
1
OBSTETRICS
Lec: 11
Anemia in pregnancy
Dr. Haider Al Shamma’a
Objectives
•
Understand the normal physiological changes in pregnancy
•
Understand the scientific bases of pathophysiology of anemia
•
appreciate
the
importance
of
anemia
in
obstetrics
and
know
the
risks
to
the
fetus
and
mother
•
The
student
should
be
able
to
diagnose
anemia
and
it’s
type
and
severity
effectively
and
accurately
•
The
student
should
be
able
to
justify
the
management
of
anemia
according
to
type
,
severity
and
gestational
age
•
The
student
should
be
able
to
prevent
the
development
of
anemia
specially
iron
deficiency
and
folate
deficiency
•
The
student
should
be
able
to
avoid
inappropriate
treatment
that
may
compromise
patient
health
-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐-‐
•
It is the most common medical disorder in pregnancy
•
Anemia
in
pregnancy:
-‐
is
a
pathological
condition
in
which
the
oxygen
–
carrying
capacity
of
the
red
blood
cells
is
insufficient
to
meet
the
body’s
needs.

2
•
Hb < 11g/100ml
Physiological changes in pregnancy (normal changes)
•
Increase plasma volume by 40 -‐ 50%
•
Increase RBC mass by 18 – 25%
•
→
consequent
fall
in
Hb
concentration
haemodilution
inspite
of
increase
RBC
mass
this
gives
the
physiological
anemia
in
pregnancy
11g/100ml
•
MCV ↑
•
MCHC ±
•
S. Fe , ferritin ↓
•
Total iron-‐binding capacity ↑
•
Iron requirement ↑ ( 2.5 mg/day 1
st
trimester , 6.6mg /day at 3
rd
trimester ) = 1000 mg / total pregnancy
•
Moderate ↑ Fe absorption
•
Increase folate requirements
Incidence
•
30 – 50 % of pregnant women become anemic during pregnancy
•
90% is iron deficiency
•
Folate deficiency 5%
•
other causes are 5%

3
Effects of anemia on pregnancy
• ↓
oxygen supply to the fetus
•
↑ cardiac output of the mother → cardiac failure
•
Predispose to infection
•
↑ chance of abortion & PTL 2-‐3 times
•
Aggravate complications of bleeding should it occur
•
↑ chance of fetal hypoxia during labor
•
Not allow women to start labor with Hb of less than 10g/100ml
Iron deficiency anemia
•
Is the commonest type of anemia during pregnancy 90% of cases
Iron metabolism
•
Iron in diet 10 – 15 mg/day
•
10 -‐15 % absorbed ( duodenum , upper jejunum )
•
Ferrous is absorbable , ferric less absorbed
•
Bound to apoferritin at the bowel mucosa to form ferritin
•
Transported
as
transferrin
to
b.
marrow
to
form
Hb,
to
all
tissues
to
form
cytochrome
oxidase.
Muscles
myoglobin
•
mucosal absorption capacity 1.5 -‐ 4 mg/day
•
Requirements more than absorption 6.5 mg/day
•
Mobilization of iron stores
•
If depleted cause anemia
•
Stores depleted after few pregnancies

4
Iron excretion
•
No mechanism of excretion
•
Loss with menstruation
•
Desquamation of skin hair etc.
Causes of iron deficiency anemia
•
Decrease intake
•
Decrease absorption
•
Increase demands repeated pregnancy
Features of Iron deficiency anemia in pregnancy
•
Asymptomatic in majority
•
Fatigue,
palpitation,
(may
regarded
as
normal
symptoms
related
to
preg.)
•
Pallor
not
common
due
to
peripheral
vasodilatation
associated
with
pregnancy
•
So diagnosis depends on Hb level ( booking , 28 wks , 37 wks
•
If anemic
Investigations
• ↓
Hb , MCV, MCHC, RBC count
•
Microcytic hypochromic
•
In severe cases → poikylocytosis, anisocytosis

5
•
S Fe < 50 micro g/100ml
•
IBC > 450 micro g / 100ml
•
S ferritin < 12 micro g / l
Treatment
•
Depend on gestational age , severity and compliance
•
Oral iron (in mild cases , early pregnancy)
•
Frerrous sulfate Fe SO4 200 – 350 mg / day
•
Max increase is 0.8 g / week
•
Advantage of oral
•
Cheap, effective and safe
•
Disadvantage
•
Slow
•
Side effects GIT,
•
Poor compliance
•
Ferrous
fumarate
,
ferrous
gloconate
etc.
….
Less
side
effects
but
less
absorption
•
Continue Rx for 3-‐6 months to correct stores
Late pregnancy
•
No time for slow correction
•
Parentral Rx !!!!!
•
Iron
sorbitol
((
im))
each
250
mg
correct
1
g
Hb
+
500
mg
for
the
stores
correction
((correct
3g/month))

6
•
Iron succarose (( iv )) total dose infusion
•
Indications poor compliance, no time for oral correction
After 30 weeks
•
No time for parenteral Rx
•
Blood
transfusion
needed
(
packed
RBC
transfusion
)
each
unit
1-‐
2gHb
•
Add iron to correct stores
•
Add folic acid prophylaxis
Folic acid deficiency anemia
•
Requirement in non preg . 50 microg/day
•
Pregnant 350 microg /day
•
Important in nucleic acid synthesis (rapidly divided cells
Etiology
•
Decrease intake
•
Decrease Decrease absorption
•
Decrease utilization
•
Increase demand (twins hemolytic anemia…)
Symptoms and signs
•
Fatigue
,
palpitation
,
very
ill
,
painful
tongue
,
flattened
papillae
,
ulcers
,hepatosplenomegaly
anorexia
,
diarrhea

