Original Article www.jpedhc.

org

Anemia: Diagnosis Anemia is a pathologic condi-

tion in which there is a decrease in
red blood cell mass or a decrease

and Management
in the amount of hemoglobin (Car-
ley, 2003; Kumar, Cotran, & Rob-
bins, 2003). Anemia is a common
occurrence in the United States. As
many as 20% of children have ane-
Sharon M. Coyer, PhD, APN, CPNP mia, and ethnic groups may have a
higher incidence, such as African-
American children (24.6%) and
Hispanic children (18.4%) (Car-
ABSTRACT ley). Anemia may develop in over-
Anemia is a pathologic condition produced by a decrease in red blood cell mass weight children (Nead, Halterman,
or a decrease in the amount of hemoglobin. Anemia is a common occurrence in Kaczorowski, Auinger, & Weitz-
the United States. Children from some ethnic groups have a higher incidence of man, 2004). Iron-deficiency ane-
anemia, but anemia also can affect overweight children and children with chronic mia can produce long-term devel-
illnesses. Iron-deficiency anemia, which is the most common cause of anemia and
opmental outcomes and continues
can produce long-term developmental outcomes, continues to be prevalent in
some groups of children. This article will review the procedures for taking a
to be prevalent in some groups of
history, determining the etiology, and providing initial treatment for the anemia. J children (Childs, Aukett, Darby-
Pediatr Health Care. (2005) 19, 380-385. shire, Ilett, & Livera, 1997; Lozoff,
Jimenez, Hagen, Mollen & Wolf,
2000).
Anemia continues to occur in
groups of children with an inade-
quate diet, although supplemental
food programs have helped some
parents provide their children with
foods with higher iron content
(Kahn, Binns, Chen, Tanz, & List-
ernick, 2002; Sherry, Bister, & Yip,
1997; Sherry, Zuguao, & Yip,
2001). Children living in high-alti-
tude locations and some ethnic
groups have different criteria for
evaluating the normal hemoglobin
(Hoekeleman, Adam, Nelson,
Weitzman, & Wilson, 2001). If the
child has a chronic condition, such
as cystic fibrosis, the child may re-
quire a higher hemoglobin and he-
matocrit to avoid the problems as-
sociated with anemia.
For nurse practitioners, the
evaluation of the hemoglobin and
Sharon M. Coyer is Assistant Professor, Northern Illinois University, School of Nursing, hematocrit of a child requires not
DeKalb, Ill. only evaluating the normal range
Reprint requests: Sharon M. Coyer, PhD, APN, CPNP, School of Nursing, Northern for the child’s age but also whether
Illinois University, 1240 N Normal Rd, DeKalb, IL 60115; e-mail: scoyer@niu.edu the child’s hemoglobin and hemat-
0891-5245/$30.00
ocrit has changed significantly
since the last visit. This article will
Copyright © 2005 by the National Association of Pediatric Nurse Practitioners. review the procedures for taking a
doi:10.1016/j.pedhc.2005.07.014 history, determining the etiology,
380 Volume 19 • Number 6 Journal of Pediatric Health Care

