Iron deficiency anemia

Iron deficiency anemia

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  Anemia, Iron deficiencyanemia Dr. Kalpana Malla MD Pediatrics Manipal Teaching Hospital Download more documents and slide shows on The Medical Post [ www.themedicalpost.net ]
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  ANEMIA
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  What is Anemia? •Reduction of the red blood cell (RBC) volume or hemoglobin concentration below reference level for the age and sex of the individual • Hb < - 2SD or 95th centile for age and sex
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  Anemia Basics All anemiasare either due to…. 1. Ineffective RBC production or 2. Accelerated destruction of the RBC
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  Classification • By RBCmorphology and By Etiological factors responsible for anemia
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  Microcytic hypochromic anemia 1.Iron deficiency anemia – nutritional, - posthemohragic 2. Ineffective Erythropoiesis - hemoglobinopathies, Thalassemia - Lead poisoning, Sideroblastic anemia - Cu deficiency, Pyridoxine deficiency -Chronic ds - infection, inflammations , renal ds
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  Macrocytic anemia • MegaloblasticErythropoiesis a) Nutritional - Folate deficiency, B12 deficiency b) Toxic – Treatment with antifolate compound – methotrexate,, and drugs that inhibit DNA replication – zidovudine, phenytoin c) Congenital disorders of DNA synthesis like Orotic aciduria etc. d) Malabsorption - liver ds
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  Macrocytic anemia Non- Megaloblastic Erythropoiesis a) Chronic hemolytic anemia b) Liver ds c) Hypothyroidism d) Diamond blackfan syndrome
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  Normocytic, Normochromic anemia 1.Impaired cell production (low reticulocyte count) - aplastic anemia - pure red cell aplasia - physiological anemia of infancy - infections - Systemic diseases like endocrinal, renal and hepatic diseases - bone marrow replacement – leukemia, tumors, storage ds, myelofibrosis, osteopetrosis 2 Hemolytic anemia ( reticulocyte count high)
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  DIMORPHIC ANEMIA • Whentwo causes of anemia act simultaneously, e.g : macrocytic hypochromic due to hookworm infestation leading to deficiency of both iron and vitamin B12 or folic acid • following a blood transfusion
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  ETIOLOGICAL CLASSIFICATION OFANEMIA • Blood loss Acute Chronic • Decreased iron assimilation - Nutritional deficiency - Hypoplastic or aplastic anemia - Bone marrow infiltration like leukemia & other malignancies, - Myelodysplastic syndrome - Dyserythropoietic anemia
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  ETIOLOGICAL CLASSIFICATION OFANEMIA • Increased physiologic requirement - Extracorpscular - - Alloimmune & isoimmune hemolytic anemia - Microangiopathic anemias - Infections - Hypersplenism
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  ETIOLOGICAL CLASSIFICATION OFANEMIA - Intracorpsular defect – Red cell membranopathy i.e. congenital spherocytosis,elliptocytosis – Hemoglobinopathy like HbS, C,D,E etc. Thalassemia syndrome – RBC enzymopathies like G6PD deficiency, PK deficiency etc.
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  Follow-up • Re-check CBC4-6 weeks (to confirm response) • Continue iron 3-4 months (to replace stores) • If no improvement on adequate iron therapy, consider evaluating the child for lead poisoning or thalassemia
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  Differential of Anemia Hgb, indices, retic count and smear Inadequate response (RPI<2) Adequate response (RPI>3) r/o blood loss/hemolytic dis Hypochromic, microcytic Normochromic,normocytic Macrocytic hemoglobinopathy iron def chronic dis B12/folate def enzymopathy thalssemia Ca/BM failure Liver disease membranopathy chronic disease Transient erythroblastopenia Down Syndrome extrinsic factors of childhood (DIC,HUS,TTP) lead poisoning Renal disease Drugs (etoh) Immune Hemolytic anemia
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  IRON DEFICIENCY ANEMIA
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  IDA • Most commoncause of anemia worldwide • Most important cause of iron deficiency anemia is parasitic infection - hookworms, whipworms and roundworms
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  GENERAL FEATURES  Newborncontains 0.5g of iron, adult contains 5g  A diet containing 8–10mg of iron daily is necessary for optimal nutrition  1mg of iron must be absorbed each day - Absorbed in the proximal small intestine  Absorbed 2-3 times more efficiently from human milk than from cow's milk
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  Iron sources: • Meat •Liver • Kidney • Egg-yolk • Green vegetables • Fruits **** Cow’s milk- poor source of iron
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  Iron metabolism: Distribution ofbody iron: (adults) - Hemoglobin: 2.3 gm - Storage (ferritin / haemosiderin) : 1.0 gm - Non-available tissue iron: 0.5 gm - Transport iron: 3-4 mg - Total : ~5 gm
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  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
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  Iron Metabolism: Figure 16-8: Iron metabolism
