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8/13/2019 Anemia in Obs-gyn
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ANEMIA IN OBSTETRI
Sulchan Sofoewan
Departement of Obstetrics and
Gynecology Faculty of MedicineGadjah Mada University
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Pendahuluan
Eropa Amerika Afrika As-teng Total
1019
4657
35.6
Prevalensi Anemia Dunia ( )
WHO, 2000
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ANEMIA IN PREGNANCY
Definition:
Non pregnant : Hb < 12g/dl
Pregnant : Hb < 10g/dl
Hb concentr lower in midpregnancy
In early and near term : 11g/dl
CDC criteria: anemia as less than 11g/dl inthe 1stand 3rdtrim, and less than 10,5g/dl
in the 2ndtrim
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PHYSIOLOGICAL ANEMIA
Fall in Hb level during pregnancy causedby a relatively greater expansion ofplasma volume compared with theincrease in Hb mass and red cell volume,called hydremia / hemodlution
The disproportion between the rates atwhich plasma and erythrocyte are added
to the maternal circulation during the 2ndtrim
The long-used term: physiological anemia
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HYDREMIA/HEMODILUTION
During 10 weeks of pregnancy to 7 day
after delivery:
Plasma : 30%
Red cells : 18%
Hb : 19%
Cause: physiological anemia
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THE ADVANTAGES OF
HYDREMIA
The need of circulation is fulfilled
To decrease the function of heart
To decrease the peripheral resistency To minimized the iron loss during
hemorrhage
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THE PREVALENCE OF ANEMIA
Pregnant women : 50.9%
Young persons : 57.1%
Child schools : 47.2% Under 5 yrs child : 40.5%
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Prevelansi
Di US: 5-10% wanita 20 to 44 th menderita defisiensibesi
Lebih tinggi, pada kelompok berisiko: Wanita hamil, apalagi berulang dengan interval pendek
Paritas tinggi Soial ekonom dan edukasi rendah
Wanita dengan riwayat menoragi
Kehamilan ganda
Diet rendah daging dan vitamin C
Donor darah lebih dari 3 kali per tahun
Adolesent
Pengguna aspirin
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Prevalensi anemia di Indonesia, 1995 (%)
Semua Wan hamil Pra sekolah
35.9
63.555.5
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THE INFLUENCES OF ANEMIA
TO THE PREGNANCY, DELIVERY
AND PUERPURIUM
To increase the morbidity and mortality ofmaternal and perinatal
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CLASSIFICATION OF ANEMIA
Iron deficiency anemia
Megaloblastic anemia
Hypoplastic anemia Hemolytic anemia
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IRON DEFICIENCY ANEMIA
Iron deficiency anemia:
The most common anemia in pregnant
women, especially in the 3rdtrim
Iron metabolisme depend on dynamic
equilibrium
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DYNAMIC EQUILIBRIUM
Influenced by:
Hb destruction
Up take of bone marrow for Hb synthesis Utilization / deposition in the tissue
Absorption in the intestine
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Fisiologi perubahan kadar
hemoglobin selama kehamilan Perubahan fisiologis volume intravaskular
Volume plasma meningkat 50-70 %
Mulai minggu ke 6, puncak ke 32, plato sampaipersalinan
Sel darah merah meningkat 20-35 %
Mulai minggu ke 12
Kenaikan vol plasma melebihi sel darah merahhemodilusi
Ameneorea dan kenaikan absorpsi besi dan folat
menaikan cadangan besi
Penurunan fisiologis kadar hemoglobin dan hematokrit
Anemia: penurunan lebih dari 2 SD
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Sumber besi
Jenis besi diet Penghambat
absorpsi
Penguat absorpsi
Heme iron Highbioavailability): daging danjeroan
Kalsium dan
mangane yang ada
dalam diet sehari-
hari
Protein sehari-hari
Nonheme iron Lowbioavailability): daun-
daunan, produk makanan
dan garam yang
difortifikasi besi,kacang-
kacangan, buncis, bayam,lobak, kentang, labu,
pisang, strawberi, cherries,
melon dll
Tanin (teh, kopi
dan coklat)
Asam fitat (biji-
bijian, kacang-
kacangan, beras)
Serat, proteinkedelai
Protein, asam amino
Asam yang mereduksi
feri ke fero: asam
