ANAEMIA in peadiatrics and adolescentppt

Anaemia in children

1. ANAEMIA
PRESENTR
O. MALIYAMA

2. OBJECTIVES

3. Formation of Red Blood cells
•Formation of Red Blood cells in the foetus called
embryonic hematopoiesis begins by the 20th day of
gestation.
•It is characterized as blood islands in the yolk sac
• In mid-gestation, erythropoiesis occurs in the liver
and spleen of the foetus
•In the last trimester the bone marrow becomes the
predominant site hematopoiesis

4. Formation of Red Blood cells
•Hemoglobin concentration increases from 8 to 10
g/dL at 12 weeks to 16.5 to 18 g/dL at 40 weeks
gestation
•Erythropoietin hormone is responsible for the
production of Red Blood Cells in the foetus and the
concentration of this hormone increases with fetal
hypoxia and anemia

5. Formation of Red Blood cells
•After birth, hemoglobin levels increase transiently at
6 to 12 hours, then decline to 11 to 12 g/dL at 3 to 6
months.
•A premature infant (<32 weeks' gestational age) has
a lower hemoglobin concentration and a more rapid
postnatal decline of hemoglobin level, which
achieves a nadir 1 to 2 months after birth.
• Fetal and neonatal RBCs have a shorter life span (70
to 90 days) and a higher mean corpuscular volume
(110 to 120 fL) than adult cells.

6. Formation of Red Blood cells
•In the fetus, hemoglobin synthesis in the last two trimesters
of pregnancy produces fetal hemoglobin (hemoglobin F),
composed of two alpha chains and two gamma chains.
• Immediately before term, the infant begins to synthesize
beta-hemoglobin chains; the term infant should have some
adult hemoglobin (two alpha chains and two beta chains).
•Fetal hemoglobin represents 60% to 90% of hemoglobin at
birth, and the levels decline to adult levels of less than 5%
by 4 months of age.
• 

7. •The time of presentation of hemoglobinopathy depends on
the timing of chain synthesis. α-Thalassemia caused by a
four-gene defect produces no alpha chains and presents as
severe anaemia and hydrops (Bart hemoglobin, composed
of four gamma chains)

•Hemoglobin H is caused by a thalassemia three-gene defect
resulting in four beta chains and appears with haemolysis
and anaemia in infants
• In contrast, infants with beta-chain abnormalities, such as
Cooley anemia (β-thalassemia major) and sickle cell
anaemia, do not manifest anaemia in the neonatal period

8. •The blood volume of a term infant is 72 to 93 mL/kg
•Preterm infant, blood volume is 90 to 100 mL/kg.
•The placenta and umbilical vessels contain
approximately 20 to 30 mL/kg of additional blood that
can increase neonatal blood volume and haemoglobin
levels transiently for the first 3 days of life if clamping
or milking ("stripping") of the umbilical cord is delayed
at birth
•Delayed clamping increases the risk for Polycythaemia,
increased pulmonary vascular resistance, hypoxia, and
jaundice, but improves glomerular filtration

9. •Early clamping may lead to anaemia, a cardiac murmur,
poor peripheral perfusion but lower pulmonary vascular
pressures, and less tachypnoea
• To prevent the above situations, the cord should be
clamped at approximately 30 to 45 seconds after birth.
•Hydrostatic pressure affects blood transfer between the
placenta and the infant at birth
•An undesired fetal-to-placental transfusion occurs if the
infant is situated above the level of the placenta
 

10. •The physiologic anaemia noted at 2 to 3 months of age in
term infants and at 1 to 2 months of age in preterm
infants is a normal process that does not result in signs of
illness and does not require any treatment.
•It is a physiologic condition believed to be related to
several factors, including:
• increased tissue oxygenation experienced at birth
• shortened RBC life span and
• low erythropoietin levels

