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5/14/2018 Anemia Pregnancy (3) - slidepdf.com
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ANEMIA IN PREGNANCY -IDA: CHANGING CONCEPT
Dr Veena AgrawalM.S., MICOG, WHO Fellow (USA)
Professor & HOD, Obst. & Gynecology,G. R. Medical College
Core faculty of human Genetics,
Jiwaji UniversityGwalior, M.P.
Dr Sonali AgrawalDGO
Consultant Agrawal Hospital & Research CentreGwalior, M.P. India
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Anemia is a sign, not a diseaseof dynamic process
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World Health Organization
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Anemia – a major killer
Incidence is about 50% in general population, (in
India 80%).
Iron deficiency anemia is the most common
medical disorder during pregnancy.
In pregnancy, it is one of the leading causes ofmaternal mortality in developing countries.
It affects both mother and fetus.
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PREVALENCE OF anemia in
India Available studies on prevalence of nutritional anemia
show that:
65% infant and toddlers, 60% 1-6 years of age,
88% adolescent girls (3.3% has hemoglobin <7 gm./dl;severe anemia) and
85% pregnant women (9.9% having severe anemia) prevalence higher in lactating than pregnant women
The most common is iron deficiency anemia.
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Causes: Physiological - disproportionate ↑se of plasma
volume apparent reduction of RBC, Hb & Hct.Picture is normochromic normocytic.
Acquired:
Nutritional
Iron deficiency anemia (60%),
Macrocytic anemia (10%) due to def of folic acidand/or vitamin B12
Dimorphic and protein deficiency anemia (30%) inextreme malnutrition
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Causes of Anemia Hemorrhagic
acute blood loss,
chronic (hook worm, bleeding piles) Infections
Acute (e.g., malaria)
Chronic (e.g., tuberculosis)
Genetic conditions (e.g., thalassemia, sickle cell) Enzyme disorders (e.g., sideroblastic anemia)
Anemia of chronic disease (e.g., malignancy, chronicrenal failure
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Criteria for Physiologic Anemia Hb: 10gm%
RBC: 3.2 million/mm3
PCV: 30% Peripheral smear showing normal morphology of
RBC with central pallor
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Significance of Hypervolemia1. To meet the demands of the enlarged uteruswith its greatly hypertrophied vascular system.
2. To protect the mother, and in turn the fetus,against the deleterious effects of impairedvenous return in the supine and erect positions.
3. To safeguard the mother against the adverseeffects of blood loss associated with parturition.
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IDA
12th most important risk factor for all mortality globally.
9th
most important risk factor for the global burden of disease.
associated with 115,000 of the 510,000 maternal deaths(22%) and 591,000 of the 2,464,000 perinatal deaths
(24%) occurring annually around the world.
Mason, Rivers and Helwig Food and Nutrition Bulletin 26: 57-162, 2005..
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1/3 world’s population suffers from anemia, mostly iron deficiency anemia.
India continues to have a very high prevalence.
National Family Health Survey (NFHS-3) reveals theprevalence of anemia to be 70-80% in children, 70% inpregnant women and 24% in adult men.
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Definition of Anemia in Pregnancy
WHO-Hb conc <11gm/dl & Hct < 33%
CDC definition-Hb con <11gm/dl & Hct < 33% duringthe 1st trimester & < 10.5 gm/dl Hct < 32% during the2nd trimester
Absolute iron deficiency is defined as ferritin <200µg/L with or without iron saturation <20%,
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CDC definition:
Pregnancy
Trimester
Hemoglobin Hematocrit
First 11.0 33.0
Second 10.5 32.0
Third 11.0 33.0
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Factors required for erythropoiesis
• Proteins (erythropoietin)
• Minerals (iron)
• Trace elements: (Zinc, Cobalt, Copper etc)
• Vitamins: Folic acid, Cyanocobalamin (B12), Vitamin C, Pyridoxine
(B6), Riboflavin, Vitamin A
• Hormones: Androgens & Thryoxine
Letsky E. 1995
Prasad AS. J. Am. Coll. Nutr. 1996
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Anemia
Acc to ICMR
Mild 10-11mg%
Moderate 7-10.9mg% Severe 4 - 6.9mg%
Very severe <4mg%
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Normal Iron
depletion
Iron
deficient
erythropoiesis
Iron
deficiency
anemia
Storage iron
Transport iron
Erythorin iron
Marrow iron
Plasma ferritin (µg/l)
Transferrin saturation(%)
Iron absorption
2-3+ 0 trace 0 0
100±60 < 20 10 <10
35±15 Normal Normal Microcytic
hypochromic
Normal ± + +
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Hb 13.5 – 14 gm %
R.B.C. 4.5 – 4.7 million/cu mm
