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Pediatric Acute Anemia Workup

  • Author: Susumu Inoue, MD; Chief Editor: Robert J Arceci, MD, PhD  more...
 
Updated: Oct 09, 2015
 

Approach Considerations

To evaluate anemia, obtain initial laboratory tests, including the complete blood count (CBC), reticulocyte count, and review of the peripheral smear. (See the diagram below.)

An overwhelming majority of acute anemia is normocytic, although marked reticulocytosis may raise mean corpuscular volume (MCV). If microcytic, it has an underlying chronic anemia component, and one needs to know the cause.

Algorithm for diagnostic approach and workup of an 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.

Chest radiography is performed in patients who may have CHF and to rule out mediastinal mass (associated with acute leukemia).

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.

Radioactively tagged RBC radionuclide scans are occasionally used to localize the site of GI bleeding when the source is unclear (a common example in pediatrics is the Meckel scan, used in the diagnosis of Meckel diverticulum).

Family studies, such as sending the CBC count, smear review, and hemoglobin electrophoresis from parents, may be helpful in making a diagnosis of conditions such as hereditary spherocytosis or thalassemia.

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 white blood cell (WBC; neutrophil) count, in association with anemia, often warrants an examination of the bone marrow.

Magnetic resonance imaging in research settings

Recently an MRI change termed acute silent cerebral ischemic events (ASCIE) in patients who developed acute anemia with and without sickle cell disease has been described.[1] The MRI abnormality is detected by diffusion-weighted imaging. The lesion may be temporary or long-lasting. If it is a permanent MRI lesion and the patient has no over clinical symptoms attributable to that lesion, then it is called a silent infarct. The fact that it occurs in children without sickle cell disease may indicate that in acutely severely anemic children regardless of the cause, ASCIE may not be a very rare event, and it does raise a question if some of these lesions are permanent and may cause subtle neurological dysfunction. Although MRI cannot be a routine imaging study for acute severe anemia, it may be a worthwhile test under a research setting.

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Complete Blood Count

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. 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] and 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.

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Reticulocyte Count

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. Note that in some autoimmune hemolytic anemias, reticulocytopenia is present due to lysis of reticulocytes by the same antibodies.

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, as follows: corrected reticulocyte count = patient hematocrit/normal hematocrit x %reticulocyte count.

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Peripheral Smear

Examination of the peripheral smear helps to identify the cause of the anemia through recognition of abnormal cell morphology (this is particularly helpful in normocytic anemia). The following are examples of abnormal cell morphology:

  • Schistocytes or fragmented cells (microangiopathic hemolytic anemia)
  • Spherocytes (hereditary spherocytosis, autoimmune hemolytic anemia)
  • Ghost, helmet, blister, or bite cells (G-6-PD deficiency)
  • Sickle-shaped cells (sickle cell disease)
  • Target cells (hemoglobin C): These can be seen nonspecifically in other conditions, such as thalassemia, other hemoglobinopathies, and with liver disease; however, hemoglobin C is the classic, most common example
  • Stippled red blood cells (nonspecific, but may suggest lead poisoning; occurs in any condition with reticulocytosis)
  • Increased polychromasia (reticulocytosis)
  • Crenated or spiculated cells (liver disease, uremia, abetalipoproteinemia)

Recognizing that normal RBC morphology does not rule out hemolysis is important.

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Additional Laboratory Tests

Additional laboratory tests that may be indicated in the diagnosis and treatment of patients with acute anemia include the following:

  • Bilirubin level, lactate dehydrogenase (hemolytic anemia)
  • Direct antiglobulin or Coombs test (autoimmune hemolytic anemia)
  • Hemoglobin electrophoresis (hemoglobinopathies) (many unstable hemoglobins, such as Hb KÖLN, cannot be detected by hemoglobin electrophoresis)
  • Red cell enzyme studies (eg, G-6-PD, pyruvate kinase)
  • Osmotic fragility (spherocytosis)
  • Iron, total iron-binding capacity (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)
  • Blood urea nitrogen (BUN) and creatinine levels to assess renal function
  • Thyroxine (T 4)/ thyroid-stimulating hormone (TSH) to rule out hypothyroidism
  • "Fetaldex test" on maternal blood (Kleihauer-Betke test), when fetomaternal transfusion is suspected
  • Stool for occult blood (on multiple specimens)
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Contributor Information and Disclosures
Author

Susumu Inoue, MD Professor of Pediatrics and Human Development, Michigan State University College of Human Medicine; Clinical Professor of Pediatrics, Wayne State University School of Medicine; Director of Pediatric Hematology/Oncology, Associate Director of Pediatric Education, Department of Pediatrics, Hurley Medical Center

Susumu Inoue, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Clinical Oncology, American Society of Hematology, American Society of Pediatric Hematology/Oncology, Society for Pediatric Research

Disclosure: Nothing to disclose.

Coauthor(s)

Margaret T Lee, MD Associate Professor, Department of Pediatrics, Division of Pediatric Hematology/Oncology/SCT, Children's Hospital of New York, Columbia University College of Physicians and Surgeons

Margaret T Lee, MD is a member of the following medical societies: American Society of Hematology

Disclosure: Nothing to disclose.

