Immediate Questions

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A. What are the vital signs? With no hypotension or severe tachycardia, transfusion therapy is not emergently indicated.

B. Is patient symptomatic? In the absence of congestive heart failure, syncope, presyncope, or hemodynamic compromise, transfusion therapy is not emergently indicated.

C. Is there evidence of acute or recent blood loss (eg, hemateme-sis, melena, or hematochezia)? GI blood loss can be divided into acute or chronic, upper GI and lower GI. Acute upper GI blood loss is more often life-threatening than lower GI blood loss.

D. History of hematuria? Long-standing hematuria can cause iron deficiency anemia. Hemoglobinuria is found in hemolytic anemias with brisk intravascular hemolysis.

E. What medication(s) does patient take? Aspirin and NSAIDs may lead to GI blood loss. Chemotherapy drugs, immunosuppressives, folate antagonists (trimethoprim-sulfamethoxazole), anticonvulsants (carbamazepine, valproate, dilantin), and anti-inflammatory drugs (phenylbutazone) may cause marrow suppression or aplasia. Penicillin, sulfonamides, or oxidants may cause hemolysis. Alcohol, isoniazid, and trimethoprim may cause maturation defects.

F. Is there significant organ dysfunction or active inflammatory disease? Severe liver, kidney, adrenal, and thyroid dysfunction cause anemia. Rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease, vasculitides, and chronic osteomyelitis are associated with anemia of chronic disease.

G. How old is patient? Nutritional iron deficiency is never responsible for anemia in term infants before 6 months of age or in premature infants before doubling birthweight. In the newborn period, anemia often results from recent blood loss, isoimmunization, congenital hemolytic anemia, or congenital TORCH infection. Anemia first detected at ages 3-6 months is likely congenital (initially not detected because of fetal hemoglobin).

H. Gender and ethnicity? Consider glucose-6-phosphate dehydroge-nase (G6PD) deficiency in male patients and those of Mediterranean and African origin; thalassemia syndromes in those of Mediterranean and Asian origin; hemoglobin S and C in those of African origin.

I. Neonatal history? Jaundice in the newborn period suggests hemolytic anemia (hereditary spherocytosis or G6PD deficiency).

J. Dietary history and milk intake? An excessive volume of cow's milk in a toddler (> 24 oz/day) commonly results in iron deficiency Goat's milk is deficient in folate.

K. Other medical problems that may cause pseudoanemia? Conditions associated with excess total body water (eg, congestive heart failure) may cause pseudoanemia. In the setting of increased plasma volume, anemia may be made more apparent. History or family history of anemia, splenomegaly, jaundice, thalassemia, sickle cell anemia, or G6PD deficiency? Patients with hereditary disorders of RBCs usually present nonacutely. History of autoimmune disease or immunodeficiency? May be associated with direct Coombs-positive hemolytic anemias or anemia of chronic disease.

III. Differential Diagnosis. CBC with differential, visualization of peripheral smear, RBC indices, and reticulocyte count are essential and show whether anemia results from decreased RBC production, blood loss, or increased RBC destruction.

A. Pancytopenia. All cell lines (hemoglobin, platelets, and WBCs) are decreased. Usually the result of marrow invasion, failure, or suppression caused by drugs, metastatic tumor, hematologic malignancies, and inflammatory diseases. Bone marrow failure (aplastic anemia) may be idiopathic.

B. Low Mean Corpuscular Volume (MCV) Anemias. Iron deficiency is the most common etiology, especially in menstruating girls and toddlers. Hypochromic, microcytic RBCs; target cells; basophilic stippling; marked anisocytosis; and poikilocytosis are seen with thalassemias. Lead poisoning, sideroblastic anemia, and anemia of chronic disease are also associated with low MCV. Red blood cell distribution width index (RDW) is normal in thalassemia trait but high in iron deficiency.

C. Normal MCV Anemias. Anemia of chronic disease is most common. Other etiologies include acute blood loss; chronic infections; collagen vascular diseases; malignancies; kidney, liver, thyroid, and adrenal dysfunction; and transient erythroblastopenia of childhood.

D. High MCV Anemias. Folate and vitamin B12 deficiencies are most common. Vitamin B12 deficiency may be secondary to pernicious anemia, bacterial overgrowth, ileal disease, and (rarely) dietary deficiency (eg, vegan diet). Folate deficiency is associated with dietary deficiency (eg, goat's milk diet), pregnancy, hyperthyroidism, and hemolytic anemias. Consider malabsorption if there is no obvious cause of folate deficiency. Peripheral smear demonstrates hyper-segmented neutrophils and nucleated RBCs. Increased MCV may result from a markedly increased reticulocyte count.

E. Anemias With Increased Reticulocyte Count. Indicates bone marrow that is producing RBCs faster than normal, usually to compensate for loss of RBCs with a shortened life span or from acute blood loss. Reticulocytes appear 24-48 hours after significant acute blood loss. Causes include autoimmune hemolytic anemias and congenital hemolytic anemias (sickle cell anemia, thalassemias). Correction of a deficit (eg, iron deficiency) also leads to transient reticulocytosis.

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