Practice Essentials
Pediatric anemia refers to a hemoglobin or hematocrit level lower than the age-adjusted reference range for healthy children. Physiologically, anemia is a condition in which reduced hematocrit or hemoglobin levels lead to diminished oxygen-carrying capacity that does not optimally meet the metabolic demands of the body.
Anemia is not a specific disease entity but is a condition caused by various underlying pathologic processes. It may be acute or chronic.
This article provides a general overview of anemia, with an emphasis on the acute form. In addition, conditions are emphasized in which anemia is the only hematologic abnormality. The combination of anemia with leukopenia, neutropenia, or thrombocytopenia may suggest a more global failure of hematopoiesis, caused by conditions such as aplastic anemia, Fanconi anemia, myelofibrosis, or leukemia, or may suggest a rapid destruction or trapping of all blood elements, such as hypersplenism, autoimmune disease, localized coagulopathy in a large hemangioma, or hemophagocytic lymphohistiocytosis (HLH) or macrophage activation syndrome (MAS). (See Etiology.)
The main physiologic role of red blood cells (RBCs) is to deliver oxygen to the tissues. Certain physiologic adjustments can occur in an individual with anemia to compensate for the lack of oxygen delivery. These include (1) increased cardiac output; (2) shunting of blood to vital organs; (3) increased 2,3-diphosphoglycerate (DPG) in the RBCs, which causes reduced oxygen affinity, shifting the oxygen dissociation curve to the right and thereby enhancing oxygen release to the tissues; and (4) increased erythropoietin to stimulate RBC production.
The clinical effects of anemia depend on its duration and severity. When anemia is acute, the body does not have enough time to make the necessary physiologic adjustments, and the symptoms are more likely to be pronounced and dramatic. In contrast, when anemia develops gradually, the body is able to adjust, using all 4 mechanisms mentioned above (1, 3, and 4 in most cases), ameliorating the symptoms relative to the degree of the anemia. (See History and Physical Examination.)
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Emergent Management of Acute Anemia
Complications in pediatric acute anemia
Acute and severe anemia can result in cardiovascular compromise. Moreover, if individuals with acute anemia are not treated immediately and appropriately, the resulting hypoxemia and hypovolemia can lead to brain damage, multiorgan failure, and death. Long-standing anemia can result in failure to thrive in children. (See Prognosis.)
Many studies have shown the deleterious effects of iron deficiency anemia or iron deficiency without anemia on the neurocognitive and behavioral development in children. Other complications can include congestive heart failure, hypoxia, hypovolemia, shock, seizure, and acute silent cerebral ischemic event (ASCIE; see Magnetic resonance imaging in research settings in Workup).
Workup in pediatric acute anemia
To evaluate anemia, obtain initial laboratory tests, including the complete blood count (CBC), reticulocyte count, and review of the peripheral smear.
Chest radiography is performed in patients who may have congestive heart failure (CHF) and to rule out mediastinal mass (associated with acute leukemia and lymphoma).
Abdominal ultrasonography is used to assess for gallstones or splenomegaly in hemolytic anemia, while computed tomography (CT) scanning is used to evaluate occult bleeding in blunt trauma (eg, splenic rupture, subcapsular hemorrhage of the liver) or a bleeding disorder. Abdominal Doppler study is used to detect portal vein thrombosis.
Management of pediatric acute anemia
Transfusion with packed red blood cells (PRBCs) is the universal treatment for most individuals with severe acute anemia. The indication to transfuse should not be based solely on the hemoglobin or hematocrit levels; more importantly, one must consider the clinical effects or the signs and symptoms of the individual with anemia.
Patient education
Girls with heavy and/or prolonged menstrual periods should seek medical attention (should tell parents to obtain CBC). One of the most common reasons for fainting spell or syncope in adolescent girls is rapidly developing anemia due to menstrual blood loss.
Toddlers who drink more than 24 oz of milk a day most likely have iron deficiency. Primary care physicians should inquire about the amount of milk intake.
Children diagnosed with anemia should be taught to look at their stool color and to report to their parents if it is tarry or bloody.
Educate the patient and/or the family about the specific disease that causes the anemia. For example, provide a list of drugs, food, and other agents to avoid because of their effect of triggering acute hemolysis in glucose-6-phosphate dehydrogenase (G-6-PD) deficiency.
In pediatrics, beyond the immediate neonatal period, acute anemia is rare in otherwise healthy children. In most instances, it is due to blood loss, usually through the GI tract or via a heavy menstrual period, occurs as a result of an acute hemolytic episode in a child with undiagnosed G-6-PD deficiency, or is due to autoimmune hemolytic anemia. The most common reason for hospitalization because of acute anemia is so-called aplastic crisis in children with chronic hemolytic anemia who otherwise had been stable. The most common varieties are hereditary spherocytosis and sickle cell disease. Therefore, it would be prudent to educate parents regarding this complication, at the time when the diagnosis is established.