AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

Section 2 of 11  

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Background

Anemia refers to a hemoglobin or hematocrit level lower than the age-adjusted reference range for healthy children. In adolescents and adults, normal values vary according to sex. Racial differences are apparent, with black children having lower normal values than white and Asian children of the same age and socioeconomic background. With a statistical threshold set at 2 standard deviations lower than the mean for the healthy population, 2.5% of the healthy population is classified as anemic. Physiologically, anemia is a condition in which reduced hematocrit or hemoglobin levels leads to diminished oxygen-carrying capacity that does not optimally meet the metabolic demands of the body. These points must be considered when evaluating a child for possible anemia.

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; these diagnoses are considered in more detail in other eMedicine articles.

Pathophysiology

The main physiologic role of 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, ameliorating the symptoms relative to the degree of the anemia.

The underlying pathologic processes that cause anemia can be broadly categorized as (1) decreased or ineffective red cell production, (2) increased red cell destruction, or (3) blood loss.

Frequency

United States

Among all races, ages, and socioeconomic groups studied, an overall steady decline (from 7.8% in 1975 to 2.9% in 1985) in prevalence of anemia in the US pediatric population (aged 6 mo to 6 y) has been observed. Data show continued decline in the prevalence of anemia from the mid 1980s to the mid 1990s.¹ Iron deficiency is the most common etiology.

International

In developing nations, the prevalence of anemia is extremely high. This is particularly true in preschool-aged children, in whom the prevalence reached as high as 90% of the sample population studied. Although iron deficiency is identified as the major factor, the etiology is often multifactorial, including recurrent or chronic infections (bacteria, parasites), malnutrition, and reduced immunity.

In addition, the prevalence of certain hereditary forms of anemia (eg, thalassemia, sickle cell disease) varies with ethnicity and, thus, with geography. For instance, α thalassemia, which may be the most common single gene disorder in the world, has a frequency of as much as 68% in the southwest Pacific, 20-30% in western Africa, and 5-10% in the Mediterranean region. β thalassemia mutations have high frequencies in the Mediterranean, northern Africa, southeast Asia, and India, but they have low frequencies in Great Britain, Iceland, and Japan.

Mortality/Morbidity

Mortality and morbidity rates vary according to the underlying pathologic process causing the anemia, the degree of severity, and the acuteness of the process. When a precipitous drop in the hemoglobin or hematocrit level occurs (eg, due to massive bleeding or acute hemolysis), the clinical presentation is typically dramatic and can be fatal if the person is not immediately treated. In addition to the signs and symptoms of anemia, patients can present with congestive heart failure (CHF) or hypovolemia.

Race

Acute anemia is universal, but the likely underlying etiologies are influenced by race. Inherited red cell disorders are predominant in certain racial populations, such as sickle cell disease in black persons, β thalassemia in persons of Mediterranean ethnicity, and α thalassemia in Asians, African Americans, and others.

Sex

Sex predisposition to anemia varies according to the underlying etiology. For instance, certain hereditary X-linked red cell disorders (eg, G-6-PD deficiency) are observed in males. Anemia caused by blood loss can be observed in males with an X-linked bleeding disorder (eg, hemophilia). Females with the autosomally inherited von Willebrand disease may be anemic because of heavy blood loss during menstruation. Acquired hemolytic anemia related to autoimmune disorders such as systemic lupus erythematosus is more common in females because of their relative predisposition to autoimmune disease.

Age

• The newborn period is one age group in which acute anemia most commonly occurs. Significant blood loss can occur from birth trauma or blood exchange from the baby's mother or the placenta. Isoimmune anemia can result from maternal antibodies crossing the placenta. Neonates have a shorter red cell life span and limited erythropoiesis that can aggravate any hemolytic process. Abnormalities of fetal hemoglobin may cause anemia that resolves with the normal shift to adult-type hemoglobins.
• Nutritional anemia is common in infancy because of the associated rapid growth (necessitating an increase in red blood cell mass) and dietary adjustments.
• With exposure to new infections in early childhood, the anemia of acute infection is common. Rarely, severe autoimmune hemolytic anemia can be triggered by certain infections.
• Adolescence is characterized by rapid growth and vulnerability to nutritional anemia. In addition, blood loss with heavy menstruation can be observed in adolescent girls.

CLINICAL

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• Clinical
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History

History of the individual with anemia must include data that demonstrate the acuteness and severity of the condition and suggest a cause of the anemia.

