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Anaemia in pregnancy
 

Anaemia in pregnancy

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o&g update course 2012 hospital segamat

o&g update course 2012 hospital segamat

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    Anaemia in pregnancy Anaemia in pregnancy Presentation Transcript

    • ANAEMIA COMPLICATING PREGNANCY DR:HUSSEIN H AKL O&G SPECIALIST HOSPITAL SEGAMAT
    • Definition Anemia - insufficient Hb to carry out O2 requirement to the tissues. WHO definition : Hb conc. 11 gm % CDC definition : Hb conc. < 11gm % in 1st and 3rd trimesters and < 10.5 gm% in 2nd trimester For developing countries : cut off level suggested is 10 gm % - WHO technical report Series no. 405, Geneva 1968 Centre for disease control, MMWR 1989;38:400-4
    • ANAEMIA IN PREGNANCY Definition: By WHO Hb. < 11 gm /dl (or haematocrit <32%). Mild anaemia -------- 9 -10.9 gm /dl Moderate anaemia--- 7-8.9 gm /dl Sever anaemia-------- < 7gm /dl Very sever anaemia-- < 4gm/dl
    • Degree Hb% Haematocrit (%) Moderate 7-10.9 24-37% Severe 4-6.9 13-23% Very Severe <4 <13% WHO Classification of Anaemia
    • Magnitude of Problem Globally, is about 30 % In developing countries & India, incidence is around 40 – 90%. Responsible for 40% of maternal deaths in third world countries. Important cause of direct and indirect maternal deaths - Vitere FE Adv Exp Med Biol 1994;352:127
    • Infection Lack of Concentration Weakness Irritability Palpitation Fatigue Dizziness Symptoms
    • Clinical Features Pallor of skin And m/m Edema Platynychia Koilonychia Glossitis Stomatitis Tachycardia Soft ejection systolic murmur Signs
    • IRON DEFICIENCY ANEMIA GENERAL ANEMIA’S SYMPTOMS: •FATIGABILITY •DIZZENES •HEADACHE •SCOTOMAS •IRRITABILITY •ROARING •PALPITATION
    • pallor
    • Conjunctival Pallor
    • Koilonychia
    • CHARACTERISTICS SYMPTOMS •GLOSSITIS, STOMATITIS • DYSPHAGIA ( Plummer-Vinson syndrome) •ATROPHIC GASTRITIS •DRY, PALE SKIN •SPOON SHAPED NAILS, KOILONYCHIA, •BLUE SCLERAE •HAIR LOSS •PICA (APETITE FOR NON FOOD
    • Physiological Pathological Causes of Anaemia Nutritional Haemorrhagic Haemolytic
    • Common Anaemias in pregnancy Common types: Nutritional deficiency anaemias - Iron deficiency - Folate deficiency - Vit. B12 deficiency Haemoglobinopathies: - Thallassemias - SCD Rare types: - Aplastic - Autoimmune hemolytic - Leukemia - Hodgkin’s disease - Paroxysmal nocturnal haemoglobinurea
    • Iron Requirement Iron Absorption 1 Amount of iron in the body Iron Loss Skin Urine Feces Menstruation 1-2mg/d 20-30mg/c
    • Physiological changes in pregnancy • Plasama volume 50% (by 34weeks) • But RBC mass only 25% • Results in haemodilution : • Hb Haematocrit RBC count No change in MCV or MCH 2-3 fold increase in Fe requierment. 10-20 Fold increase in folate requirement
    • Criteria for Physiologic Anemia Hb: 10gm% RBC: 3.2 million/mm3 PCV: 30% Peripheral smear showing normal morphology of RBC with central pallor
    • Significance of Hypervolemia 1. To meet the demands of the enlarged uterus with its greatly hypertrophied vascular system. 2. To protect the mother, and in turn the fetus, against the deleterious effects of impaired venous return in the supine and erect positions. 3. To safeguard the mother against the adverse effects of blood loss associated with parturition.