Chief Editor

Robert J Arceci, MD, PhD Director, Children’s Center for Cancer and Blood Disorders, Department of Hematology/Oncology, Co-Director of the Ron Matricaria Institute of Molecular Medicine, Phoenix Children’s Hospital; Editor-in-Chief, Pediatric Blood and Cancer; Professor, Department of Child Health, University of Arizona College of Medicine

Robert J Arceci, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American Association for Cancer Research, American Pediatric Society, American Society of Hematology, American Society of Pediatric Hematology/Oncology

Disclosure: Nothing to disclose.

Acknowledgements

Steven K Bergstrom, MD Department of Pediatrics, Division of Hematology-Oncology, Kaiser Permanente Medical Center of Oakland

Steven K Bergstrom, MD is a member of the following medical societies: Alpha Omega Alpha, American Society of Clinical Oncology, American Society of Hematology, American Society of Pediatric Hematology/Oncology, Children's Oncology Group, and International Society for Experimental Hematology

Disclosure: Nothing to disclose.

J Martin Johnston, MD Associate Professor of Pediatrics, Mercer University School of Medicine; Director of Pediatric Hematology/Oncology, Backus Children's Hospital; Consulting Oncologist/Hematologist, St Damien's Pediatric Hospital

J Martin Johnston, MD is a member of the following medical societies: American Academy of Pediatrics and American Society of Pediatric Hematology/Oncology

Disclosure: Nothing to disclose.

John T Truman, MD, MPH Professor Emeritus of Clinical Pediatrics, Columbia University College of Physicians and Surgeons

John T Truman, MD, MPH is a member of the following medical societies: American Academy of Pediatrics, American Association for the History of Medicine, American Society of Pediatric Nephrology, and New York Academy of Medicine

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

References
  1. Dowling MM, Quinn CT, Plumb P, et al. Acute silent cerebral ischemia and infarction during acute anemia in children with and without sickle cell disease. Blood. 2012 Nov 8. 120(19):3891-7. [Medline]. [Full Text].

  2. Parkin PC, DeGroot J, Maguire JL, Birken CS, Zlotkin S. Severe iron-deficiency anaemia and feeding practices in young children. Public Health Nutr. 2015 Jun 1. 1-7. [Medline].

  3. Niemeyer CM, Baumann I. Myelodysplastic syndrome in children and adolescents. Semin Hematol. 2008 Jan. 45(1):60-70. [Medline].

  4. Ballin A, Hussein A, Vaknine H, Senecky Y, Avni Y, Schreiber L. Anemia associated with acute infection in children: an animal model. J Pediatr Hematol Oncol. 2013 Jan. 35(1):14-7. [Medline].

  5. Sherry B, Mei Z, Yip R. Continuation of the decline in prevalence of anemia in low-income infants and children in five states. Pediatrics. 2001 Apr. 107(4):677-82. [Medline].

  6. Cusick SE, Mei Z, Freedman DS, et al. Unexplained decline in the prevalence of anemia among US children and women between 1988-1994 and 1999-2002. Am J Clin Nutr. 2008 Dec. 88 (6):1611-7. [Medline].

  7. Mujica-Coopman MF, Brito A, Lopez de Romana D, Ríos-Castillo I, Coris H, Olivares M. Prevalence of Anemia in Latin America and the Caribbean. Food Nutr Bull. 2015 Jun. 36 Suppl 2:S119-28. [Medline].

  8. Cusick SE, Mei Z, Cogswell ME. Continuing anemia prevention strategies are needed throughout early childhood in low-income preschool children. J Pediatr. 2007 Apr. 150(4):422-8, 428.e1-2. [Medline].

  9. Hare GM, Tsui AK, McLaren AT, Ragoonanan TE, Yu J, Mazer CD. Anemia and cerebral outcomes: many questions, fewer answers. Anesth Analg. 2008 Oct. 107(4):1356-70. [Medline].

  10. Gibson BE, Todd A, Roberts I, Pamphilon D, Rodeck C, Bolton-Maggs P. Transfusion guidelines for neonates and older children. Br J Haematol. 2004 Feb. 124(4):433-53. [Medline].

  11. Amendments and corrections to the 'Transfusion Guidelines for neonates and older children' (BCSH, 2004a); and to the 'Guidelines for the use of fresh frozen plasma, cryoprecipitate and cryosupernatant' (BCSH, 2004b). Br J Haematol. 2007 Feb. 136(3):514-6. [Medline].

  12. Bateman ST, Lacroix J, Boven K, et al. Anemia, blood loss, and blood transfusions in North American children in the intensive care unit. Am J Respir Crit Care Med. 2008 Jul 1. 178(1):26-33. [Medline].

  13. Carson JL, Carless PA, Hebert PC. Outcomes using lower vs higher hemoglobin thresholds for red blood cell transfusion. JAMA. 2013 Jan 2. 309(1):83-4. [Medline].

  14. Villanueva C, Colomo A, Bosch A, Concepcion M, Hernandez-Gea V, Aracil C. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013 Jan 3. 368(1):11-21. [Medline].

  15. Ohlsson A, Aher SM. Early erythropoietin for preventing red blood cell transfusion in preterm and/or low birth weight infants. Cochrane Database Syst Rev. 2006 Jul 19. CD004863. [Medline].

 
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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.
 
 
 
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