Serum Iron 50 – 150 μgm / dL
TIBC 300 – 360 μgm / dL
Transferrin saturation 25 – 50 %
S. Ferritin level 30 μg / Lit
Red Cell protoporphyrin 30 μg / dL
Erythropoietin 15.20 U / Lit
MCV 76 – 100 L
MCH 27 – 33 pg
MCHC 33.37 gm / dL
PCV 32 – 40 %
Normal Levels
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Requirement of Iron
IRON in mg THAT SHOULD be ABSORBED DAILY
ADULT FEMALES
MENSTRUATION 2.8
PREGNANCY(1st HALF) 0.8
(2nd HALF) 3.5
LACTATION 2.4
POSTMENOPAUSE 0.7
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Iron Requirements in Pregnancy Amountmg
Total cost of pregnancy
Fetus 270
Placenta 90
Expansion of red blood cell mass 450
Obligatory basal losses 230 Sum 1040
Maternal blood loss at delivery 150
Total cost 1190
Net cost of pregnancy
Contraction of maternal red blood cell mass -450
Absence of menstruation during pregnancy -160
Subtotal -610
Net cost 580
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Normal Iron Requirements Iron requirement for normal pregnancy is 1gm
200 mg is excreted300 mg is transferred to fetus
500 mg is need for mother
Total volume of RBC inc is 450 ml
1 ml of RBCs contains 1.1 mg of iron
450 ml X 1.1 mg/ml = 500 mg
Daily average is 6-7 mg/day
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Early Pregnancy
20 – 32 weeks 32 – 40 weeks
2.5 mg. / day 5.5 mg. / day 6.8 mg / day
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Overall needs are about 2 to 4.8 mg iron/day.
Must consume 20 to 48 mg of dietary iron to absorbthis quantity of iron daily.
Average vegetarian diet provide 10-15 mg iron/day.
Amount of iron absorbed from diet+iron mobilized
from stores, is usually insufficient to meet thedemands.
Therefore, iron supplementation during pregnancy isrecommended universally even in non anemic women.
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Maternal Anemia:A Preventable Killer
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Decreasedabsorption
Increasedblood loss
Poor diet
Increased
requirements
Causes ofIDA
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Anemia: Etiologies Inadequate dietary intake
Poor nutrition
Chronic alcoholism
Decreased consumption ofanimal protein and ascorbicacid
Increased iron demands
Multiparity
Diarrhea, HIV/ AIDS and UTI
Recurrent Infections-Tuberculosis, Amoebiasis ,Giardiasis, Roundworm
other infectious diseases
Inadequate GIT absorption
Malabsorption syndromes
Certain drugs/foods
Blood loss Hookworm infestation
Malaria
Bleeding piles &gums
Surgery
Gastrointestinal bleeding Trauma
Dialysis
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Low Iron Intake or Low Iron Absorption
Haemolysis due to malaria
worm infestations (hookworm)
Multiparity
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Effects of Anemia on Pregnancy
Pathophysiology - Fetus
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Fetal Effects
Mild and moderate anemia may not show significanteffects.
Iron is actively transported across the placenta.
Fetal iron and ferritin levels > maternal levels 3 times
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Effects of Anemia on Fetus
• PROM,
• IUGR,
• IUFD,
• Prematurity,
• Abnormal trophoblast invasion
• Fetal programming & disease of newborn:
behavioral abnormalities, poor performance on BayleyMental Development Index, decreased cognitive function.
• Neonatal anemia
• Adult HT associated with low birth weight & high ratio of
placenta to birth weight.•( Barker DJP, Bull AR, et all BMJ 1990; 301:259-262)
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• If maternal oxygenation is 98 – 100 %,• The fetus gets around 70 % of O2, with fetal Hb.
Fetus can compensate.
• As the maternal Hb. drops, fetal hypoxiadevelops, which leads to stimulation of fetalerythropoiesis
• Increased viscosity of blood due to raised PCV.
sluggish circulation
• End artery thrombosis
• Failure of the organs, supplied by these vessels.
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Increased PCV
Brain damage Necrotising enterocolitis
Hypoglycemia
Hypocalcemia
Hyperbilirubinimia
RDS
At Birth Hb – 18 to 20 gms %,PCV – 55 to 60 %
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Severe Anemia
Fetal hypoxia
Prolonged period
Neurological
deficit
Short duration
IQ less, slow
learner
Fetal hypoxia leads to an increase in the cord blood EPO.
Cord blood EPO correlates with perinatal brain damage.
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Release of placental stress hormones(CRH,Nor epinephrine)
Fetal release of ACTHand cortisol
Abnormal trophoblast invasion andrelease of hypoxic inducible factor
Early anaemia during
gestation
Production of uterine contraction
stimulating hormones
(estrogen, connexin) and inhibition of IGF,
an anabolic hormone
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Maternal Effects of Anemia
• Behavioral changes,irritability.