Anemia can be classified in two ways: by the
physiologic process of red blood cell loss or by
the size, color, and shape of the red blood cells.
and providing initial treatment for
the anemia.
PATHOPHYSIOLOGY OF
ANEMIA
Anemia can be classified in two
ways: by the physiologic process
of red blood cell loss or by the size,
color, and shape of the red blood
cells. The classification of anemia
based on physiologic process in-
cludes several etiologies. Anemia
can be caused by a decrease in red
cells as a result of blood loss, in-
creased rate of destruction of the
red cell, and impaired red cell pro-
duction. Blood loss occurs during
acute or chronic diseases (Ru-
dolph, Kamei, & Overby, 2002).
Increased rate of destruction of red
cells occurs in various hemolytic
anemias, resulting from both in-
trinsic factors and extrinsic factors.
Intrinsic abnormalities of red cell
can be the result of hereditary or
acquired diseases. Hereditary dis-
eases have several etiologies.
Sperocytosis and elliptocytosis are
conditions causing anemia be-
cause of a disorder in the red cell
membrane.Disorders in red cell
enzymes, such as glucose-6-phos-
phate dehydrogenase and pyru-
vate synthesis diseases, also can
cause anemia. Sickle cell anemia
and thalassemia cause anemia be-
cause red cells have structural ab-
normalities (Kumar et al., 2003).
There are extrinsic abnormali-
ties of the red blood cell that pro-
duce anemia. Other extrinsic fac-
tors causing anemia are antibody-
mediated red cell destruction
diseases, such blood transfusion
reactions. Another extrinsic factor
causing anemia are mechanical
processes causing red cell destruc-
tion, such as hemolytic anemia,
Journal of Pediatric Health Care
and thrombocytopenia purpura or
disseminating intravascular coagu-
lation. Anemia that is produced
from impaired cell production oc-
curs when there is a disturbance of
proliferation and distribution of
stem cells. This situation occurs in
aplastic anemia, anemia from renal
cell aplasia, and anemia from renal
failure or endocrine disorders. Im-
paired cell production also can
occur with a disturbance in matu-
ration and proliferation of red
The history should include an evaluation of
extremity pain, blood loss, extensive bruising,
petechia, travel, infection exposure, and drug
use.
cells. Impaired cell production oc-
curs when cells have defective
DNA synthesis such in vitamin B12
and folic acid anemia. Defective
hemoglobin synthesis is the patho-
logic process for iron deficiency
anemia, thalassemia, and the ane-
mia of chronic infections (Kumar
et al., 2003).
DIAGNOSIS OF ANEMIA
Family and Physical History
The history provides valuable
information for the diagnostic
workup. A family history should
include information about the
ethnic heritage of the family, any
history of anemias, splenectomy,
jaundice, gallbladder disease, sickle
cell trait, or thalassemia. A nutri-
tional history is an important part
of the history in the evaluation of a
child with anemia. The nutritional
history should include the moth-
er’s dietary patterns if she is breast-
feeding an infant. Infants, toddlers,
and adolescent girls share the pos-
sibility of iron deficiency anemia
resulting from nutrition and diet
deficiencies. The review of the sys-
tems should include a newborn
history of jaundice. The history
should include an evaluation of
extremity pain, blood loss, exten-
sive bruising, petechia, travel, in-
fection exposure, and drug use. A
family history of jaundice, splenec-
tomy, or cholecystectomy suggests
a hereditary etiology for hemolytic
anemia diseases (Dershewitz, 1999).
The physical examination
should include a comprehensive
review of the plotted growth charts
and a survey of the patterns of
growth of the child over a period
of time to determine the potential
for chronic anemia. The physical
examination also should include
an evaluation of the child for pal-
lor, jaundice, petechiae, bruising,
murmurs adenopathy, organo-
megaly, frontal bossing, and con-
genital anomalies (Dershewitz,
1999). The blood pressure, heart
rate, and respiratory rate also
should be evaluated using the ap-
propriate normative values for the
child’s age and height (Wong,
Hockenberry, Wilson, Winkel-
stein, & Kline, 2003).
Lack of iron stores at birth, low
level of iron in the diet during
growth, and blood loss all cause
iron deficiency and can lead to
iron deficiency anemia. Iron
stores are developed during the
November/December 2005 381
 TABLE 1. Normal values for hemoglobin, hematocrit and mean corpuscular value
Hemoglobin (g/dL) Hematocrit (%) Mean corpuscular volume

Mean Lower limit Mean Lower limit Mean Lower limit

Age (y)
0.5-1.9 12.5 11.0 37 33 77 70
2-4 12.5 11.0 38 34 79 73
5-7 13.0 11.5 39 35 81 75
8-11 13.5 12.0 40 36 83 76
12-14
Female 13.5 12.0 41 36 85 78
Male 14.0 12.5 43 37 84 77
15-17
Female 14.0 12.0 41 36 87 79
Male 15.0 13.0 46 38 86 78
18-49
Female 14.0 12.0 42 37 90 80
Male 16.0 14.0 47 40 90 80
Adapted from Hoekeleman et al., 2001.