11. Etiology
1.Decreased RBC production
2.Increased RBC destruction
3.Blood loss

12. Decreased Red Blood Cell Production
•Anaemia caused by decreased production of
RBCs appears at birth with:
• pallor
•a low reticulocyte count and
•absence of erythroid precursors in the bone
marrow
•

13. Decreased Red Blood Cell Production
•Potential causes of neonatal decreased RBC production
include:
• bone marrow failure syndromes (congenital RBC
aplasia [Diamond-Blackfan anaemia])

•infection (congenital viral infections [parvovirus,
rubella]
•acquired bacterial or viral sepsis
•nutritional deficiencies (protein, iron, folate, vitamin
B
12), and congenital leukaemia

14. Increased Red Blood Cell Destruction
 
Immunologically mediated haemolysis in utero may lead
to erythroblastosis fetalis, or the fetus may be spared,
and haemolytic disease may appear in the newborn.
 Haemolysis of fetal erythrocytes is a result of blood
group differences between the sensitized mother and
fetus, which causes production of maternal IgG
antibodies directed against an antigen on fetal cells

15. Blood loss
•Blood loss due to injuries or accidents Road Traffic
Accidents (RTAs), open fractures etc)
•Un clamped umbilical cord or loose clamps or blood
losses in utero (before birth)

16. Blood loss
•Blood loss anaemia from blood loss at birth is
manifested by two patterns of presentation, depending
on the rapidity of blood loss
•Acute blood loss after:
• fetal-maternal hemorrhage
•rupture of the umbilical cord in placenta praevia or
•internal haemorrhage (hepatic or splenic haematoma;
retroperitoneal) is characterized by pallor,
• diminished peripheral pulses, and shock

17. Blood loss
•There are no signs of extramedullary haematopoiesis
and no hepatosplenomegaly.
•The haemoglobin content and serum iron levels
initially are normal, but the haemoglobin levels
decline during the subsequent 24 hours

18. •Newborns with chronic blood loss caused by chronic
fetal-maternal hemorrhage or a twin-to-twin
transfusion present with marked:
•Pallor
•heart failure
•hepatosplenomegaly with or without hydrops
•a low hemoglobin level at birth
•a hypochromic microcytic blood smear
•decreased serum iron stores

19. •Fetal-maternal bleeding occurs in 50% to 75% of all
pregnancies, with fetal blood losses ranging from 1
to 50 mL;
•most blood losses are 1 mL or less
•1 in 400 are approximately 30 mL
•1 in 2000 are approximately 100 mL

20. Diagnosis
•The diagnosis of fetal-maternal haemorrhage is
confirmed by the Kleihauer-Betke acid elution test;
•pink fetal RBCs are observed and counted in the
mother's peripheral blood smear because fetal
hemoglobin is resistant to acid elution;
•adult haemoglobin is eluted, leaving discolored
maternal cells (patients with sickle cell anaemia or
hereditary persistence of fetal haemoglobin may have
a false-positive result, and
•ABO incompatibility may produce a false-negative
result).

21. Other types of anaemia
•Iron deficiency
•Aplastic
•Vitamin B12 deficiency

22. Management
•The treatment of symptomatic neonatal anemia is
transfusion of cross matched packed RBCs.
•If immune haemolysis is present, the cells to be
transfused must be cross matched against maternal and
neonatal plasma.
•Acute volume loss may necessitate resuscitation with
nonblood products, such as:
–saline if blood is not available
–packed RBCs can be given subsequently.

23. Management
•To correct anaemia and any remaining blood volume
deficit, 10 to 15 mL/kg of packed RBCs should be
sufficient.
•CMV-sero-negative blood should be given to CMV-sero-
negative infants, and
– all blood products should be irradiated to reduce the
risk of graft-versus-host disease;

24. Management
•blood should be screened for:
– HIV
–hepatitis B and C, and
–syphilis.
•Recombinant erythropoietin may improve the
hematocrit in infants with a hypo regenerative
anaemia after in utero transfusion.