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![INDICATIONS FOR IV IRON
• Severe symptomatic anemia requiring accelerated erythropoesis
• Failure of oral iron from GI intolerance
• Failure of oral iron due to absorption issues
H pylori infection, autoimmune gastritis, celiac disease, gastric bypass
surgery, inflammatory bowel disease
• Cancer and chemotherapy associated anemia
• Anemia with chronic renal disease (with or without[?] dialysis dependance)
• Heavy ongoing GI or menstrual blood losses](https://image.slidesharecdn.com/irondeficiencyanemiafinal-190903184556/75/Iron-deficiency-anemia-final-68-2048.jpg)
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Iron deficiency anemia final
This document provides information on iron deficiency anemia (IDA), including its global burden, pathophysiology, causes, clinical features, investigations, and management. Some key points: - IDA is the most common cause of anemia globally, with over 50% of anemias due to iron deficiency. It accounts for 8.4 lakh deaths annually, most in Africa and Asia. - IDA occurs when iron stores are decreased and total body iron is reduced. It develops in stages from initial iron deficiency without anemia to latent IDA to overt IDA. - Causes of IDA include blood loss, inadequate dietary iron intake, malabsorption, increased demands in pregnancy/growth. Daily iron requirements vary from
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Iron deficiency anemia final
- 1. DR. P.GANDIAH, MD Director Departmentof medicine SVSMC, MBNR
- 2. GLOBAL BURDEN OFIDA • Globally 50% of anemias are due to Iron deficiency. • 8.4 lakhs death annually due to IDA. • 71% of deaths due to IDA are in Africa and Asian countries.
- 4. • First mostcommonest cause of Anemia is Iron deficiency. • Second most commonest cause of Anemia is Anemia due to chronic disease. • IDA is a type of Anemia where total body iron is reduced.
- 5. • Anemia isreduction in number of Red cell mass or their Oxygen carrying capacity that is needed to meet the metabolic needs of body tissues. • IDA is a type of anemia where Iron supplied to marrow is decreased and total body iron is decreased.
- 6. ANEMIA CUT OUTPOINTS • Adult males < 13gm/dL • Adult females < 12gm/dL • Adult pregnant women < 11gm/dL • Children below 14yrs < 12gm/dL • Children below 6 yrs < 11gm/dL
- 7. THREE PARAMETERS AREUSED TO DEFINE ANEMIA • Hemoglobin level • Hematocrit percentage • RBC count
- 8. CLASSIFICATION OF ANAEMIA •Microcytic anemia – MCV < 80 fL • Normocytic anemia – MCV 80 – 95 fL • Macrocytic anemia – MCV > 95 – 100 fL • Some define Macrocytic > 100 fL
- 9. CAUSE OF MICROCYTICANEMIA • Iron deficiency (relating to blood loss, dietary deficiency and occasionally malabsorption) • Anaemia of chronic disease (also associated with normocytic anaemia) • Haemoglobinopathies, e.g. thalassaemia • Sideroblastic anaemias (rare genetic or acquired disorders)
- 10. DAILY IRON REQUIREMENTS •< 4 months ………………… 0.5 mg • Infants < 12months …………………. 1 mg • Pregnants ………………… 4mg • Menstruating females ………………. 3mg • Adult males and post menopausal females …… 1mg
- 11. • Adult malehas ~ 4 gms total body iron stores
- 12. • Heme isa porphyrin ring containing an Iron atom • Each Hb molecule can bind 4 oxygen molecules at haeme site
- 14. Iron Absorption (%of dose) 0 5 10 15 20 25 Veal muscle Hemoglobin Fish muscle Veal liver Ferritin Soy beans Wheat Lettuce Corn Black beans Spinach Rice Non-heme iron Heme iron
- 15. IRON ABSORPTION • Foodsources supply: 10 - 25 mg / day • Absorbed in the brush border of the upper small intestine • Enhanced by gastric acid • Inhibited by tannins, systemic inflammation • Most dietary iron is non-heme form, <5% bioavailability • < 10% dietary iron is heme form, >25% bioavailability
- 17. • Transferrin –plasma iron transporter protein. - Carries less than 1% of total body iron • Ferritin – intracellular storage of iron • Hemosiderin – long term iron storage pool
- 18. IRON STORAGE Ferritin multi-subunit protein primarilyintracellular some in plasma Hemosiderin insoluble form of ferritin visible microscopically
- 21. IRON LOSSES • Ironis closely conserved in humans <0.05% of iron is lost per day normally 1. Very small amounts in urine, bile and sweat 2. Cells shed from skin, intestinal and urinary tracts 3. Menstrual blood loss 4. Pregnancy and lactation • Humans have NO other physiologic means to excrete excess iron
- 23. • Blood loss •Occult or overt GI losses, traumatic or surgical losses • Failure to meet increased requirements • Rapid growth in infancy and adolescence • Menstruation, pregnancy • Inadequate iron absorption • Diet low in heme iron • Gastrointestinal disease or surgery • Excessive cow’s milk intake in infants
- 26. 3 STAGES OFIDA • Stage 1 : Decrease storage of Iron without any other detectable abnormality. • Latent IDA : Iron storage exhausted not anemic Diagnosed by decrease in serum Ferritin fall in Transferrin level (Normal 30%) • Iron Deficiency Anemia
- 28. • Iron deficiency •Decrease in Ferritin • Anemia is variable • Decrease Iron availability due to - lower plasma Iron level - increase phagocytosis of RBC by macrophages • Increase in Ferritin levels • Anemia is usually mild (10 – 11 gm%)
- 30. CAUSES OF IRONDEFICIENCY ANAEMIA • Obstetric/gynaecological causes • Gastrointestinal bleeding • Malabsorption • Pharmacological • Increased demand • Dietary deficiency • Other – blood donation, blood loss from non-gastrointestinal sources.
