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Transient erythroblastopenia of childhood: Implications for nurse practitioners
Transient Erythroblastopenia of Childhood: n Implications for Nurse Practitioners n Debra
M. Brewin-Wilson,
MSN,
RN, CPNP
Pediatric nurse practitioners in all areas of practice encounter anemic children. This article describes transient erythroblastopenia of childhood (TEC), a rare type of anemia that baffles health care providers and causes anxiety in parents. Understanding the cause, course, and treatment of TEC allows the nurse practitioner to educate and reassure affected children and their parents. J PEDIATR HEALTH CARE. (1989). 3, 200-203.
A
s the name implies, transient erythroblastopenia of childhood (TEC) is a temporary decrease in the number of immature erythrocytes in children. Transient erythroblastopenia is a rare disorder that pediatric nurse practitioners may encounter when caring for healthy children. Although the disorder rarely interferes with the child’s activities, parents frequently worry about the diagnosis and what it means to their child. No one knows what causes TEC. Immune suppression of erythropoiesis seems to be the culprit, with both IgM and IgG implicated (Alter, 1987; Freedman, 1983; Freedman & Saunders, 1983; Koenig, Lightsey, Nelson, & Diamond, 1979). Researchers remain uncertain of the exact role of immunoglobulins in TEC. Freedman & Saunders (1983) state that the immunoglobulins may be antibodies specific for antigens on red-cell precursors, or the antibodies may interfere with the actions of erythropoietin in erythrocyte development. Despite the mechanisms involved that cause the disorder, the outcome remains the same, with affected children recovering fully. w HISTORY
AND
PHYSICAL
EXAMINATION
Typically, children affected with TEC are toddlers with a, history of a viral illness during the previous 3 months, although children may range in age from 1 month through their teens (Alter, 1987; Zwerdling, Finlay, & Glader, 1986). Parents may bring the child to the primary health care provider because the child appears pale, or the provider may note pal-
Debra M. Brewin-Wilson was a pediatric nurse practitioner erie Fund Children’s Cancer Center at Monmouth Medical Long Branch, New jersey, at the time this article was written. Ms. Brewin-Wilson technology News,
is currently Associate Editor of Oncology Plainsboro, New Jersey.
Reprint requests: Debra M. Brewin-Wilson, Ave., Edison, NJ 08817.
200
lor and/or a systolic ejection murmur during the course of a routine examination. The child’s activity level may be decreased or normal; indeed, parents may not notice any symptoms of anemia, such as pallor or decreased activity, even when the child has a profoundly low hemoglobin of less than 3 gm/dl. The medical and family histories are usually negative for hematologic disorders and exposure to toxins (Freedman, 1983). laboratory
Findings
The practitioner should obtain a complete blood count (CBC) and reticulocyte count on the child. A child with TEC will have a decreased hemoglobin (pediatric normal, 11 to 13 gm/dl) and a normal mean corpuscular volume (MCV; pediatric normal, 80 to 94 fl). The reticulocyte count may be normal or decreased. ,These parameters indicate that although there are decreased numbers of erythrocytes, their size is normal. This helps to rule out some common anemias (Table 1). Children with iron-deficiency anemia have erythrocytes decreased in both number and size; their reticulocyte count may also be increased. Such a CBC also excludes folic acid and Vitamin Blz deficiencies, as red cells in children with these disorders are decreased in number, but their size is increased (MCV of 110 to 140 fl) (Hockenberry & Hoots, 1986).