• Symptoms of anemia include pallor, fatigue, lethargy, dizziness, and anorexia.
• Jaundice and, occasionally, dark urine may be present with significant hemolysis.
• Failure to thrive indicates a long-standing condition. It may reflect the anemia itself or the underlying cause (eg, chronic renal failure).
• Patients with acute anemia are overtly symptomatic when the condition is severe, whereas those with chronic anemia may go undiagnosed because they are asymptomatic relative to the degree of anemia.
• Age is an important clue to the etiology of the anemia. For example, blood loss, isoimmunization, and congenital red cell disorders are common causes of anemia in newborns. Although observed in older infants, toddlers, and adolescent girls, iron deficiency anemia is unlikely in newborns or infants in whom iron stores from the mother are usually adequate and in prepubertal school-aged children in whom no rapid growth and expansion of blood volume occurs.
• Some hereditary X-linked disorders are observed mainly in males. A common example is acute hemolysis in G-6-PD deficiency.
• Knowing the racial background or ethnicity can help diagnose inherited abnormalities of hemoglobin production. Examples include the following:
• • Thalassemias, hemoglobin S and C in the black population
  • β thalassemia in individuals of Mediterranean descent
  • α thalassemia and hemoglobin E disease in Asian individuals
  • Red cell enzyme defects (eg, G-6-PD deficiency) among individuals from the Mediterranean, Africa, and southeast Asia
• Review dietary history, including milk intake in infants and toddlers and the sources of other nutrients (eg, iron, folate, vitamin B-12).
• Note details about sources of blood loss, recent infections, travel, drug exposures, chemicals (eg, lead), toxins, and oxidants.
• Inquire about symptoms of hypothyroidism (eg, cold intolerance, constipation, lethargy, poor growth).
• Inquire regarding a neonatal history of anemia, jaundice, phototherapy, transfusion, any other chronic medical illnesses or complaints, and medications.
• When reviewing the family history, include questions regarding anemia, jaundice, gallbladder surgery, splenomegaly or splenectomy, autoimmune diseases, or a bleeding disorder.

Physical

• Check vital signs.
• • Patients with acute and severe anemia appear in distress with tachycardia, tachypnea, and hypovolemia.
  • Patients with chronic anemia are typically well compensated and only have tachycardia.
• To evaluate chronicity, plot growth parameters, which may affect the urgency of treatment.
• Note pallor, jaundice, edema, and signs of bleeding (eg, petechiae, bruising).
• Patients with significant anemia often have a systolic ejection murmur.
• Look for signs of CHF (eg, tachycardia, gallop rhythm, tachypnea, cardiomegaly, hepatomegaly).
• Splenomegaly can be found in many hemolytic anemias or may reflect infiltration in malignancy. In young patients with sickle cell disease, splenic sequestration can manifest with tender splenomegaly and an exacerbation of anemia. Passive congestion of the spleen may complicate CHF.
• Note any dysmorphic features and other congenital anomalies.
• • Facial bony prominences (eg, frontal bossing) are signs of extramedullary hematopoiesis associated with chronic severe hemolytic anemias and thalassemias.
  • Some congenital bone marrow failure syndromes (eg, Diamond-Blackfan anemia and Fanconi anemia) are associated with facial, limb, and other anomalies.
• Signs of hypothyroidism include low body temperature, failure to thrive, dry skin, and thinning of the hair.

Causes

Causes of anemia are either inherent in the RBCs or related to an external factor. As noted above, these can be simplified into 3 main categories, although more than one mechanism may be involved in some anemias.

• Anemia caused by decreased red cell production (generally develops gradually and causes chronic anemia)
• • Marrow failure
  • • Diamond-Blackfan anemia (congenital pure red cell aplasia)
    • Transient erythroblastopenia of childhood
    • Aplastic crisis caused by parvovirus B19 infection (in patients with an underlying chronic hemolytic anemia)
  • Impaired erythropoietin production
  • • Anemia of chronic disease in renal failure
    • Chronic inflammatory diseases
    • Hypothyroidism
    • Severe protein malnutrition
  • Defect in red cell maturation
  • • Nutritional anemia secondary to iron, folate, or vitamin B-12 deficiency
    • Congenital dyserythropoietic anemia
    • Sideroblastic anemias
    • Pure red cell aplasia/maturational arrest
• Anemia caused by increased red cell destruction (hemolysis)
• • Extracellular causes
  • • Mechanical injury (hemolytic-uremic syndrome, cardiac valvular defects)
    • Antibodies (autoimmune hemolytic anemia)
    • Infections, drugs, toxins
    • Thermal injury to RBCs (with severe burns)
  • Intracellular causes
  • • Red cell membrane defects (eg, hereditary spherocytosis, elliptocytosis)
    • Enzyme defects (eg, G-6-PD deficiency, pyruvate kinase deficiency)
    • Hemoglobinopathies (sickle cell disease, unstable hemoglobinopathies)
    • Thalassemias
    • Porphyrias
    • Paroxysmal nocturnal hemoglobinuria
• Anemia caused by blood loss
• • Obvious or occult site of blood loss: GI tract, intra-abdominal, pulmonary, intracranial (in neonates)
  • Particular risk of massive hemorrhage (internal or external) for patients with bleeding disorders

