anemia in pregnancy &role of parenteral iron therapy
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ANEMIA IN PREGNANY AND
ROLE OF PARENTERAL IRON THERAPY
Dr SUSANTA KUMAR BEHERA
SENIOR RESIDENTDEPARTMENT OF O & G
MKCG MEDICAL COLLEGEBRAHMAPUR, ODISHA; INDIA
Most Common Nutritional Disorder in the World Incidence = 40 to 60 % of pregnant women in India Commonest Medical(hematological) disorder during pregnancy 25% of direct maternal deaths Responsible for 40% of maternal deaths in third world countries. India contributes to 80% of maternal deaths due to anemia in South Asia
Pregnancy : Most dangerous journey
of mankind
Anemia begins in childhood, worsens during adolescence in girls and gets aggravated during pregnancy
Quantitative or qualitative
reduction of Hb or circulating RBC’s
or both resulting in a reduced oxygen
carrying capacity of blood to organs
and tissues
Woman Hct 33% or Hb 11g/dl – 1st &
3rd trimester and Hct 32% or Hb 10.5
g / dl in 2nd trimester(CDC/WHO)
Gm% ICMR WHO
Mild 10 – 11 10-10.9
Moderate 7 – 10 7-9.9Severe 4 – 7 <7Very severe < 4
Physiological Acquired
Nutritional deficiency anaemias - Iron deficiency (90%) - Folate deficiency - Vit. B12 deficiency
Infections : Malaria/Hookworm/UTI Hemorrhagic –acute/chronic blood loss
Bone marrow- Aplastic anemiaRenal diseases
Genetic/Haemoglobinopathies: - SCD
- Thalassaemias
COMMON ANEMIAS IN PREGNANCY
PHYSIOLOGICAL ANEMIA
• Plasma volume 50% (by 34weeks) but RBC mass only 25%
• Disproportionate increase in plasma vol, RBC vol. and hemoglobin mass during pregnancy
CRITERIA FOR PHYSIOLOGICAL ANAEMIA• Hb = 10 gm%• RBC = 3.2 million/mm3
• PCV = 30%• Peripheral smear showing normal
morphology of RBC with central pallor
IRON REQUIREMENTS DURING
PREGNANCY
Maternal req. of total Iron -1000mg
500 mg Maternal Hb. Mass
expansion
300 mg Fetus & Placenta
200mg Shed through gut., urine &
skin
2.5mg /day in early pregnancy
5.5mg /day from 20 -32 weeks
Average 4 mg/ day
6 – 8 mg/ day after 32 weeks
Increases from 1-2mg in 1st
trimester to 6-8 mg in 3rd trimester
Absorption of iron depends upon
a)Amount of iron in the diet
b)Bioavailability of iron
c) Physiological requirements
Iron sources are two types
1)Haem iron(5%) : hemoglobin
and myoglobin from red meat,
poultry and fish
2)Nonhaem iron(95%): fibers,
green vegetables
NORMAL IRON CYCLE
Dietary ironUtilization Utilization
Duodenum(average, 1 - 2 mg
per day)
Muscle(myoglobin)
(300 mg)
Liver(1,000 mg)
Bone marrow(300 mg)Circulating
erythrocytes(hemoglobin)
(1,800 mg)
Reticuloendothelialmacrophages
(600 mg)
Sloughed mucosal cellsDesquamation/Menstruation
Other blood loss(average, 1 - 2 mg per day)
Storageiron
Plasmatransferrin
(3 mg)
Iron loss
(Ferritin)
(TIBC)
FACTORS THAT MODIFY IRON ABSORPTION
Heme>Fe2+>Fe3+ Physical State
Vagotomy, pernicious anemia H2 receptor blockers, calcium-based antacids
High Gastric pH
Crohn’s disease, Celiac disease
Intestinal Structure disruption
Phytates, tannins Inhibitors
Cobalt, Lead, Strontium Competitors
Ascorbate, Citrate, Amino acids, Iron deficiency
Facilitators
EFFECTS OF ANAEMA IN PREGNANCY
ANTEPARTUMa) Pre eclampsia b) Intercurrent
