To determine the cause of a child&s anemia, focus on aspects of the history and physical examination and on a few laboratory tests, the author advocates.
|Jump to:||Choose article section...LEARNING OBJECTIVES Defining anemia Making the diagnosis More about the MCV and reticulocyte count Zeroing in on mild microcytic anemia Tying it together|
To determine the cause of a child's anemia, focus on aspects of the history and physical examination and on a few laboratory tests, the author advocates. Generally, the hemoglobin concentration, reticulocyte count, mean corpuscular volume, and peripheral blood smear tell you what you need to know.
Consider this case: You are seeing an African-American infant boy in follow-up for a 1-year screening hematocrit that is 30%. He has been healthy, with no recent infections, and has been on iron-fortified formula since 1 month of age (after breastfeeding for one month), supplemented by appropriate intake of fruits, vegetables, grains, and meat. No history of either gastrointestinal or urinary blood loss is present. The examination is normal.
After reviewing this article the physician should be able to:
Conduct the evaluation of most cases of suspected anemia in children using the triad of selective elements of the history, the physical exam, and only a few laboratory tests.
Differentiate microcytic anemia, macrocytic anemia, and normochromic-normocytic anemia based on the reticulocyte count and mean corpuscular volume.
Understand the causes and conduct the appropriate workup of mild microcytic anemia in children.
Complete blood count (CBC) reveals: white blood cell (WBC) count, 5.5 x 103/µL (30% neutrophils); hemoglobin concentration, 10.0 g/dL; mean corpuscular volume (MCV), 60 femtoliters (fL); red cell distribution width (RDW), 14%; platelet count, 270 x 103/µL; and the reticulocyte count, 1.5%. How would you arrive at a diagnosis? Would additional tests be helpful?
And another case: You are called to the emergency room to evaluate a 4-year-old Hispanic girl in moderate respiratory distress (respirations, 60/min with some nasal flaring) and fever (38.6° C). Examination demonstrates mild scleral icterus and an enlarged spleen 6 cm below the left costal margin. CBC reveals: WBC count, 20 x 103/µL (40% neutrophils, 25% lymphs, 15% bands); hemoglobin, 5 g/dL; MCV, 80 fL; RDW, 20%; platelet count, 450 x 103/µL; and the reticulocyte count, 17%. Besides attending to the acute management that she requires, what other laboratory tests might you order to establish a diagnosis?
In working through such cases of anemia as thesemild or severepediatricians often do not consider the admonition in the title of this article, which I borrowed from the title of Jane Austen's 19th century novel: They don't inject "sense and sensibility" into the proceedings. A child with anemia can be evaluated in a variety of ways, and some pediatricians rely on a host of laboratory tests. I believe in a more focused approachparticularly in managed care, where clinicians are often expected to consider a broad differential diagnosis but make do with a minimum of diagnostic testing.
The focused approach I promote can be achieved by relying on important aspects of the history, the physical examination, and, in most cases, a limited number of laboratory testsin particular, the hemoglobin concentration, MCV, and reticulocyte countand by reviewing the peripheral blood smear. Such an evaluation usually leads to a determination of the type and cause of the anemia.
Anemia can be defined as, simply, a reduction in red blood cells (RBCs), or in their hemoglobin concentration, to a level that is more than two standard deviations (SDs) below the mean in healthy children. The sole function of the RBC is to carry and release oxygen to tissues. In most cases of anemia, oxygen saturation is normal. In a child with severe anemia, however, it may be essential to measure oxygen delivery to the tissues using pulse oximetry or arterial blood gas analysis. It may also be important to assess the child for cardiopulmonary disease, which might accentuate poor oxygen exchange and delivery in the face of severe anemia.