• Loss of appetite,
indigestion, etc. due lowperformance of eachorgan.
• Increased morbidity and
mortality due to PIH, APH,PPH, if associated.
• C CF at 30-32 wks, intra-partum & post-partum.
Reduced immune function- infection, ante-partumand puerperal sepsis.
Negative thermoregulation
Increased risk of bloodtransfusion
• Preterm Labor
• Sub involution• Failing lactation
• Pulmonary Venous:thrombosis & embolism,
due to thrombophlebitis.
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ANTENATAL CARE
As a routine - No differenceRegistration
Counseling
Regular check up weight, B.P., Hb%, urinePrevention of complications
Immunizations
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Care in addition to routine ANC H & P of Anemia Investigate for
Grade of anemia Type
Severity of IDA cause
Tx of anemia Tx the cause of anemia ie. deworming, Antimalarial
I M
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Intrapartum Management
if patient comes in labor
Individuals who MUST present in labor room
Skilled Birth attendant's
Anesthesiologist
Pediatrician
Nursing Staff
―Extra Hands‖
Informed consent
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Things that should be available: US Machine
Cardiotocographic machine
Blood transfusion facility
Neonatal resuscitative measures
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Things that should be done:
IV Line should be patent
Bl arranged - PCV
Monitor pt for sign of CCF esp. immediatelypostpartum
Early cord clamping No methergin
Cut shirt 2nd stage labor
IV Diuretic Antibiotics
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Postpartum Management Monitor patient for sign of CCF
Antibiotics
Otherwise same
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Clinical Feature of AnemiaSymptoms:
Mild anemia; usually asymptomatic
Moderate anemia - weakness, fatigue, exhaustion, loss of appetite, indigestion, giddiness, breathlessness
Severe anemia-palpitation, tachycardia, breathlessness,Increased cardiac output, CHF, general anasarca,
pulmonary edema
Sharma J.B. Progress in Obst. & Gynae. (Studd) 2003.
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Clinical Features of AnemiaSigns:
Pallor
Nail changes – Koilonychia Angular cheilosis, Glossitis, Stomatitis
Oedema
Hyperdynamic circulation (short and soft systolic murmur)
Fine crepts
Sharma J.B. Progress in Obst. & Gynae. (Studd) 2003.
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What is level
Type
cause
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Anemia?
Production? Survival/Destruction?
The key test is the …..
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The Reticulocyte Count
(Kinetic Approach)
↑ reticulocytes (>2-3% or 100,000/mm3 total) are seen in
bl loss and hemolytic processes, although up to 25% ofhemolytic anemia's will present with a normal count.
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Hb Measurement & Haematocrit Peripheral smear will often reveal many diagnostic clues
Reticulocyte count
Serum ferritin most sensitive tool. Values < 10mcg/L indicateabsence of stored iron, <20 or <15 µg/L indicate depleted iron stores
Transferrin saturation (TSAT), should be above 16% with normalbeing 30%
Soluble serum transferrin receptors (sTfR) (>45 nM/Ldenote IDA),
TSAT <20%, serum ferritin <100 ng/mL & % of hypochromic RBC’s >10% indicate absolute ID,
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RBC indices - little diagnostic value unless the MCV isbelow 70fl
Serum iron - decreased in a variety of states includingiron deficiency, inflammation & stress. Variestremendously from morning to evening and from day today. value < 0.5mg/L indicate anemia, normal range:0.80 to 1.80 mg/L
Total iron binding capacity is very specific for irondeficiency (near 100%) but has poor sensitivity (<30%).
Iron saturation (Fe/TIBC x 100) can be decreased below16% in both anemia of chronic disease and iron
deficiency
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Tests used in Diagnosing Iron
Deficiency Anemia (IDA)Test Limitations
*Blood smear hypochromia Subjectivity
*MCV Insensitivity
RDW Non-specificity Serum iron Markedly lowered by fever or
inflammation
Iron binding capacity (IBC) Moderately lowered by fever; increasedby pregnancy
Iron/IBC (% saturation) Like serum iron, lowered by fever*Ferritin Mildly raised by fever or inflammation
Stool for occult blood Bleeding may be intermittent
Bone marrow for iron stores Expensive and invasive; iron depletiondoes not prove IDA
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Specific tests for etiology of the anemia
•Urine & stool examination• Test for malaria• Rarely- Endoscopic or barium studies of the GItract, bone marrow examination
Exclude other causes of hypochromic microcyticanemia
•Anemia of chronic disease• Thalassaemia trait
• Sideroblastic anemia
L b T ti f
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Lab Testing forIron Deficiency Anemia (IDA)
Patient with anemia,
Ferritin
> 100
Ferritin
20-100
Ferritin < 20,
or Iron < 50
and IBC > 450
Ferritin > 20,
or Iron > 50
and IBC < 450
sTR<45
sTR>45
IDA Workup for other
causes of anemia
Iron
therapy
Look for
source of
blood loss
Check ferritin, Iron, IBC level
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Prevention
Dietary modification
Iron supplementation of adolescent & non pregnantfemale
Tx of Hookworm infestation Control of malaria
Iron supplementation in pregnant Women
Food fortification
Antenatal care for early recognition Optimal birth spacing
E f d h
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Eat foods that are: Rich in iron - liver, beef, whole-grain breads
cereals, eggs, dark green vegetables and dried fruit. High in folic acid, such as wheat germ, beans,
peanut butter, oatmeal, mushrooms, collards,broccoli, beef liver and asparagus.
