ANEMIA IN PEDIATRICS 2019
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Iron deficiency anemia is the most common nutritional deficiency in children worldwide. It occurs most frequently in infants aged 6-24 months, especially those who are artificially fed or from low socioeconomic backgrounds. Iron deficiency anemia develops in stages from iron depletion to iron deficiency to anemia, characterized by low iron stores, serum iron, and high total iron binding capacity. Clinically, it presents with pallor, fatigue, and impact on development in children. Treatment involves oral or parenteral iron replacement therapy, addressing the underlying cause, and ensuring an adequate iron intake.
ANEMIA IN PEDIATRICS 2019
- 1. 11--ANEMIA INANEMIA IN PEDIATRICSPEDIATRICS for clinical pharmacyfor clinical pharmacy Prof Dr Hussein AbdeldayemProf Dr Hussein Abdeldayem Professor of Pediatrics,Professor of Pediatrics, Alex UniversityAlex University
- 2. FACTORS FORFACTORS FOR ERYTHROPOIESISERYTHROPOIESIS Bone MarrowBone Marrow ERYTHROPOIETIN (90%kidney,ERYTHROPOIETIN (90%kidney, 10%liver)10%liver) Nutritional factors:Nutritional factors: 1- protein: AA1- protein: AA 2- iron2- iron 3- B12, folic acid3- B12, folic acid 4- copper, cobalt4- copper, cobalt 5- ascorbic acid5- ascorbic acid
- 3. Regulation ofRegulation of ErythropoiesisErythropoiesis While the kidney produces most of theWhile the kidney produces most of the erythropoietin, the liver and othererythropoietin, the liver and other tissues also produce some.tissues also produce some. In fetal life, the liver produced all of theIn fetal life, the liver produced all of the erythropoietinerythropoietin –– as the final kidneyas the final kidney –– the metanephros - had not yetthe metanephros - had not yet completed development.completed development.
- 4. Regulation ofRegulation of ErythropoiesisErythropoiesis How many are produced:How many are produced: – 25 billion /24 hours.25 billion /24 hours. – The entering cells are reticulocytes whichThe entering cells are reticulocytes which should be 1% of the total population ofshould be 1% of the total population of circulating erythrocytes.circulating erythrocytes. – Erythrocytes last 120 days and areErythrocytes last 120 days and are destroyed by the spleen.destroyed by the spleen. – Red cell production should equal red cellRed cell production should equal red cell destruction.destruction.
- 5. Uses of erythropoietinUses of erythropoietin epoetin alfaepoetin alfa Indication: Anemia of chronic renal failure. Cancer and AIDS chemotherapy Transplant patients Chronic inflammatrory illness as SLE Prematurity . Anemia in surgical or extracorporeal proceduresAnemia in surgical or extracorporeal procedures because the pumps may have destroyed many redbecause the pumps may have destroyed many red blood cells.blood cells.
- 6. Uses of epoetin alfaUses of epoetin alfa Recommended starting dose is 80 – 120 U/kg - sc three times a week. Average maintenance dose - 75 U/kg, three times a week in most patients. The most common side effect - aggravation of hypertension
- 7. Normal CBC
- 8. Bone Marrow
- 10. Hematologic Value Hb (g/dl) Ht % RBCs Nucleated RBCs % Reticulocytes % Cord 17 55 5.3 6 5 3 m 11.5 35 4.3 0 1 6m-6y 12.5 37 4.7 0 1 7-12 y 13 39 5 0 1 Normal RBC
- 11. What is AnemiaWhat is Anemia?? Anemia is a decrease in HbAnemia is a decrease in Hb concentration or the number of redconcentration or the number of red blood cells (RBC) as measuredblood cells (RBC) as measured – 1. gm per cu mm or1. gm per cu mm or – 2. by volume of packed RBC per 100 ml2. by volume of packed RBC per 100 ml of blood. This is clinically obtained byof blood. This is clinically obtained by doing a hematocrit (HCT)doing a hematocrit (HCT) Below average of normal values for ageBelow average of normal values for age and sexand sex
- 12. ANEMIAS CLASSIFICATION OF ANEMIAS 1. Anemia from inadequate erythropoiesis. 2. Anemia of blood loss (post-hemorrhagic). 3. Anemia due to ↑ destruction (hemolytic).