Table 1 lists normal values for hemoglobin and MCV. Various references cite slightly different normal ranges; for simplicity, this article considers the lower limit of normal for the hemoglobin concentration to be 11 g/dL in a 9- to 12-month old child and the lower limit of normal for the MCV to be 70 fL in the same age range. A pediatric office that screens with a spun hematocrit should consider the lower limit of normal to be 33%.*
*The hematocrit is useful as a screening test but is a derived value: the MCV multiplied by the RBC count. If you use the hematocrit as a screening test, remember that its values are susceptible to fluid shift and postural changes (standing or prone), stress, and vasoconstrictionall of which often accompany blood drawing in small children. Because the hematocrit seems to be more affected than the hemoglobin concentration by these factors, the hematocrit is therefore not recommended as the sole laboratory means of assessing anemia.
|Hemoglobin (g/dL)||MCV (fL)|
|Age||Mean||Lower limit (2 SD)||Mean||Lower limit (2 SD)|
|6 mo2 yr||12.5||11||77||70|
The American Academy of Pediatrics recommends screening for anemia sometime at the end of the first year of life; most pediatricians do this between 9 and 12 months of age. In infants at high risk of anemia because of prematurity or anemia at birth, the evaluation often takes place earlier.
The history, physical examination, and laboratory testing form the basis for determining the cause of the anemia.
History. Table 2 summarizes important variables in the history. Age is a significant consideration in possible iron deficiency (such deficiency is rare in infants younger than 4 to 6 months unless the child was born prematurely) and in discerning the cause of anemia in the neonatal period. Anemia immediately after birth or during the first few days of life almost always relates to blood loss (fetal-maternal transfusion, abruptio placenta, intracranial hemorrhage), immune-mediated hemolysis, or infection. Anemia discovered after the first several days of life or during the neonatal period (the first 30 days of life) is most often related to heritable hemolytic anemia. The neonatal history is also essential to discern whether hyperbilirubinemia was present, suggesting an inherited hemolytic anemia or immune-mediated hemolysis.
|Age||Anemia in the first year of life may be related to blood loss (discovered within a few days of birth), congenital hemolytic anemia (discovered during the neonatal period), a hemoglobinopathy (often discovered at 36 months of age), or iron deficiency (rare in full-term infants younger than 46 months)|
|Gender||Certain conditions, such as X-linked glucose-6-phosphate-dehydrogenase (G-6PD) deficiency, are much more common in boys than in girls|
|Race or ethnicity||Sickle cell disease is most common in African-Americans, and thalassemia syndromes are found in many ethnic groups|
|Diet||Dietary deficiencies can lead to a deficiency of iron, vitamin B|
|Drugs suppression||Drugs (antibiotics, anti-inflammatory agents, anticonvulsants) can cause oxidative stress hemolysis, hemolytic anemia, and bone marrow|
|Infection||Certain infectious agents can result in bone marrow suppression (hepatitis viruses, parvovirus) or hemolytic anemia (Epstein-Barr virus cytomegalovirus,|
|Family history||Gallstones, neonatal jaundice, enlarged spleen, and transfusion in family members suggest a mechanism for an increased risk of a heritable form of anemia|
Anemia discovered at 3 to 6 months in a term infant suggests a hemoglobinopathy. All infants experience a physiologic drop in hemoglobin between 6 and 8 weeks of age, caused by normal cessation of erythropoiesis that results from the sudden increase in oxygenation and the shift from fetal to adult hemoglobin. The hemoglobin concentration can be as low as 9 to 10 g/dL and still be normal, especially if the infant was born with a low hemoglobin.
Gender is an important consideration in anemia associated with certain X-linked conditions, such as glucose-6-phosphate-dehydrogenase (G-6PD) deficiency, which occurs mainly in males. Race and ethnicity are significant factors in the diagnosis of hemoglobinopathies such as sickle cell anemia (most common in African-Americans) and ß thalassemia trait or disease (seen among many ethnic groups from Southern Europe and Africa, extending east to the Middle East, India, and South and East Asia). The
thalassemia trait can be seen in both African-Americans and South and East Asians, whereas three-gene deletion
thalassemia (hemoglobin H disease) and four-gene deletion
a thalassemia (associated with hydrops fetalis) occur exclusively among South and East Asians.