High in vitamin C, such as citrus fruits and fresh,raw vegetables. Vitamin C makes iron absorptionmore efficient.
Take prenatal vitamin and mineral supplements,especially folic acid.
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Diet
Low Bioavailability Rice, Wheat
Maize
Potato
High Bioavailability Eggs
Fish
Meat
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Dietary Components and Absorption of Iron
Dietary components Absorption
Calcium (Dairy products)
Meat, fish, poultry, sea-food
Phytate (grain products)
Polyphenols
(Tea, spices, vegetables)
Vitamin C
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Depends upon severity
and gestation
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Which Iron Compound?
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Inorganic1. Ferrous
• sulfate, fumarate, gluconate, ascorbate, succinate,glutamate, dextran, carbonyl iron, and lactate
• bis-glycinate chelate.
2. Ferric Salts – iron (III)-hydroxide polymaltosecomplex
Organic - Heme
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Ferrous vs. Ferric iron
Ferrous iron is absorbed three times more than ferric iron.
Ferric iron absorption is dependent on duodenal ferric
reductase.
Availability of duodenal ferric reductase is dependent on
ascorbic acid.
Supplementation of ascorbic acid may increase ferric iron
absorption.
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First iron pills were commonly known as Blaud's
pills, which were named after P. Blaud of Beaucaire.
He is a French physician who introduced and started
the use of these medications as a treatment for
patients with anemia.
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Goal: Hgb – 11-12g/dL
Hct – 33 – 36%
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Iron Preparations
Available with various amounts of iron, iron salts,
complexes, combinations, and dosing regimens.
Available in tablets and capsules, liquid and drops,coated and extended release tablets and capsules.
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• Different oral preparations exhibit different safety profiles.
• Greater oxidative stress is observed with oral iron (II)salts than with iron (III) complexes
• Iron salts are selected based on compliance of thetolerance, side effects, clinical situation of the pt andavailability of a particular salt.
• Fe sulphate is cheapest, best absorbed, and mostcommonly prescribed, showing a rapid rise in both serumiron concentrate and NTBI (Non transperrin bound iron) &greatest frequency of adverse events
• If not tolerated, then ferrous gluconate, fumarate and
others are the next choice.
• Oral iron must be continued for 3-6 mon after Hb hascome to normal levels – for building iron stores.
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“In small intestine ferric iron is precipitated
as ferric hydroxide which is basically RUST”
“The difficulty of absorbing rust is the main
reason for the prevalence of iron deficiency anemia in the world”
“The most readily available and cheapest natural reducing agent is ascorbic acid”
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Iron metabolism
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Iron Supplementation During Pregnancy
In developed countries like U.K., routine Iron
supplementation is not recommended.
However, it is mandatory in non-industrialized countries.
WHO - 60 mg elemental iron with 250 mg folic acid for 6
months in pregnancy and additional 3 months postpartum.
NNACP in India - 100 mg of elemental iron and 500 mcg of
folic acid for 100 days after the first trimester
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Ferrous Salts or Bivalent Iron Salts
Good bioavailability however, decreases in the presenceof dietary inhibitors like phytates, tannic acid, etc .
Efficacious and cheap
Several disadvantages:
High incidence of GI Tract side effects (~23 %).
Teeth staining with liquid preparations
Salty astringent taste which is not palatable for mostchildren
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Side Effects of Oral Iron
Nausea
Vomiting
Constipation
Abdominal cramping
Diarrhea
The tab can be given with meals or
different brands may be tried.
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Ways to Minimize Adverse
Effects of Oral Iron Recommend half the dose and gradually ↑se to the
full dose.
Take the supplement in divided doses.
Take with food to alleviate GIT distress (↓se iron
absorption by as much as 40-66%).
Change to a different iron preparation.
Concomitant use of a stool softener, such asdocusate, may help alleviate constipation.