DIFFERENTIALS

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Other Problems to be Considered

Acute blood loss
Anemia of inflammation/infection
Aplastic anemia
Autoimmune hemolytic anemia
Chronic renal failure
Congenital dyserythropoietic anemia
Diamond-Blackfan anemia
Erythrophagocytosis
Fanconi anemia
G-6-PD deficiency
Hereditary spherocytosis
Iron deficiency anemia
Microangiopathic hemolytic anemia
Osteopetrosis
Paroxysmal nocturnal hemoglobinuria
Pure red cell aplasia
Sideroblastic anemia
Unstable hemoglobinopathy

WORKUP

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Lab Studies

• To evaluate anemia, obtain initial laboratory tests, including CBC count, reticulocyte count, and review of the peripheral smear (see Media file 1).
• • Base interpretation of the hemoglobin and hematocrit levels on the reference range for the specific age group. Some laboratories provide only a uniform reference range for the entire pediatric age group and not for specific age groups. Interpret this carefully so as not to misdiagnose a patient with anemia. Hemoglobin and hematocrit levels can be used interchangeably, depending on professional preference and familiarity. Essentially, the hematocrit level is 3 times the hemoglobin value.
  • If the patient is anemic, look at the red cell indices (mean corpuscular volume [MCV], mean corpuscular hemoglobin [MCH], mean corpuscular hemoglobin concentration [MCHC]). Note that reference ranges for these parameters also vary with age. Of these, the MCV is particularly helpful in classifying anemia. Microcytic anemia suggests iron deficiency, lead poisoning, or thalassemia; macrocytosis suggests folate/B-12 deficiency or reactive reticulocytosis.
  • Another valuable parameter in classifying anemia is the RBC distribution width (RDW). This is the statistical description of the heterogeneity of RBC sizes. It is increased in anisocytosis (variable sizes of red cells), such as when increased reticulocytes are present.
  • Reticulocytes are immature nonnucleated RBCs that indicate active erythropoiesis.
  • • The relative reticulocyte count is useful in differentiating whether the anemia is caused by decreased production, increased destruction, or loss of RBCs. An elevated number of reticulocytes (eventually) is observed in individuals with anemia caused by hemolysis or blood loss; note that the absence of reticulocytosis may simply reflect a "lag" in the response to the acute onset of anemia.
    • The term reticulocyte count is often used inaccurately to refer to the percentage of reticulocytes, a value that must be interpreted in light of the degree of anemia. Thus, a finding of 2-3% reticulocytes (vs the normal value of approximately 1%) in a patient whose hemoglobin is only one third to one half of normal does not indicate a reticulocyte "response." Some clinicians prefer to use either the absolute number of reticulocytes per μL of blood or a reticulocyte percentage "corrected" for the degree of anemia. (Corrected reticulocyte count = patient hematocrit/normal hematocrit X % reticulocyte count)
  • Examination of the peripheral smear helps identify the cause of the anemia by recognizing abnormal cell morphology. The following are examples of abnormal cell morphology:
  • • Schistocytes or fragmented cells (microangiopathic hemolytic anemia)
    • Spherocytes (hereditary spherocytosis, autoimmune hemolytic anemia)
    • Ghost or bite cells (G-6-PD deficiency)
    • Sickle-shaped cells (sickle cell disease)
    • Target cells (hemoglobin C)
    • Stippled red blood cells (nonspecific but may suggest lead poisoning)
    • Increased polychromasia (reticulocytosis)
  • Recognizing that normal RBC morphology does not rule out hemolysis is important.
• Additional laboratory tests that may be indicated in the diagnosis and treatment of patients with acute anemia include the following:
• • Bilirubin level, lactate dehydrogenase (LDH) (hemolytic anemia)
  • Direct antiglobulin or Coombs test (autoimmune hemolytic anemia) 
  • Hemoglobin electrophoresis (hemoglobinopathies)
  • Red cell enzyme studies (eg, G-6-PD, pyruvate kinase)
  • Osmotic fragility (spherocytosis)
  • Iron, TIBC, ferritin (iron deficiency anemia)
  • Folate, vitamin B-12 (macrocytic/megaloblastic anemia)
  • Blood typing and crossmatching to assess possible isoimmune anemia in a neonate and to prepare for transfusion
  • Bone marrow aspiration and biopsy
  • Viral titers (eg, Epstein-Barr virus, cytomegalovirus)
  • BUN/creatinine levels to assess renal function
  • Thyroxine (T₄)/thyroid-stimulating hormone (TSH) to rule out hypothyroidism

