ANAEMIA IN PREGNANCY.ppt

1,516 views 81 slides Jan 11, 2024
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About This Presentation

Anemia in pregnancy


Slide Content

ANEMIA
IN
PREGNANCY
M.mounika
Scon

Definition of Anemia during Pregnancy.
Anemiaisreductionintheoxygencarrying
capacityoftheblood,whichmaybedueto:
-reducednumberofredbloodcells
-lowconcentrationofhemoglobin,or
-combinationofboth
WHO:11gm/dlorless

Incidence
40-80% in tropics
10-20% in developed countries

Degree of anemia
Mild –between8-10g%
Moderate-<than8-7g%
Severe-<than7g%

causes of Anemia
Ironloss:sweat,repeatedpregnancy,hookworm
infestationandmalaria
Faultyabsorptionmechanism:duetohigh
incidenceofintestinalinfestation,thereisintestinal
injury
Faultydiethabit:richcarbohydrateandhigh
phosphateindietreduceabsorptionofiron

Increase iron demand
Diminished intake of iron
Disturbed metabolism( depressed erythropoietic
function)
Pre-pregnancy health status
Excess demand(multiple pregnancy, rapid recurring
pregnancy, teen pregnancy)

Classification
Physiologic
Pathologic:
a. Deficiency: Iron, Folic Acid, Vitamin B12
b. Hemorrhagic: APH, Hookworm
c. Hereditary: Thalassemia, Sickle cell haemoglobinopathies ,
Hereditary Hemolytic Anemia
d. Bone Marrow Insufficiency: Aplastic Anemia
e. Infections: Malaria, TB
f. Chronic Renal Diseases or Neoplasm.

Concept of Physiologic Anemia
Disproportionateincreaseinplasmavol,RBC
vol.andhemoglobinmassduringpregnancy
Markeddemandofextraironduring
pregnancy.

Criteria for Physiologic Anemia
Hb:10gm%
RBC:3.2million/mm3
PCV:30%
Peripheralsmearshowingnormalmorphology
ofRBCwithcentralpallor
Erythropoesis
Ironrequirementinpregnancy

Iron Deficiency Anaemia
Causes:
poor intake:
-diet deficient in iron
poor absorption:
-vomiting in pregnancy affects absorption
-increased ph of gastric juices
-ferric ions in gut instead of ferrous
-lack of vitamin c

increaed utilization:
-demands of pregnancy
multiple pregnancy
grand multiparity
pregnancies close together
vegetarians

Clinical features:
Symptoms:
fatigue
drowsiness
Weakness
Dizziness
Headache
Malaise
Pica
Poor appetite
Changes in mood
Change in sleep pattern

Signs:
pallor
Jaundice
Orthostatic hypertension
Peripheral edema
Pale mucous membrane and nail beds
Smooth and sore tongue
Glossitis
Stomatitis
Spleenomegaly
Tachycardia or flow murmur
Tachypnea,Dyspnea on exertion

pallor

Conjunctival Pallor

Koilonychia

Smooth Tongue

Investigation
Hematologicalvalues
Haemoglobin(lowlessthan10g%)
Totalredcellcount(low<4million/mm3)
PCV(<30%)
MCVdecreased<75um3)
MCHdecreased<25pg
MCHCdecreased<30%
Sr.irondecreased<30ugper100gm

Sr.ferritindecreased<15ug/l
Sr.folatenormal
Marrowdecreasedironstore
Bloodfilm(peripheralbloodsmearstainedwithleishman
stain)
redcells:
Sizenormal
Hypochromia
anisocytosis+
poikilocytosis+
Whitecellsnormal

Examinationofstool(helminthic(hookworm
)infestation
Urineforprotein,sugar,puscells,culture,colony
count>10.5/mlinfection
ChestXray(PTB)
SR.protein(hypoproteinemiaorosmoticfragility
inhereditaryspherocytosisorheamoglobinopathic
disorders