- 13. ANEMIAS Diagnosis: Type, Severity, Etiology CLINICAL EVALUATION: 1. Common manifestations: Pallor, exercise intolerance, dyspnoea, palpitations, headache, lack of conc., irritability, syncope, hemic murmurs. 2. Less commonly: anorexia, nausea, flatulence, constipation, mild proteinuria, fever 3. Severe cases: ↑ C.O, CHF
- 14. PallorPallor
- 16. Laboratory Investigations 1. CBC * Hct, Hb * RBCs count, WBCs, Platelets * Reticulocytes •Cell morphology •* Blood Indices: MCV MCH MCHC RDW=11.5-14.5%
- 17. Primary LaboratoryPrimary Laboratory InvestigationInvestigation The increased reticulocyte count isThe increased reticulocyte count is usually accompanied by peripheralusually accompanied by peripheral smear RBC polychromasiasmear RBC polychromasia
- 18. Reticulocyte CountReticulocyte Count Is required in the evaluationIs required in the evaluation of all patients with anemia asof all patients with anemia as it is a simple measure ofit is a simple measure of productionproduction Young RBC that still containsYoung RBC that still contains a small amount of RNAa small amount of RNA Normally take 1 day forNormally take 1 day for reticulocyte to mature.reticulocyte to mature. 1/1201/120thth of RBC normallyof RBC normally
- 19. Classification according to MCV Microcytic Iron deficiency Thalassemia Lead poisoning Chronic disease Normocytic ↓ Production Macrocytic Vit. B12 Folic acid
- 20. 2. Biochemical Investigations A. Iron status Serum iron (N 60-150 µg/dl) TIBC (N 100-400 µg/dl) Serum ferritin (N 10-150 ng/dl) B. Megaloblastic anemia Serum vit. B12, folate Laboratory Investigations
- 21. Commonest Causes of Anemia Nutritional Deficiency : Iron Deficiency Acute Hemolytic: G6PDD Chronic Hemolytic: β-Thalassemia
- 24. ANEMIAS DUE TO DEFICIENCYANEMIAS DUE TO DEFICIENCY OF SPECIFIC NUTRIENTSOF SPECIFIC NUTRIENTS IRON DEFICIENCY ANEMIAIRON DEFICIENCY ANEMIA Most commonMost common nutritional deficiency innutritional deficiency in children and is worldwide.children and is worldwide. Highest :Highest : ●● 6 - 246 - 24 monthsmonths ●● artificially fed infants.artificially fed infants. ●● low socioeconomic status.low socioeconomic status.
- 25. Iron-deficiency anemia remains the mostIron-deficiency anemia remains the most common nutritional problem from a globalcommon nutritional problem from a global perspective, it is estimated that roughly 2-5%perspective, it is estimated that roughly 2-5% of the world population are anaemic.of the world population are anaemic. Prevalence of Iron Deficiency AnemiaPrevalence of Iron Deficiency Anemia
- 26. Normal Daily IronNormal Daily Iron RequirementsRequirements FT baby: with store enough for 4 moFT baby: with store enough for 4 mo PMT baby: with store enough for 2 moPMT baby: with store enough for 2 mo 1mg/kg/day elemental iron for infants and1mg/kg/day elemental iron for infants and children (max 15 mg/day)children (max 15 mg/day) 2 mg/kg/day elemental iron for low birth2 mg/kg/day elemental iron for low birth weight and newborns with very low initial Hbweight and newborns with very low initial Hb valuesvalues 6 mg/kg/day elemental iron is needed for tt6 mg/kg/day elemental iron is needed for tt for 3 mofor 3 mo