Imaging Studies

• Chest radiography in patients who may have CHF and to rule out mediastinal mass (associated with acute leukemia) or thymoma (associated with paroxysmal nocturnal hemoglobinuria)
• Abdominal ultrasonography to assess for gallstones or splenomegaly in hemolytic anemia
• CT scanning to evaluate occult bleeding in blunt trauma or bleeding disorder
• "Tagged" RBC scans (occasionally useful) to identify an anatomic site of blood loss or sequestration

Other Tests

• Examination of blood smears of the parents may be helpful in making a diagnosis of conditions such as hereditary spherocytosis or thalassemia.

Procedures

• Rarely indicated in isolated acute anemia, bone marrow aspiration and biopsy are indicated in the evaluation of possible bone marrow failure or malignancy. Suppression of the platelet count or WBC (neutrophil) count, in association with anemia, often warrants an examination of the bone marrow.

TREATMENT

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Medical Care

Acute anemia usually warrants immediate medical attention. Treatment depends on the severity and underlying cause of the anemia.

• Initial treatment begins with careful assessment of the signs and symptoms of the anemia that indicate therapy. Guidelines for the treatment of patients with critical illness apply to children with severe anemia who are in acute distress and unstable. Supportive measures, such as supplemental oxygen for decreased oxygen-carrying capacity, fluid resuscitation for hypovolemia, and bed rest or activity restriction for fatigue, may be required.
• Transfusion with packed RBCs (PRBC) 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 signs and symptoms of the individual with anemia.
• • PRBC dose is 10-15 mL/kg over 3-4 hours. The rate of transfusion can be modified according to the clinical situation. Transfusion can be administered faster in individuals with acute blood loss or slower or in smaller aliquots in persons with CHF.
  • In individuals with autoimmune hemolytic anemia, blood must be given with extreme caution, using the blood unit that is least reactive on crossmatch.
• Medications for specific forms of anemia may be indicated in addition to blood transfusion (eg, corticosteroids for autoimmune hemolytic anemia, iron therapy for iron deficiency anemia).
• Recombinant erythropoietin has been available for the treatment of certain forms of anemia. Its use can allow for avoidance or minimization of the need for blood transfusion. Indications include anemias of chronic disease (eg, renal failure), chemotherapy, acquired immunodeficiency syndrome (AIDS) treatment, preparation for surgery with anticipated significant blood loss, prematurity, and hyporegenerative anemia of erythroblastosis fetalis. It is important to note that erythropoietin is not indicated for the immediate correction of anemia. Correction of anemia with erythropoietin occurs after about 2-8 weeks.

Surgical Care

Except in cases of uncontrolled hemorrhage, surgery is very rarely indicated in acute anemia. Splenectomy is occasionally considered in persons with autoimmune hemolytic anemia that is refractory to medical treatment.

Consultations

Except for patients who have acute anemia secondary to blood loss from obvious trauma or injury, a hematology consultation is ideal for most patients with acute anemia to determine the underlying RBC disorder and provide the appropriate therapy.

• In particular, the following features in an individual with acute anemia indicate the need for a hematology consultation:
  • Concomitant abnormality in WBC and/or platelet counts (eg, neutropenia, thrombocytopenia, presence of immature WBCs)
  • Positive Coombs test result
  • Hepatosplenomegaly
  • History of underlying hematologic disorder
  • Excessive blood loss relative to the degree of injury in individuals who may have an underlying bleeding disorder
• Consider consultation with a gastroenterologist in cases of GI blood loss.

Diet

See articles on nutritional anemias (eg, Iron Deficiency Anemia).

Activity

Activity restriction or bed rest may be indicated in symptomatic individuals with severe anemia.