infectionc) Cardiac failured) Preterm laboure) APHf) PIH
INTRAPARTUM PPH Cardiac failure Shock
POSTPARTUMa) Puerperal
sepsisb) Subinvolutionc) Failing
lactationd) Puerperal
venous thrombosis
e) Pulmonary embolism
Baby a) IUGRb)Prematurity c) Increased risk of IDA early
infancyd)Still birthse)Congenital malformationsf) ↑ in Neonatal deaths/Perinatal
mortalityg)Intra uterine deaths(severe
maternal anoxemia)h)Abnormal Social and Emotional
behaviourEFFECT OF PREGNANCY IN ANAEMIA• Pt. Mildly anemic progresses to
marked Anaemia• Pt. Who is severely anemic becomes
symptomatic by the end of 2nd trimester
IDA IN PREGNANCYa)Grandmulti b)Hook worm infestationc) Blood loss : Menorrhagia 20-30% d)Increase demand for iron
particularly in 2nd & 3rd trimestere)Higher risk with morning sicknessf) Aspirin/NSAIDSg)Multiple pregnanciesh)Intolerance for red meati) Low dietary intake (Vegetarians, Vit.
C & Calcium)j) Malabsorption (Hypo-or
achlorohydria)k)Losses can increase with colorectal
cancer, polyps
STAGES OF IRON DEFICIENCY
Prelatent(Depletion) :a) Stores are depleted without a change
in hematocrit or serum iron levels .b) Reduced stored iron e.g. serum
ferritin with normal hemoglobin Latent(iron deficient erythropoisis) : c) Serum iron drops and the TIBC
increases without a change in the hematocrit.
d) Reduced stored and transport irone) Increased erythrocyte protoporphyrin
concentrationf) Detected by a routine check of the
transferrin saturation.
Frank IDA :a)Associated with erythrocyte
microcytosis and hypochromia.b)Stage of deficiency of stored,
transport and functional ironc) Reduction of hemoglobin and
serum ferritind)Low serum transferrin saturatione) Increased erythrocyte
protoporphyrin concentrationf) Iron deficiency attracts medical
attention most commonly at this stage.
SYMPTOMS Fatigue Weakness Headache Loss of appetite Dysphagia Palpitations Dyspnea on exertion Ankle swelling Paresthesia Leukoplakia Cold intolerance irritability
CLINICAL FEATURESSIGNS Glossitis Stomatitis Heart murmurs Increased JVP Tachycardia Tachypnea Postural hypotension Pallor Dryness or roughness of the skin Koilonychia Dry & cracked lips & Brittle hair
DIAGNOSIS OF IDA Low hemoglobin Low serum ferritin<15 mcg/dl Microcytic & hypochromic in absence of chronic diseases/hemoglobinopathies Low serum iron content(< 30mcg/dL) Low PCV, MCV, MCH, MCHC High TIBC > 400 mcg/dl
Increased ZPP (>40 mmol/mole heme) Low transferrin saturation(<15%) Increased serum transferrin(>350mg/dL) Increased serum soluble transferrin binding receptors(> 8 mg/L) increased serum neopterin concentration
PENCIL CELLS
INVESTIGATIONS• Haematocrit• RBC Indices: - Low MCV
- Low MCH - Low MCHC - Low PCV• Peripheral blood
• Urine for haemturia(R&M/C&S)
• Stool examination• Hb electrophoresis• X-ray Chest(PA View)
• Serum iron < 50 μgm/dl
• TIBC is increased - > 400 μgm/dl
• Serum ferritin is < 12 μgm/dl
• Serum transferrin saturation<20%
• Red cell Zinc Protoporphyrin
• Stainable iron in the bone marrow is reduced-Gold Standard
• Serum transferrin receptor(TfR) : Increased
• Bone marrow examination.