Dietary assessment can help establish the diagnosis of iron deficiency (early and excessive cow's milk ingestion), vitamin B12 deficiency (strict vegetarian diet), and folic acid deficiency (goat's milk as the sole source of milk protein). Most physicians know about the association between pica and iron deficiency but are often unaware that this condition is associated with eating ice chips as well as with ingesting dirt and clay.
It is essential to take a detailed drug history when assessing the cause of anemia. Many antibiotics, anti-inflammatory medications, and anticonvulsant drugs can cause oxidative stress hemolysis, other hemolytic anemias, or bone marrow suppression. Infection with various agents may cause hemolytic anemia (Epstein-Barr virus, cytomegalovirus, Mycoplasma pneumoniae) or anemia resulting from bone marrow suppression (hepatitis viruses and parvovirus).
Careful questioning of the family may elicit a history of gallstones, neonatal jaundice, or an enlarged spleen. It may be helpful simply to ask if anyone in the family has ever been told that he (or she) has anemiataking care to explain what you mean by "anemia."*
*When explaining anemia and the essentials of RBC mass and hemoglobin concentration to parents or family members, consider using the analogy of a train: The purpose of the circulation (the train) is to deliver oxygen (freight or passengers) to the body; the RBCs (the boxcars) contain crates or boxes (hemoglobin) in which the oxygen is stored.
Also ask if the patient has received any treatment for anemia, such as transfusions or supplemental iron. Often overlooked, questions about travel outside the continental United States (particularly to tropical areas where malaria is endemic) can be helpful. Symptoms of malabsorption that are seen in inflammatory bowel disease may point toward anemia of inflammation.
Last, question patient and parents carefully to elicit a description of any signs and symptoms of anemia, such as pallor, irritability, dyspnea, and fatigue. Do not overlook hematologic symptoms such as jaundice, scleral icterus, bone pain, and blood in the stool and urine, which are classically associated with anemia.
Physical examination. By performing a careful physical examination, the circumspect pediatrician goes beyond obvious physical findings to uncover subtle clues to the cause of anemia (Table 3). Frontal bossing and maxillary overgrowth, for example, are signs of increased bone marrow expansion, which is characteristic of many congenital hemolytic anemias. Inspection of the extremities can reveal abnormalities of the forearm and hand found in Fanconi anemia and the triphalangeal thumb of RBC aplasia (Blackfan-Diamond anemia). Valvular heart disease (such as aortic stenosis) and congenital heart disease (such as a ventricular septal defect) may contribute to microangiopathic hemolytic anemia, which is characterized by fragmented RBCs.
|Abdomen||Splenomegaly||Congenital hemolytic anemia Portal hypertension|
|Extremities||Abnormal forearm or hand|
|Head and face||Frontal bossing and maxillary overgrowth||Congenital hemolytic anemia|
|Heart||Aortic stenosis and ventriculoseptal defect||Fragmented RBCs|
|Skin anemia||Cavernous hemangioma Petechiae and bruising Caf-au-lait spots||Microangiopathic hemolytic Bone marrow failure syndrome Fanconi anemia|
|Central nervous system||Posterior column defects||Vitamin B|
The abdominal exam can define the presence of hepatosplenomegaly (often associated with heritable hemolytic anemia), and the digital rectal exam can reveal the hemorrhoids that might reflect portal hypertension (suggested with liver disease that is possibly associated with anemia). Petechiae and bruising suggest bone marrow failure. Café-au-lait spots may be seen in Fanconi anemia, while cavernous hemangioma, although sometimes small at the surface of the skin, may be the only clue to the diagnosis of microangiopathic hemolytic anemia. Last, ataxia and posterior column signs on the neurologic exam may be the only physical finding that helps establish a diagnosis of vitamin B12 deficiency.