MEDICATION

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Refer to articles on the specific forms of anemia, including Aplastic Anemia; Iron Deficiency Anemia; and Anemia, Megaloblastic caused by vitamin B-12 or folate deficiency.

FOLLOW-UP

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Further Inpatient Care

• Further inpatient care is indicated in patients with CHF who are severely anemic and in those with unstable vital signs (eg, hypotension, active bleeding). Most of these patients require admission to the intensive care unit. Patients who may be stable but have severe anemia may also be admitted for diagnostic workup.

Further Outpatient Care

• Depending on the underlying disease process, observe the patient's response to treatment. A hematologist preferably should provide outpatient care for patients who are diagnosed with a chronic RBC disorder or a bleeding diathesis.

In/Out Patient Meds

• Medications vary according to the patient's underlying disease.

Complications

• Acute and severe anemia can result in cardiovascular compromise.
• 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.
• Many studies have shown the deleterious effects of iron deficiency anemia on the neurocognitive and behavioral development in children.

Prognosis

• Prognosis depends on the severity and acuteness with which the anemia develops and the underlying cause of the anemia. 

Patient Education

• 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 G-6-PD deficiency.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Failure to recognize and treat the signs and symptoms of severe anemia (eg, cardiovascular decompensation) is a pitfall. Be aware of the risks of rapid transfusion in patients with severe anemia patients in a compromised cardiovascular state.
• Failure to discuss the risks and benefits of blood transfusion with the parents (for minors) or patients is a pitfall.
• When blood transfusion is indicated for patients who are against transfusion (eg, because of certain religious or cultural beliefs), involving hospital ethical and legal counsel for advice is prudent.
• Failure to provide genetic counseling when appropriate is a pitfall.

MULTIMEDIA

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Media file 1:  Algorithm for diagnostic approach and workup of anemia in children. Hb=hemoglobin; Hct=hematocrit; HS=hereditary spherocytosis; HE=hereditary elliptocytosis; G-6-PD=glucose-6-phosphate dehydrogenase; PK=pyruvate kinase; HUS=hemolytic uremic syndrome; TTP=thrombotic thrombocytopenic purpura; DIC=disseminated intravascular coagulation; DBA=Diamond-Blackfan anemia.
	View Full Size Image
Media type:  Graph

REFERENCES

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1. Sherry B, Mei Z, Yip R. Continuation of the decline in prevalence of anemia in low-income infants and children in five states. Pediatrics. Apr 2001;107(4):677-82. [Medline].
2. Abshire TC. The anemia of inflammation. A common cause of childhood anemia. Pediatr Clin North Am. Jun 1996;43(3):623-37. [Medline].
3. Armano R, Gauvin F, Ducruet T, Lacroix J. Determinants of red blood cell transfusions in a pediatric critical care unit: a prospective, descriptive epidemiological study. Crit Care Med. Nov 2005;33(11):2637-44. [Medline].
4. Cusick SE, Mei Z, Cogswell ME. Continuing anemia prevention strategies are needed throughout early childhood in low-income preschool children. J Pediatr. Apr 2007;150(4):422-8, 428.e1-2. [Medline].
5. Graham EA. The changing face of anemia in infancy. Pediatr Rev. May 1994;15(5):175-83; quiz 184. [Medline].
6. Lacroix J, Hebert PC, Hutchison JS, et al. Transfusion strategies for patients in pediatric intensive care units. N Engl J Med. Apr 19 2007;356(16):1609-19. [Medline].
7. Liet JM, Paranon S, Baraton L, Dejode JM, Roze JC. Is a prophylactic treatment by erythropoietin relevant to reduce red blood cell transfusion in the pediatric intensive care unit?. Pediatr Crit Care Med. Nov 2006;7(6):541-4. [Medline].
8. Ohls RK. Evaluation and treatment of anemia in the neonate. In: Christensen RD, Fletcher J, eds. Hematologic Problems in the Neonate. WB Saunders Co;2000:137-169.
9. Ohlsson A, Aher SM. Early erythropoietin for preventing red blood cell transfusion in preterm and/or low birth weight infants. Cochrane Database Syst Rev. Jul 19 2006;3:CD004863. [Medline].
10. Oski FA, Brugnara C, Nathan DG. A diagnostic approach to the anemic patient. In: Nathan and Oski's Hematology of Infancy and Childhood. 5th ed. Harcourt Health Sciences;1998:375-384.
11. Walters MC, Abelson HT. Interpretation of the complete blood count. Pediatr Clin North Am. Jun 1996;43(3):599-622. [Medline].

Article Last Updated: Nov 6, 2007