• Reticulocyte hemoglobin conc. : Count of <26pg/ cell
• LFT, RFT
• Trial of iron therapy-diagnostic & therapeutic
TREATMENT Anaemic gravidas 120 –240mg / per day Supplementation with folic acid + Vit C. Ferrous sulphate 300mg TID daily after meals X 12 months Therapeutic results after 3 weeks – rise in Hb % level of 0.8gm/dl/ week with good compliance Rise in Hb at a rate of 2-4 gm/dl every 3 weeks till normal Hb conc. is normal after 6 wks of therapy
INDICATORS OF IRON THERAPY RESPONSE
1. Increase in Reticulocyte count (Increases 3-5 days after initiation of therapy )
2. Increase in Hb levels. Hb increases 0.3 to 1 g/ week
3. Epithelial changes (esp tongue & nail ) revert to normal
Pregnancy <30wks
Pregnancy 30-36wks
Pregnancy >36wks
IDA FA def. Oral iron Oral FA
Intolerance orNon-compliance
I/M iron I/V iron
IDA FA def.
Parenteral Oral FA
I/M iron I/V iron
Blood transfusion
ORAL IRON THERAPYWHO : 60 mg elemental iron + 250 ug FA OD/BD.
Govt. of India : 100 mg Fe + 500 ug FA during 2nd half of pregnancy X 100 days.
Drawbacks: - Intolerance - Unpredictable absorption
rate. - Not suitable for patients with GI diseases/ significant bleeding
- Non Compliant patient. - Long time for improvement
Side effectsa) Nausea & Vomitingb) Gastric irritationc) Constipationd) Abdominal crampe) Diarrhoea
Response to therapy: - Sense of well being/Increased
appetite. - Increase in Hb approximately
2gm% per every 3-4 wk - Reticulocytosis with in 5-10
days - hematocrit returning to normal
.
Enteric coated/sustained release preparations to be avoided as they are carried past duodenum limiting absorption
Once hemoglobin is normal therapy is continued for further 3 months /at least 6 wks postpartum to replenish stores.
IRON SUPPLEMENTS
Taking iron tablets
Absorption helped by vitamin-C(take the tablets with glass of orange juice)
Take before or after 1 hr of meal
Don't take tea/coffee/milk
Calcium based antacids will reduce the absorption
NEW THERAPEUTIC ALTERNATIVES
• CARBONYL Iron
• Iron ascorbate
ADVANTAGES a) Outstanding GI Tolerance
b) Very safe with no poisoning even in high doses
c) No interaction with food stuffs
d) Delicious with non-metallic taste and don’t stain the patients’ teeth
e) Compliance is very high
INDICATIONSa) Failure to oral iron therapy.b) Non compliance/intolerance to oral
ironc) 1st time seen during last 8-10 wks with
severe anemiad) Malabsorbtion/IBDe) Small bowel resectionf) When hemorrhage is likely to continueg) C/I to blood transfusionh) Combination with recombinant human
erythropoietini) C/I to oral therapy
PARENTRAL THERAPY
Intravenous preparationa) Iron dextran (Imferon)b) Iron sucrose c) Sodium ferric gluconate
(ferrlecit)
Intramuscular preparationd) Iron Sorbitol Citrate in
dextrin(Jectofer)
e) Iron Dextran (imferon) Iron dextran: 50 mg/mL. Iron
sucrose: 20 mg/mL. Ferric gluconate: 12.5 mg/mL
Contraindications a)h/o anaphylaxis to
parenteral iron therapyb)1st trimester of
pregnancyc) Active acute/chronic
infectiond)Chronic liver diseases
Advantages: - Certainty of
admission. - Hb rises @1gm/wk.Disadvantage
a) Nausea and Vomitingb) Metallic taste on
tongue
IM ROUTEIron Dextran (1ml contains 50mg elemental iron
& 1amp=2ml)Dose : 100 mg IM OD/AD till the total dose overDrawbacks:
a) Painful injection (less with jactofer).b) Skin discolorationc) Local abscessd) Allergic reactione) Fe over load.f) Category C drugg) Gluteal sarcomah) Test dose needed
AdvantageCan be given in primary care set upAbsolute reticulocyte count increases in 7 daysHemoglobin increases within 1-2 wksWhole dose can be given in single setting
I/V Route :
a)Repeated Injections
b)Total dose infusion
Side effects:
- Anaphylactic reaction.
