2. Iron defeiciency Anemia
• Anemia is defined as reduced amount of hemoglobin and reduction in oxygen carrying capacity
of RBCs
• High prevalence is seen in preschool children (6–36 months of age).
• 90% cases are from developing countries.
• Approximately 50% of cases are due to iron deficiency
• Risk factors include limited iron stores at birth,
• Immediate umbilical cord clamping at birth,
• Delayed introduction of complementary foods and
• Chronic infections
• Iron deficiency anaemia develops when the supply of iron is inadequate for the requirement of
haemoglobin synthesis.
• m/c cause of anemia in the world.
3.
4. ETIOLOGY
• DECREASED IRON STORES-Preterm ,Small for date babies,Twins
• INADEQUATE DIETARY INTAKE - Delayed introduction of complementary
feeds,Malnutrition/Iron-poor diet.
• INCREASED BLOOD LOSS- Gastrointestinal e.g. peptic ulcer, haemorrhoids
hookworm infestation,malaria,bleeding diathesis,Menstrual loss in adolescent girls.
• DECREASED ABSORPTION - malabsorption syndromes ,Chronic infection/ chronic
diarrhea, Gastrointestinal surgery.
• INCREASED REQUIREMENTS - Spurts of growth in infancy, childhood and
adolescence, Prematurity, LBW babies ,Recovering from protein energy malnutrition
(PEM).
5. • Healthy newborns have body iron stores of 250 mg or approximately 80 parts per
million (ppm); this decreases to approximately 60 ppm in the first 6 months of life,
as milk is a poor source of iron.
• Infants consuming cow milk are more likely to have iron deficiency than breastfed
infants because
• (i) the iron contained in cow milk has lower bioavailability;
• (ii) bovine milk has a higher concentration of calcium that competes with iron for
absorption
• (iii) due to gastrointestinal blood loss with cow milk allergy.
6.
7.
8. Clinical features
• Careful history including type of milk, timing of introduction of complementary
foods in infants should be noted.
• Peak incidence - between 6 months and 3 years followed by adolescents 11–17
years
Clinical findings are related to the severity and rate of development of anemia.
• SYMPTOMS
• Irritability and anorexia usually precede weakness, fatigue, leg cramps,
breathlessness and tachycardia.
• Exertional dyspnoea Palpitations
• Inability to concentrate, somnolence,
giddiness
• Features of the causative condition,
for example epigastric pain (peptic
ulcer)
• Constipation
• Pica
• Delayed mental and motor
development
9. • SIGNS
• Pallor(EYES,PALM)
• Atrophy of tongue papillae, Angular stomatitis, Glossitis,
• Koilonychias, and Platynychia.
• Hair: Dry, lustreless hair, excess loss of scalp hair.
• CVS: • Severe cases may have breathlessness, tachycardia and a soft systolic hemic flow
murmur at the cardiac base,can progress to ‘high output’ congestive cardiac failure
10. Angular stomatitis
.
• Growth is invariably affected in severe cases causing ‘failure to thrive’.
• Rare presentations = diarrhea, pseudotumor cerebri and splenomegaly
• Craving and ingestion of inedible substances (Pica) is present in 70%–80% of cases. Common
substances include clay (geophagia), dirt, ice (pagophagia), chalk etc. Pica improves with iron
therapy. Pica increases the risks of lead poisoning and helminthic infections.
• IDA also impairs cognitive abilities and can affect mental, social and emotional development.
• Fe = cofactor for many enzymes in cellular metabolic pathways, depress immunity,secondary
infections.
11. Investigations
1. PBS= Microcytic, hypochromic red cells with anisocytosis and poikilocytosis
2. Red cell distribution width (RDW) (>15%) n=11.5-14.5%
3. MCV and MCHC
4. Total RBC count is reduced, unlike in thalassemia where it is increased.
5. The serum iron <60 microgram/dl and ferritin is low.
6. TIBC >350 microg/dl
7. S.transferrin saturation is reduced to less than 16%. (N= 25-50%)
8. The reduction in serum ferritin occurs early and correlates well with the total body
iron stores. (May ^| in pneumonia)
12. • High free erythroprotoporphyrin
(FEP>70)precedes the anemia
• Reticulocyte count is normal unless the child has
received iron therapy.
• Severe cases= Chest X-ray, and Echo Heart ( for
Cardiomegaly and signs of LVF )
• Iron containing enzymes low( monoamine
oxidase, catalase, cytochrome peroxidases )
• Investigations to determine the cause of
anaemia
1. Stool examination: Stool for occult blood,
ova,cyst (hookworms).
2. Gastrointestinal studies for bleeding, polyp,
etc.
3.Barium meal examination, upper/lower GI
endoscopy, etc.
13. Treatment
• Cause of anemia should be identified and treated
• Dietary counseling and treatment for the cause.
1. Oral therapy
• Ferrous sulfate is most effective and started at 3–6 mg/kg/ day.
• Reticulocyte count increase in 72–96 h after initiating treatment .
• Continue oral iron 4-6 months to replenish stores.
• Absorption is best if taken on an empty stomach .
• Side-effects = –nausea, vomiting, diarrhea, constipation, abdominal
cramps, staining of teeth and tongue and discoloration of stools
.
• Hemoglobin rise following oral iron therapy is around 0.1 g/dL/da
14.
15. 2. Parenteral therapy
• Indications for parenteral therapy
Intolerance to oral iron –
• Commercially available preparations – Iron
dextran – Iron sucrose – Iron ferric gluconate –
Ferric carboxymaltose injection .
