Anaemia in children

1. BY
DR DIKSHA KUMARI
MD 2ND YEAR

2.  Anemia is defined as a decrease in the red cell
volume or total hemoglobin level below the
normal range for that age and sex.
 WHO cut-off values of hemoglobin for defining
anemia in children are as follows:-
1. 6 months to 6 years : hemoglobin<11g/dl.
2. 6 years to 14 years : hemoglobin <12g/dl.

3. STEM CELLS PROGENITOR CELLS
HEMATOPOEITIC
GROWTH FACTORS
RED BLOOD CELLS,
PLATELETS,MONOCYTES,
MACROPHAGES, LYMPHOCYTES,
NEUTROPHILS, EOSINOPHILLS AND
BASOPHILLS.

5. Anemia decreased oxygen carrying capacity
of blood increased red cell production by
secreting more erythopoeitin from JG cells
Stimulates bone marrow hypercellular
resulting in the release of more immature red cells
into the peripheral
circulation.

6.  Body also compensates for the decreased oxygen
carrying capacity of blood:-
 Increasing stroke volume, heart rate.
 Shunting of blood towards vital organs.
 Shifting the oxygen dissosciation curve to right.

7.  Microcytic anemia.
 Macrocytic anemia.
 Normocytic anemia.
 Microcytic Anemia :-
 Defect in RBC formation mainly affecting the
hemoglobin synthesis.
 MCV is less than the lower limit of normal for
age.
 MCV <80fl (after 6 months of age is considered
microcytosis.)
 MCH and MCHC are also decreased leads to
hypochromia.

8.  MACROCYTIC ANEMIA:-
a. Defect lies in the DNA synthesis instead of
hemoglobin synthesis.
b. MCV> 96fl (after 6 months of age is defined as
macrocytosis.)
c. MCH and MCHC are normal.
d. RBCs are usually normochromic.
 CAUSES OF MACROCYTIC ANEMIA:-
A. Megoblastic Erythropoiesis:-
1. Nutritional:- Vitamin B12 deficiency, folate
deficiency, kwashiorkor.
2. Toxic :- Methotrexate, phenytoin.
3. Malabsorption.

9.  Iron deficiency anemia in infancy and older
children may be nutritional and post hemorrhagic.
 Ineffective erthyropoesis due to
a. Thalassemia.
b. Pyridoxine responsive anemia.
c. Dyserythropoetic anemia.
d. Lead poisoning.

10. b. Non- megoblastic erythropoeisis:-
1. Chronic hemolytic anemia.
2. Liver diseases.
3. Hypothyroidism.
4. Diamond Blackfan syndrome.
c. Normocytic Anemia :-
1. MCV, MCHC and MCH are within normal
limits.
2. RBC are normochromic.
 Causes of normocytic anemia:-
1. Impaired cell production.
2. Acute hemolysis.

11. Due to impaired cell production:-
a. Deficiency of essential nutrients – Iron , vitamin B12,
folic acid deficiency.
b. Reduced erythropoesis:-
 Aplastic anemia.
 Bone marrow infiltrations.
Excessive red cell destruction:-
a.Intracorpuscular defects:- Thalassemia, red cell enzyme
deficiency.
b. Extracorpuscular defects :- Immune hemolytic
anemia, hypersplenism.
Blood loss:-
a. Acute.
b. Chronic.

12.  Tiredness.
 Lassitude.
 Easy fatigability.
 Generalized muscular weakness
 Poor feeding.
 Irritability.
 Inadequate school performance.
 Dyspnea on exertion.
 Tachycardia.
 Palpitation.

13.  Pallor of nail beds, oral mucous membrane and
conjuctivae.
 Hemic murmurs.
 Systolic bruits.
 Postural hypotension.
 Congestive heart failure.
 Dizziness, fainting.
 Headache, drowsiness.
 Humming in ears, tinnitus.
 Lack of concentration
 Clouding of consciousness.

