Anaemia And Thrombocytopenia in pregnancy and its treatment and control

Anaemia in pregnancy              (1)

                                                          Prophylaxis 

recommendation to give 40–60 mg elemental Fe/d which
will increase availability of dietary absorbable Fe and protect against
chronic Fe deficiency; debated whether supplements required by all
pregnant women or only for those in at-risk socio-economic and
nutritionally deficient groups. Folate supplementation is recommended
for all and also appears to reduce incidence of neural tube defects.

 Dilutional anaemia —Hb seldom <10.0g/dL (requires no therapy).

 Fe deficiency —may occur with normal MCV because of 4 MCV associated
with pregnancy; check serum ferritin and give Fe replacement;
assess and treat the underlying cause.

 Blood loss —sudden 5 in Hb may signify fetomaternal bleeding or
other forms of concealed obstetric bleeding.

 Folate deficiency —macrocytic anaemia in pregnancy almost invariably
will be due to folate deficiency (B12 deficiency is extremely rare during
pregnancy).

 Microangiopathic haemolysis/DIC may be seen in eclampsia or following
placental abruption or intrauterine death. HELLP syndrome
 is rare but serious cause of anaemia.

 Anaemia may also arise during pregnancy from other unrelated causes
and should be investigated.

Cause of  requirements Amount of additional Fe

 Red cell mass ~500mg
Fetal requirements ~300mg
Placental requirements ~5mg
Basal losses over pregnancy (1.0–1.5mg/d) ~250mg
Folate requirements
are increased during pregnancy because of
increased cellular demands; folate levels tend to drop during pregnancy

Physiological changes in red cell and plasma volume occur during
pregnancy.

1 Red cell mass 4 by ≤30%.
2 Plasma volume 4 ≤60%.
3 Net effect to 4 blood volume by ≤50% with lowering of the normal

Hb concentration to 10.0–11.0g/dL during pregnancy. MCV increases

during pregnancy.

4 Iron deficiency is a common problem and cause of anaemia in pregnancy.
These result in a total requirement of ≤1000 mg Fe requiring an average
daily intake of 3.5–4.0mg/d. Average Western diet provides <4.0mg Fe/d
so that balance is marginal during pregnancy. Diets with Fe mainly in nonhaem
form (e.g. vegetables) provide less Fe available for absorption. Thus
a high risk of developing Fe deficiency anaemia which is exacerbated if preconception
Fe stores are reduced
.

symptom of anaemia

                                                               (2)

Thrombocytopenia in pregnancy     

A normal uncomplicated pregnancy is associated with a platelet count in
the normal range though up to 10% of normal deliveries may be associated
with mild thrombocytopenia (>100 ¥ 109/L). Detection of thrombocytopenia
in a pregnant patient requires consideration not only of the
diagnoses listed in the previous section but also the conditions associated
with pregnancy which cause thrombocytopenia. An additional important
consideration is the possible effect on the fetus and its delivery.
If thrombocytopenia is detected late in pregnancy, most women will have
a platelet count result from the booking visit (at 10–12 weeks) for comparison.
Mild thrombocytopenia (100–150 ¥ 109/L) detected for the first
time during an uncomplicated pregnancy is not associated with any risk to
the fetus nor does it require special obstetric intervention other than hospital
delivery.

Non-immune thrombocytopenia

2 Thrombocytopenia may develop in association with pregnancy-induced
hypertension, pre-eclampsia or eclampsia. Successful treatment of
hypertension may be associated with improvement in thrombocytopenia
which is believed to be due to consumption. Treatment of
hypertension, pre-eclampsia or eclampsia may necessitate delivery of
the fetus who is not at risk of thrombocytopenia.
l HELLP syndrome (haemolysis, elevated liver enzymes and low
platelets) may occur in pregnancy.
2 A number of obstetric complications, notably retention of a dead fetus,
abruptio placentae and amniotic fluid embolism, are associated with
DIC

Immune thrombocytopenia

may occur in pregnancy and women with
chronic ITP may become pregnant. Therapeutic considerations must
include an assessment of the risk to the fetus of transplacental passage
of antiplatelet antibody causing fetal thrombocytopenia and a risk of
haemorrhage before or during delivery. There is no reliable parameter
for the assessment of fetal risk which, although relatively low, is most
significant in women with pre-existing chronic ITP. Note: the severity of
the mother’s ITP has no bearing on the fetal platelet count.
Women with a platelet count
<20 ¥ 109/L due to ITP should receive
standard prednisolone therapy or IVIg.If prednisolone fails
or is contraindicated, IVIg should be administered and may need to be
repeated at 3 week intervals. Splenectomy should be avoided (high rate
of fetal loss). Enthusiasm has waned for assessing the fetal platelet
count during pregnancy by cordocentesis followed by platelet
transfusion. Fetal scalp sampling in early labour is unreliable and
hazardous. Delivery should occur in an obstetric unit with paediatric
support and the neonate’s platelet count should be monitored for
several days as delayed falls in the platelet count occur.