askorbat (tomat dan
jeruk), asam sitrat,
malat , laktat dantartarat
Hasil fermentasi:
yoghurt
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Elemen Besi
Iron Salt Elemental Iron
Content
Required to Provide
30 mg of Iron
Ferrous sulfate 20% 150 mg
Ferrous sulfate, dry 30% 100 mg
Ferrous gluconate 12% 250 mg
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Diagnosis
Klinis: tanda dan gejala klinis
Laboratori
Hemoglobin dan hematokrit turun
Mikrositosis dan hipokromia
Feritin serum turun (
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Terapi
Tujuan: 1. koreksi hemoglobin dan cadangan besi
2. memperbaikipregnancy outcome
Sifat: preventif atau kuratif Preventive: optimasi intakebesi & suplementasi rutin besi
Kuratif: hanya diberikan pada wanita hamil dengan anemiaatau cadangan besi rendah
Women with prepregnancy ferritin levels >20 mg/L didnot have a marked decline in serum ferritin throughoutthe course of pregnancy in contrast to
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PROT BOUND IRON & TOTAL
IRON BINDING CAPACITY
Prot bound iron (BI):
90120 ug / 100ml
Total iron binding capacity (TIBC): 300360 ug / 100 ml
Iron deficiency anemia:
BI : decrease TIBC : increase
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IRON LOSS DURING DELIVERY
Newborn : 400 mg Placenta : 150 mg
Hemorrhage : 200 mg
Lactation / day : 1,5 mg Total : 750 mg
Hb: 0.245 Fe= 34 mg Fe, Iron loss during
delivery 220 g Hb or 39% from Hb levelbefore
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CAUSE OF IRON DEF ANEMIA
Decrease iron intake
Intestinal absorption disturbence
Ancylostomiasis Hemorrhage
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TX OF IRON DEF ANEMIA
60 mg Fe + 400 ug folic acid / day is better
than:
1. Folic acid only
2. Folic acid + Fe + Zn 30 ug
3. Folic acid + Fe + Zn + 11 micronutrients
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THE INFLUENCE OF
SUPLEMENTATION
To decrease the prevalence of anemia in
3rdtrim
To decrease the prevalence of anemia in 3
months after delivery
To increase ferritin in newborn
The length and Apgar score of the
newborn more higher than the placebo
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SOLVE THE ANEMIA PROBLEM
IN INDONESIA
1950 the focus efforts to the pregnant
women
1970 through the UPGK in the primary
health care
Suplementation of : Fe; Fe + folic acid and
promoting of health and nutrition,
especially to the women workers
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THE RESULTS OF EFFORTS
1996 the prevalence of iron deficiencyanemia 63,5%
Cause of fail:
Incontinuity of intake iron tabletsconsumption
Low animal protein consumption
Iron deficiency The low of role of micronutrients
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Program Penanggulangan
Anemia Ibu Hamil
Program suplementasi zat besi belum
berhasil menurunkan anemia
Rendahnya kepatuhan minum tablet besi
merupakan kendala utama
Alasan tidak patuh:
Kebanyakan lupa
Efek samping yang tidak disukai
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CAUSES OF ANEMIA DURING
PREGNANCY
Acquired
Iron-def anemia
Acute blood loss Inflammation or malignancy
Folic acid def/megaloblastic anemia
Hemolytic anemia Aplastic/hypoplastic anemia
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CAUSES OF ANEMIA DURING
PREGNANCY
Hereditary
Thalassemias
Sickle-cell hemoglobinopathies
Other hemoglobinopathies
Hereditary hemolytic anemias
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EFFECT OF ANEMIA ON
PREGNANCY
Increased risk of :
Abortion
Preterm IUGR
Stillbirth
Obstetrical hemorrhage Maternal deaths
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Efek anemia terhadap ibu
Mudah lelah
Kinerja menurun (10% vs 5%)
Stres kardiovaskular (hb dan saturasi oksgen rendah)palpitasi, sesak nafasdekompensasi jantung
Tidak tolerans thd kehilangan darahshockhemoragikMMR meningkat
Kesulitan persalinan: partus lama, partus dengantindakan
Infeksi postpartum meningkat Transfusi meningkatrisiko tertular penyakit
Muncul setelah kadar Hb turun di bawah 7-8 g/dL
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Efek terhadap janin dan neonatus