Laboratory testing. Most cases of anemia can be discerned by simple determination of the hemoglobin concentration, MCV (one of the three RBC indices that define the size and hemoglobin content of the RBC), reticulocyte count, and a review of the peripheral blood smear. Regrettably, some pediatricians fall into the habit of becoming inextricably entwined in an unfortunate tangle of testing, such as osmotic fragility, haptoglobin, methemalbumin, urine porphyrin, and the like, while initially attempting to unravel the cause of their patient's anemia. Neither quality medical care nor managed care allows a shotgun laboratory approach to the evaluation of anemia. Nor should our patients endure such extensive and unnecessary evaluation.
Almost every laboratory utilizes some form of electronic blood cell counting, which provides rapid, precise, and reproducible CBC results on a large number of patients. Most laboratories rely on a Coulter Counter, which applies principles of electrical impedance to directly measure hemoglobin, MCV, and the reticulocyte count.
The RDW, a derived value, quantifies variability in the size of RBCs around a normal MCV. In a normal patient, RBC size is quite uniform and the RDW ranges from 11.5% to 14.5%. The relationship between the RDW and the MCV, which indicates the average volume of RBCs, may help the busy clinician to differentiate cases of anemia characterized by erythrocytes of varying sizes. In iron deficiency anemia, for example, the RDW is high (much variation in the size of RBCs) in combination with a low MCV (small RBCs). This compares with
and ß thalassemia trait, which is also characterized by a low MCV but demonstrates a normal RDW. Other, more severe microcytic anemias that have a high RDW, such as homozygous ß thalassemia disease and sickle ß thalassemia, might be missed if only RBC indices are used. The RDW may also be elevated in immune hemolytic anemia, sickle cell disease, and hereditary spherocytosis. In these states, however, the MCV should be normal.
The reticulocyte count is essential in determining whether a patient has hemolytic anemiain which production of RBCs increases in response to increased destruction or loss of existing RBCs. Modern CBC analyzers provide automated reticulocyte counting that is more accurate than manual counting. At the upper level of normal, reticulocytes may represent 3% of the RBC population.
A review of the peripheral blood smear provides additional clues for discerning the most likely cause of anemia (Table 4), especially in conditions in which an empiric trial of iron fails or if anemia is moderate (hemoglobin, <9.5 g/dL). If you are unable to review a smear personally, arrange to have a laboratory technologist or pathologist examine it.
|Cell size is not uniform||Anemia of inflammation|
|Folate deficiency (or other cause of increased MCV)|
|Iron deficiency (small cells)|
|Acanthocytes||Vitamin E deficiency, liver disease|
|Bizarre shapes||RBC membrane defects, thalassemia syndromes|
|Blister or bite cells||G-6PD deficiency|
|Helmet cells (fragmented cells)||Microangiopathic anemia, such as hemolytic uremic syndrome; disseminated intravascular coagulation|
|Pseudopods||Thalassemia trait or disease|
|Rouleaux (stacking of RBCs)||Inflammation or immune hemolytic anemia|
|Stomatocytes||Liver disease, Rh null blood group, stomatocytosis|
|Target cells||Hemoglobinopathy, liver disease|
|Tear-drop cells||Bone marrow failure|
|Hyperchromia (presence of spherocytes)||Hereditary spherocytosis, immune hemolytic anemia cytomegalovirus or other infection, or any condition that damages the RBC membrane (such as oxidant stress hemolysis)|
|Polychromasia (elevated reticulocyte count)||Hemolytic anemia* or acute blood loss|
|Basophilic stippling (ribosomes)||Lead poisoning|
|Heinz bodies (seen only on supravital stain, such as methyl violet)||G-6PD deficiency or unstable hemoglobin (oxidant stress hemolysis)|
|Howell-Jolly bodies (nuclear remnants)||Absence of splenic function|
|Sideroblasts (deposits of iron in RBCs)||Increased iron|
Table 5 proposes how the MCV and the reticulocyte count can be used to evaluate anemia. A caution: As in most systems developed to be a diagnostic tool, some anemias do not fit neatly into this framework.
