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Pediatric Acute Anemia Clinical Presentation

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

History

The acute development of anemia in the pediatric age group commonly occurs in 2 situations, (1) acute blood loss and (2) acute hemolysis.

Acute blood loss

In neonates, blood loss can occur through the placenta, abruption, placenta previa, and fetomaternal transfusion. The former 2 can be known by history, while fetomaternal transfusion cannot be discerned from history findings. Iatrogenic blood loss through multiple blood samplings in extremely low birth weight infants can cause anemia rapidly.

In older children, the GI tract is the most common site of blood loss; common causes include esophageal and gastric varices (inquire about a history of umbilical vein catheterization during neonatal ICU stay), ulcerative colitis, and Crohn disease. Menstruating girls’ blood loss due to dysmenorrhea is an extremely common cause of acute blood loss (may or may not be associated with von Willebrand disease; ask about easy bruisability, frequent epistaxis, and family history of similar bleeding history).

A history of trauma is important (eg, rupture of spleen)

Rapid hemolysis

When taking the history, keep the following factors in mind:

  • Isoimmune or alloimmune hemolytic anemia (ABO incompatibility or Rh incompatibility in neonates) – (1) Mother’s blood group (ABO) and type (Rh); (2) minor Rh antigen incompatibility such as c, E, may cause severe hemolytic anemia (even if there is no ABO or D incompatibility), therefore do direct antiglobulin test (DAT) whenever there is a suspicion
  • Autoimmune hemolytic anemia – (1) History of a viral infection such as mycoplasma or Ebstein-Barr virus (EBV) may precede paroxysmal cold hemoglobinuria; (2) an infection with Streptococcus pneumoniae may cause autoimmune hemolytic anemia due to exposure of cryptic T antigen on the red blood cells by the bacterial neuraminidase
  • Transfusion reaction due to major blood group incompatibility - Usually due to clerical error or misidentification of patient delayed transfusion reaction due to previously unrecognized antibodies to red blood cell antigens (may occur a few days to 1 wk after previous transfusion)
  • Ingestion of strong oxidants in a child with G-6-PD deficiency - Ingestion or sniffing of a mothball is most common
  • Splenic sequestration in a child with sickle cell anemia or hereditary spherocytosis - Sudden onset of severe abdominal pain; shocklike state with a drop in hemoglobin and platelet count

Other history considerations

Symptoms of anemia include pallor, fatigue, lethargy, dizziness, and anorexia. Jaundice and, occasionally, dark urine may be present with significant hemolysis. Syncope and fainting are quite common in a teenager.

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.

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.

Next

Physical Examination

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 usually asymptomatic.

To evaluate chronicity, plot growth parameters; this may affect the urgency of treatment. Also, note pallor, jaundice, edema, and signs of bleeding (eg, stool occult blood, frequent epistaxis, petechiae, bruising).

Patients with significant anemia often have a systolic ejection murmur. Look for signs of congestive heart failure (CHF), such as tachycardia, gallop rhythm, tachypnea, cardiomegaly, wheezing, cough, distended neck vein, and 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 a sudden enlargement of the spleen and/or abdominal pain and distension together with an exacerbation of anemia and thrombocytopenia. 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, Fanconi anemia and, less often, Diamond-Blackfan anemia) may be associated with facial, limb, and other anomalies. Signs of hypothyroidism include low body temperature, failure to thrive, dry skin, constipation, and thinning of the hair.

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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
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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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