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Factors that Affect Absorption ↓ as doses get larger - supplement in 2 or 3 divided doses.
Enteric-coated and long-acting supplements may be ineffective. notdissolve in the stomach hence not absorbed in duodenum or upper jejunum
Ascorbic acid is enhanced absorption by forming a chelate with ferriciron at acid pH that remains soluble at the alkaline pH of theduodenum. & reverse the inhibiting effects of substances such as teaand calcium.
Taken with food decreased absorption by as much as 40-66%.
Food ↓ absorption- Tannins from foods, such as tea
Iron forms an insoluble complex with several other drugs - decreasedabsorption of both iron and the other drugs, e.g. tetracycline,pencillamine, methyldopa, levodopa, bisphosphonates quinolones,calcium and antacids, phosphates, etc.
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Effectiveness of Iron Supplementation
Clinical improvement
laboratory indices
Reticulocyte count
Hemoglobin
Ferritin levels
TAST
Newer measurements: Reticulocyte hemoglobin content
Percent hypochromic RBCs
Soluble transferrin receptors (sTfR)
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Reticulocytosis occurs within 7-10 days afterinitiation of iron therapy.
Hb usually ↑es within 2-3 wks of starting Iron
Therapeutic doses should ↑se Hb 0.7-1.0 g/dL / wk.
Serum ferritin level is a more accurate measure of
total body iron stores. Adequate iron replacement has typically occurred
when the serum ferritin level reaches 50 µg/L.
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Reasons for Failure to Respond
1. Non compliance2. Concomitant folate deficiency
3. Continuous loss of blood through hookworm infestation or
bleeding hemorrhoids
4. Co-existing infection
5. Faulty iron absorption
6. Inaccurate diagnosis
Non iron deficiency microcytic anemia
a. Thalassaemia
b. Pyridoxine deficiencyc. Lead poisoning
d. Sideroblastic anemia
e. AtransferrinemiaPrema K. Obst. & Gynaecol 1992
Sharma JB, In Progress in Obst. & Gynaec,
2002
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Foods and Drugs that Impair
Oral Iron Absorption Taking oral iron with food reduces absorption
Caffeinated beverages, (especially tea)
Calcium containing foods and beverages
Calcium supplements
Antacids
H-2 receptor blockers
Proton pump inhibitors
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3 months postpartum to replenish the ironstores
Follow up
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Follow up:
Iron status (ferritin, TIBC, & TSAT) and RBC indicesmust be checked periodically to re-evaluate the pt'sneed for additional iron supplementation.
Parenteral iron should not be administered topatients with ferritin > 800 ng/mL or transferrinsaturation > 50%.
P t l I Th
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Parenteral Iron Therapy
Indicated: when unable to take iron due to side effects
Non compliant
Suffers from inflammatory bowel disease
Near term
With chronic renal disease
Postpartum, especially in those who have hadsignificant blood loss at delivery
Pre – post operative anemia can also be cured
Its main advantage is certainty of administration
Rise in Hb is similar to oral iron (up to 1gm per wk)
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Postpartum High EPO state in postpartum anemia
IV iron supplementation in such period ↑es the
erythropoiesis 5 times
The Hb rise will be evident in as early as 5 days
Harrisons principles of medicine
Contraindications:
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Contraindications:
Hypersensitivity to any of the Parenteral ironproducts
Liver disease or acute renal failure, Nephritis,
Cardio respiratory disease
Pts with ferritin > 800 ng/mL or transferrin saturation> 50%.
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Disadvantages
Pain
Nausea vomiting, headache
Skin discoloration
Abscess formation Fever
Lymphadenopathy
Allergic reaction
Anaphylaxis
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Precaution
Oral Iron to be suspended 48 hours before parenteraltherapy.
Emergency measures like injection hydrocortisoneadrenaline, oxygen cylinder etc., should be keptready.
Look for a reaction while giving infusion.
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Parenteral Iron Preparations Iron- sorbitol -citric acid complex (jectofer (1.5ml) 75mg –
Available in Europe, Asia & Canada. It is not yetapproved by US FDA. IM use only
HMW Iron Dextran – both IM & IV use
LMW Iron Dextran - both IM & IV use
Sodium ferric gluconate – IV use only
Iron sucrose - IV use only
Ferric carboxymaltose - IV use only
Newer
Iron isomaltoside 1000 - IV use only
Ferumoxytol - IV dose of 510 mg, followed by 2nd dose 3 –8days later. (Undiluted, at a rate of 1 ml/second (30
mg/sec)).
