Iron-Deficiency

Anemia

 Dr Abdifatah Ahmed
 Supervisor: Prof Silva
 September 2022
 Outline
2

1. Introduction to anemias
2. Classification of anemias
3. Iron deficiency anemia: Etiology, epidemiology and pathogenesis
4. Risk factors
5. Clinical features
6. Diagnosis
7. Treatment and follow up
8. Prevention
9. References
 Introduction

 Anemia (An-without,emia-blood)is a decrease in the RBC

count, hemoglobin and/or Hematocrit values resulting in a
lower ability for the blood to carry oxygen to body tissues .
 Normal ranges for HGB and HCT vary with age and sex.
The threshold for defining anemia is an HCT or HGB at or
below the 2.5th percentile for age and sex based upon
normative data from healthy individuals.
Cont.
 PATIENT CHARACTERISTICS

 Causes of anemia in children vary based upon age at

presentation, sex, race, and ethnicity.
 Age of patient — The age of the patient is important to
consider because normal values of hematocrit (HCT) and
hemoglobin (HGB) vary greatly with age and because
different causes of anemia present at different ages
 Cont.

 Birth to three months – The most common cause of anemia

in young infants is "physiologic anemia," which occurs at
approximately six to nine weeks of age.
 Pathologic anemia in newborns include blood loss, immune
hemolytic disease (ie, Rh or ABO incompatibility),
congenital infection, twin-twin transfusion, and congenital
hemolytic anemia
 Cont.

 Infants three to six months – Anemia detected at three to

six months of age suggests a hemoglobinopathy.
 Nutritional iron deficiency is an unlikely cause of anemia
before the age of six months in term infants.
 Cont.

 Toddlers, children, and adolescents – In toddlers, older

children, and adolescents, acquired causes of anemia are
more likely, particularly iron deficiency anemia.
 Cont.

 Sex — Some inherited causes of anemia are X-linked (eg,

G6PD deficiency and X-linked sideroblastic anemia) and
occur most commonly in males.
 In postmenarchal girls, excessive menstrual bleeding is an
important cause of anemia
 Cont.

 Race and ethnicity — Race and ethnic background are

helpful in guiding the work-up for hemoglobinopathies and
enzymopathies (eg, G6PD deficiency).
 HGB S and C are most commonly seen in Black, Hispanic,
and Middle Eastern populations.
 Cont.

 Thalassemia syndromes are more common in individuals of

Mediterranean and Southeast Asian descent; G6PD
deficiency is more common among Sephardic Jews,
Filipinos, Greeks, Sardinians, Kurds, and Black populations
PATHOPHYSIOLOGY
CLASSIFICATION
 Based on Morphology

 Normochromic, normocytic anemia (normal MCHC,

normal MCV).These include:
⚫ Anemias of chronic disease
⚫ Hemolytic anemias (those characterized by accelerated
destruction of RBC's)
⚫ Anemia of acute hemorrhage
⚫ Aplastic anemias (those characterized by disappearance of
RBC precursors from the marrow)
 Cont.

 Hypochromic, microcytic anemia (low MCHC, low

MCV).These include:
⚫ Iron deficiency anemia
⚫ Thalassemias

⚫ Anemia of chronic diseases

 Cont.

 Normochromic, macrocytic anemia (normal MCHC,

high MCV).These include:
⚫ Vitamin B12 deficiency
⚫ Folate deficiency
 Based on Cause
 I. Increased Blood Loss
⚫ Trauma

⚫ Peptic ulcer
⚫ Uterine bleeding
⚫ Disturbance in blood coagulation
 Cont.
 2. Accelerated destruction as in:
⚫ Chronic hemolytic anemias
⚫ Hemolytic anemia due to infections and poisons
 Cont.
 3. Decreased Blood Formation
 a. Depression of marrow function in:
⚫ Idiopathic aplastic anemia
⚫ Cachexia, chronic intoxication, metabolic disturbances,
poisons, radioactive substances, malignancy
 Cont.
 b. Deficiency in specific substances necessary for normal
red cell formation as:
⚫ Deficiency in specific anti-anemic factor of liver leading
to pernicious and other macrocytic anemias.
⚫ Deficiency in iron and perhaps other unknown
substances necessary for hemoglobin formation as in
chronic hemorrhage, dietary deficiency in iron, and
disturbance in absorption or assimilation of iron (
 Definitions

 Iron deficiency anemia (IDA) in children can thus be

defined as:
 Children 6 months to <5 years:
⚫ Ferritin <15 micrograms/L and
⚫ Hemoglobin <11 g/dL (for children 0.5 to 5 years)
 Cont.