prenatal period. In the first 6
months of life, full-term infants
have sufficient iron stores, but
these stores gradually are being
depleted (Hoekeleman et al.,
2001; Kohli-Kumar, 2001). In pre-
term infants, anemia may de-
velop earlier than 12 months
from insufficient iron stores (Al-
kalay, Galvis, Ferry, Simmons, &
Krueger, 2003). Dietary intake of
iron replaces the loss of stored
iron from prenatal life.
Preschool-aged children in
low-income families, newly im-
migrant children, or refugee chil-
dren are at high risk for iron de-
ficiency. They should be
screened at 9 to 12 months of age
and 6 months later (Bogen, Dug-
gan, Dover, & Wilson, 2000).
High-risk groups of children
should be screened annually
from 2 years to 5 years (Graham
& Uphold, 2003; Kohli-Kumar,
2001). During the school age
years, only high-risk children
need to be screened. Adolescent
boys also do not need to be
screened unless they are at risk.
Adolescent girls should be
screened every 5 to 10 years.
Children with any other condi-
tions that suggest the potential
for anemia should have routine
screening to assess for chronic
anemia, blood loss, or low iron
intake (Graham & Uphold).
Laboratory Evaluation of
Anemia
The American Academy of Pedi-
atrics recommends screening all
children for anemia by the 12-
month visit (Behrman, Kliegman, &
Jenson, 2004). The normal values of
hemoglobin and hematocrit vary by
age (Table 1). Measurements of he-
moglobin, hematocrit, and red cell
indices provide information about
the red cells that assists in the diag-
nosis of the underlying cause of ane-
mia. Red cell indices include the
mean cell volume, mean hemoglo-
bin, mean cell hemoglobin concen-
tration, and red blood cell distribu-
tion width (Hoekeleman et al.,
2001). Serum ferritin concentration
is the measurement of iron storage
and contributes to the diagnosis of
iron deficiency. Transferrin satura-
tion measures dietary iron absorp-
tion and transport (Graham & Up-
hold, 2003).
Describing cell morphology is a
method of classification of anemia.
Cell morphology can be determined
by a peripheral film and mean cor-
puscular volume. The red blood cell
can be described as microcytic, nor-
mocytic, or macrocytic. Understand-
ing the description of the cell and
additional information about other
red blood cell indices can assist with
diagnosing the etiology of the ane-
mia, leading to treatment options
(Behrman et al., 2004; Hoekeleman
et al., 2001).
Microcytic Anemia
Several diseases produce micro-
cytic red blood cells, iron defi-
ciency anemia, thalassemia trait,
lead poisoning, chronic inflamma-
tion, and sideroblastic anemia. In
most children who have microcytic
red blood cells, there is a defect in
hemoglobin synthesis (Behrman et
al., 2004).
Iron deficiency anemia is a fre-
quent problem in pediatrics and is
most commonly treated by nurse
practitioners (Graham & Uphold,
2003). When iron is in short sup-
ply, the body decreases the pro-
duction of hemoglobin. The red
cells become hypochromatic and
microcytic. Iron deficiency pro-
duces a chronic anemia that may
have long-term psychological, mo-
tor, and behavioral functioning
(Kazal, 2002; Lozoff et al., 2000).
Iron deficiency also can develop in
the first year of life in children who
are fed low-iron formula.
Young boys may be most af-
fected by iron deficiency (Abelson,
2001; Doemellof et al., 2002). Chil-