- 31. • Obs &Gynaecological causes – Menorrhagia, Normal menstruation combined with a deficient diet, Pregnancy. • Gastrointestinal bleeding – Oesophagitis, Varices, Ulcerated hernia, PUD , IBD, malignancy, Angiodysplasia. • Malabsorption – Celiac disease, Atrophic gastritis, H. pylori infection • Pharmacological – medicines that cause gastric erosions/ulceration, e.g. NSAIDs, Steroids, Anticoagulants, SSRIs. • Increased demand – Pregnancy, growth spurts (uncommon) • Dietary deficiency – vegans, older people, toddlers fed exclusively milk • Other – blood donation, blood loss from non-gastrointestinal sources, e.g. nosebleeds, trauma, surgery.
- 32. RED FLAGS INIRON DEFICIENCY ANAEMIA • Upper and lower GI investigations should be considered in all males and post-menopausal females with iron deficiency anemia unless there is an obvious alternative cause. N.B. fecal occult blood testing is not beneficial for investigating people with iron deficiency anemia as it is insensitive and non-specific. • Patients with gastrointestinal symptoms and unexplained anemia, require urgent referral, particularly those aged over 50 years or with a family history of colorectal cancer • Males with Hb < 11 g/dL and non-menstruating females with Hb levels < 10 g/dL require urgent referral. • Patients who do not respond to a trial treatment of iron replacement should be referred for further investigation.
- 33. CHRONIC DISEASES –ASSOCIATED WITH MICROCYTIC ANEMIA • Situations of chronic inflammation • Chronic infections • Autoimmune conditions, e.g. rheumatoid arthritis, SLE, inflammatory bowel disease • Malignancy • Chronic heart failure • Chronic kidney disease
- 34. LATENT IRON DEFICIENCYANEMIA • Iron deficiency without Anemia. • Iron deficiency does not always develop into anaemia. • low Iron and normal Hb levels. • three times more common than iron deficiency anaemia.
- 35. INVESTIGATING THE CAUSEOF MICROCYTIC ANAEMIA • Serum Ferritin should be done in microcytic anemia. • Ferritin is an acute phase protein. • Ferritin is an iron storage protein. • Keeps iron in a soluble and non-toxic form. • Ferritin reflects true iron stores in uncomplicated iron deficiency. • Ferritin might raised in - Inflammation - Infection, - Chronic diseases - Malignancy - Liver diseases.
- 36. • A serumferritin below 15 – 20 micrograms/L in a person with microcytic anaemia confirms iron deficiency anaemia
- 37. Iron deficiency Anaemia ofchronic disease Haemoglobinopathies, e.g. thalassaemia, Sideroblastic anaemia Serum ferritin Decreased Increased Increased Serum iron Decreased Normal or decreased Normal or increased TIBC Normal or increased Normal or decreased Normal Transferrin saturation Decreased Normal or decreased Normal or increased Serum soluble transferrin receptor Increased Normal or decreased Increased
- 38. FEATURES OF IRONDEFICIENCY ANEMIA •Depends on the degree and the rate of development of anemia •Symptoms common to all anemias: • pallor, fatigability, weakness, dizziness, irritability
- 39. OTHER FEATURES OFIDA • Pagophagia - craving ice • Pica - craving of nonfood substances • e.g., dirt, clay, laundry starch • Glossitis - smooth tongue • Restless Legs • angular stomatitis - cracking of corners of mouth • Koilonychia - thin, brittle, spoon-shaped fingernails
- 40.