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Classification of IV Iron Carbohydrate
Complex Preparations (Geisser ) TYPE I TYPE II TYPE III TYPE IV
Example Ferriccarboxymalt
ose Iron dextran
Ironsucrose
Sodiumferric
gluconate
Iron(III)-citrateIron(III)-sorbitol
Iron(III)-citrate +iron(III)-sorbitol + iron dextrinSodium ferric gluconate+iron sucrose
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HMW ID LMW ID Iron
Saccharate
Ferric
Gluconate
Type of ironcomplex
IronIII-dextran
IronIII-dextran
IronIII-sucrose
IronIII-gluconate insucrose
Mg iron per
ml
50 mg/ml 50 mg/ml 20 mg/ml 12.5 mg/ml
Preservative No No No Yes, 9 mg of benzyl alcoholper ml
Relativestability of iron complex
Robust/
strong
Robust/
strong
Half robust/mediumstrong
Weak/labile
HMW ID = high molecular wt iron dextran;,LMW ID = low molecular wt iron dextran;TDI = total dose infusion.
HMW ID LMW ID Iron Ferric
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Saccharate Gluconate
pH 4.5 - 7.0 5.2 - 6.5 10.5 - 11.1 7.7 - 9.7
T½
9.4 - 87.4 hr.
(average 58.9hr.)
5-20 hr. 6 hr. 1 hr.
Standarddosage
Injection timefor undil. adm.
100 mg
2 min
100 - 200 mg
2 min or
10 min
100 - 200 mg
5-10 min
125 mg
10 min
Maximumsingle dose
Infusion
time/Injectiontime.
100 mg
2 minundil. adm.
20 mg/kgbody weight
4-6 hrs. adm.
200 mg
10 min undil.adm.
125 mg
10 min undil.adm.
TDI adm.possible
Yes Yes No No
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Complex stability:
Iron dextran > iron sucrose > iron gluconate
Strongest iron complexes allow for the largest doseof iron in one infusion.
Toxicological potential Iron sucrose > iron gluconate >> low Mw iron dextran
Fe-carbohydrate agents mix with plasma, enter the RES directly from
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y g p , yintravascular fluid compartment
Within Phagocytes of RES,Fe released from the iron-carbohydrate compound into anLMW iron pool
LMWFe either is incorporated by ferritin into intracellular iron stores or
released from the cell to be taken up by the extracellular iron-binding protein transferrin.
Transferrin delivers iron to transferrin receptors on the surface of erythroidprecursors.
Transferrin delivers iron to transferrin receptors on the surface of erythroidprecursors.
Iron-transferrin-transferrin receptor complex supplies Fe for Hb synthesis &maturation of the red cell
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Safety ProfileMost of the iron is deposited in the Reticulo-endothelial
system than in parenchyma.
This gives the advantage of not having free-radicalinduced lipid peroxidation which takes place withinparenchyma only.
Practically no liver injuries occur as confirmed byexperimental histological results.
Iron dextran has the highest incidence of modest andsevere life-threatening side effects.
Hypersensitivity Reactions:
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Hypersensitivity Reactions: Anaphylactic reactions
Almost exclusively with iron dextran, independent ofdose - 0.6 to 0.7%
Mechanism is unknown but some possibilities are:
Dextran itself is immunogenic, cause allergic reactions
including anaphylaxis & anaphylactoid reactions, Availability of free iron after administration.
Antidextran antibody mediated mast cell activation
Alternate pathway complement activation
Direct stimulation of mast cell degranulation
.
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Controversies severe adverse allergic
reactions with iron dextran component but other formulations are also not safe
Pts with a h/o of allergy may be at risk of developingundesired immunological reactions such as asthma
(Meyler 14th edition, page 701). Iron toxicity is more if amount of free iron released into
plasma exceeds plasma iron-binding capacity (morelikely to occur when using iron sorbitol – citric acid
complex, since the iron is less firmly bound than withiron dextran (Meyler 14th edition, page 701).
Conditions associated with low iron-
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binding capacity of parentral iron- More
reaction Malnutrition & previous or simultaneous oral iron
therapy
Folic acid def - likely mechanism - disturbance of iron
utilization. (Side Effects of Drugs, Annual 9, 516).
Different parenteral iron differ experimentally in theircomparative toxicity related to free radical generation& severe ATP depletion. Iron sucrose has greater
potential for this than iron dextran (Zager et al, 2002).
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Both Iron gluconate & sucrose are associatedwith anaphylactoid type reactions, dose related.
Reactions were due to over saturation of thetransferrin molecule resulting in the circulation offree iron.
This theory is still uncertain.
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Iron sucrose is also associated with
anaphylactoid type reactions, but these seem tobe dose related
Reactions that occur are due to over saturationof the transferrin molecule resulting in the
circulation of free iron
This theory is still uncertain
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How to give IM
Intravenous Iron Therapy IV PUSH in divided doses
Diluted
Undiluted
TDI
Parenteral Iron Therapy (IM or IV) with recombinanthuman erythropoietin (rHuEPO)
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How to Calculate TDI: Total dose of infusion of iron is calculated as:
(15- pt s Hb%) x body wt in Kg x3 = Fe in mg.