- Chest pain, rigors, chills, fall in BP, dyspnoea, hemolysis.
Treatment:
a) Stop infusion.
b) Give antihistaminics, corticosteroids & epinephrine.
IRON DEXTRANa)Colloidal solution of ferric
oxyhydroxide complexed with polymersised dextran
b)Advantage : patients total iron requirement is given in one administration
c) Higher rate of adverse effects like delayed hypotension/ arthralgia/abdominal pain
d)Test dose is necessarye)Patients should be monitored 1
hr following a test dose of 25 mgf) Can given as IV infusion with rate
less than 50 mg/ming)Category B drug
TDI – TOTAL DOSE INFUSION
I/V : (IRON DEXTRAN)
TDI=(Normal Hb - Patients Hb) X Blood Volume(65ml/kg)X3.4
100
TDI= (Normal Hb – Pt. Hb) X Wt in Kg X 2.21+1000
TDI=[10 × (target Hb-actual Hb ) × (0.24 × bodyweight )] +0/500
Dose given I/V by slow push 100mg / day or the entire dose given in 500 ml N/S slow I/V infusion over 1-6 hours
FERRIC GLUCONATE COMPLEX IN SUCROSE
1)Given as IV injection/infusion
2)Standard dose of 125 mg may be given IV injection over 10 min
3)Rate should be < 12.5mg/min
4)Dose can be repeated if ferritin < 100ng/ml or saturation < 20%
5)Can be safely given to Dextran sensitive patients
IRON SUCROSE• Commonly used in chronic kidney
diseases• MW 34,000-60,000 D• Iron hydroxide sucrose complex in
water• Given as IV injection/infusion• Each ml contains 20 mg of Fe• After IV administration it
dissociates into iron & sucrose• T 1/2 is 6hrs
• Category B drug
• Total iron deficit = Body weight x (Target Hb – Actual Hb) x 2.4 + Iron stores [mg]
• Administered 100 mg IV over 5 minutes, thrice weekly until 1000 mg
• 200mg max dose per Sitting• Rate of administration should not
more than 20 mg/min• Infusion : 50 mg to be injected
slowly over 2 minutes, wait for 2-3 min ,then give another 50 mg over 2 min
• 100mg-200 mg to be diluted with 100ml NS, infuse at least 15 min
• Marked increase in reticulocyte count expected in 7-14 days
Advantages of IRON SUCROSE over othersa)All iron preparations were capable of
causing tissue peroxidation except iron sucrose
b)Less oxidative injuryc) Less risk of tissue parenchymal injury by
free iron.d)Higher availability for erythropoiesis
than iron Dextran e) IV iron supplementation increases the
erythropoiesis 5 timesf) Safe in dextran sensitive patientsg)Minimal side effects
The Hb rise will be evident in as early as 5 days IV iron sucrose is safe & effective Iron sucrose is given both bolus push & infusionDisadvantage
a)Total dose administered in multiple infusions
b)Needs a set up where anaphylactic reaction can be managed.