Dasar: berkurangnya pasokan oksigen ke
rahim, plasenta dan janin
Efek: Persalinan preterm, BBLR &JMDR
(Evidence: II-b)
Ibu hamil dengan defisiensi besi tidak
menaikkan risiko kelahiran janin dengan
defisiensi besi
Plasenta menyediakan cukup cadangan besi untuk
janin
Delayed cord cramping (3 menit) menaikkan
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IRON-DEFICIENCY ANEMIA The two most common causes of anemia during
pregnancy and the puerperium: iron deficiencyand acute blood loss
Associated with poor nutritional status
Maternal need for iron induced by pregnancy
average: 800 mg, about 300 mg for the fetusand placenta and about 500 mg for maternal Hbmass expansion and about 200 mg are shedthrough the gut, urine and skin
This total amount 1.000 mg exceeds the ironstores
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Continue
With the rather rapid expansion of blood
volume duing second trimester, iron
deficiency is often manifested
In the third trimester, additional iron is
needed to augment maternal Hb and for
transport to the fetus.
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DIAGNOSIS
Classical morphological evidence of irondeficiency anemia: erythrocyte hypochromia andmicrocytosis is less prominent in the pregnantwoman compared with that in the pregnant
woman
Initial evaluation of a pregnant woman withmoderate anemia should include measuremantof Hb, Hmt and red cell indices, serum iron,ferritin.
Serum ferritin
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TREATMENT OF IRON-DEF The objective of treatment:
1. correction of the deficit in Hb mass
2. restitution of iron stores
Tx: orally of ferrous sulfate , fumarate, or
gluconat, daily dose about 200 mg element iron
If can not take oral iron, parenteral Tx is given.
Transfusion only for hypovolemia from blood
loss, or an emergency operative procedure mustbe performed on a severely anemic
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Studi tentang Pemberian Besi
Ziaei S, Norrozi M, Faghihzadeh S, Jafarbegloo E: A
randomised placebo-controlled trial to determine the effect of
iron supplementation on pregnancy outcome in pregnant
women with hemoglobin 13.2 g/dl.BJOG vol 114 (6):684-8,
2007
small-for-gestational-age birth rate and the number
of women with hypertension disorder increased
significantly in the treated group in 15.7% vs
10.3%, P = 0.035, and 2.7% vs 0,8%, P = 0.05
CONCLUSIONS: Our finding proves that routine
iron supplementation in nonanemic women is not
rational and may be harmful (Evidence Ia)
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Studi tentang Pemberian Besi
Wu Y, Weng L, Wu L (1998):
To study the efficacy of iron supplementation during
pregnancy and its influences on the outcome ofpregnancy. Preventive (Hb >11 g/dL) and treatment
(Hb
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Studi tentang Pemberian Besi
Wu Y, Weng L, Wu L (1998):
To study the efficacy of iron supplementation during
pregnancy and its influences on the outcome ofpregnancy. Preventive (Hb >11 g/dL) and treatment
(Hb
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K Mahomed. Folate supplementation in pregnancy. The
Cochrane Database of Systematic Reviews1997, Issue 3.
Art. No.: CD000183. 83 Evidence based of routine folatesupplementation
21 studies, comparing placebo or no supplementation
increased or maintained serum folate levels & red cell folate reduction in the proportion of women with low haemoglobin level in late
pregnancy & megaloblastic erythropoiesis (odds ratio 0.65, 95%confidence interval 0.45 to 0.95).
a possible reduction in the incidence of low birthweight
have no measurable effect on any other substantive measures of
pregnancy outcome. Where there is evidence that megaloblastic anaemia in pregnancy is a
common problem, particularly in areas where malarial infection iscommon for example, routine supplementation may well be justified.
Evidence: Ia
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LG Cuervo, K Mahomed. Treatments for iron deficiency
anaemia in pregnancy. The Cochrane Database of
Systematic Reviews2001, Issue 2. Art. No.: CD003094.
