ANAEMIA IN PREGNANCY

DR E. K. OKAGUA
DEPT OF OBS/GYNAE
UPTH
 THE BURDEN
 Anaemia is by far the most common
pregnancy complication worldwide
(Harrison,2001)
 It affects 2/5th of the non-pregnant
and over ½ of all pregnant women in
developing countries (WHO).
 It however affects less than 20% of
pregnant women in developed
countries, the higher figure in
developing countries due to poverty,
poor antenatal attendance and
recurrent infection.
 Anaemia in pregnancy is a major
health problem in many developing
countries where nutritional
deficiency, malaria and other
parasitic infections contribute to
increased maternal and perinatal
mortality and morbidity.
 After the puerperium, the debilitating
effect of anaemia undermines the
woman's health, lowers her economic
productivity and reduces their ability
to care for their homes and look after
their children
 DEFINATION
 Anaemia is defined by the WHO as a
haemoglobin concentration of <
11mg/dl.
 In Africa, 10mg/dl may be more
appropriate as evidence from Zaria
(Harrison, 1985) shows that the
proportion of low birth weight babies
and perinatal mortality begin to
increase with Hb less than 10mg/dl
 PREVALENCE
 62.2% of pregnant women in Ile-Ife
(Komolafe et al, 2005)
 56.1% of pregnant women in kwale,
(Oboro et al, 2002)
 15% of pregnant women at booking
at UCH, Ibadan (Aimakhu, 2003)
 Risk factors include late booking,
primigravidae, advanced maternal
age, short birth interval, wet season.
 AETIOLOGY
DECREASED ERYTHROCYTE PRODUCTION
(HYPOPROLIFERATIVE)
 1. Nuitritional deficiencies (low intake, poor
absorption)
 Haemoglobin synthesis
 (1) Heme (iron deficiency)
 DNA synthesis (megaloblastic)
 (1) Folic acid deficiency
 (2) Vitamin B12 deficiency
 2. Haemoglobinopathies – Globin
(thalassemia)
 3. Bone marrow failure
 4. Unknown (neoplasia, inflammation)
 AETIOLOGY (2)

INCREASED ERYTHROCYTE LOSS

 1. Early gestation (abortion,ectopics)

 2. Late gestation (placental

abnormalities)
 3. Parasites (hookworms)

 4. Puerperium (uterine atony)

 4. Intestinal lesions (hemorrhoids)

 AETIOLOGY (3)
INCREASED ERYTHROCYTE DESTRUCTION
(PROLIFERATIVE)
 1. Extrinsic mechanism (acquired)
 Infections and infestations
 Hypersplenism
 Mechanical (microangiopathic)
 Coombs-positive anaemia
 2. Intrinsic mechanism (inherited)
 Membrane abnormalities (spherocytosis)
 Enzyme abnormalities (G6PD)
 Globin abnormalities (sickle haemoglobin)
 3. Unknown (paroxysmal nocturnal
haemoglobinuria)
 AETIOLOGY 4
 Aetiology in many instances is
multifactorial
 In developing countries, the amount of
available iron from dietary sources may
not meet the additional demands placed
on maternal iron stores by the growing
fetus (300mg), placenta (50mg), increased
maternal red cell mass (450mg) and the
continuing maternal basal loss (200mg)
even though the increased demands are
partially offset by cessation of
menstruation and increased absorption of
 CLINICAL FEATURES
 asymptomatic in mild anaemia
 symptoms – headaches, weakness, tiredness,
faintness, dizziness, palpitations, breathlessness,
Pica.
 Signs – atrophy of buccal and tongue papillae,
glossitis, and angular stomatitis, pallor of the skin,
tongue, oral mucosa, palms of the hand, nail- bed,
hyperdynamic circulation, high pulse rate with wide
pulse pressure (bounding pulse), systolic murmurs
due to dilated cardiac chambers and turbulence of
blood flow.
 Cardiac failure – orthopnoea, engorgement of neck
veins (raised JVP), pulmonary oedema, tender
 IRON DEFICIENCY ANAEMIA
 Accounts for 75% of all anaemia
diagnosed during pregnancy (Flemming et
al 1975)
 Iron depletion without signs of anaemia is
very common during pregnancy.
 In one study, iron stores were found to be
exhausted in 25% of young, apparently healthy
women on their first prenatal visit.
 Another study demonstrated that 80% of
normal pregnant, iron-sufficient women if not
given iron supplementation were anaemic by
 IRON METABOLISM
IRON COMPARTMENTS
 Haemoglobin iron
1700mg(67%)
 Storage iron
700mg(27%)
[Ferritin & Haemosiderin]
 Myoglobin iron 130mg(3.5%)
 Labile pool 80mg
(2.2%)
 Other tissue iron
8mg(0.2%)
 Transport iron 3mg(0.08%)
 IRON ABSORPTION
 Principally absorbed in the
duodenum and proximal small
intestine.
 It is presented to the GIT in 1 of 3
forms:
 Ferrous form from elemental iron
 Haemoglobin from animal protein
sources
 Ferric form from vegetable complexes
 FACTORS AFFECTING IRON ABSORPTION
Increased Absorption Decreased
Absorption
IRON CONTENT
 Form of iron Heme iron Enteric-coated capsules
 Adequate ferrous salt
 Iron deficiency
INTRALUMINAL factors
 Intestinal secretions Hydrochloric acid Achlorhydria
 Bile
 Intrinsic factor
 Stomach contents Ascorbic and other acids, Oxalates, phytates,
phosphorus,
 cysteine carbonate
 Intestinal motility Atropine Cathartics
 Chelators EDTA, desferrioxamine
 Metallic cations Cobalt, nickel
MUCOSAL factors
 Disease states Intermittent outlet obstruction Gastrectomy,
lymphoma
 Chronic diarrhea (sprue)
 Cellular Decreased mucosal iron Increased mucosal iron
SYSTEMIC factors
 Erythropoiesis Acute blood loss Aplastic anaemia
 Hemolytic anaemia Transfusion, chronic
infection
 Hypoxia
 Iron requirements Pregnancy, growth Weight
loss, thalassemia
 Iron deficiency Hemochromatosis
 IRON SUPPLEMENTATION
 Poor compliance with iron
supplementation is a problem in clinical
practice because women feel well and thus
do not appreciate the need for medication
 Poor compliance may be also due to side
effects due to the medication and
 Alternative methods of supplementing iron
include slow release preparation and
reduced frequency as well as dosage of
the medication
 COMPLICATIONS OF
ANAEMIA
 MATERNAL
 Anaemic heart failure
 Intolerance of blood loss
 Aggravation of bacterial infections
 FETAL
 Birth asphyxia, intrapartum fetal death, ENND
 Low birth weight
 IUFD
 Immature immune system, depleted iron,
folate stores