NEWEST FAST ACTING IV MOLECULES
Iron III Carboxymaltose (FERRINJECT) :
a)Ferric hydroxide carbohydrate complex which allows for control delivery of iron within cells of the RES (primarily bone marrow) and subsequently delivery to the iron binding proteins ferritin and transferin
b)T1/2 : 16 hrc) Dose : Single dose of 1000 mg
over 15 minutes (maximum 15mg/kg by injection or 20 mg/kg by infusion)
IRON III ISOMALTOSE(MONOFER)
a)Strongly bound iron in spheroid iron-carbohydrate particle providing slow release of bioavailale iron to iron binding proteins
b)Rapidly up taken by RES and little risk of free iron for tissue damage
c) Dose : 1000 mg in a single infusion
d)Erythropoietic response seen within days
e)Serum ferritin returns to normal by 3 wks
FERUMOXYTOL
USA FDA approved this drug in 2009 for iron replacement in patients with IDA & CKD
No test dose required
Can be given as large dose (510 mg/vial) in <20 Seconds in single settings
No significant side effects
Not approved in Europe
FAILURE TO RESPOND
• Non compliance• Concomitant folate deficiency• Continuous loss of blood through
hookworm infestation or bleeding haemorrhoids
• Co-existing infection• Faulty iron absorption• Inaccurate diagnosis• Non iron deficiency microcytic
anaemia
BLOOD TRANSFUSION
Decision based on • Needs and risk of developing
complications of inadequate oxygenation
• Both clinical and hematological grounds
Indications a) Severe anemia, especially after
36 weeksb) Risk of further hemorrhage c) Associated infectionsd) Imminent cardiac compromise
Patient factors Type of surgery
Preg Preg Elective
Emergency<36wks > 36wks C/S
C/S
-Hb ≤ 5gm% - Hb ≤ 6gm% - with H/o -assess
without CHF without CHF APH,PPH, according
-Hb 5-7gm%,if -Hb 6-8gm%,if previous to situation
CHF, hypoxia, CHF, hypoxia, LSCSInfection infection
Hb 8 – 10 gm%, confirm BG & cross-matching Hb <8 gm%, 2 units to be kept ready in OT
MANAGEMENT DURING LABOUR
• Consideration for delivery in well equipped hospital.
• Avoid sympathetic stimulation and hyperventilation; prevent rightward shift of ODC.
• Supplemented with oxygen therapy
• Prophylactic forceps/Vaccum to cut short 2nd stage
• Decreased blood loss by active management of 3rd stage of labors.
• Avoid maternal stress, patient can go into CHF.
• PPH should be emergently treated(uterotonics)
ANAETHETIC CONSIDERATIONS
Pre oxygenation is mandatory with 100% O2
Oxygen supplementation should be given in peri and postoperative periods
Blood arrangements prior to surgery is must
Airway maintenance to prevent fall of PO2 due to airway obstruction
Hyperventilation to be avoided to minimize respiratory alkalosis
General/spinal anaesthesia can be given after platelet count and excluding h/o spontaneous hemorrhage.
MEGALOBLASTIC ANAEMIA
• Incidence – 0.2 – 5 %• Caused by folic acid deficiency &
Vit B12 deficiencyPathophysiologyPreg. Causes 20 -30 fold increase in
Folate requirement (150-450 microgram / day ) to meet needs of fetus & placenta.
Placenta transports folate actively to fetus even if the mother is deficient.
Vit.B12 deficiency : Occurs in patients with gastrectomy , ileitis, ileal resection, pernicious anaemia, intestinal parasites
FOLATE DEFICIENCY ANAEMIA
Folic acid reduced to DHFA then THFA, used in nucleic acid synthesis, 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.