Five trials, involving 1234 women
One trial (n=125) ,
Oral iron treatmenta reduction in the number of women with
hemoglobins under 11g/dl , mean hemoglobin level 11.3g/dl
compared to 10.5 g/dl (cmp to plasebo)
There were no data on clinically relevant outcomes
1 trial (n=74), the intravenous (IV) route of administration was
associated with an increased risk of venous thrombosis
Authors' conclusions
This review provides inconclusive evidence on the effects of treatingiron deficiency anaemia in pregnancy due to the shortage of good
quality trials
Evidence: Ia
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Pena-Rosas JP, Viteri FE. Effects of routine oral ironsupplementation with or without folic acid for women duringpregnancy. Cochrane Database of Systematic Reviews2006, Issue 3. Art. No.: CD004736 Evidence Ia)
Forty trials, involving 12706 women, were included in thereview
The data suggest that daily antenatal iron supplementationincreases hemoglobin levels in maternal blood bothantenatally and postnatally
Women who receive daily antenatal iron supplementation areless likely to have iron deficiency and iron-deficiency anemiaat term as defined by current cutoff values.
Side-effects and hemoconcentration are more common in
women who receive daily iron supplementation vs weekly. Very limited information related to clinical maternal and infant
outcomes was available in the included trials.
R i L G t GML C LG T t t f i
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Reveiz L, Gyte GML, Cuervo LG. Treatments for iron-
deficiency anaemia in pregnancy. Cochrane Database of
Systematic Reviews 2007, Issue 2. Art. No.: CD003094.
Randomized controlled trials comparing treatments for iron-deficiency anemia in pregnancy.
17 trials, involving 2578 women.
Oral iron in pregnancy showed a reduction in the incidence ofanaemia (one trial, 125 women; relative risk 0.38
No scientific basis to suggest that in otherwise healthy women,the benefits of treatments for mild anemia in pregnancy willoutweigh the adverse effects associated with them.
No evidence that in women with iron-deficiency anemia inpregnancy, improvement in womens hematological indicestranslate into clinical improvements for them or their children
Treatments are associated with frequent adverse effects suchas gastrointestinal disturbances and poor compliance.
Evidence: Ia
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FOLIC ACID DEFICIENCY Megaloblastic anemia/pernicious anemia
Megaloblastic anemia may havedeveloped nausea, vomiting and anorexia
Folic acid deficiency during prepregnancy
and 1sttrim is a cause of NTD Daily folic acid requirement is about 400
ug is recommended
Tx: 1 mg folic acid and a nutritious andiron
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VIT B12 DEFICIENCY
Megaloblastic anemia caused by lack of vit B12
Addisonian pernicious anemia: failure yo absorb
vit B12 because of lack of intrinsic factor
Following partial or total gastric resection Crohn disease, ileal resection and bacterial
overgrowth in the small bowel
Decrease of transcobalamin, serum B12-carrier
protein
ANEMIA CAUSED BY ACUTE
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ANEMIA CAUSED BY ACUTE
BLOOD LOSS
Early in pregnancy anemia caused byabortion, ectopic pregnancy andhydatiform mole
Trim-III of pregnancy and puerperiumanemia resulting from hemorrhage,antepartum bleeding: abruptio placentaeand placenta previa
Early post partum bleeding and late postpartum bleeding
ANEMIA ASSOCIATED WITH
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ANEMIA ASSOCIATED WITH
CHRONIC DISEASE
Chronic disease recognized as characteri:weakness, weight loss and pallor
Wide variety of disorders: chronic infection
and malignant neoplasms, hypochromicand microcytic erythrocytes
Tbc, endocarditis, osteomyelitis, SLE
Chronic renal failure, cancer andchemotherapy, HIV are most common
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CHRONIC RENAL DISEASE Chronic renal insufficiency can be accomp by
anemia, due to erythrpoietin deficiency
During pregnancy , red cell mass is augmented,
but less so than normal pregnancy
The degree of red cell expansion correspd to thedegree of renal impairment
Tx: recombinant erythropoietin used for anemia
caused by chronic renal insufficien, chronic
inflammation and malignancy
