ANAEMIA IN PREGNANCY

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

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

CLASSIFICATION

PHYSIOLOGICAL ANEMIA
PATHOLOGICAL


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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
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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


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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

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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



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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
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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


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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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