CHILDHOOD

ANAEMIAS
BLOOD VALUES IN INFANCY AND CHILDHOODS
Hb(g/dL) HCT MCV(fL) MCH(pd)

CORD 16.5 52 108 36

1 DAY 19.6 61 107 37

1 WEEK 18.2 58 98 33

1 MONTH 14.5 44 96 32

2 MONTH 11.5 35 94 30

6 MONTH 11.6 35 90 30

1 YEAR 11.5 35 78 27
2-5YEARS 12.5 37 80 27 1.5

ADOLESCENT

MALE 15-17 46-52 78-98 26-32 15-2

FEMALE 13-15 40-46 78-98 26-32 15-2

Diagnosis of anaemia in infancy and childhood is based upon
knowledge of changes in Hb, HCT and red cell characteristics
which occurs during growth and development.
The high Hb (physiological polycythemia) at birth reflects recent
exposure to the relative hypoxic intra-uterine life environment.
The progressive post natal decrease in Hb which reaches a nadir
between 6 -12 weeks is a physiological adjustment, more marked
in preterm infants.
Anaemia is decrease in Hb or HCT below normal for age and sex.
The main pathogenic mechanisms are:
1. Impair or ineffective blood production.
2. Haemorrghage.
3. Haemolysis.
It is not disease in itself but a manifestation of an underlying
disorder.
 Definition
Anaemia is defined as Haemoglobin (Hb) less than the lower limit of the reference range for age

Lower limit of normal range

Age
Hb (g/L)
2 months 90
2 – 6 months 95
6 – 24 months 105
2 – 11 years 115
female – 120
>12 years
male - 130
ANAEMIA IN NEW-BORN
Dfn: as Hb < 14gm\dl in full term baby, most commonly due to
haemolysis, bld loss or infection.
Evaluation of aetiology include detailed history of pregnancy and
delivery, with particular reference to infections, blood loss and drug
ingestion .
History of previous anaemic or jaundiced infants, miscarriage or
blood transfusions are particularly important in relationship to
hereditary haemolytic anaemia (Rh and ABO incompatibility).
Jaundice and hepatospleenomgally suggest haemolysis or
infection whereas pallor, shock or overt bleeding indicate
haemorrhagic anaemia. Cephaelhaematoma and bleeding into
organ eg spleen, liver should be excluded. Twin-twin transfusion
should be excluded.

CAUSES OF ANAEMIA
 IMPAIRED RBC PRODUCTION
• NEW BORN
INFECTION, TORCH, HIV, NNS ,Red cell aplasia, congenital
leukemia
 • INFANCY AND PRESCHOOL
Fe def, folate def, infection, idiopathic, fanconi (familal
hypoplastic anaemia) acute leukeumia, solid tumour.

• LATE CHILDHOOD
Fe def, folate def, infections, systemic diseases eg JRA,
Nephropathies, infections, idopathic, drugs, fanconi anaemia,
Acute leukemia lymphomas and solid tomours.

 BLOOD LOSS
• NEW BORN
Feto-feltal transfusion, feto-maternal transfusion, cord
accident, cephalhaematoma, HDN , blood sampling.
 • INFANACY/CHILDHOOD
GI Malformations, ulcers, parasites eg Bilharziasis,
platelet/coagulation abnormalities.

 HAEMOLYSIS
• NEW-BORN
Rh/ABO incompatibility, infection, hereditory spherocytosis,
G6PD def

• CHILDHOOD
Infection eg malaria, Autoimmune, Haemoglobinopathy,
thalasamia, G6PD def
 SIGNS
The main sign is pallor; check out in mucous membrane,
conjunctiva, mouth, nail bed, palm.
Pulse is tachy, full, bounding, pulse pressure is raised, diastolic Po is
decreased. In prolong cases there is cardiomegally - a
compensatory mechanism to increase CO.

 SYMPTOMS
CVS: Weakness, easy fatiquability, dyspnoea on exertion, andin
severe cases heart failure (CCF)
DS: Anorexia, dyspepsia, constipation
RS: DOE, orthopnea
CNS: Dizziness, faintness (syncopy) insomnia, headache
MSK: Muscular weakness
UGS: Hyposthenuria – inability to concentrate urine
 THE CAUSE OF DEATH
Cardiac failure, but in severe cases patient have cerebral
hypoxaemia with restlessness , disorientation, air hunger and
patient rapidly die from these.

 NUITRITIONAL ANAEMIA
AETIOLOGY
Poor diet leading to deficiency of haematopoitic factors Fe def
anaemia is the commonest . Fe is found mainly in animal protein –
meat , fish, egg, red meat.
Fe def
• Most common case in early childhood
• Prenatal predisposition factors: multiparity, twin birth,
LBWT, blood loss.
• Most important post natal cause is rapid intravascular
expansion due to rapid growth.
• Bacterial, viral and parasitic infections, which impair Fe
uptake and utilization or cause chronic blood loss
• At greatest risk; 6/12(months) – 3years and adolescent
Incidence – inversely with socio economic status, 5% in
developed countries, up to 50% in 3rd world.
• CF
• Vague and non specific; fatique, lethergy, irritability, anorexia,
pica and koilonychia.