P
arents diagnosis
frequently worry about the and what it means to their child.
at the ValCenter in and Bio-
MSN, RN, CPNP, 36 Brookhill
A profoundly low hemoglobin (for example, less than 6 gm/dl) may necessitate immediate admission to the hospital and a thorough hematologic workup. A hemoglobin that is moderately low (for example, JOURNAL
OF PEDIATRIC
HEALTH
CARE
Journal of Pediatric Health Care
n
TABLE
Transient
1 Comparison
of laboratory
findings
Age at onset Hgb MCV Reticulocytes FEP
Infants/toddlers Decreased Decreased Decreased* Increased
*Increased after iron therapy. **Increased during recovery phase. Data from Alter (1987); Hockenberry
n
TABLE
-
2 Characteristics
-
Age at onset W& MCV f-tgb F WBC Platelets Physical examination Data from Alter (1987);
in iron-deficiency
& Hoofs
of red-cell
of Childhood
201
vs. TEC
Toddkrs Decreasail Normal Normal or decreased** NWmt
(1986)
aplasias
Under
12 months
ktcreased Normal Norma1 or increased About 25% to 30% have congeilital anomalies Hockenberry
& Hoots
(1986);
Wang
& Mentzer
(1976).
7 to 10 gm/dl) may allow more time for outpatient testing. Individual providers establish their own parameters for referral to a specialist; a hemoglobin that one considers low may be considered moderate by another health care provider. Outpatient testing for anemia should include a free erythrocyte porphyrin (FEP) level, ferritin level, total iron-binding activity, and a serum lead level, especially for children in the toddler age group. FEP levels will be increased in both iron-deficiency anemia and lead poisoning, but will be higher in children with lead poisoning. (Hockenberty & Hoots, 1986). Hemoglobin electrophoresis is indicated if sicklecell anemia or any thalassemia syndrome is suspected through a patient’s history. Other diagnostic possibilities, such as hereditary spherocytosis or red-cell enzyme deficiencies, require more specialized testing, and the child should be referred to a pediatric hematologist/oncologist. n
anemia
Erythroblastopenia
DIFFERENTIAL DIAGNOSIS
When the only abnormal laboratory result indicates an erythrocyte hypoplasia, the hematologist must rule out further diagnostic possibilities. Aplastic anemia, congenital hypoplastic anemia (CHA), or Diamond-Blackfan anemia, and pure red-cell aplasia have many of the same presenting symptoms as TEC
(Table 2). Children with aplastic anemia have decreased numbers of all bone marrow elements. Children with CHA usually become symptomatic before 1 year of age, whereas pure red-cell aplasia occurs in adolescents and adults. Children with CHA also frequently have congenital anomalies, including triphalangeal thumbs, short stature, webbed neck, and mental retardation. These children also have increased levels of Hgb F (Alter, 1987; Hockenberry & Hoots, 1986; Wang & Mentzer, 1976). Another diagnostic possibility that must be considered is that the child has, or is developing, leukemia: either acute lymphoblastic leukemia (ALL), or acute nonlymphocytic leukemia (ANLL). A bone marrow aspiration must be done to determine the cause of the low hemoglobin. The primary care provider can give an age-appropriate explanation of the procedure to the child, or can help the parents to do so, before referring the family to the hematologist/oncologist. The time between learning the blood count results and learning the results of the bone marrow aspiration is characterized by the extreme anxiety of the parents. The primary health care provider may suspect the child has leukemia, and will inform the parents of his or her suspicions. Even if they are not told this, the parents’ imaginations frequently fill in
202
Volume 3, Number 4 July-August 1989
Brewin-Wilson
the details. Ongoing contact from the primary care provider can help provide continuity and support to the family during this difficult period. When the family meets members of the pediatric hematology/oncology team, the parents are often afraid that their child is dying. The child and parents require much reassurance during the following days, as further bloodwork is performed, a diagnosis is made, and treatment begins.