Microcytic anemia (low MCV). The list of conditions classified as the cause of microcytic anemia are easily recognizableparticularly the three that are most common: iron deficiency, thalassemia trait, and hemoglobin EE disease. In the past, lead poisoning was a common cause of microcytic anemia; today, however, screening of the blood lead level usually uncovers this condition before anemia develops. Indeed, a diagnosis of lead poisoning rendered solely on the basis of hematologic changes might be too late to permit intervention to reverse accompanying neurologic symptoms.
Hemoglobin EE has become an increasingly common cause of microcytic anemia because of the influx of immigrants from South and East Asia into the United States. Chronic infection, though listed as a cause of microcytic anemia, is more likely to present as a normochromic-normocytic anemia. Last, a membrane defect such as hereditary elliptocytosis can sometimes present with a low-normal or slightly low MCV associated with mild anemia.
Macrocytic anemia (high MCV). Most pediatricians can recognize the nutritional anemias (folate and vitamin B12 deficiency) and their association with an elevated MCV, but some practitioners may overlook bone marrow failure syndromes such as myelodysplasia, Blackfan-Diamond anemia, aplastic anemia, and drug suppression (anticonvulsants, immunosuppressive therapy) as other causes of macrocytic anemia.
Normochromic-normocytic anemia should be evaluated within the context of the reticulocyte count. An absent or very low count strongly suggests RBC aplasia or, if the neutrophil or platelet count is low, malignancy or bone marrow failure.
A normal reticulocyte count almost always reflects some type of chronic inflammation. Many observers consider anemia of inflammation the most common cause of anemia. Indeed, if it is not essential to determine quickly the cause of anemia in a child who is ill, I strongly advise that you wait until the inflammation resolves and then perform the CBC when the child is well again. Subsequent investigation can then be pursued if the hemoglobin is low.
Barring acute blood loss, the finding of a normochromic-normocytic anemia with an elevated reticulocyte count indicates a hemolytic anemia. The MCV is almost always normal in these conditions because the elevated reticulocyte count and concomitant slight increase in RBC size (MCV) are usually balanced by the smaller cells of the corresponding RBC defect. It is best to evaluate such a patient by keeping in mind the three components that constitute an RBCmembrane, hemoglobin, and enzymesor by conditions external to the RBC that cause damage to the membrane (microangiopathic or immune hemolytic anemia). Review of the peripheral blood smear will aid in discerning the type of hemolytic anemia, and should be pursued aggressively in moderate or severe anemia and in the patient whose hemoglobin concentration has not improved at follow-up.
Consideration of the findings on the peripheral blood smear, in conjunction with the MCV and reticulocyte count (Table 4 and Table 5, respectively), facilitates a reasoned approach to evaluating anemia. The anemic patient with a normal MCV, elevated reticulocyte count, and target cells on the peripheral blood smear probably has a hemoglobinopathy such as sickle cell disease. The pediatrician can now focus the evaluation to confirm the diagnosisin this case, by ordering a hemoglobin electrophoresis.
Figure 1 offers an approach to discerning the cause of mild microcytic anemia. (Before embarking on this journey, however, always consider blood loss.) As mentioned, most clinicians are now testing healthy term infants for anemia at 9 to 12 months; preterm children or children who had anemia in the nursery might be tested earlier, at 4 to 6 months. Assuming that the child consumes a normal diet, has had no recent infections, and is not in an ethnic group in which thalassemia trait is a possibility, he (or she) can be screened for anemia with a CBC.
A lower than normal hemoglobin value calls for an empiric course of iron3 mg/kg/d in one morning dosegiven with a drink that contains vitamin C, such as apple juice. For mild anemia, this dosage of iron is sufficient and eliminates some of the gastric irritation and constipation a higher dosage can cause.