Coexists with IDA
Folic acid deficiency more likely if. Woman taking
anticonvulsants.. Multiple pregnancy.. Hemolytic anemia,
thalassemia & cleft palateDiagnosis :
-Increased MCV ( > 100 fl)-Peripheral smear : -
Macrocytosis, hypochromia - Hypersegmented
neutrophils(> 5 lobes)
- Neutropenia - Thrombocytopenia
-Low Serum folate level.(<3ng/ ml)
-Low RBC folate (<20 ng/ml)
CLINICAL FEATURES• Insidious onset, mostly in last
trimester• Anorexia and occasional diarrhea• Pallor of varying degree• Ulceration in mouth and tongue• Glossitis• Enlarged liver and spleen• Hemorrhagic patches under the
skin and conjunctiva• Macrocytic Megaloblastic Anemia• Peripheral neuropathy• Subacute combined degeneration
of the Spinal cord
a)Hb < 10gm%b)Hypersegmentation of neutrophilsc)Megaloblast, Howell-Jolly bodiesd)MCV > 100 fle)MCH > 33pg, but MCHC is Normalf) Serum Fe is Normal or high, TIBC is
lowg)Serum Vit B12 levels < 100 pg /mlh)Radio active Vit B12 absorption
test (Schilling Test)
DIAGNOSIS
MEGALOBLASTIC ANEMIA(PS)
MEGALOBLASTIC ANEMIA(BM)
TREATMENT
• Replace iron and treat underlying disease.
• Oral route is preferred for replacement.
• Response can be followed by retic. increase in 1-2 weeks (5-7 days)
• Hb response to treatment– half normal by a month– returns to normal by 2-4 months
• Replacement therapy is prolonged by 6-12 months to replenish stores of iron.
• 1000 microgram Parenteral Cyanocobalamin every wk X 6 weeks
• Prophylactic : All woman of reproductive age should be given 400mcg of folic acid daily
• Curative : Daily administration of Folic acid 4mg orally up to at least 4 wks following delivery
HAEMOGLOBINPATHIESSickle cell disease a)Sickle cell anaemia (most
common & severe) b)Sickle cell beta
thalassemia,c) Haemoglobin SC diseaseThalassemia - Alpha thalassaemia. - Beta thalassaemia: .
Major .
Minor
SICKLE CELL ANAEMIA
• Valine substituted for glutamic acid at 6th position on β chain of Hb molecule
• Common variants - SS ( sickle cell anemia)
- SA ( sickle cell trait) Hb SS Hb SA
Cell trait Homozygous HeterozygousHbS 70 – 90%,
rest HbF10 – 40%, 40-60% HbA
Hb (g/dl) 6 - 9 13 -15Life expectancy
30 yrs normal
Propensity for sickling
++++ + (O2 falls < 40%)
SIGNS & SYMTOMSVaso-occlusive
complications a)Painful episodes-most
common(50%) b) Acute chest
syndrome(20%) c) Strokes d) Renal insufficiency e) Splenic sequestration f) Proliferative
retinopathy g) Priapism h) Spontaneous abortion i) Bone pains, leg ulcers,
Osteonecrosis
Complications related to hemolysis a) Anemia (Hct 15 – 30%) b) Cholelithiasis c) Acute aplastic episodesInfectious complications a) Streptococcus pneumonia
sepsis b) E.coli sepsis c) OsteomyelitisDIAGNOSIS• Hb solubility test-specific, cheap,
rapid and simple.• Sickling test• Hb electrophoresis,
MANAGEMENT Multidisciplinary approch Routine BP measurement and urinalysis
to detect hypertension and proteinuria Retinal screening/fundoscopy for
prliferative retinopathy Screening for iron overload(serum
ferritin) Screening for PAH by echocardiography Antibiotic
prophylaxis-penicillin/eruthromycin Termination planned for homozygous
state
Folic acid-5 mg should be given OD preconceptually and throughout the pregnancy
Hydroxurea if taking should be stopped 3 months prior conception
ACE inhibitors & angiotensin receptor blockers stopped before conception
Early detection and treatment of malaria and infections
Low dose Aspirin from 12 wks of gestation
Thromboprophylaxis with LMWH NSAIDS between 12 to 28 weeks Fluid and oxygen therapy(oxygen
saturation > 95%) in painful crisis BT indicated only during
complications like acute anemia/ACS/twin pregnancies, preeclampsia, septicemia, renal failure
Goals : Hb > 8gm/dl & HbA > 40% of total Hb
Iron therapy to be given if there is evidence of iron deficieny
• Vaccine : H influenza type b, conjugated menigococcal C vaccine, peneumococcal vaccine & Hepatitis-B vaccine
• Timing of deliver : 38 -40 wks of gestation either by induction of labour/elective CS
• Factors to be avoided favouring sickling
- Dehydration - Hypotension - Hypothermia - Acidosis - High conc. of HbS
CS is preferred over vaginal delivery when labour is not progressing well.
