Ministry of Higher

Education and Scientific

Research
University of Diyala
College of Medicine

Pathology Report

Subject:

Diagnosis and Treatment of

Iron Deficiency Anemia (IDA)

Supervised by:

Dr. Zahraa Najah

Prepared by:

Abdullah Essa Raham

Mustafa Muqdad Muniem

Abdullah Qussai
 Introduction
Iron (Fe) deficiency anaemia: Microcytic anaemia is common and the commonest cause is
chronic iron deficiency.

Iron physiology and metabolism

Normal (Western) diet provides 715mg of Fe/d, of which 5–10% is absorbed in duodenum and
upper jejunum. Ferrous (Fe2+) iron is better absorbed than ferric (Fe3+) iron. Total body iron
store 74g. Around 1mg of Fe/d lost in urine, faeces, sweat, and cells shed from the skin and GIT.
iron deficiency is commoner in ♀ of reproductive age since menstrual losses account for 720mg
Fe/month and in pregnancy an additional 500–1000mg iron may be lost (transferred from
mother to fetus) (see Table 2.4).
 Assessment

Clinical history—review potential sources of blood loss, especially GIT loss.

Menstrual loss—quantitation may be difficult; ask about number of tampons used per
day, how often these require changing, and duration.
Other sources of blood loss, e.g. haematuria and haemoptysis (these are not common
causes of iron deficiency). Ask patient if he/she has been a blood donor—regular blood
donation over many years may cause chronic iron store depletion.
Drug therapy, e.g. NSAIDs and corticosteroids may cause GI irritation and blood loss.
Past medical history, e.g. previous gastric surgery (l malabsorption). Ask about previous
episodes of anaemia and treatments with iron.
In patients with iron deficiency assume underlying cause is blood loss until proved
otherwise. In developed countries pure dietary iron lack causing iron deficiency is almost
unknown.
 Examination

General examination including assessment of mucous membranes (e.g. hereditary

haemorrhagic telangiectasia).
Seek possible sources of blood loss.
Abdominal examination, rectal examination, and sigmoidoscopy mandatory.
Gynaecological examination also required.

Laboratory tests

↓ Hb.
↓ MCV (<76fL) and ↓ MCHC (Note: ↓ MCV in thalassaemia and ACD).
Red cell distribution width (RDW): ↑ in iron deficiency states with a greater frequency
than in ACD or thalassaemia trait (see Fig. 2.2).
Serum ferritin (measurement of iron /TIBC generally unhelpful). Ferritin assay
preferred—low serum ferritin identifies the presence of iron deficiency but as an acute
phase protein it can be ↑, masking iron deficiency. ↓ Fe and ↑ TIBC indicates iron
deficiency (though tests are obsolete).
The soluble transferrin assay (sTfR) is useful in cases where ↑ ESR. sTfR is ↑ in iron
deficiency but ↔ in anaemia in presence of ↑ ESR (e.g. rheumatoid, other inflammatory
states). This assay is not universally available at present.
% hypochromic RBCs—some modern analysers provide this parameter. ↑ % hypo RBCs
are seen in iron deficiency but also thalassaemia, CRF on EPO where insufficient Fe
given.
Zinc protoporphyrin (ZPP)—in the absence of iron, zinc is incorporated into
protoporphyrin. ↑ ZPP in iron deficiency is a non-specific marker since ↑ ZPP is seen
in any disorder that restricts iron availability to developing RBCs, e.g. infection,
inflammation, cancer, etc.
Reticulocyte Hb concentration (CHr) appears to be a sensitive method for detecting early
iron deficiency.
Examination of BM aspirate (iron stain) is occasionally useful.
 Theoretically FOB testing may be of value in iron deficiency but results can be
misleading. False +ve results seen in high dietary meat intake.

Treatment of iron deficiency

Simplest, safest and cheapest treatment is oral ferrous salts, e.g. FeSO4 (iron gluconate and
fumarate equally acceptable). Provide an oral dose of elemental iron of 150–200mg/d. Side
effects in 10–20% patients (e.g. abdominal distension, constipation and/or diarrhoea)—try
↓ the daily dose to bd or od. Liquid iron occasionally necessary, e.g. children or adults with
swallowing difficulties. Increasing dietary iron intake has no routine place in the
management of iron deficiency except where intake is grossly deficient.
 Response to replacement

A rise of Hb of 2.0g/dL over 3 weeks is expected. MCV will ↑ concomitantly with Hb.
Reticulocytes may ↑ in response to iron therapy but is not a reliable indicator of response.

Duration of treatment

Generally 76 months. After Hb and MCV are normal continue iron for at least 3 months to
replenish iron stores.

Failure of response

Is the diagnosis of iron deficiency correct?

Consider ACD or thalassaemia trait.
Is there an additional complicating illness?
Chronic infection, collagen disorder, or neoplasm.
Is the patient complying with prescribed medication?
Is the preparation of iron adequate in dosage and/or formulation?
Is the patient continuing to bleed excessively?
Is there malabsorption?
Are there other haematinic deficiencies (e.g. B12 or folate) present?
Reassess patient: ? evidence of continued blood loss or malabsorption.

Parenteral Iron
Occasionally of value in genuine iron intolerance, if compliance is a problem, or if need to
replace stores rapidly, e.g. in pregnancy or prior to major surgery. Note: Hb will rise no
faster than with oral iron.

Intravenous Iron

Iron may be administered IV as Fe hydroxide sucrose (ferric hydroxide with sucrose) or Fe

dextran (ferric hydroxide with dextran). Facilities for cardiopulmonary resuscitation should
be available though serious adverse events are uncommon.
References:
1. Oxford Handbook of Clinical Hematology; 4th Edition; Chapter 2; p. 42-45.
2. Andrews, N.C. (1999). Disorders of iron metabolism. N Engl J Med, 341, 1986–95.
3. Brugnara, C. (2000) Reticulocyte cellular indices: a new approach in the diagnosis of
anemias
4. and monitoring of erythropoietic function. Crit Rev Clin Lab Sci, 37, 93–130.
5. Kuhn, L.C. and Hentze, M.W. (1992). Coordination of cellular iron metabolism by
posttranscriptional
6. gene regulation. J Inorg Biochem, 47, 183–95.