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ANAEMIA IN PREGNANCY

DEFINITION: HB% < 11gm%(WHO) < 10gm% ( developing countries)

Incidence: 40-80%( developing countries) 10- 20% ( developed countries)

CLASSIFICATION

PHYSIOLOGICAL ANEMIA
PATHOLOGICAL

Deficiency anemia( isolated/combined)


Iron deficiency Folic acid deficiency Vitamin B12 deficiency protein deficiency

CLASSIFICATION
Haemorrhagic - Acute - Chronic- hook worm ,piles hemolytic - familial - sickle cell anemia - acquired- malaria, severe infection

Aplastic Hemoglobinopathies

Normal blood values in non pregnant and pregnant


nonpregnant lInd half

hb RBC PCV MCH MCV MCHC S.fe TIBC


Saturation

s.ferritin

14.8gm% 5 million/mm3 39- 42% 27-32pg 75-100cu micron 32-36% 60-120 micro g 300-350 micro g 30% 20-30 mig/L

11-14gm% 4-4.5 million/mm3 32-36% 26-31pg 75-95 cu micron 30-35% 65- 75 micro g 300-400micro g < 16% 15mig/L

PHYSIOLOGAL ANEMIA
Hb- 10gm% RBC- 3.2 million/c.mm PCV- 30% RBC morphology normal with central pallor Expected Hb%= Hb%<12 wks 2gms%

ERYTHROPOISES

Pronormoblassts- normoblasts- reticulocytesRBC Life span 120 days Nutrients required Minerals- Fe, Cu, Co Vitamins- B12, folic acid, vit C B12 for RNA, FA- DNA Vit C folinic acid to folic acid Proteins- for globin moiety Erythropoitin

Causes for increased prevalence of anaemia in tropics


Faulty dietic habit Faulty absorption mechanism Iron loss 1.sweating-15mg/month 2.short interval pregnancies 3.menorrhagia 4.hook worm infestation 5.chronic malaria, piles,dysentery

Causes during pregnancy

Increased demand Diminished intake Disturbed metabolism-presence of infection Pre-pregnant health status Excess demand i) multiple pregnancy ii)rapidly recurring pregnancy iii) Teen age pregnancy Polymorphism

Clinical features
Symptoms: lassitude, weakness, anorexia, indigestion, palpitation dyspnoea, giddiness, swellings of limbs PALLOR, glossitis, stomatitis Edema- hypoproteinemia/ PIH Hemic murmur crepitations

INVESTIGATIONS

Pt with Hb < 9gm should be investigated Objectives

Degree of anaemia Type of anaemia Cause of anaemia

Degree of anaemia
HB% RBC count PCV Mild- 8- 10gm% Moderate- 8-7gm% Severe- < 7gm%

TYPE OF ANAEMIA
Peripheral blood smear Microcytic hypochromic cells Hematological indices- MCV, MCH,MCHC S.fe - <30mig/dl TIBC-400mig/dl %age saturation- <10% S.ferritin- <15mig/L S.bilirubin normal

Cause of anaemia
Stool for ova& cyst Urine CXR Bone marrow study- nonresponse to treatment, hypoplastic anaemia, kalaazar D.D : -infection -nephritis/preeclampsia -Hemoglobinopathies

COMPLICATIONS
PREGNANCY

Preeclampsia Intercurrent infection CCF Preterm labour LABOUR uterine inertia, PPH, CCF, shock PUERPERIUM sepsis, subinvolution, failure of lactation, dvt, pulmonary embolism

DANGER PERIODS
30-32 WEEKS LABOUR IMMEDIATELY AFTER DELIVERY 7-10 DAYS AFTER DELIVERY BABY LBW IUD MMR 20%

PREVENTION
FAMILY PLANNING SUPPLIMENTATION DIET TREATMENT OF INFECTION Hb % estimation at Ist visit, 30 wks,36wks

CURATIVE
Hb< 7.5g to be admitted Associated medical or obs complication with moderate anemia General treatment Diet Improve appetite Antibiotic Effective therapy

CHOICE OF THERAPY
SEVERITY OF ANAEMIA DURATION OF PREGNANCY ASSOCIATED COMPLICATIONS

IRON THERAPY ORAL PARENTERAL

ORAL THERAPY
Best absorbed in ferrous form Ferrous sulphate, fumarate,succinate 200mg, 60mg elemental 1 tid,max-6/day Maintainance dose 1 od for 100days Draw backs; 1. intolerance, 2. unpredictable absorption rate,3.stores not replinished easily Response to treatment

