The complaint of pallor indicates a perceived decrease in rubor in the skin and mucous membranes of a child, which is associated with decreased oxyhemoglobin delivery to the skin or mucous membranes. Potential causes include decreased blood flow, which may be regional (e.g., thrombosis) or systemic (e.g., shock), and normal blood flow with decreased oxygen-carrying capacity (e.g., anemia).
In most cases, the finding of pallor demands that anemia first be considered as this is the most common cause. Exceptions include children who have a constitutional cause of pallor due to their fair complexion and lack of exposure to sunlight. However, most children with pallor should be considered to have low hemoglobin, which should be measured. Ordinarily, a complete blood count with differential count, red blood cell (RBC) indices, and reticulocyte count guide the clinician in differentiating the many causes of anemia and in determining unusual situations in which pallor is not related to anemia. In addition, a peripheral smear with examination of RBC morphology may further guide the clinician in determining the etiology of anemia.
Pallor may be divided into causes involving normal hemoglobin (Table 10-1) and those involving a low hemoglobin level. The etiology of anemia may be separated into causes due to decreased RBC production, increased RBC destruction, or acute blood loss. Causes due to decreased RBC production are generally associated with low reticulocyte count while causes due to increased RBC destruction or acute blood loss are generally associated with increased reticulocyte count. Anemia may also be considered in relation to mechanism, such as trauma, toxin, metabolic tumor, congenital, or mixed etiology (Table 10-2), or in relation to RBC morphology (Table 10-3).
Table Graphic Jump Location Table 10-1. Pallor with Anemia. ||Download (.pdf)
Table 10-1. Pallor with Anemia.
Decreased erythrocyte or hemoglobin production
Folic acid and vitamin B12 deficiency or associated metabolic abnormalities
Aplastic or hypoplastic anemias
Transient erythroblastopenia of childhood
Malignancy: leukemia, lymphoma, neuroblastomaa
Anemia of chronic disease
Abnormal heme and hemoglobin synthesis
Increased Erythrocyte Destruction
Erythrocyte membrane defects: hereditary spherocytosis, elliptocytosis, stomatocytosis, pyknocytosis, paroxysmal nocturnal hemoglobinuria
Erythrocyte enzyme defects
Defects of hexose monophosphate shunt: G6PD deficiency most common
Defects of Embden-Meyerhof pathway: pyruvate kinase deficiency most common
Sickle cell syndromea
Immune hemolytic anemia
Autoimmune hemolytic anemia (e.g., Evans syndrome)
Isoimmune hemolytic anemia
Viral: mononucleosis, influenza, coxsackie, measles, varicella, cytomegalovirus
Bacterial: Escherichia coli, Pneumococcus, Streptococcus, thyphoid fever, Mycoplasma
Drugs: antibiotics, methyldopa
Inflammatory and collagen vascular disease
Disseminated intravascular coagulationa
Hemolytic uremic syndromea
Thrombotic thrombocytopenic purpura
Idiopathic pulmonary hemosiderosisa