Diagnosis of anemia part 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

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

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.

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.

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 procedures (e.g.:Anemia in surgical or extracorporeal procedures (e.g.:
CABG and AVM) because the pumps may haveCABG and AVM) because the pumps may have
destroyed many red blood cells.destroyed many red blood cells.

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

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

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

ANEMIAS
CLASSIFICATION OF ANEMIAS
1. Anemia from inadequate erythropoiesis.
2. Anemia of blood loss (post-hemorrhagic).
3. Anemia due to ↑ destruction (hemolytic).

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

Laboratory Investigations
1. CBC
* Hct, Hb
* RBCs count, WBCs, Platelets
* Reticulocytes
•Cell morphology
•* Blood Indices:
MCV MCH MCHC
RDW=11.5-14.5%

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

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

Classification according to MCV
Microcytic
Iron deficiency
Thalassemia
Lead poisoning
Chronic disease
Normocytic
↓ Production
Macrocytic
Vit. B12
Folic acid

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

Commonest Causes of Anemia
Nutritional Deficiency : Iron Deficiency
Acute Hemolytic: G6PDD
Chronic Hemolytic: β-Thalassemia

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.

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

Normal daily requirements ofNormal daily requirements of
ironiron
 Iron stores of term sufficient for 4 msIron stores of term sufficient for 4 ms
Iron supplementation should be given to:Iron supplementation should be given to:
 Term breast fed: starting from 4 ms.Term breast fed: starting from 4 ms.
 PT & Formula fed: from 1 - 2 months.PT & Formula fed: from 1 - 2 months.
 1 mg/kg/day1 mg/kg/day elemental iron for normalelemental iron for normal
infants and children (max 15 mg/day).infants and children (max 15 mg/day).
 2 mg/kg/day2 mg/kg/day elemental iron: LBW,very lowelemental iron: LBW,very low
HbHb

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),

Etiology of IDAEtiology of IDA
I. Inadequate supply of iron.I. Inadequate supply of iron.
A. Inadequate iron stores atA. Inadequate iron stores at
birth:birth:
 Premature.Premature.
 multiple births.multiple births.
 Severe maternal iron def.Severe maternal iron def.
 Fetal blood loss.Fetal blood loss.
II. Impaired absorption ofII. Impaired absorption of
iron:iron: chronic diarrhea andchronic diarrhea and
celiac disease.celiac disease.
III. Excessive demands forIII. Excessive demands for
iron:iron:
A‑ Blood loss during infancy:A‑ Blood loss during infancy:
 Cow milk allergy.Cow milk allergy.
 Acute or chronicAcute or chronic
hemorrhages.hemorrhages.
 Parasitic infestations asParasitic infestations as
hookhook worms.worms.
B. Inadequate dietary intake:B. Inadequate dietary intake:
 Early cow milk.Early cow milk.
 Exclusive breast feeding afterExclusive breast feeding after
6 months.6 months.
 Low intakeLow intake
 B‑ Failure to meet increasedB‑ Failure to meet increased
demands for growth:demands for growth:
 premature.premature.
 adolescenceadolescence ..

Pathogenesis: sequence ofPathogenesis: sequence of
eventsevents
 ↓↓ iron stores.iron stores.
 ↓↓ iron‑storage protein (ferritin) in ts , serum.iron‑storage protein (ferritin) in ts , serum.
 ↓↓ serum ironserum iron →→ ↑iron binding capacity TIBC.↑iron binding capacity TIBC.
 Anemia, prog. hypochromia,microcytosis.Anemia, prog. hypochromia,microcytosis.
 ↓↓ activity of iron‑containing intraactivity of iron‑containing intracellularcellular
enzymes (e.g. CNS -MAO).enzymes (e.g. CNS -MAO).

 Critical element in function of cellsCritical element in function of cells
 Hb facilitates O2 transfer to tissuesHb facilitates O2 transfer to tissues
 Myoglobin transfer O2 to muscle cellsMyoglobin transfer O2 to muscle cells
Functions of ironFunctions of iron

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

Clinical manifestationsClinical manifestations
1- Manifestations of underlying etiology:1- Manifestations of underlying etiology:
 prematurity, feeding pattern.prematurity, feeding pattern.
2- General manifestations of anemia2- General manifestations of anemia
3- Particular findings d.t effect of iron def. on3- Particular findings d.t effect of iron def. on
systems:systems:
 GIT:GIT: Anorexia, atrophic glossitis, dysphagia, PicaAnorexia, atrophic glossitis, dysphagia, Pica
(ingestion of wall plaster, clay), Geophagia(ingestion of wall plaster, clay), Geophagia
(earth), Pagophagia (ice), leaky gut synd,(earth), Pagophagia (ice), leaky gut synd,
malabs.lactose int.malabs.lactose int.
 CNS:CNS: Short attention span, irritability, breathShort attention span, irritability, breath
holding,holding,
↓↓ alertness, ↓ learning ability and schoolalertness, ↓ learning ability and school
performance.performance.
 Epithelial structuresEpithelial structures in adults such as spoonin adults such as spoon
shaped or concave nails and brittle nails.shaped or concave nails and brittle nails.