ORAL THERAPY
Rate of improvement : should be evident with in 3 wks. 0.7gm/wk Causes for failure of improvement: 1. Improper typing 2. Defective absorption 3. Poor compliance 4. Concurrent blood loss 5. Infection 6. Coexistant folate deficiency Contraindications: intolerance, severe anemia

PARENTERAL THERAPY
INTRAVENOUS: I.REPEATED INJECTIONS II. TDI INTRAMUSCULAR INDICATIONS: 1. C.I. to oral therapy 2. Non co-operative pt 3. Last 8-10 wks with severe anemia Advantage : stores replinished early Rate of improvement: 0.7-1gm/wk

TDI
Iron dextran Advantages: 1.eliminates repeated painful injections 2.Treatment completed in single day 3.Less costly Limitations : 1.max response 4-9wks 2.h/o reaction Estimation: 0.3xW(100-Hb%)+50%

IM therapy
Iron dextran Iron sorbital citrate Oral therapy should be suspended atleast 24hrs before Test dose Z technique Draw backs: 1) painful, 2) abcess, 3) reactionfever, headache, lymphaedenopathy, allergy

BLOOD TRANSFUSION
INDICATIONS Blood loss anaemia Severe anemia >36wks Refactory anaemia Associated infection Packed cells Advantages 1.increase in o2 carrying capacity 2. substrate for hemopoises 3.stimulates erythropoises 4.Improvement in 3 days

BLOOD TRANSFUSION
Precautions: 1. antihistaminics 2. diuretics, 3. drip rate 10/min, 4. pulse,r.r., creps Drawbacks: 1. preterm labour, 2. CCF, 3.reaction EXCHANGE TRANSFUSION CCF, SURGERY, HCT<13%

MANAGEMENT OF LABOUR
IST STAGE: bed rest,o2 inhalation,asepsis II STAGE: cut short ii stage by forceps, iv methergin III STAGE: packed cell trans fusion, Puerperium : antibiotics, continue hemotherapy, counseling about next pregnancy

MEGALOBLASTIC ANAEMIA
There is derangement in RBC maturation with production of abnormal precursors (megaloblasts) due to impaired DNA synthesis Normal requirement= 3microgm Causes: 1. temperate, 2. tropical, 3.addsonian pernicious 3. malabsorption addsonian is due to lack of IF

FOLIC ACID DEFICIENCY

Inadequate Intake: emesis, dietary, cooking Daily requirement- 50-100microgm, during pregnancy- 400 microgm Diminished absorption Abnormal demand; twins,infection, bleeding Failure of utilisation Diminished stores Iron defficiency anaemia

Clinical features

Pallor,glossitis,hemorrhagic patches, hepatosplenomegaly, PIH Hyper segmented neutrophils, macrocytosis,gaint polymorphs, megaloblasts, ^mcv,^mch, Pancytopenia folate,<3ng/ml S.B12<90pg/ml BM- megaloblastic erythropoises

COMPLICATIONS
Abortion, IUGR, preterm, abruption, malformation( NTD). TREATMENT Folic acid 4mg daily , till 4 months after delivery

SICKLE CELL ANAEMIA


HEREDITARY DISORDER Red cells contain Hb-s Valine for glutamic acid at 6 on beta chain Homozygous Hb-SS, .Heterozygous Hb-AS

Pathophysiology: deoxygenated state hb aggregates polymerises & distort RBC to sickle Blocks micro circulation Ppted by infection, acidosis, hypoxia & cooling Decreases life span Increased destruction- hemolysis, anemia, jaundice

DIAGNOSIS

Refactory hypochromic anemia Sickling test Persistent reticulosis High fasting fe Electrophoresis Effects on pregnancy: abortion, IUGR,fetal loss Maternal death ^ to 25% due to pulmanary infarction, CCF, embolism Effects on disease- hemolytic crisis, painful crisis

MANAGEMENT
PRECONCEPTIONAL COUNSELLING During pregnancy- anc, avoid air travelling, folate 1mg daily, fe tobe restricted, B.T. at 6 monthly intervals,hydroxyurea During labour- o2, avoid anoxia, fluids, antibiotic, Contraception- sterilisation, barrier ideal

THALASSEMIA SYNDROMES
Basic defect is reduced rate of synthesis of globin synthesis RBC with deficient Hb content Deficient erytropoises, hemolysis, ultimately anemia Alfa, beta minor / major

Beta thalassemia major (cooley anemia)


Progressive hepatosplenomegaly, impaired growth, anemia, CCF, intercurrent infection PGD, B T small Good maternal & fetal out come

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