7
Investigations
•
Low Hb
•
Low RBC count
•
MCV Increases
•
MCH ±
•
MCHC decrease
•
WBC == and increase segmentation
•
Decrease serum folate
Treatment
•
Folic
acid
5
mg
/day
gives
rapid
improvement
within
2
days
see
increase
reticulocyte
count
•
Also give iron because Rx may unmask iron dif.
B 12 deficiency
•
Rare
•
More in vegetarians and poor families
•
Same
as
folate
even
respond
to
large
dose
folate
but
may
cause
neurological
lesion
in
spinal
cord
Hemolytic anemia
•
There
is
reduced
life
span
of
RBCs
“
normally
120
days“
the
RBCs
destroyed
and
removed
from
circulation
rapidly

8
Congenital spherocytosis
•
Cell
membrane
defect
“
spectrin
deficiency
“
cause
swelling
of
RBC
and
become
oval
shape
instead
of
biconcave
disc
•
RBCs
become
stiff
and
cannot
tolerates
mechanical
stress
when
pass
through
the
capillaries
•
Excessive hemolysis in the spleen and liver
•
Rapid turnover of bone marrow
•
Increase reticulocytes count
•
Respond to splenectomy
•
Autosomal dominant (( 50% of newborn will be affected))
Glucose 6 phosphate dehydrogenase deficiency
•
More than 400 types
•
Most common is an X linked recessive
•
Rarely women become affected ( homozygous )
•
Deficiency
of
NADH
(
produced
by
hexose
monophosphate
pathway
of
glycolysis
)
•
Oxidative damage of cell membrane
•
Episodic hemolytic anemia (drug, infection, fava beans, etc……)
•
Male fetus 100% affected , female 50% carrier
Hemoglobinopathies
•
Inherited defects in Hb synthesis cause hemolysis

9
Sickle cell anemia
•
HbS
•
replacement
of
glutamic
acid
by
valine
at
position
6
in
the
β
globin
chain
of
the
Hb
•
HbSS
(
homozygous
sickle
)
when
deoxygenated
,
acidosis
,
or
dehydration
it
become
insoluble
crystals
→
deformity
of
the
RBC
which
becomes
like
a
sickle
•
Repeated sickle → hemolysis
•
Cells become rigid block capillaries → further sickling
•
tissue ischemia and infarcts
Clinical features of sickle cell disease
•
Chronic hemolytic anemia
•
Painful crisis
•
Hypersplenism – autosplenectomy
•
Increase risk of infection
•
Avascular bone necrosis
•
CVA
•
Chest syndrome
Diagnosis of HbSS
•
Sickling test ( incubation with 2% Na metabisulphate)
•
Hb electrophoresis → HbSS, HbSA

10
Management during pregnancy
•
Crisis more frequent
•
Higher risk of
1. Abortion
2. Infection
3. IUGR
4. Pre-‐eclampsia
5. Prematurity
6. Thrombo-‐embolism
7. Perinatal mortality
8. Maternal mortality
Management of HbSS
•
Joined clinic obst. + haematologist
•
Pre-‐pregnancy counseling !!!
•
stop iron chelation
•
Echo
•
Folic acid 5mg
•
Penicillin prophylaxis
•
Regular check for renal , hepatic functions
•
Hb,
Hb
electrophoresis
±
top
up
transfusion
(
HbS
<
60%)
,
exchange
transfusion
???
•
Look for and treat infection aggressively

11
•
Avoid cold exposure , dehydration,
•
Crisis
and
chest
syndrome
,
treated
with
hydration
+
O2
+
opiate
+
top
up
transfusion
•
Thrombo prophylaxis !!
•
Fetal monitor by Doppler U/S
•
C/S for obstetrical reason , use epidural anesthesia
Management of labor in HbSS
•
Iv fluid to avoid dehydration
•
O2
•
Analgesia
•
Continuous fetal monitoring
•
Prophylactic Antibiotics ??!!
•
Prophylactic anticoagulation ! ?
•
Maternal mortality 2%
Sickle cell trait HbSA
•
Similar but mild
•
Fetal outcome like normal
•
Maternal complication usually rare
•
Avoid acidosis and hypoxia
β thalassemia
•
Deficiency in β chain synthesis

12
Hb compose of 4 globin chains
Hb A 2 α + 2β ……….adult Hb
HbF 2 α + 2 γ ………….fetal Hb
HbA2 2 α + 2 Δ
HbH 4 β chains
HbBart 4γ
•
Deficiency in β chain → ↑% of other Hb
•
↑hemolysis
•
In homozygous form (severe form , β thalassemia major)
•
Hepatosplenomegaly
•
Severe anemia
•
Repeated blood transfusion since age of 4-‐5 months
•
Usually die early!! Hemosiderosis
β thalassemia minor
•
Heterozygous mild form Hb 7-‐8 g/100ml
•
Microcytic , hypochromic anemia , mild hemolysis
•
Avoid iron Rx unless deficiency confirmed
•
May need repeated transfusion during pregnancy
•
Folic acid 5mg/day
•
During labor maintain Hb of 10 g/100ml
α thalassemia

13
•
Rare
•
Wide range of severity ( controlled by 4 alleles )
•
HbH
•
HbBarts
•
Major cause stillbirth in southeast Asia