Pediatric Acute Anemia Clinical Presentation
- Author: Susumu Inoue, MD; Chief Editor: Robert J Arceci, MD, PhD more...
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)
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.
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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