 Children 5 to <12 years:

⚫ Ferritin <15 micrograms/L and
⚫ Hemoglobin <11.5 g/dL (for children 5 to 12 years)
 Epidemiology

 Iron deficiency is the most widespread and common

nutritional disorder in the world.

 It is estimated that 30–50% of the global population has

iron-deficiency anemia, and most of these individuals live in
developing countries.
 Cont.

 Over 273 million children under – five, suffer from anaemia

worldwide. The Sub-Saharan Africa is one of the most
affected regions - with more than half (53.8%) of children
under - 5 years old suffering from anaemia.
 In Uganda, some hospital-based data is available, however,
there is a paucity of data on anaemia in school children and
community based surveys. Nevertheless, in a few of the
studies, anaemia prevalence ranges from 38 to 46%
 Pathophysiology
 Iron deficiency anemia is the most common form of anemia
and it develops over time if the body does not have enough
iron to manufacture red blood cells.

 Without enough iron, the body uses up all the iron it has
stored in the liver, bone marrow and other organs.
 Cont.

 Once the stored iron is depleted, the body is able to make

very few red blood cells.
 If erythropoietin is present without sufficient iron, there is
insufficient fuel for red blood cell production
 The red blood cells that the body is able to make are
abnormal and do not have a normal hemoglobin-carrying
capacity, as do normal red blood cells.
 Risk factors for IDA
28

Period Risk factors

 Maternal iron deficiency
 Prematurity
Perinatal
 Administration of erythropoietin for anemia of prematurity
 Perinatal hemorrhagic events (eg, twin-twin transfusion or fetal-maternal hemorrhage)

Dietary risk factors

Lack of iron supplements for breastfed infants
Use of low-iron infant formula
Feeding of unmodified (non-formula) cow's milk, goat's milk, or soy milk
Infancy Insufficient iron-rich complementary foods

 Other risk factors

 Disorders with GI blood loss (eg, milk protein-induced proctocolitis)
 Malabsorptive disease

 Dietary risk factors:Excessive intake of cow's milk◊

 Insufficient iron in foods§

1 to <12 years  Other risk factors:Disorders with GI blood loss (eg, inflammatory bowel disease, or chronic gastritis)
 Malabsorptive disease (eg, celiac disease, or chronic intestinal infections)
 Obesity
 Stages of iron deficiency 

 IDA is a microcytic, hypochromic, and hypoproductive state.

 There is progression from normal iron status to iron deficiency,
followed by iron-limited erythropoiesis and finally to IDA.
 With iron deficiency, storage sites are depleted, but there is
sufficient iron in the "labile" iron pool from the daily turnover of
red cells for normal hemoglobin synthesis, unless further iron
losses occur.
 Cont.

 Anemia develops only in the final stage of iron deficiency. 

 Clinical features

 Most children with IDA are asymptomatic and are identified

by routine laboratory screening.
 Anemia:
 Pallor is the most recognized clinical sign of IDA but is not
usually visible until the hemoglobin falls to 7-8 g/dL.
 It is most readily noted as pallor of the palms, palmar
creases, nail beds, or conjunctivae.
 Clinical features

 Parents often fail to note the pallor because of the typical slow
decline of hemoglobin over time.
 Mild to moderate iron-deficiency anemia (Hb 6-10 g/dL)
 Few symptoms of anemia aside from mild irritability are noted.
 Compensatory mechanisms: increased levels of 2,3-
diphosphoglycerate and a shift of the oxygen dissociation
curve, may be so effective.
 Clinical features

 When the hemoglobin level falls to <5 g/dL,

 Irritability, anorexia, and lethargy develop, and systolic
flow murmurs are often heard.
 If the hemoglobin continues to fall, tachycardia and high
output cardiac failure can occur.
 Clinical features
34

 Neurodevelopmental 
 In young children, IDA is associated with impaired
neurocognitive development, including decreased visual and
auditory processing time.
 Neurocognitive outcomes are worse for children with more
severe and chronic IDA.
 Clinical features
35