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  Pathogenesis of IDA: Increasedphysiological demand: - growing children (6-24 months) - adolescence - women during reproductive ages Pathological blood loss: -chronic loss Inadequate intake of diets rich in iron: -nutritional deficiency -decreased absorption- gastroenterostomy/ tropical sprue/ coeliac disease
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  • High Hbconc of the newborn falls during the first 2– 3 mo - considerable iron is stored - usually sufficient for blood formation in the first 6–9 mo of life in term
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  ETIOLOGY • The mostimportant cause world-wide is infestation with parasitic worms (hookworms- suck 0.03- 0.2 ml of blood per worm /day ),whipworms, roundworms • Dietary insufficiency • Malabsorption
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  ETIOLOGY • Chronic bloodloss - occult bleeding : peptic ulcer, Meckel diverticulum, polyp, hemangioma, inflammatory bowel disease, Intravascular hemolysis and hemoglobinuria • Chronic diarrhea • Milk allergy
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  Risk factors forIDA • Demograpghic – Eldery, Teenager, Female • Dieatary – low Iron, low Vit C, excess phytate,tea coffee, • Social and physical – poverty,alcohol abuse,GIT ds
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  CLINICAL FEATURES Pallor isthe most important sign Look for pallor : FACE, nails, palms, conj, mucus membranes Pagophagia (pica for ice) / pica Anxiety , Poor appetite Below 5g/dL: irritability and anorexia are prominent Tachycardia and systolic murmurs- dyspnea , Palpitations
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  CLINICAL FEATURES • Hair loss and lightheadedness • Fainting • Sleepiness, Tinnitus • Mouth ulcers, Glossitis ,Angular cheilitis • Constipation • Depression, Twitching muscles, Tingling, numbness or burning sensations
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  CLINICAL FEATURES • Koilonychia(spoon-shaped nails) , • Platynychia • Weak,brittle nails • Pruritus • Dysphagia due to formation of esophageal webs (Plummer-vinson syndrome
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  Koilonychia - spoonshaped nail
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  CLINICAL FEATURES Neurologic andintellectual function Affects attention span, alertness, Verbal learning and memory Monoamine oxidase (MAO), an iron dependent enzyme, has a crucial role in neurochemical reactions in the CNS breath-holding spells
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  Response to lowHb: First:  Tissue iron stores represented by bone marrow hemosiderin disappear  Serum ferritin decreases Next:  Serum iron level decreases  Serum transferrin,S. iron-binding capacity of the - increases  Percent saturation (transferrin saturation) falls below normal  Free erythrocyte protoporphyrins (FEP) accumulates
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  Response to lowHb: Later: Microcytosis, hypochromia, poikilocytosis, and increased RBC distribution width (RDW)
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  Diagnosis - LABORATORYINVESTIGATIONS 1.complete blood count (CBC) - High RBC distribution width (RDW) - reflecting an increased variability in the size of red blood cells (RBCs). - A low MCV,MCH and MCHC 2. Hemoglobin (Hb)&hematocrit (Hct) value – low 3. Reticulocyte - normal or moderately elevated
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  Diagnosis - LABORATORYINVESTIGATIONS 3.Peripheral blood smear – microcytic hypochromic anemia, target cells, hypochromic pencil-shaped cells, and occasionally small numbers of nucleated RBC • Thrombocytosis -activate thrombopoietin receptors in precursor cells which make platelets
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  LABORATORY INVESTIGATIONS 4. Diagnostictests – - Serum ferritin- low - Serum iron - low - Serum transferrin -elevated - Total iron binding capacity (TIBC) - high 5.Stool for occult blood 6.Stool R/M/E - hookworm and whipworm
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  LABORATORY INVESTIGATIONS • Ratioof serum iron to TIBC (called iron saturation or transferrin saturation index - is the most specific indicator of iron deficiency - < 5% - indicates iron deficiency
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  DiagnosisLABORATORY INVESTIGATIONS Goldstandard • Bone marrow aspiration, with the marrow stained for iron -Bone marrow is hypercellular, with erythroid hyperplasia • Leukocytes and megakaryocytes are normal • No stainable iron in marrow reticulum cells
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  TREATMENT • Oral administration- ferrous salts (sulfate, gluconate, fumarate) -4–6mg/kg of elemental iron • Consumption of milk should be limited • Blood loss from intolerance to cow's milk proteins is reduced • The amount of iron-rich foods is increased
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  Oral iron failure? •Incorrect diagnosis (eg, thalassemia) • Patient is not taking the medication • Not absorbed (enteric coated?) malabsorption syndromes gastrectomy/celiac disease • Rapid iron loss? • Anemia of chronic disease-impairs bone marrow response
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  TREATMENT • Parenteral ironpreparation (iron dextran) : Intolerance to oral iron, severe gastrointestinal complaints • Packed or sedimented RBCs : with Hb values < 4g/dL • congestive heart failure: fresh-packed RBCs should be considered
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  RESPONSES TO IRONTHERAPY 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
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