IRON DEFICIENCY ANEMIA

Definition Reduced RCBs, Hemoglobin & Hematocrit Level

 most widespread and common nutritional disorder in the world
 30-50% has IDA globally; mostly in developing countries
 Full term newborn contains 0.5 g of iron; Adults (5 g)
 Infant requires 0.8 mg of iron absorbed daily for the first 15 years of
life
 1 mg to consider normal losses; to maintain positive iron balance in
childhood
 Breast fed infants can absorb 2-3x more iron than fed with cow’s milk
 Since growth is most rapid in infancy, breastfed infants are still at risk
of developing IDA without intake of iron fortified food by 6 months of
age
Causes - Dietary deficiency
- Chronic blood loss (most common)
- Increased demands during growth periods
- Low birth weight
- Excessive consumption of cow’s milk (cow’s milk is low in iron)
Epidemiology most widespread and common nutritional disorder in the world.

30–50% of the global population has iron-deficiency anemia, and most of

these individuals live in developing countries.

In the United States, 8–14% of children ages 12-36 mo are iron

deficient, and 30% of this group progresses to iron-deficiency anemia.

Approximately 2% of adolescent girls have iron-deficiency anemia,

largely as a result of their adolescent growth spurt and menstrual blood
loss. The highest risk of iron-deficiency anemia (>30%) is among
teenagers
who are or have been pregnant
PATHOPHYSIOLOG1. Iron deficiency has 3 stages:
Y 2.
3. The 1st stage is the iron depletion stage. In this stage, there is a
negative iron balance, in which the demands for iron exceed the
body’s ability to absorb iron from the diet. At this point, there is
mobilization of iron from reticuloendothelial storage sites. This is
reflected by the decrease of serum ferritin level and increase in TIBC.
However, there are still no signs and symptoms present in this stage.

The second stage is the iron-deficient erythropoiesis. iron stores

become depleted, the serum iron begins to fall hence impaired
hemoglobin synthesis. Marrow iron stores are absent as defined by the
serum ferritin level is <15ug/L. laboratory findings include serum
ferritin level of <15ug/L, transferrin saturation falls to 15–20%,
microcytic , hypochromic rbc. TIBC increases also. Feelings of a low
energy level, reduced capacity to do physical work, slow cognitive function
are signs that anemia is developing.

The 3rd stage is iron-deficiency anemia. The transferrin saturation at

this point is <10–15%. When moderate anemia is present (hemoglobin
10–13 g/dL), the bone marrow remains hypoproliferative. Consequently,
with severe prolonged iron-deficiency anemia, erythroid hyperplasia of
the marrow develops. Also With more severe anemia (hemoglobin 7–8
g/dL), hypochromia and microcytosis become more prominent, target
cells and poikilocytes appear on the blood smear as elliptocytes (cigar-
or pencil-shaped form), and the erythroid marrow becomes increasingly
ineffective. Symptoms include fatigue upon exertion, weakness,
headaches, apathy, pallor, poor resistance to cold temperatures, low
physical work capacity, and poor immune function.
*SIMPLIFIED:
The progression to iron deficiency can be divided into three stages
1. first stage is negative iron balance,
2. in which the demands for (or losses of) iron exceed the
body’s ability to absorb iron from the diet.
3. This stage results from a number of physiologic
mechanisms, including blood loss, pregnancy (in which the
demands for red cell production by the fetus outstrip the
mother’s ability to provide iron), rapid growth spurts in the
adolescent, or inadequate dietary iron intake. Blood loss
in excess of 10–20 mL of red cells per day is greater than the
amount of iron that the gut can absorb from a normal diet.
4. Under these circumstances, the iron deficit must be made
up by mobilization of iron from RE storage sites.
5. During this period, iron stores—reflected by the serum
ferritin level or the appearance of stainable iron on bone
marrow aspirations—decrease.
6. As long as iron stores are present and can be mobilized, the
serum iron, total iron-binding capacity (TIBC), and red cell
protoporphyrin levels remain within normal limits.
7. At this stage, red cell morphology and indices are
normal.
7. This is a period of iron-deficient erythropoiesis.
 iron stores become depleted, the serum iron begins to fall.
o TIBC increases, as do red cell protoporphyrin levels.
o By definition, marrow iron stores are absent when
the serum ferritin level is <15ug/L.
o As long as the serum iron remains within the normal
range, hemoglobin synthesis is unaffected despite
the dwindling iron stores.
o Once the transferrin saturation falls to 15–20%,
hemoglobin synthesis becomes impaired.
o Careful evaluation of the peripheral blood smear
reveals the first appearance of microcytic cells, and
if the laboratory technology is available, one finds
 hypochromic reticulocytes in circulation.