Treatment
Preventive:-
Regularironbearingfoodindiet
Animal(redmeat,whitemeat,fish,egg)
Plant(lentils,darkgreenleafyvegetables,beans,wholewheat,green
plantains,onionstocks,jaggery.
Ironandfolicacidsupplements
Avoidfrequentchildbirth
Eradicatehookworminfestation,treatdysentery,malaria,bleeding
pilesandUTI
Earlydetectionoffallinghb

Curative:
generaltreatment:
dietrichiniron,proteinandvitamins
acidpepsintds(improvesappetiteanddigestion)
prophylacticantibiotictherapy(avoidsepticfocus)
specifictherapy:
oraltherapy
parenteraltherapy
intramusculartherapy
bloodtransfusion
exchangetransfusion

Treatment
Specific therapy
The principleis to raise the HB level as near to normal as
possible before mother goes in Labour
Choice of therapy depends on
Severity of anemia
Duration of pregnancy
Associated complicating factors
Iron Therapy
Oral Therapy
Parenteral Therapy

Treatment
Oral Therapy
Aim of the treatment is to get the maximum benefit in the
minimum possible time.
Cap. Ferrous Sulphate 200mg 3 times a day along with food helps in
absorption.
Disadvantages
Intolerance ( Evidenced by epigastic pain, nausea, vomiting &
Diarrhea or constipation)
Unpredictable absorption rate (Small percentage of the iron given is
absorbed and utilized for haemoglobin formation. Antacids, oxalates
& Phosphates will reduce absorption, Ascorbic Acid, lactate & various
amino acids-increase absorption)

Treatment
Parenteral Therapy:
It includes IM and IV
IV therapy includes repeated injections, total dose infusion. (TDI)
Indications of Parenteral Therapy.
Contraindications of oral therapy (Intolerance & Severe Anemia)
Mother is not co-operative to take oral iron
Severe Anemia
Advantages
Increase the iron storage
Expected rise in the Hb. Concentration after Parenteral therapy is 0.7 to 1gm/100 ml
per week

Treatment
TDI
CalculatetheIrondeficit.
Irondextron1mlcontains50mgofelementalIron
Theinjectionshouldbegivenslowly
Takingcarenottoinfiltrateintosurroundingtissues
Morethan200mgatatimeisnotrecommended.

Advantages
Iteliminatesrepeated&painfulintramuscularinjections
treatmentiscompletedinaday&mothermaybedischarged
muchearlier.
LesscostlycomparedtotherepeatedIMtherapy.
Disadvantages
MaximumHb.responsedoesnotappearbefore4to9weeks(
Methodisunsuitableifatleast4weekstimeisnotavailable
.Mostlysuitable30-36weeksofpregnancy)
Previoushistoryofreactioniscontraindicated

Pre requisites
Correct Diagnosis
Adequate Supervision
Facilities for management of anaphylactic reaction.

Procedure
Themotherisadmittedinthemorningforinfusion.
Therequiredironismixedwith500mlof0.9%saline
Dividethedose1stdaystartwith50mg,2
nd
day100mg,3
rd
day200mg
andfromthenoneveryotherday200mgtilltheirondeficitismade
good.Morethan200mgatatimeisnotrecommended.
Precautionslikethoseofbloodtransfusionaretobetakenbothpriorto&
duringtheinfusionprocess.
Thedriprateshouldbe10dropsperminuteduringthefirst20mts.&
thereafterisincreasedto40dropspermt.
Anyadversereactionlikerigor,chestpainorhypotension–stopthedrip

Intramuscular Therapy
The compounds used are
Iron dextran (Inferon) 50 mg.
Iron sorbitol citric acid complex is dextrin (Jectofer) 50
mg
Total dose to be estimated.

