The physical examination may point to the potential causes (see Table 150-2). The physiologic stability of the patient may be abnormal with acute blood loss and acute hemolysis, manifesting as tachycardia, blood pressure changes, and, most ominously, an altered state of consciousness. The presence of jaundice suggests hemolysis. Petechiae and purpura indicate a coagulopathy. Hepatosplenomegaly and adenopathy suggest infiltrative disorders. Growth failure or poor weight gain suggests an anemia of chronic disease. An essential element of the physical examination is the investigation of the stool for the presence of occult blood.
A hemoglobin or hematocrit test indicates the severity of the anemia. Once anemia has been substantiated, the workup should include a complete blood count with differential, platelet count, indices, and reticulocyte count. Examination of the peripheral blood smear assesses the morphology of RBCs (Fig. 150-2), white blood cells (WBCs), and platelets. All cell lines should be scrutinized to determine whether anemia is the result of a process limited to the erythroid line or a process that affects other marrow elements. Using data obtained from the indices and reticulocyte count, the workup can be organized on the basis of whether RBC production is adequate or inadequate and whether the cells are microcytic, normocytic, or macrocytic (see Fig. 150-1).
An appropriate bone marrow response to anemia would be an elevated absolute reticulocyte number, suggestingincreased production and implying either hemolysis orblood loss. Anemia with a normal reticulocyte number suggests decreased or ineffective production for the degree ofanemia. Reticulocytopenia signifies an acute onset so thatthe marrow has not had adequate time to respond, thatreticulocytes are being destroyed in the marrow (antibodymediated), or that intrinsic bone marrow disease is present.The best indicators of the severity of hemolysis are the hemoglobin level and the elevation of the reticulocyte count. Biochemical evidence of hemolysis includes an increase inlevels of bilirubin and lactate dehydrogenase and a decreasein haptoglobin.
Head Frontal bossing Thalassemia major, severe iron deficiency, chronic subdural hematoma Microcephaly Fanconi anemia
General Small stature Fanconi anemia, HIV infection, malnutrition
HIV, Human immunodeficiency virus; SLE, systemic lupus erythematosus.
Figure 150-2 Morphologic abnormalities of the red blood cell. A, Normal. B, Hypochromic microcytes (iron deficiency). C, Schistocytes (hemolytic uremic syndrome. D, Blister cells (glucose-6-phosphate dehydrogenase deficiency). E, Sickle cells (hemoglobin SS disease). F, Spherocytes (autoimmune hemolytic anemia). (Courtesy B. Trost and
J. P. Scott.)
Hypochromic, Microcytic Anemia
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Etiology. Infants fed cow’s milk when younger than 1 year of age, toddlers fed large volumes of cow’s milk, and menstruating teenage girls who are not receiving supplemental iron are at high risk for iron deficiency. Dietary iron deficiency anemia is most common in bottle-fed toddlers who are receiving large volumes of cow’s milk and eat minimal amounts of food high in iron content. (See Chapters 28 and 31.) Iron deficiency anemia also may be found in children with chronic inflammatory diseases, even without chronic blood loss.