If, one month later, the hemoglobin concentration has risen by 0.5 to 1.0 g/dL, make a presumptive diagnosis of iron deficiency and prescribe the same dosage of iron for two additional months.
If, however, the hemoglobin level does not increase more than 0.5 g/dL, then assess for blood loss and seek a skilled interpreter to review the smear and determine what to do next. In addition, consider performing the laboratory tests listed in Figure 1. If the reticulocyte count and the smear are normal, the child might have so-called statistical anemiameaning that he is more than 2 SDs below the mean and that the anemia has no apparent cause. Truly unexplained mild anemia might also be attributable to one-gene deletion a thalassemia or resolving anemia of inflammation.
Last, also perform the suggested laboratory tests if the initial screening hemoglobin concentration is <9.5 g/dL, the history indicates a higher than normal risk of anemia or iron deficiency, or the child is younger than 6 months or older than 18 months.
The evaluation of anemia calls for an infusion of "sense and sensibility." Instead of resorting to a myriad of laboratory tests, focus on the history, physical examination, CBC, peripheral blood smear, MCV, and reticulocyte count. This approach makes it possible to evaluate children like the ones described at the beginning of the article (for a review of the evaluation they should likely undergo, see "Reaching a diagnosis"). Last, for practice using the approach I've outlined in this article, try to determine the cause of the anemia in the cases described in "Why are these eight children anemic?"below.
Abshire TC: The anemia of inflammation. A common cause of childhood anemia. Pediatr Clin North Am 1996;43:623
Ezekowitz RAB, Stockman JA III: Hematologic manifestations of systemic disease, in Nathan DG, Orkin SH, Oski FA (eds): Nathan and Oski's Hematology of Infancy and Childhood, ed 5. Philadelphia, WB Saunders, 1997, p 1841
Oski FA, Brugnara C, Nathan DG: A diagnostic approach to the anemic patient, in Nathan DG, Orkin SH, Oski FA (eds): Nathan and Oski's Hematology of Infancy and Childhood, ed 5. Philadelphia, WB Saunders, 1997, p 375
Walters MC, Abelson HT: Interpretation of the complete blood count. Pediatr Clin North Am 1996;43:599
Here are suggested approaches to the two patients whose cases are described at the beginning of this article.
The best management approach for this child is to obtain a hemoglobin electrophoresis study (the history suggests that iron deficiency is unlikely) and a CBC and reticulocyte count on both parents at the outset. This is appropriate because the MCV is disproportionately low compared with the hemoglobin level and because the child is African-American, both suggesting thalassemia trait. The hemoglobin electrophoresis helps differentiate
and ß thalassemia trait: ß thalassemia trait is most often characterized by an elevated fetal hemoglobin or hemoglobin A2, or both, whereas the hemoglobin electrophoresis is normal in a thalassemia.
Review of this child's peripheral blood smear reveals target cells and mild hypochromia, which would also suggest thalassemia trait. Alternatively, you could place him on an empiric trial of iron for one month and repeat the CBC. If the hemoglobin level did not rise, you could then proceed with the evaluation proposed in Figure 1.
In conclusion, this infant probably has
thalassemia trait (two-gene deletion).
The fact that this child is female makes an X-linked hemolytic anemia, such as G-6PD deficiency, unlikely. Review of the blood smear reveals many hyperchromic RBCs, making it prudent to obtain a direct and indirect Coomb's test to rule out immune hemolytic anemia. The RDW and mean corpuscular hemoglobin concentration (an RBC index) might both be elevated in hereditary spherocytosis. This patient probably has hypersplenism and, possibly, increased destruction of RBCs because of infection. Although an aplastic crisis could contribute to the anemia, an appropriately elevated reticulocyte count rules out this possibility.
In light of the respiratory distress in the face of severe anemia, it would also be prudent to administer an RBC transfusion. This child probably has hereditary spherocytosis, and an osmotic fragility test should be performed three or four months after transfusion to confirm your suspicion.
(The answersthe diagnosis for each of these patientsare given below.)
