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Pediatric Acute Anemia Clinical Presentation: Hi...

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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) Mothers 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.

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.

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Signs of hypothyroidism include low body temperature, failure to thrive, dry skin,
constipation, and thinning of the hair.
Differential Diagnoses

Contributor Information and Disclosures


Author
Susumu Inoue, M D 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)
M argaret 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, Childrens Center for Cancer and Blood Disorders, Department of
Hematology/Oncology, Co-Director of the Ron Matricaria Institute of Molecular Medicine, Phoenix Childrens
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.
M ary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of
Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.

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