382 Volume 19 • Number 6 Journal of Pediatric Health Care

 TABLE 2. Laboratory values in microcytic anemia in children
Hemoglobin
Mean corpuscular value
Red blood cell count
Relative distribution width
Hb
Electrophoresis
Ferritin
Adapted from Rudolph et al., 2002.
dren between 12 and 24 months of
age are at the highest risk of any
age group for iron deficiency ane-
mia because of their rapid growth
and lack of dietary sources of iron
(Abelson; Doemellof et al.). Ado-
lescence is another period of rapid
growth when iron stores can be
depleted because the diet does not
replace the loss of iron. Adolescent
girls are at greatest risk if they have
heavy menstrual periods (Graham
& Uphold, 2003). Lead poisoning
is another cause of microcytic ane-
mia. Lead inhibits the synthesis of
hemoglobin, causing an anemia
similar to iron-deficiency anemia.
Lead levels are high and target
cells and basophilic stripling may
be present in the red cell, resulting
in anemia (Centers for Disease
Control and Prevention, 1997).
Normocytic Anemias
Normocytic red cell morphol-
ogy in the presence of anemia is
caused by increased destruction of
red blood cells or decreased pro-
duction of red blood cells. The
normocytic cells can be associated
with a low reticulocyte count or a
high reticulocyte count. Determin-
ing the reticulocyte count in nor-
mocytic anemia assists in diagnosis
of selected diseases. If the cell
morphology is normocytic and as-
sociated with a low reticulocyte
count, the most common diseases
occurring in childhood are Dia-
mond-Blackfan anemia and tran-
sient erythroblastopenia (Crocetti,
Hwit, & Kato, 2002).
Other diseases that have the cell
morphology of normocytic cells in-
Journal of Pediatric Health Care
Iron deficiency Thalassemia
Low/very low Low
Low/very low Very low
Low High
High Normal
Normal Normal; ␤ ⫽ more A2
Low Normal
clude panocytopenias and chronic
hemolytic anemia. Children with
anemia from panocytopenia will
have severe anemia, low platelets,
and a low white blood cell count.
A white blood cell count with dif-
ferential is indicated when the ane-
mia is very severe. In panocytope-
nia the symptoms are acute: a
sudden drop in hemoglobin,
weakness, pallor, fatigue, and pos-
sibly shock. Chronic hemolytic
anemia occurs in children with
sickle cell disease or hereditary
spherocytosis. When the red cell
production decreased suddenly,
these children experience an acute
drop in the hematocrit, producing
the symptoms of shock or an
aplastic crisis (Hoekeleman et al.,
2001).
Anemia can occur in conjunc-
tion with chronic illness. This ane-
mia produces a normocytic, nor-
mochromatic red cell. When red
cells are destroyed, there is a cor-
responding increase in production
of red blood cells. The anemia pro-
duced has normocytic cell mor-
phology with an elevated reticulo-
cyte count. Anemia conditions that
produce this clinical picture are
disseminating intravascular coagu-
lation, hemolytic uremic syn-
drome, cardiac prosthetic devices,
and autoimmune system diseases
that cause hemolysis. The periph-
eral film reveals cell destruction,
with small fragments of red cells
frequents evident (Hoekeleman
et al.).
Normocytic cells are seen in au-
toimmune hemolytic anemia, but
this disease is rare in children after
Hemoglobin E
Low
Very Low
High
Normal
Normal
Normal
the newborn period of life. A child
with autoimmune hemolytic ane-
mia usually is jaundiced and has
splenomegaly. A positive Coombs
test is diagnostic for this problem.
The child should be evaluated for
an underlying systemic disorder,
such as a malignancy, immune de-
ficiencies, collagen vascular dis-
ease, drugs, Mycoplasma pneumo-
nia, Epstein-Barr virus, and human
immune deficiency virus. Pred-
nisone often is the treatment of
choice for autoimmune hemolytic
anemia (Hoekeleman et al., 2001).
Enzyme deficiencies in red
blood cells produce a normocytic
anemia with an elevated reticulo-
cyte count. Glucose-6-phosphate
dehydrogenase is the most com-
mon disease resulting from en-
zyme deficiencies that occurs in
childhood. Normocytic cell mor-
phology is present in anemia
caused by hemoglobinopathies.
Hemoglobinopathies are a group
of hemolytic disorders in which
there are abnormalities in the ␣ or
␤ chain of the hemoglobin mole-
cule (Hoekeleman et al., 2001).
Macrocytic Anemias
Macrocytic anemia is very rare
in children. Vitamin B12, folate de-
ficiencies, inborn errors of metab-
olism that inhibit folate absorption,
and poor nutritional intake can
cause malabsorption syndromes
that produce anemia. In the pe-
ripheral blood smear, the red
blood cells are macrocytic and the
MCV is 100 to 140 fL. Serum levels
of B12 or folate can be evaluated
to determine the etiology of a mac-
November/December 2005 383
rocytic anemia. Large red blood
cells occur in several disease pro-
cesses such as hypothyroidism.
Children with Down syndrome
and newborns have macrocytosis
(Hoekeleman et al., 2001).
MANAGEMENT OF ANEMIA