LAB FINDINGS
Microcytic hypochromic (MCV < 70fl, MCH 26pg, serum fe
(<40ug\dl) ↑ fe binding cap (>450ug/dl), ↓ transferrin
saturation<16%, ↓ serum ferritin , increased RDW Retic is
increased if it is due to hemorrhage.
DD
Thalasemia, lead poisoning, anaemia of chronic inflamation

TREATMENT
Elemental fe 1mg/kg/day will correct anaemia in 4 – 6 weeks.
Additional 4week to replenish the Fe store.
MEGALOBLASTIC ANAEMIA
Macrocytic anaemia due to def of B12 or folate or both. Gen not
common in children.
CAUSE: Nutritional def or intestinal malabsorption of B12
usually due to intestinal malabsorption Crohn dx, chronic
pancreatitis , bacteria overgrowth in small bowel, fish tape worm
infestation, surgical resetion of terminal ilum def of
transcobolamni 2 and IF ( rare in children children.
FOLIC ACID DEFINITION
Inadequate intake, malabsorption, increased folate
requirement, anticonvulsants eg phenytoin, phenobarb,
cytotoxic drugs eg metotriaxate (interfere with absortion and
metabolism) Haemolytic anaemia and rapid growth.
CF
As outlined earlier, for comparable anaemia, children with
megaloblastic anaemia are usually more ill than children with fe
def anaemia. Older childern with cobalamine def may complain
of paresthesia, weakness, unsteady gait and decreased vibratory
sensation and proprioception.
LAB INV
Increased MCV and MCH, Bld film; anisocytosis, poikoliocytosis,
hyper segmented and large nutrophiles.
Rx
B12; 50-100ug im monthly for long term replenishment

Folate
1mg daily for 2/52. To correct Def and another 2/52 for store
replenishment.
ANAEMIA OF PEM
Regular feature of PEM
Aetiology – varried.
CAUSE ↓ protein, fe normal initially but dev with Rx. folate def
may occur.
Parasitic and bacteria infection
LAB
Monocytic normochromic
Transient ↓ is Hb coincides with loss of edema.
Rx: Nutritional Rehab
ANAEMIA OF INFECTION AND INFESTATION
MALARIA
Potent cause in Nigeria. The parasite lives in RBC destroys it
directly and immunologically. Toxin depresses marrow , cause
vomiting and diarrhea
Lab
Normocytic normochromic, this is because BM suppression is
most important.
Rx the cause.
HELMINTHIASIS
Esp Hookworm, feed on blood, suck about .1ml of blood/day. But
actualy need plasma. Pass out RBC that is lost in stool.
Rx
Deworm the pt and give Fe replacement therapy.

ANAEMIA OF CHRONIC DISORDER

Chronic inflamatory disorder like JRA, hepatic, renal and endocrine
disorders.
Usually moderate normocytic, normochromic anaemia. There is
often low grade sub clinical haemolysis, impaired BM response
and decrease fe utilization, serum fe and transferin are ↓
BM Fe increased and utilization of Fe is impaired, Fe therapy is
inecfective
Rx
the underlying cause.
APLASTIC ANAEMIA
conj
BM
Acquired

CONGENITAL: eg DIAMOND - BLACKFAM ANAEMIA

uncommon in Nigeria

ACQUIRED CAUSES
 Idiopathic >50%
 Antibiotic s: cphenicol, sulfonomides
 Anticonvulsant : phenobarb, phenythoin
 Antimalaria: quinine amodiaquine
 Cancer chemotherapeutic agents
 Chemicals: Benzene, carbon tetrachloride
 Insecticides: DDT, chlordane, parathion
 Infections: HAV, HIV, EBV Rubella, measles
mumps, influenza virus
 PEM
 Irradiation
• Pre leukemic condition
Clinical Features
Onset insidious with pallor, lethargy, easy bruising, petechia
progressing to overt hemorrhage and serious intercurrent
infections.
Dig. BM biopsy
Rx immunosuppresion
BM Transplant
Prognosis - poor
HAEMOLYTIC ANAEMIA
HA are characterized by increased RBC destruction (anaemia
uroblinuria, haemoglobunuria and increased BM activity,
reticulocytosis)
Long standing HA → extramedullary haemoposis in liver and
spleen →hepatosplenomegally and expanded BM cavities from
erythroid hyperplasia → skull bossing, thinning of cortex of long
bone.
RBC destruction in RES →jaundice/pallor;
intravascular space (IVS)→haemoglobunuria /pallor
AETIOLOGY
Hereditary and Acquired
Hereditary
Membrane – spherocytosis
Enzyme– G6PD, pyruvate kinase
Hb – SCA, thalassemia
ACQUIRED
Iso immune
HDN
Auto immune
viral, bacterial infection
Penicillins, sulfonamides, cephalosporin
Non immune
malaria, burns Hyperspleenism
Hereditory Spherocytosis. Inherited as OD
Lack of spectin → spherical shape, ↑ Na permiability.
The affected RBC is easily destroyed in the spleen, Hence
spleenectomy→ cure.
CLINICAL FEATURES
Vary: From asymptomatic →severe recreant anemia needing
bld tx
Often a cause NNJ
LATER CHILDHOOD
Episodic jaundice pptd by infection is a common presentation.
frequently it is associated with splenomegaly.
Complication: transient aplastic crises usually pptd by infection
gallstone, leg ulcer a (more common from adolescent )
Usually no clinical or hematological abnormality until exposed to
oxidant stress. Typical attack takes 3-4 days after ingestion of drugs
or onset of illness.
Jaundice, haemoglobinuria and low Hb.
LAB
Mod anemia 8 – 10mg/dl can be severe in crisis.
Bld film shows spherocyte, presence of osmotic fragility