33--Particular findings d.t effect ofParticular findings d.t effect of
iron def. on systems (contiron def. on systems (cont.(:.(:
 ImmunologicaImmunologicall:: URTI common but bact.URTI common but bact.
infections↓.infections↓.
 SpleenSpleen slightly enlarged in 15%slightly enlarged in 15%
 GrowthGrowth retardation and signs of otherretardation and signs of other
deficienciesdeficiencies
 CVS:CVS: ↑↑ HR , cardiac hypertrophyHR , cardiac hypertrophy
↑↑Plasma volumePlasma volume
 Musculoskeletal System:Musculoskeletal System:
impaired performanceimpaired performance
rapid lactic acidosisrapid lactic acidosis
Wide diploic spaces in XrayWide diploic spaces in Xray
↓↓Fracture healingFracture healing

Laboratory findingsLaboratory findings
A. (CBC) :A. (CBC) :
 Hypochromic microcytic anemiaHypochromic microcytic anemia (Hb > RBC(Hb > RBC
formation):formation):
 ↓↓ Hematocrit. Hb< 9 g/dl.Hematocrit. Hb< 9 g/dl.
 Red cell count 3 ‑ 5 millions/mm3Red cell count 3 ‑ 5 millions/mm3
(slightly).(slightly).
 Red blood cell indices : All are ↓: but FEPRed blood cell indices : All are ↓: but FEP
isis ↑↑
 ↓↓ MCV:MCV: < 78 fl (N 78-95 fl)[fl = 10-15L.< 78 fl (N 78-95 fl)[fl = 10-15L.
 ↓↓ MCH:MCH: < 26 pg (N 26-32 pg) [pg = 10-12< 26 pg (N 26-32 pg) [pg = 10-12
g]. , RDW >14.5%,g]. , RDW >14.5%, ↑↑FEP >40mg/dlFEP >40mg/dl
 ↓↓ MCHC:MCHC: < 30 g/ dl (N 32-36 g/dl).< 30 g/ dl (N 32-36 g/dl).

B. Plasma:B. Plasma:
 Plasma iron ↓ 10 ‑ 50Plasma iron ↓ 10 ‑ 50 µµg/dlg/dl
(normally 60-150 ugm/ dl).(normally 60-150 ugm/ dl).
 Serum ferritin: absent (N 10 -Serum ferritin: absent (N 10 -
150 ng/ ml) [ng =10-9 g].150 ng/ ml) [ng =10-9 g].
 ↑↑ TIBC 450TIBC 450 µµg/dl (N: 100-400g/dl (N: 100-400
µµg/dl).g/dl).
 Others:Others: ↑↑STfR , RBC zincSTfR , RBC zinc
protoporphyrin / heme ratioprotoporphyrin / heme ratio

Diagnosis of IDADiagnosis of IDA
1-1- Clinical manifestationsClinical manifestations..
2- Laboratory findings.2- Laboratory findings.
3- Therapeutic trial:3- Therapeutic trial: Best diagnostic.Best diagnostic.
 Improvement in NS function after 24 - 48 hrs.Improvement in NS function after 24 - 48 hrs.
 Reticulocytosis 48 - 72 hrs, peak: 5th - 10th d.Reticulocytosis 48 - 72 hrs, peak: 5th - 10th d.
 ↑↑ Hb after 4-30 days ( 0.25 - 0.4 g / dl/ day).Hb after 4-30 days ( 0.25 - 0.4 g / dl/ day).
 ↑↑ hematocrit (1 % / day).hematocrit (1 % / day).
 Repletion of Iron stores in 1 - 3 ms.Repletion of Iron stores in 1 - 3 ms.
Differential Diagnosis:Differential Diagnosis:
 causes ofcauses of hypochromic microcytichypochromic microcytic anemia asanemia as
thalassemia minor and anemia of chronic dis.thalassemia minor and anemia of chronic dis.

TreatmentTreatment
Oral Iron saltsOral Iron salts:: 6 mg/kg/day elemental for 36 mg/kg/day elemental for 3
ms/3 doses.ms/3 doses.
 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).

