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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
child with anemia. The nutritional
history should include the moth-
Anemia can be classified in two ways: by the er’s dietary patterns if she is breast-
physiologic process of red blood cell loss or by feeding an infant. Infants, toddlers,
and adolescent girls share the pos-
the size, color, and shape of the red blood cells. sibility of iron deficiency anemia
resulting from nutrition and diet
deficiencies. The review of the sys-
tems should include a newborn
and providing initial treatment for and thrombocytopenia purpura or history of jaundice. The history
the anemia. disseminating intravascular coagu- should include an evaluation of
lation. Anemia that is produced extremity pain, blood loss, exten-
PATHOPHYSIOLOGY OF from impaired cell production oc- sive bruising, petechia, travel, in-
ANEMIA curs when there is a disturbance of fection exposure, and drug use. A
Anemia can be classified in two proliferation and distribution of family history of jaundice, splenec-
ways: by the physiologic process stem cells. This situation occurs in tomy, or cholecystectomy suggests
of red blood cell loss or by the size, aplastic anemia, anemia from renal a hereditary etiology for hemolytic
color, and shape of the red blood cell aplasia, and anemia from renal anemia diseases (Dershewitz, 1999).
cells. The classification of anemia failure or endocrine disorders. Im- The physical examination
based on physiologic process in- paired cell production also can should include a comprehensive
cludes several etiologies. Anemia occur with a disturbance in matu- review of the plotted growth charts
can be caused by a decrease in red ration and proliferation of red and a survey of the patterns of
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- The history should include an evaluation of
dolph, Kamei, & Overby, 2002).
Increased rate of destruction of red extremity pain, blood loss, extensive bruising,
cells occurs in various hemolytic petechia, travel, infection exposure, and drug
anemias, resulting from both in-
trinsic factors and extrinsic factors. use.
Intrinsic abnormalities of red cell
can be the result of hereditary or
acquired diseases. Hereditary dis- cells. Impaired cell production oc- growth of the child over a period
eases have several etiologies. curs when cells have defective of time to determine the potential
Sperocytosis and elliptocytosis are DNA synthesis such in vitamin B12 for chronic anemia. The physical
conditions causing anemia be- and folic acid anemia. Defective examination also should include
cause of a disorder in the red cell hemoglobin synthesis is the patho- an evaluation of the child for pal-
membrane.Disorders in red cell logic process for iron deficiency lor, jaundice, petechiae, bruising,
enzymes, such as glucose-6-phos- anemia, thalassemia, and the ane- murmurs adenopathy, organo-
phate dehydrogenase and pyru- mia of chronic infections (Kumar megaly, frontal bossing, and con-
vate synthesis diseases, also can et al., 2003).
cause anemia. Sickle cell anemia genital anomalies (Dershewitz,
and thalassemia cause anemia be- 1999). The blood pressure, heart
cause red cells have structural ab- DIAGNOSIS OF ANEMIA rate, and respiratory rate also
normalities (Kumar et al., 2003). Family and Physical History should be evaluated using the ap-
There are extrinsic abnormali- The history provides valuable propriate normative values for the
ties of the red blood cell that pro- information for the diagnostic child’s age and height (Wong,
duce anemia. Other extrinsic fac- workup. A family history should Hockenberry, Wilson, Winkel-
tors causing anemia are antibody- include information about the stein, & Kline, 2003).
mediated red cell destruction ethnic heritage of the family, any Lack of iron stores at birth, low
diseases, such blood transfusion history of anemias, splenectomy, level of iron in the diet during
reactions. Another extrinsic factor jaundice, gallbladder disease, sickle growth, and blood loss all cause
causing anemia are mechanical cell trait, or thalassemia. A nutri- iron deficiency and can lead to
processes causing red cell destruc- tional history is an important part iron deficiency anemia. Iron
tion, such as hemolytic anemia, of the history in the evaluation of a stores are developed during the
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 anemia, blood loss, or low iron additional information about other
months of life, full-term infants intake (Graham & Uphold). red blood cell indices can assist with
have sufficient iron stores, but diagnosing the etiology of the ane-
these stores gradually are being mia, leading to treatment options
depleted (Hoekeleman et al., Laboratory Evaluation of (Behrman et al., 2004; Hoekeleman
2001; Kohli-Kumar, 2001). In pre- Anemia et al., 2001).
term infants, anemia may de- The American Academy of Pedi-
velop earlier than 12 months atrics recommends screening all
from insufficient iron stores (Al- children for anemia by the 12- Microcytic Anemia
kalay, Galvis, Ferry, Simmons, & month visit (Behrman, Kliegman, & Several diseases produce micro-
Jenson, 2004). The normal values of cytic red blood cells, iron defi-
Krueger, 2003). Dietary intake of
hemoglobin and hematocrit vary by ciency anemia, thalassemia trait,
iron replaces the loss of stored
age (Table 1). Measurements of he- lead poisoning, chronic inflamma-
iron from prenatal life.
moglobin, hematocrit, and red cell tion, and sideroblastic anemia. In
Preschool-aged children in
indices provide information about most children who have microcytic
low-income families, newly im-
the red cells that assists in the diag- red blood cells, there is a defect in
migrant children, or refugee chil-
nosis of the underlying cause of ane- hemoglobin synthesis (Behrman et
dren are at high risk for iron de-
mia. Red cell indices include the al., 2004).