A
bone marrow aspiration must be done to determine the cause of the low hemoglobin.
child to be transfused. For some, no amount of reassurance about screening blood donors or donated blood may convince them. If a transfusion is medically indicated, a designated donor from the family may be used, provided there is sufficient time for the blood donation and processing to occur without compromising the child’s health status. Parents need to know that they did nothing to cause the TEC. It is not related to diet or hereditary factors. Parents may feel guilty for not noticing their child’s pallor or decreased activity level. The nurse can help by listening as they express their feelings, then reassuring them that they did nothing to cause their child’s illness. n
The hematologist will first perform another CBC and will examine a smear to determine which elements are low. A bone marrow aspiration will then be performed. Members of the hematology/oncology team will reinforce explanations given of the procedure. Depending upon the individual caregiver’s philosophy and the parents’ feelings, parents sometimes stay with their child during the procedure. Parents should be there only to emotionally support their child-not for physical restraint. In TEC, the bone marrow aspirate reveals a decreased percentage of erythroid elements, but normal percentages of other cell types (Alter, 1987; Freedman, 1983; Freedman & Saunders, 1983; Zwerdling, Finlay, & Glader, 1986). This contrasts with aplastic anemia, in which all cell types are decreased, and also with ALL, in which the lymphoblasts, and ANLL, in which the myeloblasts, crowd out other normal cell types. n
TREATING THE CHILD WITH TEC
Once the diagnosis is made, the physician determines if treatment will be needed. Children with TEC fully recover from the disorder, usually within 1 to 2 months. Some children require no treatment at all, having reached their lowest hemoglobin levels by the time they are diagnosed. Others require a transfusion of packed red blood cells, especially if evidence of cardiac compromise exists (Alter, 1987). Some patients have atypical presentations or courses and require steroids (Freedman, 1983; Zwerdling, Finlay, & Glader, 1986). The majority of children with TEC, however, do not require steroids (Alter, 1987). Parents require a great deal of information and reassurance after the diagnosis is made, especially if a blood transfusion is needed. In today’s AIDSconcerned society, parents may refuse to allow their
PLANNING
FOLLOW-UP
CARE
Parents need reassurance about the temporary nature of TEC. Most children with TEC who receive one blood transfusion will not require another. Reticulocytosis (an increase in reticulocytes) shortly occurs, and the hemoglobin returns to a normal level and sustains itself. “Rebound” levels may be seen on the complete blood count, with an increased number of reticulocytes and erythrocytes. The erythrocytes may also increase in size, so the MCV will be increased. Higher levels of fetal hemoglobin (Hgb F) may also be found during the recovery period (Alter, 1987).
C hildren
with TEC fully recover from the disorder, usually within 1 to 2 months.
Although most children with TEC have had a viral illness in their recent past, the role that plays in the development of TEC is not clear. It may not be related at all, because viral illnesses frequently develop in most toddlers, especially if they are in group care situations. Nevertheless, some physicians may recommend that complete blood counts be obtained whenever the child has a viral illness. Recurrent erythroblastopenia has been reported (Alter, 1987; Freedman, 1983). Once discharged from the care of the pediatric hematologist/oncologist, the child can return to the primary health care provider. The hemoglobin will be periodically followed until it returns to normal. Routine follow-up should include checking for resolution of any cardiovascular compromise, as well as determining how the illness and treatment experience have affected the family. The primary health care
lournal of Pediatric Health
Care
provider has an excellent opportunity to reassure parents that their child is healthy once more. Case Study
A 23-month-old white child was admitted to the hospital by his pediatrician with a hemoglobin of 3.1 gm/dl and a reticulocyte count of 0.1%. The patient’s medical history was negative except for an upper respiratory tract infection the week before his hospital admission. The physical examination was normal, except for pallor and a grade II/VI systolic ejection murmur. A bone marrow aspiration revealed decreased erythroid cells but was otherwise normocellular.
M
ost children with TEC who receive one blood transfusion will not require another.