    • Normal hemoglobin by gestational age in pregnant women taking iron supplement 12 wks 12.2 [11.0-13.4] 24wks 11.6 [10.6-12.8] 40 wks 12.6 [11.2-13.6]
    • Early Pregnancy 2.5 mg / day 32 to 40 weeks 6.8 mg / day TOTAL 800 – 1000 mg 20 to 32 weeks 5.5 mg / day Iron Requirement During Pregnancy
    • IRON DEFICIENCY ANAEMIA Iron required for fetus and placenta ------- 500mg. Iron required for red cell increment ------- 500mg Post partum loss --------- 180mg. Lactation for 6 months - 180mg. Total requirement -------1360mg 350mg subtracted (saved as a result of amennorrhoea) So actual extra demand ----------------------1000mg Full iron stores --------------------------------1000mg
    • Hb 13.5 – 14 gm % R.B.C. 4.5 – 4.7 million/cu mm Serum Iron 50 – 150 μg / dL TIBC 300 – 360 μg / dL Transferrin saturation 25 – 50 % S. Ferritin level 30 μg / Lit Red Cell protoporphyrin 30 μg / dL Erythropoietin 15.20 U / Lit MCV 76 – 100 fL MCH 27 – 33 pg MCHC 33.37 gm / dL PCV 32 – 40 % Normal Levels
    • ETIOLOGY OF IRON DEFICIENCY ANAEMIA Depleted iron stores – dietary lack, chronic renal failure, worm infestation, chronic menorrhagia Chronic infections: ( like malaria) Repeated pregnancies : - with interval < 1 year - blood loss at time of delivery - multiple pregnancy.
    • IRON DEFICIENCY ANEMIA ETIOLOGY: –CHRONIC BLEEDING •MENORRHAGIA •PEPTIC ULCER •STOMACH CANCER •ULCERATIVE COLITIS •INTESTINAL CANCER •HAEMORRHOIDS
    • CLINICAL FEATURES Symptoms usually in severe anaemia - Fatigue - Giddiness - Breathlessness
    • EFFECTS OF ANAEMA IN PREGNANCY . Mother : – High output- due to inadequate tissue oxygenation, increase cardiac failure (more likely if reqirement for excessive blood flow ) – PPH – Predisposes to infection – Risk of thrombo-embolism – Delayed general physical recovery esp after c. section
    • Fetus: . IUGR . Preterm birth . LBW . Depleted Fe store . Delayed Cognitive function.
    • IUGR IUD ABOR TION CCF INFECTION PRETERM LABOUR PIH Medical Disorder Complications - Pregnancy
    • Instrumental delivery PPH Foetal DistressCCF MATERNAL PERINATAL Morbidity Mortality Complications - Labour
    • Laboratory Diagnosis of Anaemia IDA Thalassemia Chronic Diseases Serum Iron Decreased Normal / Increased Decreased TIBC Increased Normal Decreased or N Transferrin Saturation Decreased N or Increased N or Decreased Serum Ferritin Decreased N or Increased N Marrow Iron Decreased / absent N or Increased N Therapeutic test with oral iron Rise in Hb No rise in Hb No rise
    • Serum iron decreased (<12 micro mol / l) Total iron binding capacity :TIBC in non-pregnant state is 33% saturated with iron .when serum iron level fall ,<15% ofTIBC saturated.by fall in saturation,the TIBC INCREASED. S. ferritin :In healthy adults ferritin circulate in plasma in range of 15_300 pg/l. in iron deficiency anemia it is the first test to become abnormal. INVESTIGATIONS
    • Serum transferrin receptor(TfR) : present on all cells as transmembrane protien that binds transferrin iron and transfer it to cell interior. Increased in iron def. anemia. Bone marrow examination. RFTS/LFTS. Urine for haemturia. Stool examination for ova ,cyst and occult blood.
