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Anemia in Pregnancy-Objectives
To know the normal physiological hematological changes in pregnancy. To define anemia in pregnancy To list the common causes of pregnancy anemia To know the investigations to confirm the diagnosis of the different types of anemia To be able to manage pregnancy anemia
Anemia: Objectives
Definition: WHO (Hb<11g/dL)vs CDC(<10.5g/dL), HCT< 30%. Causes: acquired vs congenital Clinical features Pathogenesis Diagnosis: IDA/Folate/B12/HbSS. Management
Physiological Changes
Where is iron absorbed in the GIT & in what form is it absorbed? In pregnancy, additional demands for iron represent:
Fetus+ placenta RBC increase Postpartum bleeding/lactation Loss thru gut, urine & skin 500mg 500mg 180mg 200mg
IDA
Most common cause of pregnancy anemia(75%-90%). Most pts present 3rd trimester when Fe demands reach their peak(1-2mg/day non-pregnant,2.5mg/day 1st trimester,6.6mg/day 3rd trimester). IDA common in pregnancy because many enter it with depleted Fe stores (MBL,PEM-inadequate diet, previous recent pregnancies). Multiple pregnancy IDA. Blood loss at delivery IDA in puerperium Birth spacing & avoidance of teenage pregnancies allow deposition of Fe stores after pubertal growth spurt or a previous pregnancy
IDA-Presentation/Prevention
Revise Haematology/ Internal medicine Lectures for Clinical Presentation Prevention of IDA:1998-WHO/UNICEF recommend routine supplements (60mg Fe & 400g folate daily to all pregnant women for 6/12 & extending to 3/12 postpartum in areas with a high prevalence(>40%) of anemia
Investigations IDA
Visualization of peripheral blood smear RBC indices MCV;MCH;MCHC(<30)- All NB. Hb estimation alone is unreliable. Serum Fe <12mol/l, TIBC saturation<15%, serum ferrritin<12g/l Stool /Urine for M/C/S
Treatment of IDA
Dietary advice-red meat/fish/green leafy vegetables/avocadoes Fe therapy-oral vs parenteral(I.M. or I.V.) vs blood transfusion. NB Jehovah Witnesses- Blood substitutes/ parenteral Fe/Recombinant erythropoetin. Moderate reticulocytosis in 7-10 days confirms a satisfactory response.
Folate-deficiency Anemia
Normal dietary folate inadequate to prevent megaloblastic changes in the BM in~25% pregnant women. Incidence- function of SES & the nutrition of the population. FDA-more likely if pt on AEDs, or has hematological conditions like hemolytic anemiaHS/thalassemia;intestinal malabsorption/gluten sensitivity/overcooking of fresh green vegetables/excessive alcohol consumption, grand multiparity with short intervals between pregnancies
FDA
FDA =macrocytic anemia with megaloblastic change in the BM NB a MCV can be a feature of normal pregnancy. Confirm by (serum &) RBC folate levels PMN hypersegmentation, megaloblasts & Howell-Jolly bodies in peripheral blood smear;neutropenia/thrombocytopenia NB: All women planning a pregnancy are advised to take 400g of folate 3/12 before & 3/12 after conception to risk of NTDs & other fetal abnormalities (MRC Vitamin Study Research Group-1991). Pts with FDA or with a prev fetus with NTD or those on AEDs to take 5mg /day thru-ot pregnancy.
Aplastic anemia/Leukemia
These 2 conditions are rarely seen during pregnancy. Aplastic anemia characterized by anemia, thrombocytopenia & agranulocytosis with a markedly hypocellular BM. Drugs, chemicals, infection, irradiation, leukemia & immunological disorders ay trigger it.Rx inlude repeated transfuions of rbc, plts & granlocytes. Steroids have a role as well as BM transplantation. In acute leukemia chemoRx should continue as appropriately chosen drugs are well tolerated by the mother & fetus without evident teratogenic effects.
Haemoglobinopathies
Sickle-cell Hemoglobinopathies include: 1. Sickle-cell anemia(HbSS disease) 2. Sickle-cell hemoglobin C disease (HbSC) 3. Sickle-cell beta Thalassemia. These are autosomally inherited with substitution of glutamic acid by valine in the -chain.
Sickle-cell Haemoglobinopathies
Factors responsible for sickling include: Hypoxia due to poor oxygenation/circulation Acidosis Dehydration/Cooling Severe infections General anaesthesia