Anemia is a disorder that results in a decrease in the ability of the blood to carry

oxygen. Anemia by itself is not a diagnosis but merely a sign of underlying disease. The

first classification of anemia is best done by examination of the blood smear. Initial

clinical diagnosis of anemia is generally based upon classification of the anemia as

regenerative or nonregenerative. Regenerative anemias are characterized by increased

production of erythrocytes, while nonregenerative anemia show nothing of erythrocyte

production. In addition, anemias are classified by certain indices that give the clinician

some knowledge of cell size (microcytic, normocytic, microcytic) as well as hemoglobin

content (hypochromic, normochromic, or hyperchromic). This paper will focus on

microcytic anemias.

The mean corpuscular volume (MCV) or average erythrocyte size is usually

determined directly by automated hematology analyzers, but it can be calculated

manually by the formula:

(Hct x 10)/ RBC count (millions) = MCV

Microcytosis is indicated by a MCV value that is below the reference interval.

Furthermore, microcytosis often is accompanied by a high red blood cell distribution

width (RDW) value. This value is a measure of anisocytosis or variation in erythrocyte

size.

Several factors influence the MCV value. Factors that associated with

microcytosis include immature animals, iron lack or deficiency, portosystemic shunts,

The primary focus of this discussion is microcytic anemia.

The only way to diagnose anemia is with a blood test. Generally, a full blood

count is done. Apart from reporting the amount of red blood cells and the hemoglobin

level, the automatic counters also measure the size of the red blood cells, which is an

important tool in distinguishing between the causes.

The most common type of anemia overall is iron deficiency anemia, which is

most often microcytic. Much rarer causes are hemoglobinopathies such as sickle cell

anemia and thalassemia.

Iron deficiency anemia is caused when the dietary intake or absorption of iron is

insufficient. Iron is an essential part of hemoglobin, and low iron levels result in

decreased incorporation of hemoglobin into red cells. Body iron is regulated by the rate

of iron absorption rather than iron excretion. In addition, iron absorption is regulated by

the amount of storage iron and rate of erythropoiesis. Ceruloplasmin, a copper containing

protein, is necessary for the transfer of iron from intestinal epithelium and macrophages

to plasma transferrin. Iron is transported in the plasma bound to transferrin and is

measured clinically as serum iron. The total serum transferrin concentration is measured

as total iron binding capacity (TBIC). Usually only 1/3 of the transferrin binding sites are

occupied by iron. This is expressed as percent saturation.

Iron is stored in macrophages as ferritin and hemosiderin. Ferritin is a water

soluble, iron-protein complex. Small amounts of ferritin circulate in the plasma and can
be measured as an indirect indicator of the storage iron pool. However, the laboratory test

to measure ferritin concentration is species-specific and only available for specimens

from dogs, cats, horses, and human beings. Serum ferritin is usually decreased in iron

deficiency. It is important to note that ferritin is also an acute phase protein; its

concentration can be elevated in inflammation and some forms of neoplasia.

Cytologically, hemosiderin can be demonstrated in the bone marrow of most healthy

animals except cats by Perl’s (Prussian blue) staining. Hemosiderin is insoluble in water

and will persist in processed cytologic and histologic bone marrow specimens. In iron

deficiency anemia, there is a paucity or absence of stainable iron (hemosiderin) in the

bone marrow.

In iron deficiency, a decrease in the MCV will precede a decrease in the mean

corpuscular hemoglobin concentration (MCHC). Hypochromic cells have a narrow rim of

lightly stained hemoglobin and greater than normal central pallor due to decreased

hemoglobin (Hg) concentration and cells being thin (leptocytes). Affected erythrocytes

also may be smaller or microcytic because extra cell divisions occur before a critical

hemoglobin concentration is reached to arrest mitosis.

Another cause for microcytic anemia is blood loss. Blood sucking parasites (fleas,

ticks, hookworms), bleeding intestinal neoplasms, transitional cell carcinoma with

urogenital bleeding, gastrointestinal ulcers, thrombocytopenia, inherited hemostatic

disorders, hemorrhagic colitis, chronic intravascular hemolysis with hemoglobinuria, and

excessive blood draws for blood donation and diagnostic purposes can promote iron

deficiency anemia.
In acute blood loss, some degree of erythrocyte regeneration (reticulocytes, except in

horses) may keep the MCV within the reference interval. With chronic blood loss, iron is

progressively depleted resulting in insufficient iron stores for reticulocyte production.

The MCV subsequently decreases. A negative iron balance can occur with loss of as little

as 3-4 ml of blood per day. A decreased serum protein concentration or

panhypoproteinemia (low normal to low albumin and globulin concentrations) if the

blood loss is sustained. Concurrent thrombocytosis due to an increase in erythropoietin

production.

Since milk does not contain much iron, dietary iron deficiency may be seen in

nursing animals. In young, rapidly growing animals on an all-milk diet, transient iron

deficiency may lead to mild anemia. This situation occurs within first week of life in

piglets that are reared on concrete flooring without access to soil. Cautious parental or

oral supplementation with iron may be necessary. Deficiencies of vitamin E, which is

required for heme synthesis, also result in hypoferremia (low concentration of circulating

iron). Excessive iron supplementation, in the presence of hypoferremia, may increase free

iron concentration in the circulation causing peroxidation of cellular membranes and

necrosis within the heart, liver, and skeletal muscle.

Copper deficiency is another cause of microcytic anemia. Ceruloplasmin is a

copper-containing protein that is synthesized by liver. This protein is necessary for

transfer of iron from gut epithelium and macrophages to transferring (an iron transporting

protein). Generally, copper deficiency is rarely encountered.

predisposed to the development of copper storage disease. Affected individuals may

become copper deficient as a result of long term dietary copper restriction and

administration of copper chelating drugs. Microcytic, hypochromic anemia has been

documented with long-term copper restriction and chelation therapy. This condition may

be due to chelation of copper and other bivalent cations including iron.

Lastly, Pyridoxine or vitamin B6 is a cofactor for heme synthesis. Deficiency of

this vitamin is rare but may leads to failure of iron utilization.

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