8. iron-deficiency anemia
 hemoglobin begins to fall
 The transferrin saturation at this point is <10–15%.
 When moderate anemia is present (hemoglobin 10–13
g/dL), the bone marrow remains hypoproliferative.
 With more severe anemia (hemoglobin 7–8 g/dL),
hypochromia and microcytosis become more prominent,
target cells and misshapen red cells (poikilocytes)
appear on the blood smear as cigar- or pencil-shaped
forms, and the erythroid marrow becomes increasingly
ineffective.
 Consequently, with severe prolonged iron-deficiency
anemia, erythroid hyperplasia of the marrow develops,
rather than hypoproliferation.

Clinical  Most patients with mild to moderate anemia are asymptomatic .

Manifestations  In mild to mod iron deficiency (hb levels of 6-10g/dl) mild
irritability may be seen
 When hb levels reach 7-8g/dl : pallor, which is the most important
sign of ID may be seen
 When hb levels fall below 5g/dl irritability and anorexia are
prominent, there is also lethargy, easy fatigability, systolic flow
murmurs and a high output cardiac failure
 Other signs may include koilonychia, pica, pagophagia, and
irreversible neurocpgnitive defects

LABORATORY  In progressive iron deficiency, tissue iron stores are depleted. This
depletion is reflected by reduced serum ferritin, an iron-storage protein,
which provides an estimate of body iron stores in the absence of
inflammatory disease.
 Next, serum iron levels decrease, the iron-binding capacity of the serum
(serum transferrin) increases, and the transferrin saturation falls below
normal. As iron stores decrease, iron becomes unavailable to complex with
protoporphyrin to form heme. Free erythrocyte protoporphyrins
accumulate, and hemoglobin synthesis is impaired. At this point, iron
deficiency progresses to iron-deficiency anemia. With less available
hemoglobin in each cell, the red cells become smaller and varied in size.
 The variation in red cell size is measured by an increasing red cell
distribution width. This is followed by a decrease in mean corpuscular
volume and mean corpuscular hemoglobin. The red blood cell count also
decreases.
 The reticulocyte percentage may be normal or moderately elevated, but
absolute reticulocyte counts indicate an insufficient response to the degree
of anemia.
 The blood smear reveals hypochromic, microcytic red cells with
substantial variation in cell size.
 White blood cell count is normal, and thrombocytosis is often present.
 Stool for occult blood should be checked to exclude blood loss as the cause
of iron deficiency.
  A presumptive diagnosis of iron-deficiency anemia is most often made by a
complete blood count demonstrating a microcytic anemia with a high red
cell distribution width, reduced red blood cell count, normal white blood
cell count, and normal or elevated platelet count.

MANAGEMENT  Calcium and fiber decreases absorption of Fe thus Vit C

administration is done to counter
 Daily total dose of 3-6 mg/kg elemental iron at 1 or 2 doses
 Maximum dose: 150-200mg elemental iron
 Ferrous sulfate (20% elemental iron)
o Administer between meals
o Give together with Vit C containing juice
 Watch out for;
o Increase malaria virulence
o Gram neg infection
o Yersinia Infection in overdosage
 MILD ANEMIA
o Repeat blood count 1 month after initiation of therapy
 Expect 1-2 g/dL increase or Normalization of blood
count
 SEVERE ANEMIA
o Confirm via: presence of RETICULOCYTOSIS withing 48 to
96 hours of initiating treatment
o Expect an increase of Hgb by 0.1-0.4 g/dL/day
o Continue medication 2 to 3 months after normalization of
blood count
 Poor Response
o Consider other Dx other than IDA
 Blood Transfusion
o Rarely necessary unles;
 Imminent heart failure
 Severe anemia with BLEEDING
o If given, administer slowly to avoid CHF

DIFFERENTIALS
Anemia of Inflammation or  Found in conditions with ongoing immune activation
ACD  Wide range of disorders: infections, malignancies,
chronic renal disease, autoimmunity
 Mild-moderate, normocytic normochromic,
hypoproliferative, with decreased serum iron, low
transferrin saturation
 Clin manifestations: depends on underlying disease
 Lab findings:
o 6-9mg/dL
o Normochromic, normocytic, some with
hypochromia & microcytosis if with iron
deficiency
 o Normal-low absolute reticulocytosis
o Leukocytosis
o Low serum iron level, no increase in transferrin
o Ferritin levels may be elevated secondary to
inflammation
 Soluble transferring receptor (sTfR) – diagnostic test to
distinguish ACD from IDA
o High in IDA
o Normal in ACD

Sideroblastic Anemia
Megaloblastic Anemia diverse group of genetic blood diseases characterized by
absent or decreased production of normal hemoglobin,
resulting in a microcytic anemia of varying degree.