Pallor - Case 10-2: 12-Month-Old Girl
I. History of Present Illness
A 12-month-old Caucasian girl presented to the emergency department with pallor.
The grandparents had just arrived from Florida. When they were greeted by the
child at the airport, they were alarmed at her appearance, prompting a visit to
the emergency department. The child had last been seen by her grandparents at
Thanksgiving, and at that time she appeared well. The parents conceded that the
child did appear more pale than usual. There was no fever, rash, vomiting, or
diarrhea. There was no jaundice. Her activity level had been normal. She had
not traveled anywhere, but the parents had visited Puerto Rico 2 weeks earlier;
their trip was uneventful.
II. Past Medical History
The birth history was unremarkable. She had a febrile illness at 6 months of
age. Evaluation at that time included a blood culture that was positive for
Staphylococcus epidermidis. This was believed to be a contaminant. A complete blood count was also obtained
(see later discussion). She had not required hospitalization. Her immunizations
were appropriate for age. There were no pets. Her development was normal. She
was breast-fed until 6 months of age, after which she began drinking whole
milk. She was a finicky eater but had been growing well.
III. Physical Examination
T, 36.1°C; RR, 38/min; HR, 145 bpm; BP, 97/53 mm Hg; SpO2, 99% in room air
Weight, 79th percentile; height, 50th percentile
She was pale but alert and playful. The conjunctivae were pale but without
injection or discharge. There was no lymphadenopathy. Her neck was supple. A
II/VI systolic murmur was heard at the left upper sternal border without
radiation. The lungs were clear to auscultation. There was no splenomegaly or
hepatomegaly. There were no rashes or petechiae.
VI. Diagnostic Studies
The complete blood count obtained when the child was 6 months of age revealed
the following: 15,200 WBCs/mm
3 (71% segmented neutrophils, 25% lymphocytes, and 4% monocytes); hemoglobin,
11.2 g/dL; and 365,000 platelets/mm
3. At that time, the MCV was 78 fL and the RDW was 17.3.
Her current studies revealed the following: 8,300 WBCs/mm3 (58% segmented neutrophils, 31% lymphocytes, and 11% monocytes); hemoglobin,
3.4 g/dL; and 410,000 platelets/mm
3. The MCV was 59 fL, and the RDW was 15.1. The reticulocyte count was 1.4%.
Stool was Hemoccult negative.
VII. Course of Illness
The history, examination, and laboratory findings suggested a diagnosis that was
subsequently confirmed.
Discussion: Case 10-2
I. Differential Diagnosis
Table 10-4 lists the differential diagnosis of microcytic anemia in children.
Causes of iron deficiency include poor bioavailability, decreased iron
absorption, disruption of enteric mucosa or loss of functional bowel, blood
loss, and insufficient intake. Alkaline gastric pH reduces the solubility of
inorganic iron, impeding absorption. Chronic use of acid pump blockers,
vagotomy (for severe gastroesophageal reflux), and impaired gastric parietal
cell function in pernicious anemia may compromise iron absorption. Iron
absorption may also be disrupted after surgical bowel resection, often
performed because of volvulus or intussusception. Iron deficiency in such cases
develops slowly and may not become evident for several years. Blood loss is a
leading cause of iron deficiency. Common causes of gastrointestinal blood loss
in children include Meckel diverticulum, cow
's milk protein allergy, and parasitic infestation. Blood loss from hematuria or
pulmonary hemorrhage can also occur. In this case, the dietary history
suggested a likely cause.
II. Diagnosis
On examination, the child was extremely pale. The combination of a hypochromic microcytic anemia and paucity of dietary iron
implicated iron deficiency as a cause of this child
's pallor. Subsequent tests, including iron level, ferritin, and total iron-binding
capacity, supported this diagnosis. The child received a packed RBC transfusion
followed by daily iron supplements. Studies performed 1 month later revealed a
hemoglobin level of 9.7 g/dL. This case illustrates the importance of the RDW
as a marker of iron deficiency that precedes anemia.
III. Incidence and Epidemiology
In developed countries, routine iron fortification of formulas and cereals has
led to a significant decrease in early childhood anemia. However, iron
deficiency remains a leading cause of anemia. Currently, the prevalence of iron
deficiency is approximately 7%. One third of affected children develop anemia.
