1. Anemia, Iron deficiency anemia
Dr. Kalpana Malla
MD Pediatrics
Manipal Teaching Hospital
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2. ANEMIA

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

5. Classification
• By RBC morphology and By Etiological
factors responsible for anemia

6. Microcytic hypochromic anemia
1. Iron deficiency anemia – nutritional,
- posthemohragic
2. Ineffective Erythropoiesis
- hemoglobinopathies, Thalassemia
- Lead poisoning, Sideroblastic anemia
- Cu deficiency, Pyridoxine deficiency
-Chronic ds - infection, inflammations ,
renal ds

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

12. ETIOLOGICAL CLASSIFICATION OF ANEMIA
• Increased physiologic requirement
- Extracorpscular -
- Alloimmune & isoimmune hemolytic anemia
- Microangiopathic anemias
- Infections
- Hypersplenism

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

16. IRON DEFICIENCY
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

22. Iron Metabolism:
Figure 16-8: Iron metabolism

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

26. ETIOLOGY
• Chronic blood loss - occult bleeding : peptic
ulcer, Meckel diverticulum, polyp, hemangioma,
inflammatory bowel disease, Intravascular
hemolysis and hemoglobinuria
• Chronic diarrhea
• Milk allergy

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

31. Koilonychia - spoon shaped nail

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

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 ]