 Febrile seizures 
 Serum ferritin levels are significantly lower in children with
febrile seizures compared with those with fever alone.
 Clinical features
36

 Immunity and infection 

 Iron deficiency appears to be associated with mild to moderate
defects in leukocyte and lymphocyte function, including
defective IL-2 and IL-6 production.
 There is some evidence that iron supplementation results in
increased susceptibility to or reactivation of dormant
infections, such as malaria or tuberculosis
 Clinical features
37

 Exercise capacity 
 Moderately severe IDA is associated with decreased work
capacity, in part because iron is an essential cofactor for
enzyme-driven aerobic metabolism.
 Pica and pagophagia
 Pica is the intense craving for nonfood items.
 Pagophagia, or craving for ice, is particularly common and
specific for the iron-deficient state.
Laboratory findings
Cont.
 Cont.

 Bone marrow iron staining is the most accurate method of

diagnosing iron-deficiency anemia but is invasive and
expensive and usually unnecessary.
 On CBC white blood cell (WBC) count is normal, but
thrombocytosis is often present.
 Thrombocytopenia is occasionally seen with iron deficiency,
potentially confusing the diagnosis with bone marrow failure
disorders.
 Cont.

 The blood smear :

 Hypochromic, microcytic RBCs with substantial variation
in cell size.
 EVALUATION OF IDA
42

Review history
For risk factors for IDA (dietary, blood loss, obesity, or malabsorptive disease)
For evidence of other causes of anemia (acute infection, chronic diseases, or family
history of anemia or hemoglobinopathy)

Initial laboratory testing 

If the presentation is typical for IDA (age <3 years, with any dietary risk factors for
IDA), a CBC is sufficient.
 If the presentation is atypical, more extensive laboratory testing may be appropriate. 

Trial of iron therapy 

If the history and laboratory testing is consistent with IDA, perform an empiric trial of
iron therapy.
Reevaluate
Within four weeks to confirm a response to the iron therapy.
 EVALUATION OF IDA
43

 Empiric trial of iron therapy 

 Initiate ferrous sulfate, 3 mg/kg of elemental iron, once daily
between meals.
 In addition to iron therapy, provide dietary counseling to
ensure adequate intake of iron, and avoid dietary risk factors
such as excessive milk intake
 Confirm the response to iron therapy by a repeat CBC within
four weeks from initiation of iron treatment:
 Empiric trial cont..
 An appropriate response :
 Rise in hemoglobin of >1 g/dL within 4 wk for children
with mild anemia (Hb 9 to 11 g/dL) or
 Within two weeks for those with moderate or severe anemia
(hemoglobin <9 g/dL).
 DIFFERENTIAL DIAGNOSIS
45

 Other causes of microcytic anemia:

 α- or β- Thalassemia and other hemoglobinopathies,
including hemoglobins E and C
 Prevention

 Breastfeeding should be encouraged, with the addition of

supplemental iron at 4 mo of age.
 Infants who are not breastfed should only receive iron-
fortified formula (12 mg iron/L) for the 1st yr.
 Thereafter cow's milk should be limited to <20 -24 oz
dially.
 TREATMENT
47

 A daily total dose of 3-6 mg/kg of elemental iron in 1 or 2 doses

is adequate , with the higher dose used in more severe cases.
 The maximum dose is 150-200 mg of elemental iron daily.
 Ferrous sulfate is 20% elemental iron by weight and is ideally
given between meals with vitamin C–containing juice, although
this timing is usually not critical with a therapeutic dose.
 TREATMENT
48

 Parenteral iron preparations are considered when

malabsorption is present or when compliance is poor,
because oral therapy is otherwise as effective, much less
expensive and less toxic.
 TREATMENT
49

 In addition to iron therapy, dietary counseling is usually

necessary.
 Excessive intake of milk, particularly cow's milk, should be
limited.
 Dietary iron should also be increased.
Cont.
 COMPLICATIONS OF
51
TREATMENT
 Iron therapy may increase the virulence of malaria and
certain gram-negative bacteria, particularly in developing
countries.
 Iron overdose is associated with Yersinia infection.
 References

 Nelson textbook 21th edition

 Uptodate 2022