Children living below the poverty level are at greatest risk. More worrisome is
the increasing recognition of anemia as only one manifestation of iron
deficiency. Even in the absence of anemia, children with iron deficiency may
have neurocognitive and behavioral problems. Only some of these problems are
reversible with iron supplementation, suggesting the importance of prevention.
IV. Clinical Presentation
The clinical examination in children with mild iron deficiency is usually
normal. With moderate or severe iron deficiency, the findings may be similar to
those seen with other causes of anemia, including fatigue and pallor. If the
anemia develops gradually, as in the child presented here, immediate family
members may not notice changes in pigmentation. Other findings may include
pica, the compulsive consumption of nonnutritive substances such as soil or
ice. Long-standing iron deficiency may lead to angular stomatitis and
glossitis. Softening of the fingernails leads to concave deformities
descriptively termed
“spooning” (koilonychia).
V. Diagnostic Approach
Complete blood count. In children, an elevated RDW is usually the earliest hematologic finding in iron
deficiency. As the deficiency progresses, other hematologic parameters are
affected (Table 10-4).
Peripheral blood smear. Peripheral blood smear in early disease may reveal anisocytosis. As the iron
deficiency progresses, cells become hypochromic and microcytic. With severe
iron deficiency, RBCs may be deformed and misshapen and demonstrate
poikilocytosis.
Other studies. In the absence of a concurrent inflammatory disease state, the ferritin level
decreases, reflecting diminished total tissue iron stores. With continued iron
deficiency, reticuloendothelial macrophage iron stores become depleted and
serum iron levels decrease. At this point the total iron-binding capacity
increases without a change in hemoglobin levels. When the transferrin
saturation decreases to approximately 10%, the availability of iron becomes the
rate-limiting step for hemoglobin synthesis. This leads to the accumulation of
heme precursors called free erythrocyte protoporphyrins. Ultimately, the RBCs
become smaller as their hemoglobin content decreases.
VI. Treatment
Treatment of iron deficiency depends on its cause. For children with suspected
dietary deficiency, treatment consists of supplemental iron. In children with
anemia, an initial therapeutic trial often eliminates the need for expensive
laboratory testing in determining the diagnosis. The reticulocyte count usually
increases within several days and the hemoglobin concentration within 3 weeks.
Patients should be treated until the hemoglobin reaches the normal range and
then for at least one additional month to replete the iron stores. Failure of
the hemoglobin level to rise within 1 month indicates either poor compliance
with iron therapy or incorrect diagnosis.
VII. References
1. Oski FA. Iron deficiency in infancy and childhood. N Engl J Med 1993;329:190–193.
2. Segel GB, Hirsh MG, Feig SA. Managing anemia in pediatric office practice:
part I.
Pediatr Rev 2002;23:75–83.
3. Andrews NC. Disorders of iron metabolism and sideroblastic anemia. In:
Nathan DG, Orkin SH, Ginsburg D, et al., eds.
Nathan and Oski's hematology of infancy and childhood, 6th ed. Philadelphia: WB Saunders, 2003:456–497.
4. Lozoff B, Jimenez E, Wolf AW. Long-term developmental outcome of infants
with iron deficiency.
N Engl J Med 1991;325:687–694.
5. Aslan D, Altay C. Incidence of high erythrocyte count in infants and young
children with iron deficiency anemia: re-evaluation of an old parameter.
J Pediatr Hematol Oncol 2003;25:303–306.
6. Centers for Disease Control and Prevention. Iron deficiency—United States, 1999–2000. MMWR Morb Mortal Wkly Rep 2002;51:897–899.
Pictures
Book Source Details
- Book Title: Pediatric Complaints and Diagnostic Dilemmas
- Author(s): Samir S Shah MD; Stephen Ludwig MD
- Year of Publication: 2003
- Copyright Details: Pediatric Complaints and Diagnostic Dilemmas, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright Details: Pediatric Complaints and Diagnostic Dilemmas, Copyright © 2008 Williams & Wilkins.
More About Causes of Paleness
» Next page: Pallor - Case 10-3: 5-Month-Old Boy (Pediatric Complaints and Diagnostic Dilemmas)
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