Family history X-linked: G6PD deficiency and genetic Autosomal dominant: spherocytosis considerations Autosomal recessive: sickle cell anemia, Fanconi anemia Family member with history of cholecystectomy (for bilirubin stones) or splenectomy at an early age Ethnicity (thalassemia in persons of Mediterranean origin; G6PD deficiency in blacks, Greeks, and people of Middle Eastern origin) Race (β-thalassemia in persons of Mediterranean, African, or Asian descent; α-thalassemia in those of African and Asian descent; SC and SS in African descent)
Nutrition Cow’s milk diet: iron deficiency Strict vegetarian: vitamin B12 deficiency Goat’s milk diet: folate deficiency Pica: plumbism, iron deficiency Cholestasis, malabsorption: vitamin E deficiency
Drugs G6PD: oxidants (e.g., nitrofurantoin, antimalarials) Immune-mediated hemolysis (e.g., penicillin) Bone marrow suppression (e.g., chemotherapy) Phenytoin, increasing folate requirements
Diarrhea Malabsorption of vitamin B12 or E or iron Inflammatory bowel disease and anemia of inflammation (chronic disease) with or without blood loss Milk protein intolerance–induced blood loss Intestinal resection: vitamin B12 deficiency
Infection Giardia lamblia infection: iron malabsorption Intestinal bacterial overgrowth (blind loop): vitamin B12 deficiency Fish tapeworm: vitamin B12 deficiency Epstein-Barr virus, cytomegalovirus infection: bone marrow suppression, hemophagocytic syndromes Mycoplasma infection: hemolysis Parvovirus infection: bone marrow suppression HIV infection Chronic infection Endocarditis Malaria: hemolysis Hepatitis: aplastic anemia
G6PD, Glucose-6-phosphate dehydrogenase.
tolerated in children because of their cardiovascular reserve. Usually, children with chronic anemia will have minimal tachycardia and a flow murmur on examination. The urgency of diagnostic and therapeutic intervention, especially the use of packed RBC transfusion, should be dictated by the extent of cardiovascular or functional impairment more than the absolute level of hemoglobin.
The causes of anemia often can be suspected from a careful history adjusted for the patient’s age (Tables 150-1 and 150-2). Anemia at any age demands a search for blood loss.
A history of jaundice, pallor, previously affected siblings,drug ingestion by the mother, or excessive blood loss at thetime of birth provides important clues to the diagnosis innewborns. A careful dietary history is crucial. The key findings in patients with hemolytic anemias are jaundice, pallor, and splenomegaly. Because of increased bilirubin production, gallstones (bilirubinate), a result of chronic hemolysis,are a common complication. Systemic complaints suggestacute or chronic illnesses as probable causes of anemia. Inlater childhood and adolescence, the presence of constitutional symptoms, unusual diets, drug ingestion, or bloodloss, especially from menstrual bleeding, often points to adiagnosis. Congenital hemolytic disorders (enzyme deficiencies and membrane problems) often present in the first6 months of life and frequently are associated with neonatal jaundice, although these disorders often go undiagnosed. A careful drug history is essential for detecting problemsthat may be drug induced. Pure dietary iron deficiency israre except in infancy, when cow’s milk protein intolerancecauses gastrointestinal blood loss and further complicates analready inadequate iron intake.