- 27. Dietary ironDietary iron I:Heme iron compoundsI:Heme iron compounds (hemoglobin and(hemoglobin and myoglobin) :myoglobin) : foods of animal origin:foods of animal origin: 1.5 - 6 mg1.5 - 6 mg iron /100 giron /100 g meat, liver, poultry, fish, etc.meat, liver, poultry, fish, etc. Easily digested and readily absorbed.Easily digested and readily absorbed. Absorption is not affected by diet.Absorption is not affected by diet. II:Non-heme ironII:Non-heme iron ( ferric iron salts ) :( ferric iron salts ) : egg yolk, green vegetables, whole grains, legumes,egg yolk, green vegetables, whole grains, legumes, nutsnuts (( ++ 1.5 mg/100 g)1.5 mg/100 g). ferric. ferric →→ ferrous beforeferrous before absorption.absorption. Absorption (50% : breast milk , 10% of cowAbsorption (50% : breast milk , 10% of cow ’’s milks milk iron .iron . AbsorptionAbsorption ↑↑ : Vitamin C, sugar, amino acids (meat,: Vitamin C, sugar, amino acids (meat, poultry, fish) & HCl.poultry, fish) & HCl. AbsorptionAbsorption ↓↓ : Fibers (bran), tannate (tea),: Fibers (bran), tannate (tea),
- 28. Iron is used inIron is used in:: Hemoglobin: transfer O2 to tissuesHemoglobin: transfer O2 to tissues Heme enzymes, e.g., cytochromes, catalase,Heme enzymes, e.g., cytochromes, catalase, peroxidaseperoxidase Myoglobin:transfer O2 to muscle cellsMyoglobin:transfer O2 to muscle cells Metalloflavoprotein enzymes such as xanthineMetalloflavoprotein enzymes such as xanthine oxidaseoxidase The mitochondrial enzyme alpha-The mitochondrial enzyme alpha- glycerophosphate oxidase and otherglycerophosphate oxidase and other mitochondrial enzymes.mitochondrial enzymes. Other enzymes and processesOther enzymes and processes
- 29. Most commonMost common nutritional deficiency innutritional deficiency in children and is worldwide.children and is worldwide. More common at:More common at: ●● 6 - 246 - 24 monthsmonths ●● artificially fed infants.artificially fed infants. ●● low socioeconomic statuslow socioeconomic status IRON DEFICIENCYIRON DEFICIENCY ANEMIAANEMIA
- 30. STAGESSTAGES Iron stores S.IronIron stores S.Iron AnemiaAnemia (s. ferritin)(s. ferritin) Stage of IRONStage of IRON Low Normal NoneLow Normal None DEPLETIONDEPLETION Stage of IRONStage of IRON Absent Low NoneAbsent Low None DEFICIENCYDEFICIENCY Stage of IRONStage of IRON Absent Low PresentAbsent Low Present DEF. ANEMIADEF. ANEMIA
- 31. ↓↓ iron stores.iron stores. ↓↓ iron‑storage protein (ferritin)iron‑storage protein (ferritin) ↓↓ serum ironserum iron ↑↑iron binding capacity TIBC.iron binding capacity TIBC. Anemia: hypochromia,microcytosis.Anemia: hypochromia,microcytosis. ↓↓ activity of iron‑containing intraactivity of iron‑containing intra cellular enzymes (e.g. CNS -MAO).cellular enzymes (e.g. CNS -MAO). PathogenesisPathogenesis
- 32. Clinical manifestationsClinical manifestations - Particular CP due to effect of iron def. on- Particular CP due to effect of iron def. on systems:systems: GIT:GIT: Anorexia, glossitis, Pica (ingestion of wallAnorexia, glossitis, Pica (ingestion of wall plaster, clay), Geophagia (earth), Pagophagiaplaster, clay), Geophagia (earth), Pagophagia (ice,(ice, CNS:CNS: Short attention span, irritability, breathShort attention span, irritability, breath holding,holding, ↓↓ alertness, ↓ learning ability and schoolalertness, ↓ learning ability and school performance.performance.