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ACQUIRED HEMOLYTIC ANEMIA 1. Autoimmune hemolytic anemia:
Due to warm-active, cold-active antibody or a
combination, classified as primary/idiopathic,
Secondary to underlying diseases, or
other factors: lymphomas, leukemia, connective-tissue diseases, infections, chronic
inflammatory diseases, or drug induced
factors
Tx: prednison, 1 mg/kg per day
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Continue 2. Drug-induced hemolytic anemia:
Must be differentiated from other forms
of autoimmune hemolytic anemia
Hemolysis typically is mild, it resolves
upon withdrawing the drug
The severity depand on the degree of
hemolysis
Tx: corticosteroid quesenable efficacy,
transfusion for severe anemia
Related to a congenital erythrocyte enzimatic defect
glucose-6-phosphate dehydrogenase (G6PD) defic
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Continue 3. Pregnancy-induced hemolytic anemia:
Unexplained hemolytic anemia during
pregnancy is a rare, severe hemolysis
develop early in pregnancy and resolves
within months after delivery
Fetus-infant also demonstrated transient
hemolysis, immunological cause is suspected
Tx: corticosteroid is effective
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OTHER ACQUIRED ANEMIAS
Microangiopathic hemolysis:
Complicated PE-E: HELLP syndrome
Exotoxin of clostridium perfringes or group
A-beta-hemolytic streptococcus
Gram neg bacterial endotoxin , or
liposaccharide especially with severe
acute pyelonephritis
INHERITED ERYTHROCYTE
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INHERITED ERYTHROCYTE
DEFECT
Inherited red cell membrane defect or enzymedeficiencies result in destabilizatn of the
membrane lipid bilayer
Loss of lipid from the erythrocyte membrane,surface area deficiency poorly deformable cells
that undergo hemolysis
Inherited membrane defect will cause accelerat
destruction: hereditary spherocytosis,pyropoikilocytosis, ovalocytosis
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RED CELL ENZYME DEFICIENCY Erythrocyte enzyme are necessary for its
anaerobic utilization of glucose
Hereditary nonspherocytic anemia
G6PD deficiency
Pyruvat kinase deficiency, most commonenzyme deficiency it is inherited as anautosomal recessive trait
Enzyme deficiency are reduced by drugsor infections
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APLAST & HYPOPLAST ANEMIA Dx: anemia with thrombocytipenia, leucopenia,
hypocelluler bone marrow
Anemia is induced by drugs and other
chemicals, infection, irradiation, leukemia and
immunological disorders Fanconi anemia and Diamond Blackfan
syndrome inherited autosomal recessive
Tx: glucocorticoid most are transfusion, severe:
bone marrow or stem cell transplantation
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HEMOGLOBINOPATHIES Sickle-cell hemoglobinopathies:
1) Sickle-cell anemia (SS disease),2) Sickle-cell hemoglobin C disease (SC
disease), 3)Sickle-cell beta-thalassemia
disease (S-beta-thalassema disease)
are the most common of sickle-cellhemoglobinopathies, increased matern/perinatalmorbidity and mortality, infection, abortion,stillbirth, neonatal death
Tx: folic acid and prophylactic transfusion
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THALASSEMIA Alfa-thalassemia:
Genetically determined hemoglobinopathiy
characterized by impaired production of one or
more of the normal globin peptide chain
Abnormal synthesis rates may results inineffective erythropoeisis, hemolysis and anemia
2 major forms alfa-thalassemia and beta-
thalassemia
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Continue Fetus with alfa-thalassemia at 25, 26 and
32 weeks: ascites, hydrops fetalis
Alfa-thalassemia minor characteristic byminimal-moderate hypochromic microcytic
anemia, tolerate pregnancy quite well Beta-thalassemia:
Decrease beta-chain production and
excess alfa-chains precipitate to cause cellmembrane damage
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Continue Thalassemia major neonate is healthy at
birth, but as the hemoglobin F level falls,
become severely anemia
Beta-thalassemia minor during pregnancy:
mother and fetus are satisfactory
Prophylactic iron 60 mg, folic acid 1 mg
Prenatal Dx: CVS can be carried out at 9
to 13 weeks.
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TERIMA KASIH