Continuous FHR monitoring due to increases rate of still births/abruption/compromosed placental reserve
Counseling the parents regarding partner screening for carrier detection.
Contraceptivesa) Porgesterone only pillb) Injectable contraceptivesc) LNG-IUS d) Barrier methodse) Sterilization
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• Microcytic haemolytic anaemias• Reduced synthesis of one or more
of polypeptide globin chains.• Higher transfusion requirements in
pregnancy worsen haemosiderosis & cardiac failure.
CLINICAL FEATURES• Usually asymptomatic
• Weakness, fatigue, exhaustion, loss of appetite, indigestion, giddiness, breathlessness
• Palpitations, tachycardia, breathlessness, increased cardiac output, cardiac failure, generalised anasarca, pulmonary edema
a) Pallorb) Nail changesc) Cheilosis, Glossitis, Stomatitisd) Edemae) Hyperdynamic circulation (short & soft
systolic murmur)f) Fine crepitations
Women with hemoglobinopathy should be offered oral iron therapy if serum ferritin<30 mcg/L
Referral to secondary/tertiary care to be done if
a)Severe anemia
b)Significant symptoms
c) Late gestation(34 wks)
d)Failure to respond to oral iron
TREATMENT
WHO - 60 mg Elemental iron + 400 micro gram Folic acid / day up to 3 months postpartum
GOI - 60 mg elemental Iron + 500 mcg Folic acid as Prophylactic supplementation x 100 days in 2nd trimester up to 3 months postpartum
ANAEMIA ASSOC. WITH CHRONIC INFECTIONS / DISEASE
• Common in developing countries• Poor response to Haematinics
unless primary cause is treated• Worm infestations is common
( Diagnosed by stool examination )• Urinary tract inf, & asymptomatic
bacteriuria in preg. is assoc. with refractory anaemia
• Chronic renal disorders = due to erythropoietin def.
• Identifying the etiology and treat accordingly
• Deworming with mebendazole/albendazole/levamisole
• Treated with recombinant Erythropoietin for renal disease.
• ATT to a patients with tuberculosis
• Antibiotics to treat UTI according to sensitivity
TREATMENT
PREVENTION
• Dietary advice and modification(red meat/ poultry/fish)
• Germination and fermentation of cereals and legumes improve the bioavailability of iron in food
• Green peas/Whole wheat/Green vegetables/Jaggery
• Iron supplementation of adolescent girls & non pregnant women
• A nutritious diet in a pregnant woman should be providing about 40 mg elemental iron daily.
• Food fortification
a)Fortification of staple food like wheat flour which is technically simple(USA)
b)Fortification of curry powder, salt and sugar, dried and liquid milk(SA)
c) Fortification of infant foods (INDIA)
d)Fortification of complimentary foods (USA)
Treatment of hookworm Infestation, malaria,TB
Avoidance of Hypoxia, Acidosis, Infection, Dehydration Stress , Exercise, Extreme, Temperature
Avoidance of frequent child birth.
Supplemented Viamin-C (250-500mg/day) with iron
Adequate treatment for any infection like UTI
Early detection of falling Hb level, levels should be estimated at 1st A/N visit, 30th & finally 36th week
Mandatory monthly screening for anemia should be done in all antenatal clinics(especially at booking and at 28 wks with FBC)
Screening and effective management of obstetric and systemic problems in all pregnant women
THANK Q
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