14.  Relevant history .
 Detailed examination.
 Association of anemia with bleeding.
 Presence or absence of hepatosplenomeagly.
RELEVANT HISTORY :- Age of onset.
- Progression.
- Blood loss.
- Jaundice.
- Bleeding tendency.
- Blood transfusion.
- Family history.
DETAILED EXAMINATION:- Degree of Pallor.
- Icterus.

15. - Petechiae and ecchymotic patches.
- Presence of lymphadenopathy.
- Bony tenderness.
 HEPATOSPLENOMEAGLY:-
a.Hepatosplenomeagly with lymphadenopathy in
malignancy. ( leukemia and lymphoma.)
b. Hepatosplenomeagly without
lymphadenopathy in hemolytic anemias and
infective pathology (malaria).

16.  Hemoglobin estimation.
 Red blood cell indices- Hematocrit, MCV,MCH,
MCHC, RDW.
 Reticulocyte count.
 Examination of bone marrow.
 Special investigations includes :- serum iron
studies, serum folate and Vitamin B 12 levels for
deficiency anemias and hemoglobin
electrophoresis for hemoglobinopathies and
thalassemia.

17.  General Management:-
 Deworming the children regularly.
 Special supplementation need to be started in case of
nutritional anemia.
 Children with fever in the endemic zone for malaria
should be treated with antimalarials.
 Emergency Management:-
a. Child in congestive cardiac failure should be
managed promptly and aggressively.
b. Child should be nursed in a propped up position.

18.  Oxygen should be supplemented .
 Iv furosemide in a dose of 1-2 mg /kg to decrease
the pulmonary edema.
 Packed red blood cell transfusion 10-15 ml/kg
has to be urgently given at the rate of 5-7 ml/kg/h.
 Iv furosemide should be given during transfusion
to avoid circulatory overload.

19. a. Blood loss >15% of total blood volume.
b. Hb< 13 g/dl in severe cardiopulmonary disease.
c. Hb< 8 g/dl in severe infection, perioperative
period, marrow failure, symptomatic chronic
anemia, signs of hypoxia, congestive cardiac
failure.
d. Hb< 4g/dl.

20.  Nutritional deficiency of iron is the most common
cause of anemia in children.
 Most vulnerable age is 6 to 24 months.
IRON METABOLISM:- Storage:-
Iron H Hemoglobin, plasma iron and tissue
iron.
1. Hemoglobin – part of body iron released
into plasma when the RBCs gets
lysed.
2. Plasma iron reutilized for synthesis

21. of hemoglobin.
3. Tissue iron ferritin and hemosiderin in
liver, spleen and bone marrow and myoglobin in
muscles and cellular enzymes.
4. Iron absorbed by mucosal cells Ferritin.
TRANSPORT:-
1. Iron one storage to another storage site
with the help of transferrin.
2. Transferrin on the desired site attaches
itself to the transferrin receptors

22. and iron is released into the cells.
• ABSORPTION:-
1.Absorption of iron mainly takes place in the
duodenum and the proximal jejunum.
2. This mechanism can be up or down regulated
through a feedback system depending upon iron
stores.
3. Body absorbs iron from animal sources i.e.
heme iron, better than iron from plant sources i.e.
non- heme iron.

23.  Decreased intake.
 Increased demand- prematurity, twins, multiple
gestation, infancy, adolescence, cyanotic
congenital heart diseases.
 Chronic blood loss-Worm infestations,
esophageal varices,
cow’s milk protein intolerance, hemorrhoids, rectal
polyp and peptic ulcer.
 Impaired absorption- Celiac diseases,
inflammatory bowel diseases, severe prolonged
diarrhea.

24.  Child may stop eating well.
 Irritable.
 Lethargic.
 Failure to thrive.
 Pallor and paleness of body gradually increases in
severity.
 History of repeated infections.
 Pica.
 Pagophagia.
 Platonychia.
 Koilonchyia.

