QUESTIONS AND ANSWERS FOR CLINICAL INSIGHTS

(See page 157 for data.)

1. Based on the histoy and physical examination, what would you include in the differential diapaosis? a. Iron deficiency anemia b. Other anemias c. Lead poisoning

2. What additional information would you obtain? a. Answers to questions about family history of ane-

mia or other blood disorders b. Answers to further questions about the history

of pica c. Complete blood cell count with peripheral smear

if available Results: White blood cell count, 8500 ~1; hemoglobin, 9.1 g/dl; hematocrit, 27.5%; red blood cell count, 4.6 ~1; platelets 300,000 ~1; mean corpuscular volume, 70 /.Ld; mean corpuscular hemoglobin concentration, 30% Hb/cell; reticulocyte, 0.5%; smear reveals hypo- chromic, microcytic red cells with marked poikilocy- tosis. Normal values for a 2-year-old child: White blood cell count, 6.0 to 17.5 ~1; hemoglobin, 10.5 to 14.0 g/dl; hematocrit, 32% to 42%; red blood cell count, 3.7 to 5.3 ~1; platelets, 150,000 to 400,000 ~1; mean cor- puscular volume, 70 to 86 pm3; mean corpuscular he- moglobin concentration, 31% to 37% Hbicell; retic- ulocyte, 0.1% to 1.3% (Behrman & Vaughn, 1987).

d. Serum lead level. Result: 4.0 pg/dl (less than 10.0 pg/dl normal [CDC Guidelines, 19911). 3. What is the diagnosis?

Iron deficiency anemia Anemia caused by lack of sufficient iron for synthesis

of hemoglobin is by far the most common hematologic disease of infancy and childhood. It most often results from the increased requirement for iron during growth periods. The disease rarely appears before 6 months of life and is most common during year 2. The most com- mon causes of iron deficiency are low intake, disturbed absorption on the basis of various intestinal disorders, and blood loss. The usual dietary pattern observed in infants and voung children with iron deficiencv anemia is the cons&mption of large amounts of milk and of carbohydrates unsupplemented with iron. The adoles- cent age group should also be screened for iron defi- ciency because of rapid growth, blood loss in men- struating females, and increased nutritional needs of ath- letes.

Blood loss must be considered in every case of iron deficiency anemia. Chronic iron deficiency anemia from occult bleeding may be caused by a lesion in the gas- trointestinal tract, such as a peptic ulcer, Meckel diver-

JOURNAL OF PEDIATRIC HEALTH CARE

ticulum, polyp, or hemangioma. In some geographic areas, hookworm infestation is an important cause.

As manv as one third of infants in the United States with severe iron deficiency have chronic intestinal blood loss induced by exposure to a heat labile protein in whole cow milk. Loss of 1 to 7 ml of blood in the stools each day can be shown not to be influenced by iron replacement or transfusion. It can, however, be prc- vented by either reducing the quantitv of whole co\\ milk to 1 pint or less daily or by using heated or evap- orated milk or milk substitute. This gastrointestinal re- action is not related to enzvmatic abnormalities in the mucosa such as lactase deficiency or to typical milk al- lergy (Behrmann & Vaughn, 1987).

Pallor is the most common clue to iron deficiency. The spleen is palpably enlarged in 10% to 15% of pa- tients. When the hemoglobin level falls below 5.0 g/dl, tachycardia and cardiac dilitation occur, and svstolic murmurs are often present. The child mav be obese or underweight, with other evidences of undernutrition. Pica, irritability, and anorexia mav also occur. These svmptoms mav reflect deficiencv in iissue iron; with iron i therapy, strikiTng improvemen; in behavior frequentlv occurs along with significant hematologic improve- ment. Iron deficiency may also have effects on neuro- logic and intellectual function. A number of reports suggest that iron deficiency anemia and even iron de- ficiency without significant anemia may affect attention span, alertness, and learning (Chow et al., 1984).

Iron deficiency must be differentiated from other hy- pochromic microcytic anemias. In lead poisoning the red cells are morphologically similar, but coarse baso- philic stippling of the red cells is prominent. Many casts of lead poisoning have concomitant iron deficiencv.

The regular response of iron deficiency anemia to adequate amounts of iron is an important diagnostic feature, as well as a therapeutic feature. Oral adminis- tration of simple ferrous salts provides inexpensive and satisfactory therapy. The therapeutic dose should bc cal- culated in terms of elemental iron: ferrous sulfate is 20%, and ferrous gluconate is 10% to 12% elemental iron by weight. A daily total of 6 mg/kg of elemental iron in three divided doses provides an optimal amount of iron for the stimulated bone marrow to use. Bcttcr absorption may result when medicinal iron is given be- tween meals. Ingestion of large amounts of milk ma! significantly decrease absorption of iron. Vitamin C (200 mg per 30 mg of iron) may also enhance absorp- tion. Liquid iron preparations may stain teeth; therefore giving it with a dropper or a straw is best. Iron prcp- arations may cause constipation, dark stools, nausea,

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174 Clinical Insights (Q&A) Volume 6, Number 3

May-June 1992

and epigastric pain. Anticipatorv guidance about these possible effects is warranted (Chow et al., 1984).

Appropriate nutrition education is an important component of treatment as well. A diet containing 8 to 15 mg of iron daily is necessary to maintain a positive iron balance in childhood. Consumption of milk should be limited, and iron-rich foods should be increased. 4. What is the poflnosis?

Within 72 to 96 hours after administration of iron to the anemic child, peripheral reticulocytosis is seen. The height of this response is inversely proportional to the severitv of the anemia. Reticulocvtosis is followed by a rise in the hemoglobin level, which mav increase as much as 0.5 gmidl124 hours. If available, the fret erythrocyte protoporphyrin (FEI’) should be monitored also. When the red blood cell does not have enough iron to make hemc, the FEP becomes elevated and rises markcdhf as the concentration of hemoglobin falls. Val- ues abo;.e 3 kg/g-m of hemoglobin are abnormal and occur in iron deficiency, chronic inflammatorv disease, and lead intoxication. Subjective improvement mav also be noted within a day or two after starting treatment. Irritability is less prominant; pica is corrected. and ap- petite returns (Behrmann & Vaughn, 1987).

Iron medication should be continued for at least 6 to 8 weeks after blood values are normal to increase iron stores. Prognosis for recovery is excellent unless an incorrect original diagnosis is made, the prescribed med- ication is not given or is poorly absorbed, continuing or unrecognized blood loss occurs, or dietary recom- mendations are not followed. Further evaluation and/or consultation may be necessary if blood values do not improve after 3 to 6 months.

Continued follow-up of hemoglobin levels is war- ranted at routine well child visits, or more frequently if the anemia is a recurrent problem. Reinforcement of nutrition information is crucial for prevention of repeat occurrences.

REFERENCES Behrman, R.E., Vaughan, V.C. (1987). Nelson 7‘extbook of Pedtatrics

(13th cd., pp. 1042-44) Philadelphia: WB Saunders. Center for Disease Control. (1991, October). Pvevetiting leadpoisoninn

in yunp children. A statement by the Centers of Disease Control. Atlanta: US Department of Health and Human Set-vices/Public Health Service/Centers for Disease Control.

Chow, M.P. Durand, B.A. Feldman, M.N., Mills 1M.A. (1984). Hand- book ofl’ediatvic Ptimaq Care (2nd ed., pp. 759-765). New York: John Wilev and Sons.