The child received a total of 250 ml of packed red blood cells in two aliquots, thus exposing him to only one blood donor. His hemoglobin rose from 3.1 gm/dl to 9.4 gm/dl. During his hospital stay, his mother met the mother of a child with ALL who was receiving chemotherapy. The patient’s mother became visibly distraught after the meeting, crying and tightly holding her son. She required reassurance from the members of the pediatric hematology/oncology team that her son did not have leukemia. He recovered fully, with no residual problems related to his once-compromised cardiac status. n
DISCUSSION
The case study emphasizes several points about the child with TEC and the nurse’s role. The pediatric
Transient
Erythroblastopenia
of Childhood
203
nurse practitioner, whether the primary care provider or one involved through a referral, has an excellent opportunity to assist the family by providing information about the disorder, its diagnosis, and its treatment. The PNP can reassure parents about the temporary nature of the disorder, and can also provide necessary follow-up care for the child. TEC is not a common disorder. Its onset is so gradual that one wonders how many children may develop the disorder and spontaneously recover. Perhaps there are degrees of severity of TEC, and only the more severely affected children are identified and treated. Research on this disorder continues, and perhaps these questions will be answered in the future. n I wish to acknowledge sistance in the preparation
Cindy Steele, MD, for her asof this manuscript.
REFERENCES Alter, B. P. (1987). The bone marrow failure syndromes. In D. G. Nathan & F. A. Oski (Eds.), Hematology o$%jzq and Childhood, ThirdEd. (pp. 159-241). Philadelphia: W.B. Saunders Company. Freedman, M. H. (1983). ‘Recurrent’ erythroblastopenia of childhood: An @M-mediated BBC aplasia. Amricm Jout-n.~ of Dkemes in Childhood, 137, 458-460. Freedman, M. H. & Saunders, E. F. (1983). Transient erythroblastopenia of childhoocl varied pathogenesis. Am&an JOUYml OfHemutol~g, 14, 247-254. Hockenbeny, M. J. & Hoots, W. K. (1986). Childhood anemia. In M. J Hockenbeny and D. K. Goody (Eds.), Pediakc Oncology and Hema~olo~: Perspectives on Care (pp. 172-214). St. Louis: The C.V. Mosby Company. Koenig, H. M., Lightsey, A. L., Nelson, D. P., & Diamond, L. K. (1979). Immune suppression of erythropoiesis in transient erythroblastopenia of childhood. Blood, 54, 742-746. Wang, W. C. & Mentzer, W. C. (1976). Differentiation of transient erythroblastopenia of childhood from congenital hypoplastic anemia. The Jaurnul of Pediatrb, 88, 784-789. Zwerdling, T., Finlay, J., & Glader, B. E. (1986). Transient erythroblastopenia of adolescence. Clinical Pediuti, 25, 563-565.
M. Brewin-Wilson,
MSN,
RN, CPNP
Pediatric nurse practitioners in all areas of practice encounter anemic children. This article describes transient erythroblastopenia of childhood (TEC), a rare type of anemia that baffles health care providers and causes anxiety in parents. Understanding the cause, course, and treatment of TEC allows the nurse practitioner to educate and reassure affected children and their parents. J PEDIATR HEALTH CARE. (1989). 3, 200-203.
A
s the name implies, transient erythroblastopenia of childhood (TEC) is a temporary decrease in the number of immature erythrocytes in children. Transient erythroblastopenia is a rare disorder that pediatric nurse practitioners may encounter when caring for healthy children. Although the disorder rarely interferes with the child’s activities, parents frequently worry about the diagnosis and what it means to their child. No one knows what causes TEC. Immune suppression of erythropoiesis seems to be the culprit, with both IgM and IgG implicated (Alter, 1987; Freedman, 1983; Freedman & Saunders, 1983; Koenig, Lightsey, Nelson, & Diamond, 1979). Researchers remain uncertain of the exact role of immunoglobulins in TEC. Freedman & Saunders (1983) state that the immunoglobulins may be antibodies specific for antigens on red-cell precursors, or the antibodies may interfere with the actions of erythropoietin in erythrocyte development. Despite the mechanisms involved that cause the disorder, the outcome remains the same, with affected children recovering fully. w HISTORY
AND
PHYSICAL
EXAMINATION
Typically, children affected with TEC are toddlers with a, history of a viral illness during the previous 3 months, although children may range in age from 1 month through their teens (Alter, 1987; Zwerdling, Finlay, & Glader, 1986). Parents may bring the child to the primary health care provider because the child appears pale, or the provider may note pal-
Debra M. Brewin-Wilson was a pediatric nurse practitioner erie Fund Children’s Cancer Center at Monmouth Medical Long Branch, New jersey, at the time this article was written. Ms. Brewin-Wilson technology News,
is currently Associate Editor of Oncology Plainsboro, New Jersey.