25.  Tachycardia.
 Cardiomeagly.
 Functional systolic murmurs.
 Congestive cardiac failure
 Pedal edema.
 Dyspnea.
 Increased jugular venous pressure.
 Congestive hepatomeagly.
 Basal crepts.

26.  Peripheral smear will show microcytic and
hypochromic anemia when Hb level<10g/dl.
 Red blood cell indices :-MCV<82fl.
MCH<27pg.
MCHC<30%.
 Assessment of iron status:- Serum
iron<10umol/l.
- Serum ferritin<12ng/ml.
- Percentage saturation
of transferrin<16%.

27.  TIBC>350ug/l.
 FEP>40mg/dl.
TREATMENT:-
1. Diet rich in iron should be advised.
2. Oral iron supplementation is administered at
the dose of 3-6 mg/kg/day of elemental iron.
3. Ferrous sulphate has the best iron
absorption.
4. Rise in the reticulocyte count indicating the
bone marrow response can be demonstrated
after 2-3 days of supplementation.

28. 4.A rise in hemoglobin is seen by the end of the first
week.
5. The iron stores are repleted after 2-3 months of
therapy.
6. Blood transfusion (transfusion of packed red
cells) in case of severe anemia if Hb<4g/dl,
congestive cardiac failure, assosciated
superimposed severe infection.

29. PREVENTION:-
• Supplementary food rich in iron should be
initiated as soon as complementary feeding is
started preferably at 6 months of age.
• Preterm low birth infants need to be supplemented
with iron in a dose of 2-4 mg/kg/day starting from
4-6 weeks of age.
• Deworming should be done every 6 months .

30.  Lead poisoning- High blood pressure, muscles
and joints pains ,memory loss
and seizures.
 Sickle thalessemias - Pulmonary hypertension,
Acute chest sundrome,
stroke, enlarged spleen or
liver.
.
 Sideroblastic anemia- iron inside red blood cells is
inadequately used to make
hemoglobin,despite normal amounts
of iron.

31.  ANEMIA OF CHRONIC INFECTIONS:-Usually
normocytic,
but can be microcytic sometimes, serum iron is also
low, normal or increased serum ferritin, and
decreased TIBC.

32.  Anemia can be correlated with pandu
 Pandu are classified into four types:-
 Vataj Pandu.
 Pittaj Pandu.
 Kapahj Pandu.
 Sannipataj Pandu.

33. दोष ाः पित्तप्रध न स्तु यस्य क
ु प्यन्ति ध तुषु|
शैपिल्यं तस्य ध तून ं गौरवं चोिज यते||४||
ततो वर्णबलस्नेह ये च न्येऽप्योजसो गुर् ाः|
व्रजन्ति क्षयमत्यिं दोषदू ष्यप्रदू षर् त्||५||
सोऽल्परक्तोऽल्पमेदस्को पनाःस राः पशपिलेन्तियाः|
वैवर्ण्यं भजते, तस्य हेतुं शृर्ु सलक्षर्म्||६||
(ch chi
16/4-5-6)

34. सम्भूतेऽन्तिन् भवेत् सवणाः कर्णक्ष्वेडी हत नलाः|
दुबणलाः सदनोऽन्नपिट् श्रमभ्रमपनिीपडताः||१३||
ग त्रशूलज्वरश्व सगौरव रुपचम न्नराः|
मृपदतैररव ग त्रैश्च िीपडतोन्मपितैररव||१४||
शून पक्षक
ू टो हररताः शीर्णलोम हतप्रभाः|
कोिनाः पशपशरिेषी पनद्र लुाः ष्ठीवनोऽल्पव क
् ||१५||
पिन्तिकोिेष्टकट्यूरुि दरुक्सदन पन च|
भवन्त्य रोहर् य सैपवणशेषश्च स्यवक्ष्यते||१६||

35. 1. Snehna
2. Vamana and virechna.
YOGAS IN PANDU ROGA:-
1. Dadima ghrita.
2. Navayasha churna.
3. Gomutra Haritaki.
4. Punarnava mandoor.
5. Draksha ghrita.

36. THANK
YOU