Procedure for injection
Test dose 1 ml injection , watch for 20 to 30 mts any anaphylactic
reaction then administered full dose
Prevent dark staining of skin
Use ‘Z’ technique
Oral Iron should be stopped at least 24hrs prior to therapy to avoid
reaction.
Disadvantage
The injections are painful
Chance of abscess formation & discoloration of the skin

Blood Transfusion
Indications:
Tocorrectanemiaduetobloodloss
Motherwithsevereanemiaseeninbeyond36weeks
Anemianotrespondingtoeitheroralorparenteraltherapy.
Advantages
Increaseoxygencarryingcapacityoftheblood
Stimulateerythropoieses
Suppliesthenaturalconstituentsofbloodlikeproteins,
antibodiesetc
Improvementisseenafter3days

Disadvantages
Prematurelaborduetobloodreaction
Thereisincreasedchanceofcardiacfailurewith
Pulmonaryedema.
Precautions
Antihistaminic(Phenargan25mg)
Diuretics(Frusemide20mg)IM.
Driprateshouldbe10drops/mt
Monitorpulse,respiration

Nursing Management
Assessment
Nutritional History
Client Education
Nutritional counseling
Serum Ferrites levels should be obtained after the 20
th
week. It
should be repeated 6 to 8 weeks intervals.
7 days diet history is taken to evaluate the pregnant women's
general nutritional status & the quantity of iron available through
nutritional sources

Complications
MaternalriskduringAntenatalperiod:
Poorweightgain
pretermlabor
PIH
placentaprevia
Accidentalhemorrhage
Eclampsia
Prematureruptureofmembrane.

MaternalcomplicationduringIntra-natal
period:
Dysfunctionallabor.
Intra-natalhemorrhage.
Shock.
Anesthesiarisk.
Cardiacfailure.

Postnatal period:
postnatal sepsis
Sub involution
Embolism.

NEONATAL AND FETAL COMPLICATIONS
Prematurity
Low birth weight.
Poor APGAR
Fetal distress
Failure to thrive
Poor intellectual development
Higher rates of morbidity.

Megaloblastic Anemia
ItisastatewhereimpairedDNAsynthesis,resultsinderangement
inRedCellmaturationwithproductionofmegaloblast(abnormal
precussor)frombonemarrow.
ItmaybeduetodeficiencyofVitB12orFolicAcidorboth.
MegaloblasticanemiainpregnancyisalmostalwaysduetoFolic
Aciddefeciency.
VitaminB12defeciencyisrareinPregnancybecozitsneedisless
inamountanditismetwithanydietthatcontainsanimalproducts.

Vitamin B12 deficiency
CAUSES:-
gastrectomy
ileal resection(crohn’s disease)
pernicious anaemia
Addisonian pernicious anemia(auto immune disease –lacks
intrinsic factor –lack of vitamin B12 absorption)

Folic acid deficiency
Definition:-
Leadstoreductionincellproliferationduetolackof
nucleicacidformation.
Causes:-
Inadequateintake
-dietdeficientinfolates
-vomitinginpregnancy
Increasedutilization
-demandsofpregnancy
-rapidgrowthoffetal,placentalanduterinetissues.

Diminished absorption
-gastro –intestinal upsets
-oral antibiotics
-intestinal malabsorption syndrome(gluten induced enteropathy i.e.
coeliac disease.
Excessive demand
-multiple pregnancy
-multiparity
-rhesus incompatibility(fetal hemolysis)
-infection(reduces life span of red cellsand increases demand of folic
acid)
-maternal haemorrhagic condition(peptic ulcer, hookworm infestation

-maternal hemolytic condition(malaria, sickle cell anemia,
thalassaemia
Diminished utilization
-analgesics
-antibiotics
-anticonvulsant drugs
-sulfasalazine
-methotrexate
Diminished storage
-hepatic disease
-vitamin c deficiency,Iron deficiency anemia

