2. Iron deficiency anemia develops when
body stores of iron drop too low to support
normal red blood cell (RBC) production.
Inadequate dietary iron,
impaired iron absorption,
bleeding, or loss of body iron may be the
cause.
Iron equilibrium in the body normally is
regulated carefully to ensure that sufficient
iron is absorbed in order to compensate for
body losses of iron
3. Either diminished absorbable dietary iron or
excessive loss of body iron can cause iron
deficiency.
Diminished absorption usually is due to an
insufficient intake of dietary iron in an absorbable form.
Hemorrhage is the most common cause of
excessive loss of body iron, but it can occur with
hemoglobinuria from intravascular hemolysis.
Malabsorption of iron is relatively uncommon in the
absence of small bowel disease (sprue, celiac disease,
regional enteritis) or previous GI surgery.
9. Dietary factors
HEME IRON VS NON HEME IRON
Meat provides a source of heme
iron.
Substances that diminish the absorption of
ferrous and ferric iron include phytates, oxalates,
phosphates, carbonates, and tannates.
ascorbic acid increases the absorption of ferric
and ferrous iron
10. Globin degradation products diminish heme
polymerization, making it more available for
absorption. They also increase the absorption of
nonheme iron because the peptides from
degraded globin bind the iron to prevent both
precipitation and polymerization
Heme and nonheme iron uptake by intestinal
absorptive cells is noncompetitive.
11.
12. Iron absorption from food
Iron Absorption (% of dose)
0 5 10 15 20 25
Meat muscle
Hemoglobin
Fish muscle
liver
Ferritin
Soy beans
Wheat
Lettuce
Corn
Black beans
Spinach
Rice
Non-heme
iron
Heme
iron
13. Hemorrhage
Bleeding for any reason produces iron
depletion.
If sufficient blood loss occurs, iron deficiency anemia
ensues.
A single sudden loss of blood produces a post hemorrhagic
anemia that is normocytic. The bone marrow is stimulated to
increase production of hemoglobin, thereby depleting iron in body
stores. Once they are depleted, hemoglobin synthesis is impaired
and microcytic hypochromic erythrocytes are produced.
14. Malabsorption of iron
Prolonged achlorhydria may produce iron
deficiency because acidic conditions are
required to release ferric iron from food.
Starch and clay eating produce
malabsorption of iron and iron deficiency
anemia.
15. Extensive surgical removal of the proximal
small bowel or chronic diseases (eg, untreated
sprue or celiac syndrome) can diminish iron
absorption.
In patients who have undergone bariatric
surgery, postoperative gastric hypochlorhydria
impairs iron absorption; in those who have
undergone Roux-en-Y gastric bypass surgery,
bypass of the duodenum impairs reduction of
iron to the ferrous (absorbable) state.
16. Iron-refractory iron deficiency
(IRIDA)
A hereditary disorder marked by with iron
deficiency anemia that is typically unresponsive to
oral iron supplementation and may be only partially
responsive to parenteral iron therapy.
IRIDA results from variants in the TMPRSS6
gene that lead to uninhibited production of
hepcidin.
IRIDA is characterized by microcytic, hypochromic
anemia and serum hepcidin values that are
inappropriately high for body iron levels.
17. Most patients with IRIDA are women.
Age at presentation, disease severity, and
response to iron supplementation are highly
variable, even within families, with a few patients
responding to oral iron but most requiring
parenteral iron supplementation.
An uncommon form of IRIDA occurs in
postmenopausal women with androgen
deficiency that leads to primary defective iron
reutilization. This condition only responds to
androgen replacement.
18. Prognosis
Iron deficiency anemia is an easily treated
disorder with an excellent outcome;
however, it may be caused by an underlying condition
with a poor prognosis, such as neoplasia.
Similarly, the prognosis may be altered by a comorbid
condition such as coronary artery disease.
20. SYMPTOMS AND SIGNS
Fatigue and diminished capability to perform
activities
deficiency or dysfunction of nonhemoglobin
proteins leading to
muscle dysfunction,
pagophagia,
dysphagia with esophageal webbing,
poor scholastic performance,
altered resistance to infection
Pica ( clay and starch eating )
21. Severe anemia due to any cause may produce
hypoxemia and enhance the occurrence of
coronary insufficiency and myocardial ischemia.
Likewise, it can worsen the pulmonary status
of patients with chronic pulmonary disease.
Restless leg syndrome
22. Cold intolerance develops in one fifth of patients
with chronic iron deficiency anemia and is
manifested by vasomotor disturbances, neurologic
pain, or numbness and tingling.