    • BLOOD AND BONE MARROW SMEAR BLOOD: microcytosis, hipochromia, anisocytosis poikilocytosis BONE MARROW high cellularity mild to moderate erythroid hyperplasia (25-35%; N 16 – 18%) polychromatic and pyknotic cytoplasm of erythroblasts is vacuolated and irregular in outline (micronormoblastic erythropoiesis) absence of stainable iron
    • MANAGEMENT Objectives: 1- To achieve a normal Hb by end of pregnancy 2- To replenish iron stores Two ways to correct anaemia: I- Iron supplementation . Oral Fe . Parenteral Fe II- Blood transfurion
    • Choice of method: It depends on three main factors: Severity of the anaemia Gestational Age . Presence of additional risk factor
    • National Nutrition Anaemia Prophylaxis Programme (NNAPP 1971 - 72) Anaemia continues – Major health problem Nutritional Anaemia : Major Health Problems FS + FA Pregnancy Lactating mothers Family planning acceptors Children – 1 to 11 years
    • Reason For Increased Incidence Of Anemia Poor pre-pregnancy iron balance due to – untreated systemic diseases & menstrual disorders Improper supplementation of iron in pregnancy ( late registration and poor follow up) Repeated childbearing Lack of awareness and illiteracy
    • Low socioeconomic status and poor hygiene Chronic malnutrition Poor availability of iron due to predominantly veg diet, diet low in calories but rich in phytates. Food and religious taboos GI infections and infestations (e.g. Kala azar, worm infestations) Reason For Increased Incidence Of Anemia
    • Management Options Pre – pregnancy : Treat the cause before conception Pre-pregnancy balanced diet, education and health support. Build up iron stores during adolescent phase
    • Oral Iron Blood transfusionParenteral Injectable Iron Human Recombinant Erythropoietin Modalities of Management
    • 100 mg elemental Iron ------- ↑ 0.18 gm % day Iron stores poor -ve Iron absorption ↓ Bioavailability of Iron Phosphate phytate Worm infestation Oral Iron
    • Oral Iron Therapy Ideal dose – 100mg per day (prophylactic) Ferrous gluconate, ferrous fumarate, ferrous succinate, ferrous sulphate, ferrous ascorbate citrate Rise in Hb – 0.8 gm / dl / week Side effects -G I upset most common Pt. compliance not guaranteed Ineffective in pts with worm infestations Inconclusive evidence on benefit of controlled release Iron preparation
    • Iron salts are dissociated into bivalent or trivalent iron salts Diffuses as free iron ions through the upper part of the gastrointestinal mucosa Taken up by transferrin and incorporated into ferritin. For binding to ferritin and transferrin ferrous iron has to be converted into ferric iron by oxidation Highly reactive free radicals are produced during this process All ionic iron including carbonyl iron are absorbed similarly • Borbolla JR. Cicero RE, Dibilox MM, Sotres RD et al.. Rev Mex Pediatr 2000; 67(2): 63-67 • Heubers KA, Brittenham GM, Csiba E, Finch CA. J Lab Clin Med 1986 ; 108 ; 473-8. Absorption of Ferrous Salts Uncontrolled Passive Absorption
    • Fe+2 Fe+2 Fe+2Fe+2 Dissociation Passive diffusion Fe+2 Fe+2 Fe+3 Fe+2 Fe+3 Gut Lumen Mucosal Cell Blood Ferritin Iron salts Fe+3 Free Radical Fe+2 Fe+2 Fe+2 Fe+2 Fe+2 Fe+2 Fe+2 Fe+3 Free Radical Transferrin Incorporation into Hb
    • ↑ Hb – 0.21 gm % Fractionated Irondextran [Iron hydroxide dextran complex] Parenteral Therapy 100 mg elemental Iron Anaphylactic reaction Anaphylactic reaction I.M. I.V.