The clinical guidelines for pedi-
atric nurse practitioners address
the procedures for management of
iron deficiency anemia (Graham &
Uphold, 2003) and suggest the in-
dications for referral. The initial
treatment depends on the etiology,
the results of laboratory tests, and
the clinical symptoms of the child.
The most common identification of
anemia is through routine screen-
ing. Additional laboratory exami-
nation should include a complete
blood cell count, reticulocyte
count, a peripheral smear, and a
mean corpuscular volume when
the hemoglobin is between 8 g/dL
to 11 g/dL (Table 2).
If the red blood cell is micro-
cytic, the most common reason for
the anemia is iron deficiency. Iron-
deficiency anemia is treated with
oral iron in the dose of 2 to 6
mg/kg per day or elemental iron.
Children younger than 5 years are
treated with Feosol that has 44 mg
of elemental iron in each 5 mL and
is divided into 3 doses per day.
Children from 5 to 12 years can be
treated with one 60 mg tablet of
elemental iron. Adolescents are
treated with one to two tablets of
elemental iron each day. Ferrous
sulfate is the form of oral iron most
easily tolerated. The hemoglobin
should be re-evaluated after 1 to 2
months of treatment. The treat-
ment should continue for 3 to 6
months after the anemia has re-
solved (Dershewitz, 1999; Graham
& Uphold, 2003).
In addition to management with
supplemental iron, the child’s diet
should be evaluated and dietary
counseling should be provided.
The family should be educated to
increase the consumption of meat
if the family does not prefer a veg-
etarian diet. Meat is the source of
384 Volume 19 • Number 6
iron that is best tolerated (Dersh-
ewitz, 1999; Graham & Uphold,
2003). Iron should be taken be-
tween meals and with vitamin C
juices. Infants should be given iron
preparations in the back of their
mouth to avoid staining their teeth.
Iron should not be taken with
dairy products, antacids, calcium
supplements, coffee, tea, bran, and
whole grains, because these prod-
ucts decrease the absorption of
iron. Iron preparation should be
out of reach of young children be-
cause accidental poisoning can oc-
cur with ingestion of iron (Graham
& Uphold). If parents are continu-
ing to provide the recommended
treatment and the anemia does not
resolve, additional testing is re-
quired (Graham & Uphold).
If the child’s anemia does not
Iron should not be taken with dairy products,
antacids, calcium supplements, coffee, tea,
bran, and whole grains, because these products
decrease the absorption of iron.
resolve after 1 month of treatment,
alternative etiologies should be
sought (Davis & Nowicki, 2004).
Nurse practitioners should obtain a
complete blood cell count with red
cell indices and a peripheral smear
and a hemoglobin electrophoresis.
When iron stores are sufficient,
these tests will help the nurse prac-
titioner to diagnosis the thalasse-
mias (Abelson, 2001). The practi-
tioner should refer to a pediatric
hematologist if the anemia is either
very severe or initial treatment is
not effective (Graham & Uphold,
2003). Other indications for refer-
ral are when the hematocrit is less
than 25%, when the anemia is un-
explained, and when there is pan-
cytopenia. The child should be
hospitalized when the hematocrit
is less than 15% to 20%, when the
hematocrit is dropping rapidly,
and when anemia occurs in a child
who is ill (Hoekeleman et al.,
2001).
Iron deficiency anemia should
be prevented as well as treated.
Primary prevention includes en-
couraging mothers to take prena-
tal vitamins with an iron prep-
aration and breastfeeding for
infants; the breastfeeding mother
should continue to take prenatal
vitamins for the first 6 months of
breastfeeding (Geltman et al.,
2004; Graham & Uphold, 2003).
After breastfeeding is discontin-
ued, children should receive two
or more servings of iron-fortified
infant cereal (Graham & Up-
hold). Infants on formula should
have iron-supplemented formula
(Baker et al., 1999).
CONCLUSIONS
Anemia often is caused by iron
deficiency, but other causes exist
as well. Pediatric nurse practitio-
ners should be aware of the etiol-
ogies of anemia, the steps to take
to diagnose anemia, and the most
common causes of anemia in
children. Iron-deficiency anemia
should be prevented as well as
treated with appropriate ongoing
assessment of diet and patterns of
growth. If the family has been able
provide the recommended treat-
ment and the anemia continues,
additional laboratory values and
assessment will provide alternative
etiologies. Children with any other
conditions that suggest the poten-
tial for anemia should have routine
screening to assess for chronic
anemia, blood loss, or low iron in-
Journal of Pediatric Health Care
take. The long-term consequences
of chronic anemia suggest that vig-
ilance is need for this disease in all
child health care.
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Journal of Pediatric Health Care November/December 2005 385