ficiency. They should be mean cell volume, mean hemoglo- Iron deficiency anemia is a fre-
screened at 9 to 12 months of age bin, mean cell hemoglobin concen- quent problem in pediatrics and is
and 6 months later (Bogen, Dug- tration, and red blood cell distribu- most commonly treated by nurse
gan, Dover, & Wilson, 2000). tion width (Hoekeleman et al., practitioners (Graham & Uphold,
High-risk groups of children 2001). Serum ferritin concentration 2003). When iron is in short sup-
should be screened annually is the measurement of iron storage ply, the body decreases the pro-
from 2 years to 5 years (Graham and contributes to the diagnosis of duction of hemoglobin. The red
& Uphold, 2003; Kohli-Kumar, iron deficiency. Transferrin satura- cells become hypochromatic and
2001). During the school age tion measures dietary iron absorp- microcytic. Iron deficiency pro-
years, only high-risk children tion and transport (Graham & Up- duces a chronic anemia that may
need to be screened. Adolescent hold, 2003). have long-term psychological, mo-
boys also do not need to be Describing cell morphology is a tor, and behavioral functioning
screened unless they are at risk. method of classification of anemia. (Kazal, 2002; Lozoff et al., 2000).
Adolescent girls should be Cell morphology can be determined Iron deficiency also can develop in
screened every 5 to 10 years. by a peripheral film and mean cor- the first year of life in children who
Children with any other condi- puscular volume. The red blood cell are fed low-iron formula.
tions that suggest the potential can be described as microcytic, nor- Young boys may be most af-
for anemia should have routine mocytic, or macrocytic. Understand- fected by iron deficiency (Abelson,
screening to assess for chronic ing the description of the cell and 2001; Doemellof et al., 2002). Chil-
dren between 12 and 24 months of clude panocytopenias and chronic the newborn period of life. A child
age are at the highest risk of any hemolytic anemia. Children with with autoimmune hemolytic ane-
age group for iron deficiency ane- anemia from panocytopenia will mia usually is jaundiced and has
mia because of their rapid growth have severe anemia, low platelets, splenomegaly. A positive Coombs
and lack of dietary sources of iron and a low white blood cell count. test is diagnostic for this problem.
(Abelson; Doemellof et al.). Ado- A white blood cell count with dif- The child should be evaluated for
lescence is another period of rapid ferential is indicated when the ane- an underlying systemic disorder,
growth when iron stores can be mia is very severe. In panocytope- such as a malignancy, immune de-
depleted because the diet does not nia the symptoms are acute: a ficiencies, collagen vascular dis-
replace the loss of iron. Adolescent sudden drop in hemoglobin, ease, drugs, Mycoplasma pneumo-
girls are at greatest risk if they have weakness, pallor, fatigue, and pos- nia, Epstein-Barr virus, and human
heavy menstrual periods (Graham sibly shock. Chronic hemolytic immune deficiency virus. Pred-
& Uphold, 2003). Lead poisoning anemia occurs in children with nisone often is the treatment of
is another cause of microcytic ane- sickle cell disease or hereditary choice for autoimmune hemolytic
mia. Lead inhibits the synthesis of spherocytosis. When the red cell anemia (Hoekeleman et al., 2001).
hemoglobin, causing an anemia production decreased suddenly, Enzyme deficiencies in red
similar to iron-deficiency anemia. these children experience an acute blood cells produce a normocytic
Lead levels are high and target drop in the hematocrit, producing anemia with an elevated reticulo-
cells and basophilic stripling may the symptoms of shock or an cyte count. Glucose-6-phosphate
be present in the red cell, resulting aplastic crisis (Hoekeleman et al., dehydrogenase is the most com-
in anemia (Centers for Disease 2001). mon disease resulting from en-
Control and Prevention, 1997). Anemia can occur in conjunc- zyme deficiencies that occurs in
tion with chronic illness. This ane- childhood. Normocytic cell mor-
Normocytic Anemias mia produces a normocytic, nor- phology is present in anemia
Normocytic red cell morphol- mochromatic red cell. When red caused by hemoglobinopathies.
ogy in the presence of anemia is cells are destroyed, there is a cor- Hemoglobinopathies are a group
caused by increased destruction of responding increase in production of hemolytic disorders in which
red blood cells or decreased pro- of red blood cells. The anemia pro- there are abnormalities in the ␣ or
duction of red blood cells. The duced has normocytic cell mor-  chain of the hemoglobin mole-
normocytic cells can be associated phology with an elevated reticulo- cule (Hoekeleman et al., 2001).
with a low reticulocyte count or a cyte count. Anemia conditions that
high reticulocyte count. Determin- produce this clinical picture are Macrocytic Anemias
ing the reticulocyte count in nor- disseminating intravascular coagu- Macrocytic anemia is very rare
mocytic anemia assists in diagnosis lation, hemolytic uremic syn- in children. Vitamin B12, folate de-
of selected diseases. If the cell drome, cardiac prosthetic devices, ficiencies, inborn errors of metab-
morphology is normocytic and as- and autoimmune system diseases olism that inhibit folate absorption,
sociated with a low reticulocyte that cause hemolysis. The periph- and poor nutritional intake can
count, the most common diseases eral film reveals cell destruction, cause malabsorption syndromes
occurring in childhood are Dia- with small fragments of red cells that produce anemia. In the pe-
mond-Blackfan anemia and tran- frequents evident (Hoekeleman ripheral blood smear, the red
sient erythroblastopenia (Crocetti, et al.). blood cells are macrocytic and the
Hwit, & Kato, 2002). Normocytic cells are seen in au- MCV is 100 to 140 fL. Serum levels
Other diseases that have the cell toimmune hemolytic anemia, but of B12 or folate can be evaluated
morphology of normocytic cells in- this disease is rare in children after to determine the etiology of a mac-