TreatmentTreatment
Parenteral iron therapyParenteral iron therapy :: Iron dextranIron dextran
mixture (mixture (ImferonImferon))®® 50 mg elemental50 mg elemental
iron / ml: only in intolerance oriron / ml: only in intolerance or
malabsorption or severe GIT disease.malabsorption or severe GIT disease.
Iron sucrose complex in RF anemiaIron sucrose complex in RF anemia
Blood transfusionBlood transfusion:: Severely anemicSeverely anemic
children with Hb < 4 g/dl givenchildren with Hb < 4 g/dl given
packed RBCspacked RBCs
Partial exchange transfusion:Partial exchange transfusion: surgicalsurgical
emergency, CHFemergency, CHF
Treatment of etiologyTreatment of etiology correct diet andcorrect diet and
®® Ancylostoma.Ancylostoma.

Failure to respond to iron RFailure to respond to iron R//
 Poor compliancePoor compliance
 Inadequate dose, preparationInadequate dose, preparation
 Persistent blood lossPersistent blood loss
 Incorrect diagnosis as;Incorrect diagnosis as;
Thalassemia minor infectionThalassemia minor infection
malabsorption malignancymalabsorption malignancy
renal disease folic, B12 , T4 def.renal disease folic, B12 , T4 def.
antacids intakeantacids intake

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.
 TreatmentTreatment:: Forced vomiting & gastric lavage withForced vomiting & gastric lavage with
sodium bicarbonate.sodium bicarbonate.
 DesferrioxamineDesferrioxamine (Desferal)(Desferal) specific chelator ofspecific chelator of
iron (antidote).iron (antidote).
 Blood and plasma transfusion, oxygen, andBlood and plasma transfusion, oxygen, and
electrolyte correctio.electrolyte correctio.

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).
 Inborn error of DNA metabolism.Inborn error of DNA metabolism.

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

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 .

Clinical manifestationsClinical manifestations
 Age : early few weeks after birth.Age : early few weeks after birth.
 General manifestations of anemia.General manifestations of anemia.
 Failure to gain weight.Failure to gain weight.
 Spleen and liver may be slightlySpleen and liver may be slightly
enlarged.enlarged.
 URTI or diarrhea (due to neutropenia).URTI or diarrhea (due to neutropenia).
 Petechiae and ecchymosesPetechiae and ecchymoses
(thrombocytopenia) in severe cases.(thrombocytopenia) in severe cases.

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.

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

* Deficiency: protein, iron, folic, vit. C, zinc
* Pleomorphic, or dimorphic:
* Hypochromic microcytic: Iron
* Megaloblastic: Folate
* Normocytic normochromic: protein, BM dep.
Anemia of PEM

Excess membrane cholesterol
RBC inclusions
Senescent RBC
Complement coated RBC
Antibody coated RBC
Rigid RBC
Functions of the Spleen

* CBC: depression of 1 or more bl. elements
* BM: Active formation
* Splenomegaly → sequestration, hormone
* Corrected by splenectomy
* 1ry: ITP,
* 2nd Splenomegaly: lymphoma, thalassemia,
leukemia, Schistosomiasis
Hypersplenism

* Heterozygous may be asymptomatic (FH)
* CBC: mild anemia 9-11 gm/dl, Hb↓ with infection
* ↓MCV, hypoch., N RDW, basophilic stip
* No response to iron HbA:90-95%mild F↑,A2>4%
β- Thalasemia intermedia
* 2-10% of homozygous
* Hb 7-10 gm/dl, med. expansion, pallor,
jaundice,hepatosplenomegaly
* ± growth retardation or hypogonadism,
* Bl. transfusion, folic, splenectomy, chelation
(1000ng/ml), tea after meals, avoid meat, liver
β- Thalasemia minor (trait)

Risks of blood TransfusionRisks of blood Transfusion
 Febrile non-hemolytic RXNFebrile non-hemolytic RXN
 Allergic reactions, urticaria,Allergic reactions, urticaria,
anaphylaxisanaphylaxis
 Bacterial contaminationBacterial contamination
 Fluid and circulatory overload,Fluid and circulatory overload,
 Hemolytic transfusion rxn FatalHemolytic transfusion rxn Fatal
 Viral Hepatitis, HIV , CMV, EBV,Viral Hepatitis, HIV , CMV, EBV,
parvovirus, malaria, Brucellosis,parvovirus, malaria, Brucellosis,
SyphilisSyphilis
 GVH, alloimmunisation, iron overloadGVH, alloimmunisation, iron overload