Ganzoni Equation
Total Iron Deficit = Weight {kg} x (Target Hb
– Actual Hb) {g/l} x 2.4 + Iron stores {mg}
{ 500 if W > 35kg }{ 15 mg/kg if W < 35kg }
Dosage Intramuscular Iron
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Dosage Intramuscular Iron
100mg/d, Max 200mg/d can be given on D 1, 3 & 5
Z shaped deep IM to avoid skin staining.
2 High doses of IM injection 250mg each at monthly with
injection T.T has been recommended in moderate anemiaof pregnancy.
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Dosage IV Iron
Divided doses (IV Push) - dosing frequency
Iron dextran agents, plasma half-lives - 30 to 60 hrs,every 2 to 7 days, (once to thrice weekly).
Ferric gluconate and iron sucrose, with 1- & 8-h half-lives, respectively, could be given as frequently asevery 24 hours.
Total Dose infusion
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INTRAVENOUS IRON THERAPY
Iron Dextran –
Test dose (25 mg Fe) is required. Diluted in 50-100 mL ofNS and infused over 15-20 minutes.
Monitor HR, RR, & BP q15 min for 1-2 hrs after test dose.
Total Fe (dose) administered
as one large dose (diluted in 500-1000 mL NS and infused over 4to 8 hrs,
or divided into many smaller doses given 1-3 times per week.Each 100-mg dose may be administered undiluted as iv push or100-mg dose is diluted in 250 mL NS and infused over 30-60 min.
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Adverse Reactions Increased incidence with TDI.
Onset is 24-48 hrs after administration.
Effects subside within 3-4 days.
Dose related:
arthralgia, backache, chills, dizziness, moderate tohigh fever, headache, malaise, myalgia, N/V.
Non-dose related: Hypersensitivity reactions characterized by
anaphylactic shock, CV collapse, cardiac arrest,bronchospasm, oral or pharyngeal edema, or
dyspnea.
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Iron Sucrose and Iron Gluconate
0.3% side effects with iron gluconate —very low
Pts who had a reaction to iron dextran are more likely tohave a reaction to iron gluconate than to iron sucrose.
Adverse reactions with iron sucrose or gluconate seen athigher doses only.
No anaphylactic death from either preparation in 35 yrs.
used in similar total doses per course of therapy,generally 1 gm/course.
Iron sucrose may be given at 500 mg/4 hours; irongluconate can only be given at 300 mg/4 hours.
Iron Sucrose
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Iron Sucrose
No test dose is required. May be administered
as iv push undiluted at the rate of 1 mL/min. 100 mg. -200 mg over 10 min.
Or 5-mL vial diluted in a max 100 mL NS (final conc =1mg/mL) and administered over at least 20 min.
200-300 mg infused over 2 hrs have been usedsafely.
Doses as 500 mg have been infused in a single 2-hour session. This rate was associated with higherincidence of side effects such as nausea,hypotension, dizziness, and lower-back pain.
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Adverse Reactions Experienced in > 5% of patients:
Hypotension
Cramps/leg cramps
Nausea
Headache
Vomiting
Diarrhea
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Precautions Iron overload or infusing too rapidly can cause:
hypotension, headache, N/V, dizziness, joint aches,paresthesia, abdominal & muscle pain, edema, & CV
collapse
Tx - IV fluids, hydrocortisone, or antihistamines
or slow down rate of infusion
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Iron gluconate No test dose is required.
Administered in:
Small installments of 125 mg Fe or less diluted in 100
mL of NS and infused over 60 min.
Or undiluted as a slow IV injection at a rate notexceeding 12.5 mg/min (1 mL/min).
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Adverse Reactions
Hypotension/flushing
Associated with rapid administration
Not associated with hypersensitivity reactions
Resolves within 1-2 hours
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Precautions Iron overload due to accumulation of iron in storage
sites.
Serum iron > 300mcg/dl with transferrin saturation
may indicate overload. Symptoms: abdominal pain, diarrhea, vomiting
leading to pallor or cyanosis, lassitude, drowsiness,hyperventilation due to acidosis, and CV collapse.
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IV IRON POLYMALTOSE
500mg in 200mls 0.9% NS.Run at 40ml/hr for 30minutes, then 80mls/hr.
Or 1000mg in 200mls 0.9% NS.Run at 20mls/hr for30 minutes, then 45mls/hr.
First 30 minutes will always be run as a test dose.
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Monitor reaction to medication:
Headache, hypotension, joint/muscle pain,
tachycardia, syncope, nausea and vomiting,circulatory collapse.
