Post on 09-Mar-2018
Dr Goudarzipour
MCV:HCT/RBC,fl MCH:Hb/RBC,pg MCHC:HCT/Hb,gd RDW:anisocytosis
Neutropenia?
Anemia?
Physiologic anemia?
NL PLT? WHATS MPV?
examples 2 Y/O male WBC:6700:PMN:60,L:40RBC:4.700.000Hb:11.7MCV:76PLT:135000
Case -2 3 month years ,female WBC:6500,L:30,P:70
Hb:8.7MCV:90
PLT:400.000
Case-3 7 y/o,female WBC:5390,P:63,L:37
RBC:5.900.000Hb:10.5MCV:64
MCH:23PLT:433.000
CASE 4 2 y/o male WBC:14500,P;78,l;22
RBC:5400Hb;8HCT:13MCV:99
MCH:32MCHC:36PLT:78000
Background Iron deficiency is the most common nutritional
deficiency in children and is worldwide indistribuiotion. The incidence of iron-deficiency anemia is high in
infancy. 40–50% of children under 5 years of age in
developing countries.
Babies are born with iron stored in their bodies.Because they grow rapidly, infants and childrenneed to absorb an average of 1 mg of iron per day. Since children only absorb about 10% of the iron
they eat, most children need to receive 8-10 mg ofiron per day. Breastfed babies need less, becauseiron is absorbed 3 times better when it is in breastmilk
Tissue Effects of IronDeficiency
I. Gastrointestinal tract Anorexia-common and an early symptom Pica-pagophagia (ice) geophagia Atrophic glossitis II. Central nervous system Irritability Fatigue and decreased activity
Tissue Effects of IronDeficiency
III. Cardiovascular system Cardiac hypertrophy IV. Musculoskeletal system Deficiency of myoglobin and cytochrome C Adverse effect on fracture healing V. Immunologic system Evidence of increased propensity for infection
Absorbtion of Iron
PREVALENCE
Peak prevalence occurs during late infancy andearly childhood • Rapid growth with exhaustion of gestational iron • Low levels of dietary iron • Complicating effect of cow’s milk-induced
exudative enteropathy
PREVALENCE
A second peak is seen during adolescence due torapid growth and suboptimal iron intake. This is amplified in females due to menstrual blood
loss
Causes of Iron-DeficiencyAnemia
I. Deficient intake Dietary (milk, 0.75 mg iron/l) II. Inadequate absorption Poor bioavailability: absorption of heme Fe.Fe2.Fe3;
breast milk iron.cow’s milk Antacid therapy or high gastric pH (gastric acid assists
in increasing solubility of inorganic iron) Cobalt, lead ingestion
Causes of Iron-DeficiencyAnemia
III. Increased demand Growth pregnancy IV. Blood loss
The best sources of iron include: Baby formula with iron Breast milk (the iron is very easily used by the
child) Infant cereals and other iron-fortified cereals Liver
symptoms Blue-tinged or very pale whites of eyes Blood in the stools Brittle nails Decreased appetite (especially in children) Fatigue Headache Irritability Pale skin color (pallor) Shortness of breath Sore tongue Unusual food cravings (called pica) Weakness Note: There may be no symptoms if anemia is mild.
P/E and lab
1. Hemoglobin: Hemoglobin is below the acceptablelevel for age 2. Red cell indices: Lower than normal MCV, MCH and
MCHC for age. 3.Increase RDWBlood smear: Red cells are hypochromic and microcytic
with anisocytosis
hemoglobin level falls below 10 g/dl.
P/E and lab
Basophilic stippling can also be present but not asfrequently The RDW is high (.14.5%) Reticulocyte count: The reticulocyte count is usually
increase in bleeding).(normal Platelet count: The platelet count varies from
thrombocytopenia to thrombocytosis. free erythrocyte protoporphyrin (FEP) levels. increase
P/E and lab
The normal FEP level is 15.56 +-8.3 mg/dl. Theupper limit of normal is 40 mg/dl Serum ferritin: The level of serum ferritin reflects
the level of body iron stores (below than 12). Normal ferritin levels, however, can exist in iron
deficiency when bacterial or parasitic infection,malignancy or chronic inflammatory conditionsco-exist .because ferritin is an acute-phase reactant
P/E and lab Serum iron and iron saturation percentage: limitations: • Wide normal variations (age, sex, laboratory
methodology) • Time consuming • Subject to error from iron ingestion • Diurnal variation • Falls in mild or transient infection.
Stages of Iron Depletion
1. Iron depletion:tissue stores are decreased without a change in hematocrit or serum iron level2. Iron-deficient erythropoiesisIron decreasereticuloendothelial macrophage
TIBC increase With out change in HCT3. Iron-deficiency anemia: Anemia Increase RDW Increase FEP
Differential Diagnosis
Differential Diagnosis
TREATMENT
Oral Iron Medication Dose: 1.5–2.0 mg/kg elemental iron three times
daily. In children with gastrointestinal side effects, iron
once every other day Duration: 6–8 weeks after hemoglobin level and
the red cell indices return to normal.
Response:
Peak reticulocyte count on days 5–10 followinginitiation of iron therapy. Following peak reticulocyte level, hemoglobin rises
on average by 0.25–0.4 g/dl/ hematocrit rises 1%/day during first 7–10 days. Thereafter, hemoglobin rises slower: 0.1–0.15
g/dl/day.
Failure to respond to oraliron:
Poor compliance – failure or irregular administration of oraliron;
Inadequate iron dose Ineffective iron preparation Insufficient durationPersistent or unrecognized blood loss Incorrect diagnosis – thalassemia, sideroblastic anemiaCoexistent disease that interferes with absorption or
utilization of iron Impaired gastrointestinal absorption due to high gastric pH
Parenteral Therapy
Noncompliance or poor tolerance of oral iron. Severe bowel disease (e.g., inflammatory bowel
disease) Chronic hemorrhage Rapid replacement of iron stores is needed. Erythropoietin therapy is necessary, e.g. renal
dialysis.
Blood Transfusion
In children with sever infection specially with cardiacdysfunction or Hb less than 4 g/dl.
References Glader B. Iron-deficiency anemia. In: Kliegman RM, Behrman RE,
Jenson HB, Stanton BF, eds. Nelson Textbook of Pediatrics. 18th ed.Philadelphia, Pa: Saunders Elsevier; 2007: chap 455.
Heird WC. The feeding of infants and children. In: Kliegman RM,Behrman RE, Jenson HB, Stanton BF, eds. Nelson Textbook ofPediatrics. 18th Ed. Philadelphia, Pa: Saunders Elsevier; 2007: chap42.
O'Connor NR. Infant formula. Am Fam Physician. 2009;79:565-570.