- 33. IRON replacement TREATMENT (oral,IRON replacement TREATMENT (oral, IM, IV)IM, IV) TREAT THE CAUSETREAT THE CAUSE TREATMENTTREATMENT
- 34. TreatmentTreatment Oral Iron saltsOral Iron salts:: 6 mg/kg/day elemental for 3 mo6 mg/kg/day elemental for 3 mo Ferrous sulfate drops for infants ( 20%Ferrous sulfate drops for infants ( 20% elemental iron).elemental iron). Ferrous gluconate drops ( 12 % elementalFerrous gluconate drops ( 12 % elemental iron).iron). ferrous fumarate (30% elemental iron) tabletsferrous fumarate (30% elemental iron) tablets or syrup for older children.or syrup for older children. Iron better between meals. fibers (e.g. wholeIron better between meals. fibers (e.g. whole bread and cereals), tannate (like tea),bread and cereals), tannate (like tea), phosphates (in bread, cow's milk and eggphosphates (in bread, cow's milk and egg yolk) and phytic acid ↓ absorption of iron.yolk) and phytic acid ↓ absorption of iron. absorption ↑ by vitamin C (e.g. citrous fruits),absorption ↑ by vitamin C (e.g. citrous fruits), sugar and amino acids (meat, poultry, fish).sugar and amino acids (meat, poultry, fish).
- 35. TreatmentTreatment Parenteral iron therapyParenteral iron therapy :: Iron dextranIron dextran mixture (mixture (ImferonImferon))®® 50 mg elemental iron / ml50 mg elemental iron / ml only in intolerance or malabsorptiononly in intolerance or malabsorption Packed RBC transfusionPacked RBC transfusion :: SeverelySeverely anemic children with Hb < 4 g/dlanemic children with Hb < 4 g/dl Treatment of etiologyTreatment of etiology correct diet , ttcorrect diet , tt parasiteparasite
- 36. These preparation are mostlyThese preparation are mostly available as ferrous(Fe+2) and someavailable as ferrous(Fe+2) and some in ferric(Fe+3)formin ferric(Fe+3)form Ferrous salt are better absorbedFerrous salt are better absorbed than ferric saltsthan ferric salts ORAL IRON THERAPYORAL IRON THERAPY
- 37. Iron is poorly absorbed in the form ofIron is poorly absorbed in the form of carbonate, citrate and pyrophosphate,carbonate, citrate and pyrophosphate, colloidal iron and iron carbohydratecolloidal iron and iron carbohydrate complexcomplex FORMS :FORMS : Tablets, capsulesTablets, capsules Sugar coated & uncoated tablets •Sugar coated & uncoated tablets • Slow release tabsSlow release tabs chewable tabs •chewable tabs • Drops &syrups—used by children'sDrops &syrups—used by children's
- 38. 1. Ferrous sulphate: 20 – 32% iron1. Ferrous sulphate: 20 – 32% iron 2. Ferrous fumarate: 33% elemental2. Ferrous fumarate: 33% elemental ironiron 3. Ferrous gluconate : 12% elemental3. Ferrous gluconate : 12% elemental ironiron 4. Colloidal ferric hydroxide:50%4. Colloidal ferric hydroxide:50% elemental iron •elemental iron • Other oral preparations are ferrousOther oral preparations are ferrous choline citrate , ferric ammoniumcholine citrate , ferric ammonium citrate , iron calcium complex, ironcitrate , iron calcium complex, iron hydroxy polymatose.hydroxy polymatose. FERRIC HYDROCHLORIDE POLYMALTOSE
- 39. It is rapidly absorbed, with a high rate of ironIt is rapidly absorbed, with a high rate of iron utilization and produces an effective increase inutilization and produces an effective increase in Haemoglobin. Due to its favourable nonionicHaemoglobin. Due to its favourable nonionic nature it has the following properties unlikenature it has the following properties unlike ionised iron salt preparations: · Ferose does notionised iron salt preparations: · Ferose does not give rise to irritation of the intestinal mucosa andgive rise to irritation of the intestinal mucosa and does not stain the teeth. · Ferose has palatable,does not stain the teeth. · Ferose has palatable, non metallic taste (Ferose chewable tablets havenon metallic taste (Ferose chewable tablets have chocolate flavour and are acceptable even by thechocolate flavour and are acceptable even by the most resistant patients of all ages). · Ferose hasmost resistant patients of all ages). · Ferose has excellent tolerance.excellent tolerance. Ferrous form of oral ironFerrous form of oral iron FEROSEFEROSE
- 40. •• Important points to remember ;ElementalImportant points to remember ;Elemental iron content and not quantity of ironiron content and not quantity of iron compound per unit dose to be consideredcompound per unit dose to be considered Sustained released preparations expensiveSustained released preparations expensive and irrationaland irrational Liquid formulations: should be put on backLiquid formulations: should be put on back of tongue and swallowedof tongue and swallowed
