Macrocytic anemia: high MCV
A high MCV may result from hemolysis, primary vitamin B12 or folate deficiency, intrinsic factor deficiency, myelodysplasia, or hepatic dysfunction, as occurs in alcoholism.1,6 Oval macrocytes are commonly observed in myelodysplasia and vitamin B12 or folate deficiencies (Figure 3).1 Alcoholic liver disease is typically associated with large target-shaped RBCs.1 A reticulocyte count and reticulocyte production index (RPI) may
also be helpful in distinguishing the causes.9,14 Increases in the reticulocyte count and RPI indicate a good response by the bone marrow to anemia. A low reticulocyte count with low RPI indicates that RBC production is ineffective to compensate for the degree of anemia present. These measures will help to identify causes of anemia related to the bone marrow itself, such as iron deficiency, B12 deficiency, and marrow failure.
Beyond iron and RBC indices
The presence of spherocytes on the peripheral smear indicates splenic culling or the extraction of immune complexes from the RBCs in the spleen. The direct antiglobulin test (DAT), formerly known as the Coombs test, detects the presence of antibodies bound to the surface of RBCs.1 If the DAT is positive, an immune-mediated hemolysis is likely the cause of the anemia.14
Other RBC morphologies, such as target cells and sickled cells in sickle cell diseases, are pathognomonic for specific diseases. The RBC indices, such as MCV and RDW, can be variable in these instances.
By evaluating the information obtained on the CBC, the etiology of most common anemias can be determined in the primary-care setting.2 Categorizing anemia based on the MCV is the first step in a systematic approach to follow-up testing and will lead to a diagnosis in a majority of cases.3 Anemias not diagnosed by this approach can be referred to a hematologist for further evaluation.
Dr. Gunder is an assistant professor in the School of Allied Health Sciences at the Medical College of Georgia in Augusta.
1. Lee GR. Anemia: a diagnostic strategy. In: Lee GR, Paraskevas F, Foerster J, et al, eds. Wintrobe’s Clinical Hematology. 10th ed. Baltimore, Md.: Williams & Wilkins; 1999:908-940.
2. Sandhaus LM, Meyer P. How useful are CBC and reticulocyte reports to clinicians? Am J Clin Pathol. 2002;118:787-793.
3. Casanova BF, Sammel MD, Macones GA. Development of a clinical prediction rule for iron deficiency anemia in pregnancy. Am J Obstet Gynecol. 2005;193:460-466.
4. Bessman JD, Gilmer PR Jr, Gardner FH. Improved classification of anemias by MCV and RDW. Am J Clin Pathol. 1983;80:322-326.
5. Oski F, Brugnara C, Nathan D. A diagnostic approach to the anemic patient. In: Nathan DG, Orkin SH, Look AT, Ginsberg D, eds. Nathan and Oski’s Hematology of Infancy and Childhood. Philadelphia, Pa.: Saunders; 2003:409-419.
6. Schnall SF, Berliner N, Duffy TP, Benz EF Jr. Approach to the adult and child with anemia. In: Hoffman RH, Benz E, Shattil S, et al, eds. Hematology: Basic Principles and Practice. 3rd ed. New York, N.Y.: Churchill Livingstone; 2000:367-382.
7. Lesperance L, Wu AC, Bernstein H. Putting a dent in iron deficiency. Contemp Pediatr. 2002;19:60-79.
8. Abshire TC. The anemia of inflammation. A common cause of childhood anemia. Pediatr Clin North Am. 1996;43:623-637.
9. Gehrs BC, Friedberg RC. Autoimmune hemolytic anemia. Am J Hematol. 2002;69:258-271.
10. Walters MC, Abelson HT. Interpretation of the complete blood count. Pediatr Clin North Am. 1996;43:599-622.
11. Cook JD. The measurement of serum transferrin receptor. Am J Med Sci. 1999;318:269-276.
12. Ferguson BJ, Skikne BS, Simpson KM, et al. Serum transferrin receptor distinguishes the anemia of chronic disease from iron deficiency anemia. J Lab Clin Med. 1992;119:385-390.
13. Savage RA. The red cell indices. Yesterday, today, and tomorrow. Clin Lab Med. 1993;13:773-785.
14. Dhaliwal G, Cornett PA, Tierney LM Jr. Hemolytic anemia. Am Fam Physician. 2004;69:2599-2606.