Rarely, severe iron deficiency anemia is
associated with papilledema, increased
intracranial pressure, and the clinical picture of
pseudotumor cerebri. These manifestations
are corrected with iron therapy.
23. Children deficient in iron may exhibit behavioral
disturbances. Behavioral disturbances may manifest
as an attention deficit disorder
Neurologic development is impaired in infants and
scholastic performance is reduced in children of school
age.
Physical Growth is impaired in infants with iron
deficiency.
24. Physical Examination
pallor of the skin and mucous membranes.
esophageal webbing,
koilonychia,
glossitis,
angular stomatitis,
25.
26.
27.
28.
29.
30. .
Laboratory diagnosis
Complete blood count (CBC)
Peripheral smear
Serum iron, total iron-binding capacity (TIBC),
and serum ferritin
Hemoglobin electrophoresis and measurement
of hemoglobin A 2 and fetal hemoglobin
Reticulocyte hemoglobin content
31. Other laboratory tests
(eg, stool testing, incubated osmotic fragility
testing, measurement of lead in tissue, and bone
marrow aspiration)
Useful for establishing the etiology of iron
deficiency anemia and for excluding or
establishing a diagnosis of the other microcytic
anemias.
32. Complete Blood Count
documents the severity of the anemia.
the cellular indices show a microcytic
and hypochromic erythropoiesis
mean corpuscular volume (MCV) and the
mean corpuscular hemoglobin
concentration (MCHC) have values below
the normal range for the laboratory
performing the test.
33. Often, the platelet count is elevated (>450,000/µL); this
elevation normalizes after iron therapy.
The white blood cell (WBC) count is usually within
reference ranges (4500-11,000/µL), but it may be elevated.
If the CBC is obtained after blood loss, the
cellular indices do not enter the abnormal range
until most of the erythrocytes produced before the
bleed are destroyed at the end of their normal
lifespan (120 d).
34. Reticulocyte hemoglobin content
CHr was the strongest predictor of iron deficiency
and iron deficiency anemia.
Measurement of CHr may be a reliable method to
assess deficiencies in tissue iron supply and, in
combination with a CBC, may be an alternative to
the traditional biochemical panel for the diagnosis
of iron deficiency in children.
35. Peripheral Smear
Examination of the erythrocytes shows microcytic
and hypochromic red blood cells in chronic iron
deficiency anemia. The microcytosis is apparent in
the smear long before the MCV is decreased after an
event producing iron deficiency.
In iron deficiency anemia, unlike thalassemia, target
cells usually are not present, and anisocytosis and
poikilocytosis are not marked.
This condition lacks the intraerythrocytic crystals seen
in hemoglobin C disorders.
37. Laboratory findings:
•Red cell indices:
Low Hb conc.
MCV, MCH, MCHC
•Blood film:
Hypochromic microcytic Picture.
Pencil shaped poikilocytes.
Normal reticulocyte count.
•Bone marrow iron:
Normal to hypercellular.
RBC precursors are increased in number.
Iron stain negative.
•Chemical testing on serum:
Serum iron Decreased
Transferrin/TIBC Normal to High
Serum ferritin Decreased (Very low)
38.
39. Sequential Changes in IDA
NORMAL
DEPLETED
IRON
STORES
IRON
DEFICIENCY
IRON
DEFICIENCY
ANEMIA
FERRITIN
IRON SATURATION
MCV & Hb & Hct
41. Stool testing
Testing stool for the presence of hemoglobin is
useful in establishing gastrointestinal (GI)
bleeding as the etiology of iron deficiency anemia.
Also stool examination may reveal ova of
schistosomes
42. Bone marrow aspiration
Although this test has largely been displaced in the
diagnosis of iron deficiency by serum iron, TIBC, and
serum ferritin testing, the absence of stainable iron in a
bone marrow aspirate is the criterion standard for the
diagnosis of iron deficiency.
43. Iron stain of bone marrow
Iron Deficient Marrow
Prussian Blue Stain
Normal Marrow
Prussian Blue Stain
45. In most patients, the iron deficiency should be
treated with oral iron therapy, and the underlying
etiology should be corrected so the deficiency
does not recur.
Avoid giving iron to patients who have a
microcytic iron-overloading disorder (eg,
thalassemia, sideroblastic anemia
Parenteral iron therapy only when immediate
hemoglobin improvement required or intolerable to
oral iron or not improving with oral iron
supplementation
Blood transfusions should be reserved for patients who
are at risk for, or who have, cardiovascular instability due to
their anemia.