Sign and symptoms
Insidiousonset,mostlyinlasttrimester
Tired,breathlessness,oedema,protractedvomiting
Anorexiaandoccasionaldiarrhoea
Pallorofvaryingdegree
Ulcerationinmouthandtongue
Hemorrhagicpatchesundertheskinandconjunctiva
Enlargedliverandspleen(jaundice)

Angular Cheilosis

Blood values
Hb<10gm%
Blood film(any two)
Hypersegmentation of neutrophils
Macrocytosis and anisocytosis
Giant polymorphs
Megaloblast
Howell-jolly bodies
MCV>100micrometer3
MCH>33pg, but MCHC is Normal
Serum Fe is Normal or high

TIBC is low
Leucopenia
Thrombocytopenia
Sr. folate is less than 3ng/ml
Sr.B12 < 90pg/ml
Sr.bilirubin raised
Bone marrow-megaloblastic erythropoiesis

Treatment
Prophylactic
-allwomanofreproductiveageshouldbegiven400mcgof
folicaciddaily
Curative
-dailyadministrationofFolicacid4mgorallyforatleast4
wksfollowingdelivery
-vitaminB12100ugim/day
-ascorbicacid100mg

complications
Megaloblastic anemia:-
Abortion
Dysmaturity
Prematurity
Abruptio placentae
Fetal malformation
Heart failure
Pancytopenia(low WBC & platelet count)
IUGR

Vitamin B12 deficiency:-
Neuropathy involving peripheral nerves and spinal
cord
Psychiatric disturbances
Visual disturbance
Fetal neural tube defects

Dimorphic anemia
Definition:-
anemiathatresultsfromdeficiencyofbothiron&folic
acidorvitaminB12(polydeficiencystate)
Causes:-
-dietaryinadequacy
-intestinalmalabsorption

Investigations:-
Red cells-
macrocytic/normocytic
hypochromic/normochromic
Bone marrow
-megaloblastic
Treatment:-
iron and folic acid in therapeutic doses

Aplastic anemia
Definition :-
it is a condition where bone marrow does not produce sufficient new cells to replenish
blood cells resulting in marked decrease in marrow stem cells(i.e.production of erythrocytes,
WBC’s, platelets fails)
Causes:-
Acquired:
unknown
immunologically mediated
autosomal recessive inheritance

Exposure to ionizing radiation
Chemical agents
Idiosyncratic reactions to drugs (chloramphenicol or quinacrine)
Infections –viral or bacterial(infectious mononucleosis, infectious
hepatitis, cytomegalovirus infections & miliary tuberculosis)
Pregnancy
Paroxysmal nocturnal hemoglobinuria
Others-preleukemia and carcinoma
Congenital
Fanconi’s anemia

pathophysiology
Reductionordepletionofhematopoieticprecursorstemcells
leadstoperipheralpancytopenia.dueto:-
-quantitativeorqualitativedamagetopleuripotentstem
cells
-abnormalhormonalstimulationofstemcellproliferation
-defectivebonemarrowmicroenvironment
-cellularorhumoralimmunosuppressionofhematopoiesis

Clinical features
Fatigue
Heart palpitations
Pallor
Infections
Petechiae
Mucosal bleeding
Tachycardia
Fever
Painful ulceration of throat

Investigations
Blood:
Pancytopenia(anemia, leucopenia, thrombocytopenia)
lymphocytosis
Normocytic,normochromic RBCs
Anisocytosis
Poikilocytosis
Decreased RBC
Hypocellular bone marrow
Biopsy:
empty bone marrow

Treatment
Repeatedbloodtransfusion(tomaintainhct>20)
Granulocytetransfusion(combatinfection)
Platelettransfusion(controlbleeding)
Packedredbloodcells
Glucocorticoidtherapy(corticosteroids)
Bonemarroworstemcelltransplantation
Antithrombocyteantibody
Immunosuppressiveagents

complications
Increased fetal wastage
Prematurity
Intrauterine fetal demise
Increased maternal morbidity
Death due to infection and haemorrhage