Delayed reactions may include:
Dizziness, syncope, stiffness (myalgia oflegs/hands/face)
Chest pain/back pain
Rash
Laboratory Testing after IV
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Laboratory Testing after IV
Iron-carbohydrate compounds interfere with clinicallaboratory determination of serum iron
Serum iron & transferrin saturation should be testedafter most or all of the IV iron agent has been
cleared. No earlier than 7 days after administration of a 100-mg
dose of iron dextran,
2 wk after a 500-mg dose of iron dextran, and
24 to 48 hrs after a 125-mg dose of ferric gluconate ora 100-mg dose of iron sucrose.
One month for ferritin or iron studies after a 500-mgdose of Polymaltose
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Dosage regimen Erythropoetin
Inj erythropoetin - Sc or iv 100-150 iu/kg
On day 1, 3 & 5 along with parenteral iron or day 1, 3& 5 6000units s/c erythropoetin and iron dextran
100mg deep im daily for 5 days. First dose after subcutaneous sensitivity test.
Adrenaline, hydrocortisone injection oxygen to bekept ready.
Produces 3gm % rise in Hb over a 2wk period
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Inj erythropoietin 18000u s/c in one dose & inj lowmolecular dextran 500mg to be dissolved in 500mlof dextrose to be given over 2 hours, as slow iv
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Indication of Erythropoetin
Used in severe anemia & renal failure for significantincrease in Hb and to avoid Blood transfusion.
Gynaecological surgeries: preop use of erythropoietinand Parenteral iron has shown to avoid the need forblood transfusion later.
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‘Transfusion should be prescribed
ONLY for conditions for which there
is NO OTHER TREATMENT’
World Health Organization
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Blood Transfusion: • Indications-
• Severe Anemia in third trimester, CCF in pregnancy,Acute hemorrhage or hemolysis in pregnancy.
• Jehovah’s Witness who refuse blood transfusion dueto religious beliefs.
• S/E of BT-
• HIV, Hepatitis B, C, malaria, rubella, etc.
• Transfusion reaction
• Risk of incorrect cross - matching and transfusionnegative impact on immune system.
• .
d f l d f
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Hazards of Blood Transfusion in USA
Hemolytic reactions 1 in 40,000
Non hemolytic febrile reactions 3-4%
Anaphylactic reactions 1 in 20,000
GVHD 0.1 to 1%
TRALI 0.1-0.2%
HBV 1 in 50,000 HCV 1 in 3000
HIV 1 in 1,50,000
Summary Protocol of Severe Anemia in Pregnancy
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Pregnancy < 30 weeks
Iron deficiency
anemia
Folic acid
deficiency
Oral irontherapy
Oral folatetherapy
Intolerance or non-
compliance
Intramuscular
iron
Intravenous
iron
Summary Protocol of Severe Anemia in Pregnancy
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Pregnancy 30-36 weeks
Iron
deficiency
Folic acid
deficiency
Parenteraliron
Oral folatetherapy
Intramuscular
iron
Intravenous
iron
Pregnancy >36 weeks
Blood transfusion
Key Points of
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y
Iron-deficiency Anemia IDA is an illness of low iron in the body.
Iron makes Hb and healthy RBC which are needed for oxygenation
Reasons of IDA: blood loss, either from disease or injury,nutritional; defective absorption, ↑ demand such as during
pregnancy. 1 in 5 women of childbearing age and > 50% pregnant women have
iron-deficiency anemia.
Most common symptoms are fatigue & weakness.
Treated by stopping the bleeding, increasing iron in the diet, andgiving iron supplements.
Eating a well-balanced diet rich in iron and vitamins can prevent.
Can be successfully treated
CONCLUSION
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CONCLUSION
Proper antenatal care and awareness programmes forprevention of anemia.
Adequate iron / folic acid prophylaxis in all antenatalcases.
Early detection and timely referral to tertiary centers.
Management to be decided depending upon the cause ofanemia, type of anemia and severity of anemia.
Logical use of blood and blood components.
Proper intrapartum and postpartum care.
Motivation of the patient for acceptance of anycontraceptive method.
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Mild and Moderate
Nutrition
Control of infestation
Control of infection
Iron and Folic acid supplement
Economic reforms
Education Cultural reforms
Infrastructure development, etc.
Severe Anemia
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Severe Anemia
Management depends on the time at hand.
If diagnosis:
Preconception - oral, if not tolerated, parenteral
First & second trimester - oral + parenteralThird trimester - parenteral + blood transfusion by PCV
Late in third trimester and/ labor, blood transfusion byPCV nasal O2, B T, digitalization and ICU
management with team approach. Clinical condition
Associated risk factors
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Motherhood . . .. . . A dream of every woman