46. Uncommonly, postmenopausal women
are unresponsive to iron
supplementation, including parenteral
iron,( IRIDA ) because they have primary
defective iron reutilization due to androgen
deficiency. This condition responds only
to androgen replacement. Danazol is a
reasonable choice for these patients, as it
is less masculinizing.
47. Iron Therapy
Oral ferrous iron salts are the most
economical and effective medication for the
treatment of iron deficiency anemia.
Of the various iron salts available, ferrous
sulfate is the one most commonly used.
To promote absorption, patients should avoid tea
and coffee and may take vitamin C (500 units) with
the iron pill once daily.
48. In July 2019, the FDA approved ferric maltol for
treatment of iron deficiency anemia in adults with
inflammatory bowel disease (IBD).
The usual benchmark for successful iron
supplementation is a 2-g/dL increase in the
hemoglobin (Hb) level in 3 weeks.
Ferric citrate (2017) for treatment of iron deficiency
anemia in adults with chronic kidney disease (CKD)
who are not on dialysis. Each tablet of ferric citrate 1
gram is equivalent to 210 mg of ferric iron.
49. Response to oral Iron
Therapy
Peak reticulocyte count 7 - 10 d.
Increased Hb and Hct 14 - 21 d.
Normal Hb and Hct 2 months
Normal iron stores 4 - 5 months
50. Parenteral iron therapy
Reserve parenteral iron for patients who are
either unable to absorb oral iron or who
have increasing anemia despite adequate
doses of oral iron.
It is expensive and has greater morbidity than
iron preparations taken orally.
51. Indications for iv iron
Severe symptomatic anemia requiring accelerated
erythropoesis
Failure of oral iron from g.i intolerance
Failure of oral iron due to absorption issues
H pylori infection, autoimmune gastritis, celiac
disease, gastric bypass surgery, inflammatory bowel
disease
Cancer and chemotherapy associated anemia
Anemia with chronic renal disease (with or without[?]
dialysis dependance)
Heavy ongoing g.i or menstrual blood losses
52. High molecular weight iron dextrans are
associated with increased risks, so their use
for IV therapy should be avoided.
The second- and third-generation IV
irons are considered equally efficacious in
treating iron deficiency in equivalent doses,
but iron isomaltoside seems to have a
lower frequency of serious and severe
hypersensitivity reactions
53. In July 2013, the FDA approved ferric
carboxymaltose injection for the intravenous
treatment of iron deficiency anemia in adults who
either cannot tolerate or have not responded well
to oral iron.
The drug is also indicated for the treatment of
iron deficiency anemia in adults with non–dialysis-
dependent CKD.
54. Ferumoxytol injection consists of a super paramagnetic
iron oxide that is coated with a carbohydrate shell, which
helps isolate the bioactive iron from plasma components
until the iron-carbohydrate complex enters the
reticuloendothelial system macrophages of the liver,
spleen, and bone.
In January 2018, the FDA expanded the indication for
ferumoxytol injection to include all eligible adults with iron
deficiency anemia who have intolerance or unsatisfactory
response to oral iron. ( previously to CKD ) Ferumoxytol
was effective and well tolerated in patients with iron
deficiency anemia of any underlying cause in whom oral
iron was ineffective or could not be used
55. BLOOD TRANSFUSION
Reserve transfusion of packed red blood cells
(RBCs) for patients who either are
experiencing significant acute bleeding or are
in danger of hypoxia and/or coronary
insufficiency.
56. Management of Hemorrhage
Surgical treatment consists of stopping
hemorrhage and correcting the underlying defect
so that it does not recur.
This may involve surgery for treatment of
either neoplastic or nonneoplastic disease of
the gastrointestinal (GI) tract, the
genitourinary (GU) tract, the uterus, and the
lungs.
57. Prevention
Certain populations are at sufficiently high risk for iron
deficiency to warrant consideration for prophylactic iron therapy.
pregnant women,
women with menorrhagia,
consumers of a strict vegetarian diet,
infants and children in growth spurt,
adolescent girls and
regular blood donors.
58. Long-Term Monitoring
To ensure that there is an adequate response to iron
therapy and that iron therapy is continued until after
correction of the anemia to replenish body iron
stores.
Follow-up also may be important to treat any underlying
cause of the iron deficiency.
Response to iron therapy can be documented by
an increase in reticulocytes 5-10 days after the
initiation of iron therapy. The hemoglobin
concentration increases by about 1 g/dL weekly
until normal values are restored. These responses
are blunted in the presence of sustained blood loss or
coexistent factors that impair hemoglobin synthesis.