Haemolytic anemia
Definition:-
itisabnormalbreakdownofredbloodcells
(RBCs)eitherinbloodVessels(intravascular
hemolysis)orelsewhereinthebody(extravascular)
Classification:
hereditary(inherited)
acquired

causes
Hereditary:-
defects in haemoglobin production(thalassemia and sickle
cell disease
defects of red blood cell membrane production(hereditary
spherocytosis & hereditary elliptocytosis)
defective red cell metabolism(G6PD & pyruvate kinase
deficiency)

Acquired:-
immune mediated
transient factors –mycoplasma pneumoniae infection(cold agglutinin
disease)
permanent factors –autoimmune(SLE, chronic lymphocytic
leukemia)
Hyperspleenism(portal hypertension)
burns
Infection
Runners(footstrike hemolysis) venous destruction of RBC at foot.

Clinical features
Pallor
Fatigue
Shortness of breath
Heart failure
chronic hemolysis( excretion of bilirubin
–gallstones)
Continuous release of haemoglobin (PHT-Syncope, chest pain,
breathlessness-RHF,ascites, peripheral edema)

Investigation
Peripheral smear microscopy
Fragments of red blood cells(schistocytes)
RBC smaller and rounder(spherocytes)
Elevated reticulocytes
Elevated unconjugated bilirubin
Increased LDH
Decreased haptoglobin
Positive direct coomb test

Urine testing
Presence of hemosiderin
Urobilinogen

Treatment
Stop use of offending drug
Corticosteroids(prednisone)
Iv immunoglobulin infusion
Immuno suppressive(azathioprine &
cyclophosphamide)
Erthyropioetin( to increase RBC production)
Splenectomy(extra vascular hemolysis)

Hemoglobinopathies
Aninheritedmutationoftheglobingenes
leadingtoaqualitativeorquantitative
normalityofglobinsynthesis.

Classification
Mutation causing qualitative
abnormality(sicklecellanemia)
Quantitativeabnormality(Thalassemias)

Abnormal hemoglobin synthesis
Production of structurally normal but decreased amount of globin
chains(Thalasemia)
Production of structurally abnormal globin chains(hemoglobin s, c
and e)
Failure to switch globin chain synthesis(herditary persistence of
HBF)
-Autosomal co-dominant disorders

Thalassaemia
Hereditaryabnormalityofhemoglobinproductionwherethe
primarydifficultyisquantitativedeficiency-eitherbetaglobin
leadingtobetathalassaemiaoralphaglobinleadingtoalpha
thalassaemiai.egeneticdecreseinglobinchainsynthesis.

Alpha thalassaemia
Deletionofoneormorealphagenesfrom
chromosome16.

Beta thalassaemia
Bchainproductionisdecreasedandexcessofalpha
chainsprecipitatetocauseredcellmembranedamage
i.eonlytwoglobingenesoneoneachchromosome
11.
B+genemutationcausepartialblockinBchain
synthesis
BzerogenemutationcausesabsenceofBchain
production.

SicklecellHemoglobinopathy
Hbscomprises30-40%totalHb
ThereissubstitutionofLysineforglutamicacidatthesixth
positionofBchainofHb
Redcellsinoxygenatedstatebehavenormally,butin
deoxygenatedstateitaggregates,polymerisesanddistortred
cellstosickle.
Thesecellsaremorefragileandincreaseddestructionleadsto
hemolysis,anemiaandjaundice.

Effects on pregnancy
Increaseincidenceofabortion,prematurity,IUGR
andFetalloss.
Perinatalmortalityishigh.
Incidenceofpre-eclampsia,postpartumhemorrhage
andinfectionisincreased.

Management
Carefulantinatalsupervision
Airtravellinginunpressurisedaircrafttobeavoided.
ProphylaticallyFolicA.1gmdaily.
Regularbloodtransfusionatapprox.in6weeks
interval
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