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
Heme (iron deficiency)
DNA synthesis (megaloblastic)
(1) (1) (2)
Folic acid deficiency 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)
2. Intrinsic mechanism (inherited)
Infections and infestations Hypersplenism Mechanical (microangiopathic) Coombs-positive anaemia
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 Labile pool (2.2%) Other tissue iron 8mg(0.2%) Transport iron
130mg(3.5%) 80mg
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 IRON CONTENT Form of iron
Increased Absorption Absorption
Heme iron Adequate ferrous salt Iron deficiency INTRALUMINAL factors Intestinal secretions Hydrochloric acid Bile Intrinsic factor Stomach contents Ascorbic and other acids, phosphorus, cysteine Intestinal motility Atropine Chelators Metallic cations MUCOSAL factors Disease states Intermittent outlet obstruction lymphoma
Decreased Enteric-coated capsules
Cellular SYSTEMIC factors Erythropoiesis
infection
Iron requirements loss, thalassemia
Oxalates, phytates, carbonate Cathartics EDTA, desferrioxamine Cobalt, nickel Gastrectomy,
Decreased mucosal iron
Chronic diarrhea (sprue) Increased mucosal iron
Acute blood loss Hemolytic anaemia
Aplastic anaemia Transfusion, chronic
Achlorhydria
Hypoxia Pregnancy, growth Iron deficiency
Weight 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