- 41. Iron saltsIron salts Ferrous sulfateFerrous sulfate ––least expensiveleast expensive –– treatment oftreatment of choicechoice Ferrous salts (sulfate, fumarate, gluconate,Ferrous salts (sulfate, fumarate, gluconate, succinate) are absorbed about three times assuccinate) are absorbed about three times as well as ferric salts.well as ferric salts. Vitamin C increases absorption - AscorbicVitamin C increases absorption - Ascorbic acid, 200 mg or more, increases absorption byacid, 200 mg or more, increases absorption by at least 30% (with increased incidence of sideat least 30% (with increased incidence of side effects too)effects too) Carbonyl iron: microspheres of pure ironCarbonyl iron: microspheres of pure iron –– lessless gastrointestinal toxicity than iron saltsgastrointestinal toxicity than iron salts
- 42. •• Constipation (BLACK) is commonConstipation (BLACK) is common than diarrheathan diarrhea •• Epigastric painEpigastric pain •• VomitingVomiting •• Heart burnHeart burn •• Metallic tasteMetallic taste •• NauseaNausea •• Staining of teeth.Staining of teeth. Adverse reactions to oralAdverse reactions to oral ironiron
- 43. •• Oral iron is not toleratedOral iron is not tolerated •• Failure to absorb oral ironFailure to absorb oral iron •• Non compliance to oral ironNon compliance to oral iron •• In presence of severe deficiency withIn presence of severe deficiency with chronic bleedingchronic bleeding Indications of parenteralIndications of parenteral therapytherapy
- 44. •• Parenteral iron therapy needsParenteral iron therapy needs calculation of total iron requirement ofcalculation of total iron requirement of the patient –the patient – Iron requirement (mg) = 4.4 X Body wtIron requirement (mg) = 4.4 X Body wt (Kg) X Hb deficit g/dL(Kg) X Hb deficit g/dL Calculation for parenteralCalculation for parenteral ironiron
- 45. 1. Iron dextran (Imferon): I.V/ I.M1. Iron dextran (Imferon): I.V/ I.M 2. Iron sorbitol citric acid complex:2. Iron sorbitol citric acid complex: Only I.M 3. Iron carbohydrate complexOnly I.M 3. Iron carbohydrate complex : I.M: I.M 4. Sodium ferric gluconate: Recently4. Sodium ferric gluconate: Recently approved preparation for I.V use hasapproved preparation for I.V use has much lower risk of anaphylacticmuch lower risk of anaphylactic reaction than iron dextranreaction than iron dextran Parenteral ironParenteral iron preparationspreparations
- 46. •• Iron dextran and iron sorbitol bothIron dextran and iron sorbitol both contain 50 mg/mL recommended dosecontain 50 mg/mL recommended dose is 100 mg daily 2 mL on alternate daysis 100 mg daily 2 mL on alternate days until total required dose isuntil total required dose is administered or maximum 2 g .administered or maximum 2 g . To prevent staining to skin given deepTo prevent staining to skin given deep I.M in buttock using z track techniqueI.M in buttock using z track technique I.M therapyI.M therapy Elemental iron 100 mg (As Ferric hydroxide polymaltose complex)
- 47. •• Intramuscular: – Local pain at site ,Intramuscular: – Local pain at site , pigmentation of skin , sterile abcesspigmentation of skin , sterile abcess –– Systemic: headache, fever,Systemic: headache, fever, arthralgia, backache, tachycardia,arthralgia, backache, tachycardia, flushing hemolysis and collapse theseflushing hemolysis and collapse these effects are probably due to excessiveeffects are probably due to excessive amount of free iron in plasmaamount of free iron in plasma –– Iron sorbitol may causeIron sorbitol may cause disorientation and temporary loss ofdisorientation and temporary loss of taste, urine turns black on standingtaste, urine turns black on standing Adverse effectsAdverse effects
- 48. •• Iron dextran after test dose 0.5 mLIron dextran after test dose 0.5 mL iron dextran injected I.V over 5 to 10iron dextran injected I.V over 5 to 10 minmin •• Total dose required diluted in 500 mLTotal dose required diluted in 500 mL NS & infused slowly over 6 to 8 hoursNS & infused slowly over 6 to 8 hours under supervisionunder supervision •• If required amount greater than 50If required amount greater than 50 mL given on two consecutive daysmL given on two consecutive days I.V TherapyI.V Therapy
- 49. 1- Systemic reaction:1- Systemic reaction: severe form : anaphylactoid reactionsevere form : anaphylactoid reaction severe chest painsevere chest pain respiratory distressrespiratory distress circulatory collapsecirculatory collapse 2- local: skin coloration2- local: skin coloration Adverse effects OFAdverse effects OF IntravenousIntravenous
- 50. Acute iron intoxicationAcute iron intoxication Accidental ingestion of large doses of iron:Accidental ingestion of large doses of iron: mortality rate 50%.mortality rate 50%. Early symptomsEarly symptoms :: Vomiting, diarrhea,Vomiting, diarrhea, dehydration, corrosive iron ondehydration, corrosive iron on stomach,intestines.stomach,intestines. LaterLater :: Severe irreversible CV collapse, shock,Severe irreversible CV collapse, shock, coma.coma. markedmarked ↑↑in plasma iron.in plasma iron.