- 43. • Smooth tongue •Painless and shiny
- 47.
- 50.
- 51. • Peripheral bloodsmear • Red cell indices (MCV, MCH) • Serum ferritin • Serum iron / transferrin = iron saturation • Bone marrow iron stain (Prussian blue)
- 54.
- 55. • Cell sizedecreases because of decrease in Hb Heme in IDA Globin in Thalassemia • Maturation disorders may result in microcytes if the cytoplasm is altered. • Macrocytes because of defect in nucleolus or maturation.
- 56.
- 58. Serum Bone Marrow N N N Circulation Reticulocyte Erythrocyte Spleen Macrophage Low Hgb LowSerum Fe/TS Low sFt/Liver Fe High sTfR Erythroblast TfR+ Fe Transferrin
- 59. FERRITIN IRON SATURATION MCV &Hb & Hct
- 61. • Thalassemia trait(low MCV, normal RDW) • Imbalance of globin chain production • Anemia of inflammation • Decreased iron utilization in the face of adequate iron stores • Low ferritin / serum transferrin receptor
- 62. IRON STAIN OFBONE MARROW Iron Deficient Marrow Prussian Blue Stain Normal Marrow Prussian Blue Stain
- 63. TREATMENT • Most patientsare treated initally with oral iron unless there is an absorptive problem. • Dietary sources + FeSo4 BID. • TID is very constipating and causes gastric distress; commonest cause for noncompliance • IV iron is no longer ‘dangerous’. The newer formulations such as iron sucrose, LMW iron dextran and ferric gluconate have minimal risks of infusion reactions • In very severe cases, RBC transfusion
- 64. ORAL THERAPY OFIRON DEFICIENCY • Carbonyl iron (elemental), heme-iron polypeptide (extracted from porcine RBC), polysaccharide-iron complex • Ascorbic acid increases oral iron absorption but dose is usually not in significant quantity to make a difference • Phytates (cereal grains), tannins (tea) and antacid therapy inhibit oral iron absorption
- 65. ORAL IRON SUPPLEMENTATION •100 – 200 mg elemental iron per day • In the past, recommended vitamin C tablets, evidence now suggests that the therapeutic benefit of this is minimal. • on an empty stomach. • If gastric symptoms occur, advise the patient to try taking the supplement with food • Hb should rise by approximately 1 g/L, per day, and 20 g/L higher after 3 - 4 weeks. • treatment should be continued for a further 3 months to replenish iron stores. • Ferritin levels should be checked 4 – 6 weeks after completing treatment.
- 66. Iron salt DoseElemental iron content Ferrous fumarate 200 mg 65 mg Ferrous sulfate (tablet) 325 mg 105 mg Ferrous sulfate (liquid) 150 mg (in 5 mL) 30 mg ( in 5 mL)
- 67. RESPONSE TO ORALIRON THERAPY • Peak Reticulocyte count 7 - 10 d. • Increased Hb and Hct 14 - 21 d. • Normal Hb and Hct 2 months • Normal Iron stores 4 - 5 months
- 68. INDICATIONS FOR IVIRON • Severe symptomatic anemia requiring accelerated erythropoesis • Failure of oral iron from GI intolerance • Failure of oral iron due to absorption issues H pylori infection, autoimmune gastritis, celiac disease, gastric bypass surgery, inflammatory bowel disease • Cancer and chemotherapy associated anemia • Anemia with chronic renal disease (with or without[?] dialysis dependance) • Heavy ongoing GI or menstrual blood losses
- 69. INTRAVENOUS IRON FORMULATIONS •High molecular weight Iron Dextran is not routinely used anymore due to a much poorer safety profile (anaphalyctoid reactions) in comparison to newer iron preparations • Hemoglobin iron deficit (mg) = Body Wt x (14 - Hgb) x (2.145) (formula dose not account for repletion of body stores)
- 70. LMW Iron Dextran Iron Sucrose Ferric Gluconate Ferumoxytol FerricCarboxy maltose Administered Dosage 100mg 200 mg 125 mg 510mg 750mg Total Dose Infusion 1000 mg no no 1020 mg 3d apart 1500mg 7d apart Cost Inexpensive Inexpensive Inexpensive Expensive Expensive Indication IDA IDA in CKD IDA in CKD/HD +epo IDA in CKD IDA + IDA in CKD Test dose Yes none none None None Administration Iv (preferred) or im Iv push or 15m infusion i.v push or 1hr infusion 17s i.v push or 15 m infusion 7.5 m iv push or 15 m infusion