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Uploaded byKeshav Chandra
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IRON DEFICIENCY ANEMIA

Iron deficiency anemia is the most common nutritional disorder globally, affecting 30% of the population. It is caused by inadequate iron intake or absorption, blood loss, or increased physiological demands. Common symptoms include pallor, fatigue, and impaired cognitive function. Laboratory findings show microcytic hypochromic anemia, low serum ferritin and iron, and elevated TIBC. Treatment involves oral iron supplementation, while ensuring compliance and watching for malabsorption or ongoing blood loss. Prevention through breastfeeding, iron-fortified formula, and supplements can reduce iron deficiency in at-risk groups like infants and women.

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IRON DEFICIENCY ANEMIA PRESENTED BY:- DR.KUMAR KESHAV CHANDRA
Contents:- • Definition • Classification • Role of iron • Sources of iron • Iron absorption transport and storage • Cause of IDA • Clinical manifestation • Lab findings • Treatment • Prevention
Anemia is defined as a reduction of the hemoglobin concentration or red blood cell volume below the reference level for age and sex of the individual. ANEMIA Age(yr) Mean value of Hb(g/dl) Lower limit of Hb (g/dl) MCV(fl) 0.5 - 4 12.5 11 70-73 5 - 7 13 11.5 75 8-11 13.5 12.0 76 12-14(F) 13.5 12.0 78 12-14(M) 14.0 12.5 77 18-49(F) 14.0 12.0 80 18-49(M) 16.0 14.0 80
Classification A. Morphological classification :- classified as microcytic, normocytic and macrocytic based on whether the RBC size(MCV) is low, normal or high, respectively.
B. Classification based on underlying physiology . INADEQUATE PRODUCTION  Diamond-Blackfan Anemia  Acquired pure red cell aplasia  Anemia of chronic disease  Congenital dyserythropoetic anemia  Physiological anemia of infancy  Megaloblastic anemia  Iron deficiency anemia Increased destruction or loss  Hemolytic anemias: RBC Mebrane defect Enzyme dfeciencies Autoimmune hemolytic anemia Heoglobinopathies
IRON DEFICIENCY ANEMIA • Iron deficiency is the most widespread and common nutritional disorder in the world. • 30% of the global population has iron- deficiency anemia, and most of them live in developing countries
Salient points • A full-term newborn contains about 0.5 g of iron, compared to 5 g of iron in adults. • It is necessary to absorb approximately 1 mg daily to maintain positive iron balance in childhood. • Because <10% of dietary iron usually is absorbed, a dietary intake of 8-10 mg of iron daily is necessary to maintain iron levels. • Breastfed infants have an advantage because they absorb iron 2-3 times more efficiently than infants fed with cow’s milk.
Role of Iron Role in transport and storage of oxygen in form of hemoglobin and myoglobin respectively. As prosthetic group in no. of enzymes(cytochromes, cyclooxygense, ETC) Helps in maintaining healthy immune system. As a reserve(ferritin and hemosiderin, present in the liver, spleen and bone marrow) to maintain iron homeostasis.
Body Iron distribution(Adult) - Hemoglobin: 2.5 gm - Storage (ferritin / haemosiderin) : 1.0 gm - Non-available tissue iron: 0.5 gm - Transport iron: 3-4 mg - Total : ~5 gm
SOURCE OF IRON • Heme iron – mainly derived animal source include meat, fish and poultry. Our bodies easily absorb this type of iron. • Non heme iron - Plant sources ( include dried beans, peas and lentils and some fruits and vegetables) • Both cow's milk and breast milk are low in iron (around 0.2-0.5 mg /l), however the iron in breast milk offers greater bioavailability .Reasons are ;- high content of lactoferrin high levels of vitamin C and lower level of calcium and phosphate
IRON ABSORPTION Depends upon – - Body stores of iron - Rate of erythropoiesis - Iron needs of the body Increased absorption in presence of: - vitamin C - fruit juices - lactose - amino acids- cystine, lysine ,histidine, - gastric Hcl Decreased absorption : - phytates , tannic acid - calcium salts & phosphates, prolonged achlorhydria
IRON ABSORPTION, TRANSPORT AND STORAGE
Causes of Iron deficiency Increased physiological demand: - growing children (6-24 months) - adolescence - women during reproductive ages Pathological blood loss: - chronic loss(IBD, Peptic ulcer, meckel’s diverticulum -Parasitic worm infestation -Phlebotomy specially in case of preterm new born child Inadequate iron intake or absorption: -nutritional deficiency-most important cause worldwide -decreased absorption- tropical sprue/ coeliac disease/ post gastrectomy
• Each gram of Hb contains 3.47 mg of iron, so loss of each ml of blood from body result in loss of 0.5 mg of iron • Hookworms - suck 0.03- 0.2 ml of blood per worm /day
Risk factor in development of IDA • Age- infants (especially premature); adolescents • Sex- increased risk in women • Drug- aspirin and NSAIDS • Diet pattern- especially in vegetarians, infant on cow’s milk. • Physiological- pregnancy; infancy; adolescence; at age of weaning
A relatively high Hb conc. of the newborn falls during the first 2–3 month of life, considerable iron is stored – these stored iron are sufficient for blood formation in the first 6–9 month of life in term infant Stores are depleted sooner in low-birthweight infants, as their iron stores are smaller.