- 51. 1. Stomach wash with 1% NaHCO3 to render it insoluble and1. Stomach wash with 1% NaHCO3 to render it insoluble and remove undissolved iron tabletsremove undissolved iron tablets 2. IV Desferrioxamine 5 to 10 g in 100 mL isotonic saline or2. IV Desferrioxamine 5 to 10 g in 100 mL isotonic saline or calcium sodium edetate 35 to 40 mg/Kg to retard the absorptioncalcium sodium edetate 35 to 40 mg/Kg to retard the absorption from GITfrom GIT 3. Early replacement of fluids and electrolytes, correction of3. Early replacement of fluids and electrolytes, correction of metabolic acidosis and hypotension by vasopressorsmetabolic acidosis and hypotension by vasopressors 4 Diazepam and other anticonvulsa-nts if epileptic4 Diazepam and other anticonvulsa-nts if epileptic Treatment of Acute iron poisoningTreatment of Acute iron poisoning
- 52. •• Potent specific chelator of iron binds ferric iron to formPotent specific chelator of iron binds ferric iron to form ferrioxamine a stable water soluble chelateferrioxamine a stable water soluble chelate •• Ferrioxamine is excreted 2/3 in urine and 1/3 in bile colorsFerrioxamine is excreted 2/3 in urine and 1/3 in bile colors urine reddish brownurine reddish brown •• Removes iron from hemosiderin except that in bone marrowRemoves iron from hemosiderin except that in bone marrow •• Well tolerated rapid I.V may causeWell tolerated rapid I.V may cause hypotension, anaphylactic reactions andhypotension, anaphylactic reactions and tachycardiatachycardia •• Allergic reactions and cataract known with chronicAllergic reactions and cataract known with chronic administrationadministration •• Contraindicated in renal disease anuriaContraindicated in renal disease anuria Desferrioxamine MesylateDesferrioxamine Mesylate
- 54. MEGALOBLASTICMEGALOBLASTIC ANEMIASANEMIAS Megaloblasts in B.MMegaloblasts in B.M ↑↑ MCV,MCV, Hypersegmented neutrophils in peripheralHypersegmented neutrophils in peripheral blood.blood. Causes:Causes: Deficiency of :Deficiency of : folic acid (megaloblastic anemia of infancy)folic acid (megaloblastic anemia of infancy) vit.B12 (juvenile pernicious anemia).vit.B12 (juvenile pernicious anemia).
