Lymphocytes are particularly abundant in the bone marrow of young children. These are primarily B lymphocytes arising in the spleen and lymph nodes, but T lymphocytes also are present.
The diagnosis of anemia is determined by comparison of thepatient’s hemoglobin level with age-specific and sex-specific normal values (see Table 149-2). The production ofandrogens at the onset of puberty in boys causes males tomaintain a normal hemoglobin value about 1.5 to 2 g/dLhigher than girls. The easiest quantitative definition of anemia is any hemoglobin or hematocrit value that is 2 standard deviations (SDs) (95% confidence limits) below themean for age and gender. However, in certain pathologicstates, anemia may be present with a normal hemoglobinlevel (e.g., cyanotic cardiac or pulmonary disease or abnormally high hemoglobin affinity for oxygen). This is a physiologic definition of anemia. Anemia is often a manifestationof some other primary process and may accentuate otherorgan dysfunction.
Anemias are classified based on the size and hemoglobincontent of the cells (Fig. 150-1). Hypochromic, microcytic anemia is caused by an inadequate production of hemoglobin. The most common causes of this type of anemia are iron deficiency and thalassemia. Most normocytic anemias are associated with a systemic illness that impairs
Hypochromic, Microcytic ° major, minor disease Copper deficiency Sideroblastic anemia Aluminum, (?) lead
Normochromic, Normocytic • Hemoglobin SS, S-C, S-° thalassemia
DIC, HUS, TTP
Figure 150-1 Use of the complete blood count, reticulocyte count, and blood smear in the diagnosis of anemia. DIC, Disseminated intra-vascular coagulation; G6PD, glucose-6-phosphate dehydrogenase; HUS, hemolytic uremic syndrome; R/O, rule out; RPI, reticulocyte production index; TTP, thrombotic thrombocytopenic purpura.
adequate marrow synthesis of red blood cells (RBCs).Vitamin B12 and folic acid deficiencies lead to macrocytic anemia. Hemolytic diseases are mediated either by disorders intrinsic or extrinsic to the RBC that increase cell destruction. The most common RBC membrane disorders are hereditary spherocytosis and hereditary elliptocytosis. In both of these disorders, abnormalities of proteins within the cytoskeleton lead to abnormal RBC shapeand function. Numerous RBC enzyme deficiencies maylead to hemolysis, but only two are common: glucose-6-phosphate dehydrogenase (G6PD) deficiency and pyruvate kinase deficiency. Immune-mediated hemolysismay be extravascular when RBCs coated with antibodiesor complement are phagocytosed by the reticuloendothelialsystem. The hemolysis may be intravascular when antibodybinding leads to complement fixation and lysis of RBCs.
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Acute onset of anemia can result in a poorly compensated state, manifested as an elevated heart rate, a flow murmur, poor exercise tolerance, headache, excessive sleeping (especially in infants) or fatigue, irritability, poor feeding, and syncope. In contrast, chronic anemia often is exceptionally well
Age Iron deficiency rare in the absence of blood loss before 6 mo or in term infants or before doubling of birth weight in preterm infants Neonatal anemia with reticulocytosis suggests hemolysis or blood loss; with reticulocytopenia, suggests bone marrow failure Sickle cell anemia and β-thalassemia appear as fetal hemoglobin disappears (4–8 mo of age)