1. The complete blood count (CBC) of an 8-year-old girl reveals the following: hemoglobin, 11.5 g/dL; mean corpuscular volume (MCV), 102; reticulocyte count, 0.4%; WBC count, normal; platelet count, 125 x 103/µL. She is slightly short, has several large café-au-lait spots, is performing below average in school, and has short thumbs. The smear shows large RBCs, some of which are tear-drop shaped.
2. An 18-month-old girl was in good health until she developed a cold 10 days ago. Now, she is pale but without visible jaundice. The CBC shows a hemoglobin of 6.8 g/dL; MCV, 78; and reticulocyte count, 0.1%. The WBC and platelet counts are normal, as is the peripheral blood smear.
3. A 6-month-old boy has fever and irritability and a WBC count of 20 x 103/µL (67% polys, 24% bands, and 9% lymphs); hemoglobin, 9.0 g/dL; MCV, 82; and reticulocyte count, 1.0%. The smear shows rouleaux formation (stacking of RBCs atop one another) but is otherwise normal.
4. A 3-year-old Hispanic-American girl has had diarrhea, sometimes bloody, for several days. Now, she has fever, edema, petechiae, and hypertension. The CBC shows: hemoglobin, 7.5 g/dL; MCV, 79; reticulocyte count, 15%; platelet count, 35 x 103/µL; and WBC count, 13.580 x 103/µL with a normal differential count. The smear shows several helmet cells and polychromasia and confirms the thrombocytopenia.
5. A 9-month-old Caucasian boy comes to the physician's office for evaluation of a cold. Further history reveals introduction of whole cow's milk at 5 months in copious quantities (40 oz/d) and no well-baby visits. He appears quite pale and has the following findings on the CBC: hemoglobin, 5.3 g/dL; MCV, 48; platelet count, 780 x 103/µL; WBC count, 12.5 X 103/µL; and reticulocyte count, 1.7%.
6. You are asked to assist in the care of political refugees from south China. On the screening entrance exam you note that one of them, a 2-year-old girl, is very pale and lethargic. Her spleen is down to the level of the umbilicus. The hemoglobin concentration is 6.3 g/dL; reticulocyte count, 12%; MCV, 55; and WBC and platelet counts, normal. The smear shows many target cells, polychromasia, basophilic stippling, pseudopods, and hypochromia.
7. A 3-month-old African-American boy is brought to the emergency department lethargic and with a fever of 40° C. While attending to the airway, correcting hypotension, and initiating antibiotics, the nurse informs you of the CBC results: hemoglobin, 5.8 g/dL; MCV, 81; reticulocyte count, 16%; WBC count, 23.45 x 103/µL (56% polys, 24% bands, 10% lymphs, and 10% atypical lymphocytes); and platelet count, 35 x 103/µL. He has blood on a dipstick analysis of his urine with no RBCs on microscopic analysis. The blood smear shows several spherocytes, moderate blister cells, and several bite cells.
8. A 15-year-old Hispanic-American girl with a history of systemic lupus erythematosus comes to the clinic for evaluation of fatigue and pallor. Hemoglobin is 7.2 g/dL; MCV, 85; reticulocyte count, 3.5%; WBC count, 3.5 x 103/µL (50% polys, 40% lymphs, 10% atypical lymphocytes); and platelet count, 125 x 103/µL. The smear shows microspherocytes and rouleaux formation. She does not have a history of blood loss.
1. Fanconi's anemia
2. Transient erythroblastopenia of childhood
3. Anemia of inflammatory disease
4. Hemolytic uremic syndrome
5. Iron deficiency
6. Hemoglobin EE ß thalassemia
7. G-6PD deficiency
8. Autoimmune hemolytic anemia
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Date of publication: September 2001
Title: "Sense and sensibility: Approaching anemia in children"
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Thomas Abshire. CME: Sense and sensibility: Approaching anemia in children. Contemporary Pediatrics 2001;9:104.