1. Anemia, Iron deficiency anemia
Dr. Kalpana Malla
MD Pediatrics
Manipal Teaching Hospital
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3. 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
4. Anemia Basics
All anemias are either due to….
1. Ineffective RBC production
or
2. Accelerated destruction of the RBC
7. Macrocytic anemia
• Megaloblastic Erythropoiesis
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
8. Macrocytic anemia
Non - Megaloblastic Erythropoiesis
a) Chronic hemolytic anemia
b) Liver ds
c) Hypothyroidism
d) Diamond blackfan syndrome
9. 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)
10. DIMORPHIC ANEMIA
• When two 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
11. ETIOLOGICAL CLASSIFICATION OF ANEMIA
• Blood loss
Acute
Chronic
• Decreased iron assimilation
- Nutritional deficiency
- Hypoplastic or aplastic anemia
- Bone marrow infiltration like leukemia & other
malignancies,
- Myelodysplastic syndrome
- Dyserythropoietic anemia
13. ETIOLOGICAL CLASSIFICATION OF ANEMIA
- 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.
14. Follow-up
• Re-check CBC 4-6 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
15. 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
17. IDA
• Most common cause of anemia worldwide
• Most important cause of iron deficiency anemia is
parasitic infection - hookworms, whipworms and
roundworms
18. GENERAL FEATURES
Newborn contains 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
19. Iron sources:
• Meat
• Liver
• Kidney
• Egg-yolk
• Green vegetables
• Fruits
**** Cow’s milk- poor source of iron
20. Iron metabolism:
Distribution of body 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
21. 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
23. Pathogenesis of IDA:
Increased physiological 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
24. • High Hb conc 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
25. ETIOLOGY
• The most important 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
27. Risk factors for IDA
• Demograpghic – Eldery, Teenager, Female
• Dieatary – low Iron, low Vit C, excess
phytate,tea coffee,
• Social and physical – poverty,alcohol
abuse,GIT ds
28. CLINICAL FEATURES
Pallor is the 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
29. CLINICAL FEATURES
• Hair loss and lightheadedness
• Fainting
• Sleepiness, Tinnitus
• Mouth ulcers, Glossitis ,Angular cheilitis
• Constipation
• Depression, Twitching
muscles, Tingling, numbness or burning
sensations
30. CLINICAL FEATURES
• Koilonychia (spoon-shaped nails) ,
• Platynychia
• Weak,brittle nails
• Pruritus
• Dysphagia due to formation of esophageal
webs (Plummer-vinson syndrome
32. CLINICAL FEATURES
Neurologic and intellectual 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
33. Response to low Hb:
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
34. Response to low Hb:
Later:
Microcytosis, hypochromia, poikilocytosis,
and increased RBC distribution width (RDW)
35. Diagnosis - LABORATORY INVESTIGATIONS
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
36. Diagnosis - LABORATORY INVESTIGATIONS
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
37. LABORATORY INVESTIGATIONS
4. Diagnostic tests –
- 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
38. LABORATORY INVESTIGATIONS
• Ratio of serum iron to TIBC (called iron
saturation or transferrin saturation index - is
the most specific indicator of iron deficiency -
< 5% - indicates iron deficiency
39. DiagnosisLABORATORY INVESTIGATIONS
Gold standard
• 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
40.
41.
42.
43. 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
44. 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
45. TREATMENT
• Parenteral iron preparation (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
46. RESPONSES TO IRON THERAPY
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
47. Thank you
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Medical Post [ www.themedicalpost.net ]