Anaemia in Pregnancy

definition: anaemia is a pathological condition in which the oxygen-carrying capacity of red blood cells is insufficient to meet the body needs. the who define anaemia as a haemoglobin concentration of < 11.0 g/dl in the 1st trimester & < 10.5 g/dl in 2nd & 3rd trimesters. during pregnancy, although the red cell mass increases, the plasma volume expansion is relatively greater & therefore the haemoglobin concentration falls.

incidence: 30-50% of women become anaemic during pregnancy, with iron deficiency anaemia being responsible in more than 90% of cases. incidence of folate deficiency is 5%. this is due to the increased demand for the essential precursors such as iron & folate. less commonly , it may be due to chronic blood loss or haemolysis.

clinical features: anaemia is often asymptomatic during pregnancy, with the diagnosis being made on routine screening. clinical features include tiredness, dizziness, fainting & lethargy. pallor may be apparent.

screening: is by estimating haemoglobin concentration at the beginning of pregnancy & again later in the third trimester.

iron deficiency anaemia (microcytic anaemia): iron demand in pregnancy increases from 2 mg to 4 mg daily. a healthy diet contains 10 mg.
the diagnosis of iron deficiency is suspected if the mean corpuscular volume (mcv) is low, assuming electrophoresis is normal. low levels of serum iron & ferritin help to confirm the diagnosis.

consequences: impaired function of iron-dependent enzymes is the basis for the explanation of the link between iron deficiency anaemia & preterm delivery, infection, medical intervention during labour & postpartum haemorrhage.

treatment:
oral iron replacement is usually effective if there is enough time ( maximum increase in hb=0.8 g/dl per week).
the recommended dose of elemental iron is 120-240 mg daily. vitamin c taken simultaneously aid absorption, hence the common advice to take iron with fresh orange juice. side effects of oral iron are mainly gastrointestinal (gastritis & constipation) & this can effect the patient tolerance &compliance.
parenteral iron therapy can be used for those with intolerable side effect & those with poor compliance. intramuscular & intravenous preparations are available, careful administration is required because of the possibility of anaphylaxis.
blood transfusion is indicated at the end of pregnancy when there is no time to increase the hb concentration with iron therapy.

prevention: good balanced diet & identification & treatment of iron deficiency anaemia prior to pregnancy are optimal. a policy of routine iron supplementation during pregnancy is also adopted.

macrocytic anaemia:

folate deficiency: is less common as folic acid is present in many food stuffs such as green vegetables, fruits & liver. however it may be suggested by an increased mcv (> 95 fl). folate requirement is increased in pregnancy as all tissues require it for manufacture of dna. folate deficiency can occur in those with malabsorption syndrome or those with increased demand due to multiple gestation, haemolytic conditions & those taking anticonvulsant medications.

prophylaxis: all women considering pregnancy should be encouraged to use folate supplementation (0.4 mg) , as it has been shown to reduce the incidence of neural tube defect. higher supplementation (5mg) is required for women receiving anticonvulsant medication due to their antifolate activity.
treatment: folic acid 5 mg daily continued for up to 4 weeks in the peurperium.

vitamin b12 deficiency: (e.g, pernicious anaemia) is another cause of macrocytic anaemia, but such cases are more likely present with infertility. diagnosed cases should continue vitamin b12 during pregnancy.

haemoglobinopathies:

sickle-cell anaemia: an inherited disease with autosomal recessive inheritance in which abnormal haemoglobin (hbs) contains beta-chains with an amino acid substitution of glutamine in place of valine. in its deoxygenated state hbs becomes insoluble giving the red blood cells sickle shape, because of their rigid structure sickled cells block small blood vessels leading to sickling crises. it can be homozygous ( sickle cell disease) or heterozygous ( sickle cell trait).

sickle-cell disease: hbss is a severe condition & in pregnancy women are at high risk of complications. pregnancy is associated with increased incidence of sickle-cell crises that may result in episodes of severe pain, typically affecting the bones or lungs. these crisis may be precipitated by hypoxia, stress, infection & haemorrhage. mothers are at increased risk of miscarriage, pre-eclampsia, chest & urinary tract infection & preterm labour. the fetal loss rate is higher than normal, as is the incidence of growth restriction.

sick-cell trait: sickle-cell carriers have a 1:4 risk of having a baby with sickle-cell disease if their partner also has sickle-cell trait (hbas). carriers of the trait are usually fit & well, but are at increased risk of urinary tract infection.

sickle-cell haemoglobin c disease: although this condition may cause mild degrees of anemia, it is associated with very severe crises that are more common during pregnancy. the danger of this condition relate to a false reassurance because women are not as anaemic as those with ss disease thus the severity of crises may be underestimated.

antenatal management: all women should be screened at booking to detect haemoglobinopathies. if a woman is found to be heterozygote for a haemoglobinopathy, her partner should also be tested. no specific treatment exists to prevent sickle-cell crises however, hypoxia, infection & dehydration should be avoided by aggressive treatment with adequate analgesia, antibiotic, oxygen & rehydration. ideally a haemoglobin concentration of at least 10.0 g/dl with 60% normal hba will minimize the risk of crises. in some cases, blood transfusion or exchange transfusion is used to increase the percentage of circulating normal haemoglobin a.
vaginal delivery should be the aim & epidural anaesthesia advised, to reduce the stress of labour. care should be taken to avoid dehydration, cooling, infection or hypoxia during labour. continuous fetal monitoring is recommended. in the postnatal period these patients remain at increased risk of crises.



















thalassaemia:
thalassaemia syndromes are the commonest blood disorders. the defect is a reduced production of normal haemoglobin. the syndromes are divided into the alpha & beta types depending on which globin chain is affected.

in alpha-thalassaemia minor, there is a deletion of one, two or three of the four normal alpha genes required for haemoglobin production. although the effected individual is chronically anaemic, it rarely produces obstetric complications except in cases of severe blood loss. if the partner is also affected, there is a 1:4 chance of the fetus having alpha-thalassaemia major.
in alpha-thalassaemia major, there is no functional alpha chains, no normal haemoglobin is synthesized & the condition is incompatible with life. the fetus develops marked hydropings, & pregnacies are complicated by polyhydramnios & preterm delivery. if affected, the fetus will only survive few hours following delivery. these pregnancies may also be complicated by severe pre-eclampsia related to the enlarged & hydropingic placenta. there is no treatment but individuals can be offered the option of antenatal diagnosis in subsequent pregnancies.

beta-thalassaemia results from defects in the normal production of beta chains for which two genes are responsible. normal haemoglobin consist mostly of hba (2? 2?), with a small percentage of hba2 ( 2? 2?) & hbf (2? 2?) .
if one of the genes for beta-chain is missing the patient will have beta-thalassaemia minor, if the two genes are missing the patient will have beta-thalassaemia major. these conditions can be diagnosed using haemoglobin electrophoresis.
beta-thalassaemia minor is not a problem antenatally, although women tend to be mildly anaemic with low mcv. oral iron & folate should be given & the partner should be screened. if the partner has beta-thalassaemia trait, there is 1:4 chance that the fetus has beta-thalassaemia major.

the fetus produces hbf in utero while in postnatal life, normal hba cannot be produced & severe anaemia develops, requiring serial blood transfusion. eventually this leads to problems of iron overload & death.