Clinical manifestation Hematological manifestations  Pallor is the most important sign but usually not visible until Hb level falls to 7-8g/dl.  In mild to moderate anemia(Hb level of 6- 10 g/dl) only few symptoms of anemia is noted due to compensatory mechanism.  In severe anemia(Hb level<5g/dl, irritability anorexia and lethargy developed. Tachycardia and systolic flow murmur are often present and may lead to high output cardiac failure.
Non Hematological Manifestation Impaired neurocognitive function in infancy.  Some studies suggest an increased risk of seizures, strokes, breathholding spells in children, and exacerbations of restless leg syndrome in adults. Others include:-  pica, the desire to ingest nonnutritive substance  pagophagia, the desire to ingest ice.  The pica can result in the ingestion of lead- containing substances and result in concomitant plumbism . Cheilosis and koilonychia are signs of advanced iron deficiency
Dysphagia due to formation of esophageal webs (Plummer-vinson syndrome)
LAB FINDINGS Tissue iron stores represented by bone marrow hemosiderin disappear Serum ferritin decreases(stored form) Serum iron level decreases • Serum transferrin, S. iron-binding capacity of the - increases Percent saturation (transferrin saturation) falls below normal Free erythrocyte protoporphyrins (FEP) accumulate
At this point iron deficiency progresse to IDA PBS- Microcytosis, hypochromia, Anisopoikilocytosis with increased RDW. Elliptocyte and cigar shaped red cells are often seen Detection of isoluble transferrin receptor and decreased reticulocyte Hb conc are very usefull and early indicator of IDA
Diagnosis A presumptive D/g of IDA is made by; 1.CBC showing microcytic hypochroic anemia with High RDW and low MCV, MCH and MCHC. Normal WBC count with normal or elevated platelet count 2. Hb & Hct value – low OTHER TEST :- 3.Reticulocyte % - normal or moderately elevated .but absolute retic count is inadequate. 4. Reduced serum ferritin, reduced serum iron, and Elevated transferrin increased total iron-binding capacity.
Transferrin saturation index:- Ratio of serum iron to TIBC(< 16% - indicates iron deficiency) 5. Bone marrow aspiration, with the marrow stained for iron - No stainable iron in marrow reticulum cells in IDA 6.Stool for occult blood 7.Stool R/M/E - hookworm and whipworm “An increase in hemoglobin ≥1 g/dL after a month of iron therapy is usually the most practical means to establish the diagnosis.”
INDICES NORMAL IDA (CUTOFF VALUE) S. FERRITIN 50-200µg/L <12 µg/L IN AGE <5 YR <15 µg/L In age > 5yr TIBC 300-360 µg/dl >400 µg/dl S. Iron 50-150 µg/dl <30 µg/dl Transferrin saturation 30-50 % <16 % Erythrocyte protoporphyrin level <30 µg/L < 5yr age->70 µg/L >5yr age- >80 µg/L Marrow iron store 1-3 + 0 •
PBS OF IDA
Treatment Oral administration - ferrous salts (most often sulfate) - 3–6mg/kg /d of elemental iron. Ferrous sulphate contain 20% elemental iron by wt and ideally given b/w meals with juice.
Differential Diagnosis of Microcytic Anemia That Fails to Respond to Oral Iron Poor compliance (true intolerance of Fe is uncommon) Incorrect dose or medication Malabsorption of administered iron Ongoing blood loss Concurrent infection or inflammatory disorder inhibiting the response to iron Concurrent vitamin B12 or folate deficiency Diagnosis other than iron deficiency:- Thalassemias Anemia of chronic disease Lead poisoning Iron refractory iron deficiency anemia (IRIDA)
Parenteral iron preparations(iron dextran) are only used when malabsorption is present, or persistent ongoing blood loss or when compliance is poor, because oral therapy is otherwise as fast, as effective, much less expensive and less toxic. Red cell transfusion : should only be used when heart failure is imminent or if the anemia is severe with evidence of substantial ongoing blood loss. Unless there is active bleeding, transfusions must be given slowly to avoid precipitating congestive heart failure.
Responses to Iron therapy 12–24 hr • Replacement of intracellular iron enzymes; subjective improvement; decreased irritability; increased Appetite 36–48 hr • Initial bone marrow response; erythroid hyperplasia 48–72 hr • Reticulocytosis, peaking at 5–7 days 4–30 days • Increase in hemoglobin level 1–3 mo • Repletion of stores
Take home message Iron deficiency is best prevented to avoid both its systemic manifestations and the anemia Routine screening using Hb or Hct is done at 12 mo of age, or earlier at 4 mo of age, if the child is assessed to be at high risk for iron deficiency. Breastfeeding should be encouraged, with the addition of supplemental iron at 4 month of age. Infants who are not breastfed should only receive iron- fortified formula (12 mg of iron /L) for the 1st year, and thereafter cow’s milk should be limited to <600-720 ml/d. Iron medication should be continued for 2-3 mo after blood values normalize to reestablish iron stores. Good follow-up is essential to ensure a response to therapy.
IRON DEFICIENCY ANEMIA