- 55. Megaloblastic anemia ofMegaloblastic anemia of infancyinfancy Folic acid :Folic acid : Normal daily requirements :Normal daily requirements : 30 - 6030 - 60 µµgg per dayper day (10 times that of adult).(10 times that of adult). Folic deficiency in pregnant :Folic deficiency in pregnant : Fetal neural tube defectsFetal neural tube defects Preterm labour (2 folds)Preterm labour (2 folds) LBWLBW So folicSo folic should beshould be supplemented to pregnantsupplemented to pregnant mothermother
- 56. Etiology of folic acidEtiology of folic acid deficiencydeficiency 1- Inadequate intake of folic acid:1- Inadequate intake of folic acid: Feeding on goatFeeding on goat’’s milk (very poor in folic acid).s milk (very poor in folic acid). Feeding on heat-sterilized cowFeeding on heat-sterilized cow’’s milk <50% folic acid.s milk <50% folic acid. 2- Relative deficiency :2- Relative deficiency : Rapid growth : prematures.Rapid growth : prematures. Chronic hemolytic anemias, leukemias, lymphomas.Chronic hemolytic anemias, leukemias, lymphomas. 3- Defective absorption:3- Defective absorption: Chronic diarrhea.Chronic diarrhea. Prolonged antibiotics , antiepileptics (phenytoin, phenobarb.).Prolonged antibiotics , antiepileptics (phenytoin, phenobarb.). Malabsorption syndromes, congenital folate malabsorptionMalabsorption syndromes, congenital folate malabsorption syndrome.syndrome. Folic antagonists: Co-trimoxazole, methotrexate,Folic antagonists: Co-trimoxazole, methotrexate, pyrimethamine .pyrimethamine . Ascorbic acid deficiency .Ascorbic acid deficiency .
- 57. Laboratory findingsLaboratory findings 1- Peripheral blood1- Peripheral blood :: ↓↓ Hemoglobin (< 6 g/dl)., RBCs count.Hemoglobin (< 6 g/dl)., RBCs count. ↑↑ MCV to 100 fl (macrocytosis).,MCV to 100 fl (macrocytosis)., ↑↑ RDWRDW ↓↓ reticulocytic count.reticulocytic count. Neutropenia + hypersegmented nuclei ofNeutropenia + hypersegmented nuclei of mature polymorphs.mature polymorphs. Mild thrombocytopenia.Mild thrombocytopenia. Serum & RBC folateSerum & RBC folate 2- Bone marrow :2- Bone marrow : Hypercellular with predominant megaloblasts.Hypercellular with predominant megaloblasts.
- 58. TreatmentTreatment Folic acid, 2-5 mg/day P/O or inj. 3-4Folic acid, 2-5 mg/day P/O or inj. 3-4 wks.wks. Ascorbic acid if scurvy.Ascorbic acid if scurvy. Packed RBCs transfusion:Packed RBCs transfusion: ONLYONLY inin severe cases.severe cases. Folinic acid in defects d.t methotrexateFolinic acid in defects d.t methotrexate
- 59. A 6 months infant has had intermittentA 6 months infant has had intermittent diarrhoea for 1 month, after multiplediarrhoea for 1 month, after multiple formula changes, he was receivingformula changes, he was receiving goat milk. At 12 months of age hegoat milk. At 12 months of age he presented with pallor, decreasedpresented with pallor, decreased activity. Blood film was macrocytic.activity. Blood film was macrocytic. Most likely diagnosis isMost likely diagnosis is :: ThalassemiaThalassemia GiardiasisGiardiasis IDAIDA Folate deficiencyFolate deficiency G6PD deficiencyG6PD deficiency folicfolic
- 60. A 18 month old girl likes to eat dirt andA 18 month old girl likes to eat dirt and ice and her diet is cow milk with littleice and her diet is cow milk with little amount of solid foods. On exam, sheamount of solid foods. On exam, she was found to be pale with nowas found to be pale with no hepatosplenomegaly.hepatosplenomegaly. diagnosisdiagnosis Iron deficiency anemiaIron deficiency anemia Megaloblastic anemiaMegaloblastic anemia Acute hemolytic anemiaAcute hemolytic anemia Chronic hemolytic anemiaChronic hemolytic anemia
- 61. Concerning the previous girl, if Hb andConcerning the previous girl, if Hb and Hct returned to normal, when to stopHct returned to normal, when to stop iron therapy?iron therapy? Stop it as soon Hb becomes normalStop it as soon Hb becomes normal Continue for 1-2 weeksContinue for 1-2 weeks Continue for 4-8 weeksContinue for 4-8 weeks Continue for 4-6 weeksContinue for 4-6 weeks 4-84-8
- 62. Thank You