage
During puerperium
Adequate rest
Iron and folate therapy for 3 months
Infection if any should be treated energetically
Careful watch for puerperal sepsis, failing lactation; sub
involution of uterus and thromboembolism
29.
• There isderangement in red cell maturation with
the production in the bone marrow of abnormal
precursors known as megaloblasts due to
impaired DNA synthesis.
30.
• Vit B12or folate defieciency or both.
• Vit B12 deficiency is rare in pregnancy.
• In pregnancy, due to folic acid deficiency.
PROPHYLACTIC
THERAPY
• All womanof reproductive age should be given
400µg of folic acid daily.
• Additional amount (4mg) should be given where
demand is high.
• Hereditary disordersin which the red cells contain
Hb-S.
• Produced by substitution of valine for glutamic
acid at the position 6 of the β-chain of normal
haemoglobin.
43.
PATHOPHYSIOLOGY
• Red cellswith HbS in oxygenated state behave
normally but in the deoxygenated state it
aggregates, polymerises and distort the red cells
to sickle.
• These sickle shaped cells block the
microcirculation due to their rigid structure.
44.
EFFECTS ON PREGNANCY
•Increased incidence of abortion,prematurity,
IUGR and fetal loss.
• Perinatal mortality is high.
• Preclampsia, postpartum haemorrahage and
infection is increased.
45.
EFFECTS ON THEDISEASE.
• There is chance of sickle cell crisis which usually
occurs in the last trimester.
• Haemolytic crisis
• Painful crisis.
THALASSAEMIA SYNDROMES
• Commonlyfound genetic disorders of the blood.
• Basic defect is a reduced rate of globin chain
synthesis.
• As a result, the red cellsbeing formed with an
inadequate haemoglobin content.
• Types – alpha and beta (depending upon the
chain)
48.
ALPHA THALASSAEMIA
• Incompatiblewith life.
• Α-peptide chain production is controlled by 4
genes, located on chromosome 16. Depending
upon the degree of deficient synthesis – 4 clinical
types.
• Mutation of one gene: no clinical or laboratory
abnormalities. Silent carrier
49.
• Mutation in2 – 4 genes: minor. Often goes
unrecognised and pregnancy is well tolerated.
• Mutation in 3 – 4 genes: Hb H disease.
hemolytic anaemia.
• Mutation in all four genes: major. No alpha globin
chain. Fetus dies either in utero or soon after
birth.
50.
BETA THALASSEMIA
• betachain production is directed by 2 genes –
one on each copy of chromosome 11.
• Major – when mutation affect both the genes. –
red cell destruction- no erythropoiesis – blood
transfusion necessary for survival.
• Minor – mutation of one gene. – can tolerate
pregnancy –oral folic acid supplementation is
continued.