    • Parenteral Therapy : Traditional Indications Intolerance to oral iron Poor compliance to oral iron Gastrointestinal disorders Malabsorption syndromes Rapid blood loss
    • IRON DEFICIENCY ANEMIA CURE PARENTERAL IRON SUBSTITUTION Bad oral iron tolerance (nausea, diarrhoea) Negative oral iron absorption test Necessity of quick management (CHD, CHF) 50 - 100 mg daily I.v only in hospital (risk of anaphilactic shock) I.m in outpatient department iron to be injected (mg) = (15 - Hb/g%/) x body weight (kg) x 3 TDI(in mg)=2.3xWxD+500
    • Inability to maintain iron balance (haemodialysis) Patient donating large amount of blood for auto-transfusion programme ? Pregnant women with severe IDA, presenting late in pregnancy Parenteral Therapy : Traditional Indications
    • The World Health Organisation states… ‘transfusion should be prescribed ONLY for conditions for which there is NO OTHER TREATMENT’
    • FOLATE DEFICIENCY ANAEMIA At cellular level Folic acid reduced to Dihydrofolicacid then Tetrahydro-folicacid . (THF) c is required for cell growth & division. So more active tissue reproduction & growth more dependant on supply of folic acid. So bone marrow and epithelial lining are therefore at particular risk.
    • FOLATE DEFICIENCY ANAEMIA Folic acid deficiency more likely if . Woman taking anticonvulsants. . Multiple pregnancy. . Hemolytic anemia; thalasemia H.spherocytosis Maternal risk: Megaloblastic anemia Fetal risk: Pre-conception deficiency cause neural tube defect and cleft palate etc.
    • FOLATE DEFICIENCY ANAEMIA Diagnosis: Increased MCV ( > 100 fl) Peripheral smear: - Macrocytosis, hypochromia - Hypersegmented neutrophils (> 5 lobes) - Neutropenia - Thrombocytopenia Low Serum folate level. Low RBC folate.
    • FOLATE DEFICIENCY ANAEMIA Daily folate requirement for : Non pregnant women -- 50 -100 microgram Pregnant woman –-------- 300-400 microgram Usually folic acid present in diets like fresh fruits and vegetables and destroyed by cooking. Folate deficiency: - 0.5-1.0mg folic acid/day If F/Hx. of neural tube defect - 4mg folic acid/day.
    • Vitamins B12 Deficiency It is rare Occurs in patients with gastrectomy , ileitis, illeal resection, pernicious anaemia, intestinal parasites. Diagnosis: –Peripheral smear –Vitamin B12 level < 80 pico g/ml Treatment of B12 Deficiency: Vit B12 1mg I/M weekly for 6 weeks.
    • Diagnosis of Folate Deficiency Anemia (FDA) Special considerations in diagnosis • FDA is suspected when the expected response to adequate iron therapy is not achieved • Macrocytosis can occur in pregnancy in absence of FDA • If FDA + IDA present, it will be masked by IDA • Definitive diagnosis – Bone marrow aspirate
    • Megaloblastic Anemia - Diagnostic Problems HB estimation Peripheral smear MCV estimation Serum folate Red cell folate FIGLU estimations Marrow aspirate
    • Management of FDA Strong case for routine prophylaxis Prophylaxis with anti convulsants Continue routine oral therapy for hemolytic anaemia Parenteral therapy for severe deficiency
    • Worm Infestations Common cause of anaemia in developing countries Most common – hookworm infestation, Round worm, whip worm, etc. Oral iron therapy becomes ineffective Treatment by antihelminthics is a must Treatment Mebendazole : 100mg twice daily for three days Pyrantel pamoate : 10mg / kg in single dose. Albendazole : 400mg once a day for three days
    • Hemoglobinopathies A collective term for the inherited disorders of Hb synthesis Disorders of globin synthesis e.g. Thalassemia Structural Hb variants e.g. Sickle cell anemia, HbC
    • HAEMOGLOBINOPATHIES. Normal adult Hb. after age of 6 month, HbA---97%, HbA2---(1.5-3.5%), HbF2--<1%. 4 Globin chains associated with haem complex. Hb. A = 2 alpha +2 beta globin chains. Hb.A2= 2alpha+2 delta globin chains. Hb.F = 2 alpha+ 2 gamma globin chains. Hb. synthesis is controlled by genes. Alpha chains by 4 gene,2 from each parent. Beta chains by 2 genes ,1 from each parent.