G6PD
Distributed ww, more in malaria endemic areas.
Offers limited protection against falciparium malaria .
↓ RBC life span
Genetic- X linked recessive
Female heterozygous are asymptomatic carrier,
affected males and homozygous female
show full expression of the dx

CF.
NNJ often without oxidant s
OXIDANTS
Ammodiaquine, sulphanomides (phenacitine, nitrofurantoinnalidixic
acid, Aspirin/phenacitin, large doses of Vit K.)
Chemicals; naphthallin ball, Benzene
Food; fava Bean
Infection; Bacteria
Meta; DKA
DIAG: G6PD Screening
Re: Remove/avoid oxidant agents, Bld Tx in acute phase
 n
n
c
SCD
Haemoglobinopathy as result of single aa substitution in beta
chain of adult Hb resulting in S C D E depending in aa
substitution. Hb S and C exist in Nigeria. S gene in malaria area
confer a selective survival on AS.

GENETICS
AR. Heterozygous inheritance of Hbs with normal
Hb → symptomless carrier. When inherited with other abnormal
Hb like S, C, thallassemia→ dx
However SS → SCA
Hbs; valine replaces glutamic acid at B6
Hbc; Lysine ,, ,, ,, at B6
Pathogenesis Amino acid substitution → decresed solubility esp
in low 02 tension. When well oxyginated Hbs functions well but
decreased 02 tension interaction of B6 valine and complementary
region of adjacent molecule result in formation of molecular
polymer.
→ elongate to form a filamentous structure
→ aggregate to rigid crystal like rods
→ sickling of RBC.
These phenomenon has two effect:
1. Decrease RBC survival to about 20 days instead of 120days
because chronic hemolytic anaemia. Over worked RES causes
hepatosplenomegaly.
2. Vaso occlusion → ischemia/pains → infarction.

PRESENTATION
Hbf is at 6months replaced with HbA. Hand/syndrome from
thrombosis. anemia jaundice ∆∆ hepatitis
Bone pain ∆∆ trauma, osteomyelitis
Jt pain ∆∆ JRA, septic arthritis ∆∆ Abd pain, PUD IC
thrombosis→ CVA sometimes diagnosis is made while
investigating other dxs
SIGN
Pallor, jaundice, small for age, asthenic, occipital and frontal
bossing, short trunk, protuberance of upper jaw (gnathopathy),
cardiomegaly, pulse is full, rapid and collapsing,
hepatospleenomegally .
As the sickler grow older → Autospleenectomy from repeated
infarction

INVESTIGATION
Hb electrophoresis, pcv Hb 5 – 10mg/d MCHC is normal,
Retic and WBC are raised. Increased BM activity, Bld film nucleated
RBC, polychromesia, sickle shape RBC.
Major Complications is called crisis
ANAEMIA CRISIS
• Hyperhaemolytic
• Aplastic
• Sequestration

VOC
Bone pain
Hepatic crisis
Acute chest syndrome

PRECIPITANT OF CRISIS
Stress; Physical emotional
Extremes of weather
Hypoxia: high altitude, unpressurized aircraft
Acidosis
MGT

Treat various crisis accordingly:

Folate,multivitamin dly
High protein diet, malaria prophylaxis with daily
proguanil, oral penicillins
Prompt Rx of infections

RECENT ADVANCES
BM transplant, Solamine an antisickling agent 85% effective
preventing sickling
Hydroxyurea .
Prevention; Genetic counselling
Distribution of the S gene in E Nigeria; AA 74.3%, AS 24.1% ,SS
1.6%.
COMPLICATIONS
Delay sexual maturation, aseptic necrosis of head of femur,
Chronic leg ulcer, priapism, CVA, osteomyelitis, high
susceptibility to infection by encapsulated organism.
CAUSE OF DEATH
anaemia with or without infection.

PHYSIOLOGIC ANAEMIA OF INFANCY

At birth Hb is normally high. Start to decrease within 1st week of
life.
Decreasing to 9-10gm/dl 2-3 months.
FACTORS CONTRIBUTING
Decrease erythropoitin production after birth
Fetal RBC have shorten survival time
Rapid expansion vascular vol with rapid growth in first few months
of life leading to haemodilution
Def of vit E and folate may aggravate physiologic anaemia
Does not require Rx but may be exagerated in preterm to warrant
Rx.
In prem may be managed with recombinant erythropoitin