Anemia + infection + purpura but no
organomegaly

Put True or False:Put True or False:
Regarding anemia in childrenRegarding anemia in children
 Iron deficiency is the most commonIron deficiency is the most common
causecause
 Mucosal pallor is a useful clinical signMucosal pallor is a useful clinical sign
 A macrocytic blood film indicates IDAA macrocytic blood film indicates IDA
 Blood transfusion is a standard treatmentBlood transfusion is a standard treatment
 Occurs in less than 5% of populationOccurs in less than 5% of population
 A,bA,b

A child presenting with acuteA child presenting with acute
hemolysis due to inheritedhemolysis due to inherited
hemolytic anemia:hemolytic anemia:
 Anemia is present only afterAnemia is present only after
failure of hematopoiesisfailure of hematopoiesis
 Plasma conjugated bilirubin isPlasma conjugated bilirubin is
elevatedelevated
 Reticulocytes count will be < 1%Reticulocytes count will be < 1%
 Plasma haptoglobin elevatedPlasma haptoglobin elevated
 There is excess urinaryThere is excess urinary
urobilinogenurobilinogen
ee

Increased risk of pneumococcalIncreased risk of pneumococcal
infection is associated withinfection is associated with::
 Relapsed nephrotic syndromeRelapsed nephrotic syndrome
 SplenectomySplenectomy
 Sickle cell diseaseSickle cell disease
 ThalassemiaThalassemia
 Cystic fibrosisCystic fibrosis
 abcabc

TheThe following conditionsfollowing conditions
associated with hemolyticassociated with hemolytic
anemiaanemia::
 Sickle cell diseaseSickle cell disease
 Iron deficiencyIron deficiency
 G6PD deficiencyG6PD deficiency
 ITPITP
 acdacd

MatchingMatching
AnemiaAnemia::
 Aplastic anemiaAplastic anemia
 Copper deficiencyCopper deficiency
 IDAIDA
 LeukemiaLeukemia
 PerniciousPernicious
anemiaanemia
abaabcabaabc
 MicrocyticMicrocytic
 NormocyticNormocytic
 MacrocyticMacrocytic

A former 28 weeks premature presentsA former 28 weeks premature presents
with: pallor and reduced activity at thewith: pallor and reduced activity at the
age of 14 months. His diet includedage of 14 months. His diet included
cowcow’’s milk and juices. CBC reveals Hbs milk and juices. CBC reveals Hb
5.2gm/dl, MCV 50 fl, platelets5.2gm/dl, MCV 50 fl, platelets
300,000/cmm and WBCs 10,000/cmm.300,000/cmm and WBCs 10,000/cmm.
Reticulocytes count 0.8 %. The mostReticulocytes count 0.8 %. The most
likely diagnosislikely diagnosis ::
– ThalassemiaThalassemia
– Iron deficiencyIron deficiency
– SpherocytosisSpherocytosis ironiron
– Sickle cell anemiaSickle cell anemia

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 ::
 GiardiasisGiardiasis
 IDAIDA
 Folate deficiencyFolate deficiency
 G6PD deficiencyG6PD deficiency folicfolic

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. Which of thehepatosplenomegaly. Which of the
following investigations youfollowing investigations you
recommendrecommend ::
 CBC with indices and smearCBC with indices and smear
 Reticulocytes countReticulocytes count
 Lead screenLead screen
 Testing stools for occult bloodTesting stools for occult blood

Blood smear revealed microcyticBlood smear revealed microcytic
hypochromic anemia, and she receivedhypochromic anemia, and she received
iron therapy. When will be theiron therapy. When will be the
reticulocytes response maximum:reticulocytes response maximum:
 1-2 days1-2 days
 5-7 days5-7 days
 14-21days14-21days
 3-4 weeks3-4 weeks
 About 6 weeksAbout 6 weeks
 5-75-7

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
 4-84-8

If the patient did not improve in her anemia. WhichIf the patient did not improve in her anemia. Which
diseases of the following should be explored:diseases of the following should be explored:
 GIT blood lossGIT blood loss
 UTIUTI
 Parasitic infestationParasitic infestation
 Chronic diseaseChronic disease
 abdeabde

A 2 years boy referred for microcytosis thatA 2 years boy referred for microcytosis that
had not responded to iron. Findings onhad not responded to iron. Findings on
clinical exam are normal. Lab. Valuesclinical exam are normal. Lab. Values
include Hb 11.5gm%, MCV 72 fl,include Hb 11.5gm%, MCV 72 fl,
reticulocytes 1%. The most likelyreticulocytes 1%. The most likely
explanation:explanation:
 Iron deficiencyIron deficiency
 Lead exposureLead exposure
 Thalassemia traitThalassemia trait
 Chronic diseaseChronic disease
 Normal values for ageNormal values for age

ee

Diagnosis of anemia part 1

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Diagnosis of anemia part 1