    • HAEMOGLOBINOPATHIES DEFINITION: Inherited disorders of haemoglobin. Defect may be in: - Globin chain synthesis------thalassemia. - Structure of globin chains-sickle cell disease. Hb.abnormalities may be: - Homozygous = inherited from both parents. (Sufferer of disease) - Hetrozygous = inherited from one parent. (Carrier/trait of disease)
    • THALASSAEMIAS The synthesis of globin chain is partially or completely suppressed resulting in reduced Hb. content in red cells,which then have shortened life span. TYPES: - Alpha thalassaemia. - Beta thalassaemia: . Major . minor
    • Thalassemia Genetic disorders; lack or sed synthesis of globin chains Two types : & thalassemia chains encoded by 2 pairs of genes on chromosome 16 chains encoded by single pair of genes on chromosome 11 thalassemia more common and presents as either (major) or + (minor)
    • Beta thalassemia minor Beta Thalassemia trait Heterozygous inheritance from one parent. Most frequent encountered variety. Partial suppression of the Hb. synthesis. Mild anaemia. Investigations: Hb----around 10 g/dl. Red cell indices: low MCV. low MCH. normal MCHC. Diagnostic test: Hb. Electrophoresis.
    • Beta Thalassemia Minor Management: Same as normal woman in pregnancy. Frequent Hb. Testing. Iron & folate supplements in usual dose. Parenteral iron should be avoided. because of iron overload. If not responded ---I/M folic acid. blood transfusion close to time of delivery.
    • Beta Thalassaemia Major Homozygous inheritance from both parents. Sever anaemia. Diagnosed in paediatric era. T/m: is blood transfusion. ALPHA THALASSAEMIA: Both heterozygous & homozygous forms exist. Alpha thalassaemia trait. HbH disease. Alpha thalassaemia major.
    • Diagnosis of Thalassemia Hb estimations Peripheral smear sed MCV sed MCH HbA2 ( 2 2)
    • Diagnostic Strategy for Thalassemias Hb Electrophoresis + CBC Abnormal band Normal No action MCV MCH Quantitative Hb electrophoresis Raised Hb A2 B Thalassemia Normal sed Examine partners blood ? X Thalassemia DNA analysis for x gene defects
    • SICKLE CELL SYNDROME. Autosomally inherited . Structural abnormality. HbS - susceptible to hypoxia, when oxygen supply is reduced. Hb precipitates & makes the RBCs rigid & sickle shaped. Heterozygous----HbAS. Homozygous-----HbSS. Compound heterozygous---HbSC etc.
    • Sickle Cell Disease (SCD) Sickeling crises frequently occurs in pregnancy, puerperium &in state of hypoxia like G/A and Hag. Increased incidance of abortion and still birth growth restriction, premature birth and intrapartum fetal distress with increased perinatal mortality. Sickle cell trait:(carrier state) Does not pose any significance clinical problems
    • Sickle Cell Disease Structural Hb variant Exists in homo & heterozygous forms Under hypoxic conditions, HbS polymerizes, gels or crystallizes. hemolysis of cells, & thrombosis of vessels in various organs In long standing cases, multiple organ damage.
    • SCD Diagnosis: - Hb. Electrophoresis Management: - No curative Tx. - only symptomatic - Well hydration, effective analgesia, prophylactic antibiotics, O2 inhalation, folic acid, oral iron supplement (I/V iron is C/I), blood transfusion
    • Management During labour Comfortable Position Adequate analgesia O2 inhalation Low threshold of assisted delivery Avoid ergometrine Prophylactic antibiotics Continue iron &folate therapy for 3 mo after delivery Appropriate contraceptive advice
    • Take Home Message Anaemia although preventable is a global problem Anaemia still is the commonest cause of maternal mortality and morbidity in spite of easy diagnosis and treatment Anaemia can be due to a number of causes, including certain diseases or a shortage of iron, folic acid or Vitamin B12. The most common cause of anemia in pregnancy is iron deficiency. Iron therapy is best given orally
    • The youth need to be educated about diet, sanitation and personal hygiene Hookworm infestation should be treated Pregnant women should be given Iron and folate supplements Take Home Message
    • Thank You Egypt