• IV>IM
• Intravenous iron sucrose - safe and effective
Preferred in children with advanced CKD on
maintenance hemodialysis & IBD.
• The dose is 1-3 mg/kg, diluted in 150 ml of
normal saline and given as slow infusion over 30-
90 min.
• Inj Ferric carboxymaltose for malabsorption =
15mg/kg upto 1000mg given over 15-20
minutes(IV).
16. Blood transfusions
• Blood transfusions should be avoided in, stable patients.
• Red cell transfusions - emergency situations such as acute severe hemorrhage,
severe anemia with congestive cardiac failure and prior to an invasive procedure.
• Patients with very severe anemia and congestive cardiac failure should receive
transfusions at a very slow rate with hemodynamic monitoring and diuretic
administration if necessary.
Prevention
• Exclusive breastfeeding for 6 months • Timely introduction of complementary feeding at 6
months
• Iron supplementation for preterm/ LBW infants from 2 months
• Restrict cow’s milk consumption
• Intake of green leafy vegetables and sprouting green grams
• Periodic deworming in endemic areas
• Iron supplements for susceptible infants and children and at puberty, especially in girls
17. DIFFERENTIAL DIAGNOSIS
• Differential diagnosis of microcytic hypochromic anemia
• Iron deficiency
• Anemia of chronic disorders
• Sideroblastic anemias
• Thalassemia Major
• Lead Poisoning
• Hereditary pyropoikilocytosis
18. MEGALOBLASTIC ANEMIA
• Megaloblastic anemia is a distinct type of anemia characterized by macrocytic
red blood cells and erythroid precursors that show nuclear dysmaturity.
• It is commonly caused by deficiency of vitamin B12 (derived from cobalamin)
and/ or folic acid .
• Prevalence varies with dietary practices and socioeconomic condition.
• Rare metabolic causes of megaloblastic anaemia include inherited disorders
of pyrimidine synthesis (hereditary orotic aciduria), inherited disorders of
DNA synthesis, Lesch-Nyhan syndrome, etc
• Vitamin B_{12} cannot be produced in the human body and should be
obtained from the diet.
19. Pathophysiology
• Occurs due to impaired nuclear maturation.
• Methyl tetrahydrofolate, a folic acid derivative
needed for synthesis of DNA nucleoproteins. Namely
thymidine
• Deficiency of cobalamin or folate results in failure of
DNA synthesis and delayed/arrested nuclear
maturation.
• Vitamin B12 needed as cofactor for folic acid
recycling.
• Synthesis of RNA and protein is normal resulting in
normal cytoplasmic maturation.
• Thus, the nuclear maturation lags behind the
cytoplasmic maturation producing large cells called
Macrocytes
20.
21.
22. Clinical features
• Early symptoms include Anemia, Anorexia, Irritability,
and easy fatigability
• Glossitis, stomatitis
• Hyperpigmentation of skin over knuckles and terminal
phalanges are specific findings seen in this condition.
• neurological manifestations
1. Neurological symptoms often precede the onset of
anemia ,
2. Loss of position and vibratory sensation
3. Memory loss, confusion, Posterior and lateral column
deficits may appear.
4. Neuropsychiatric manifestations
5. Pins and needles sensation/numbness in thefingers
and toes due to peripheral neuropathy (paraesthesia.
23. • Psychiatric manifestations Personality or memory
changesDepression, irritability, psychosis and dementia
• Other features: Hepatosplenomegaly, signs of
malabsorption, abdominal scar due to ileal resection, etc.
• Evaluate child for malabsorption such as weightloss,
diarrhoea, abdominal distension,statorehoea
1. Subacute combined degeneration of spinal cord: Distal
sensory loss, absent ankle reflex, exaggerated knee jerk,
extensor plantar.
2. Irritability, convulsions, retrobulbar neuropathyand
intellectual disabilit.
24. Investigations
• Hemogram = Anemia, leukopenia and thrombocytopenia
(Pancytopenia seen in 40%–70% cases) ,
Macrocytic red cells (MCV >110 fl)
Hypersegmented neutrophils (nucleus >5 lobes)
Reticulocyte count—low
• Bone marrow is hypercellular because of erythroid
hyperplasia ,
• Serum vitamin B12 and folic acid reduced
• Schilling test—used to differentiate between pernicious
anemia and malabsorption
• lactate dehydrogenase and indirect bilirubin |^
25.
26. Treatment
• Therapeutic dose of folate should be administered along with vitamin B12
• Folate therapy does not correct neurological manifestations.
• Folate is given for 3–4 weeks (1–5 mg/day) and continued for 1–2 additional months for
the replenishment of body stores
• Vitamin B12 (500–1000 µg/dose) is given intramuscularly on alternate days for a period of
2–3 weeks, followed by maintenance therapy of 100–250 µg/month given intramuscularly
to prevent recurrence
• Oral vitamin B12 given is not preferred due to poor patient compliance and erratic
absorption
• Children with neurological complications should receive vitamin B12 for 2 weeks followed
by every 2 weeks for 6 months and monthly for life long
• Anemia not responding to folate or B12 may be secondary to rare metabolic disorders like
homocystinuria or due to antimetabolic drug
27. Differential diagnosis
• Aplastic anemia,
• Pure red cell aplasia
• Fanconi’s anemia
• Congenital dyserythopoietic anemia
• Hypothyroidism
• Myelodysplastic syndrome
• HIV infection