Reprint requests: Debra M. Brewin-Wilson, Ave., Edison, NJ 08817.
200
lor and/or a systolic ejection murmur during the course of a routine examination. The child’s activity level may be decreased or normal; indeed, parents may not notice any symptoms of anemia, such as pallor or decreased activity, even when the child has a profoundly low hemoglobin of less than 3 gm/dl. The medical and family histories are usually negative for hematologic disorders and exposure to toxins (Freedman, 1983). laboratory
Findings
The practitioner should obtain a complete blood count (CBC) and reticulocyte count on the child. A child with TEC will have a decreased hemoglobin (pediatric normal, 11 to 13 gm/dl) and a normal mean corpuscular volume (MCV; pediatric normal, 80 to 94 fl). The reticulocyte count may be normal or decreased. ,These parameters indicate that although there are decreased numbers of erythrocytes, their size is normal. This helps to rule out some common anemias (Table 1). Children with iron-deficiency anemia have erythrocytes decreased in both number and size; their reticulocyte count may also be increased. Such a CBC also excludes folic acid and Vitamin Blz deficiencies, as red cells in children with these disorders are decreased in number, but their size is increased (MCV of 110 to 140 fl) (Hockenberry & Hoots, 1986).
P
arents diagnosis
frequently worry about the and what it means to their child.
at the ValCenter in and Bio-
MSN, RN, CPNP, 36 Brookhill
A profoundly low hemoglobin (for example, less than 6 gm/dl) may necessitate immediate admission to the hospital and a thorough hematologic workup. A hemoglobin that is moderately low (for example, JOURNAL
OF PEDIATRIC
HEALTH
CARE
Journal of Pediatric Health Care
n
TABLE
Transient
1 Comparison
of laboratory
findings
Age at onset Hgb MCV Reticulocytes FEP
Infants/toddlers Decreased Decreased Decreased* Increased
*Increased after iron therapy. **Increased during recovery phase. Data from Alter (1987); Hockenberry
n
TABLE
-
2 Characteristics
-
Age at onset W& MCV f-tgb F WBC Platelets Physical examination Data from Alter (1987);
in iron-deficiency
& Hoofs
of red-cell
of Childhood
201
vs. TEC
Toddkrs Decreasail Normal Normal or decreased** NWmt
(1986)
aplasias
Under
12 months
ktcreased Normal Norma1 or increased About 25% to 30% have congeilital anomalies Hockenberry
& Hoots
(1986);
Wang
& Mentzer
(1976).
7 to 10 gm/dl) may allow more time for outpatient testing. Individual providers establish their own parameters for referral to a specialist; a hemoglobin that one considers low may be considered moderate by another health care provider. Outpatient testing for anemia should include a free erythrocyte porphyrin (FEP) level, ferritin level, total iron-binding activity, and a serum lead level, especially for children in the toddler age group. FEP levels will be increased in both iron-deficiency anemia and lead poisoning, but will be higher in children with lead poisoning. (Hockenberty & Hoots, 1986). Hemoglobin electrophoresis is indicated if sicklecell anemia or any thalassemia syndrome is suspected through a patient’s history. Other diagnostic possibilities, such as hereditary spherocytosis or red-cell enzyme deficiencies, require more specialized testing, and the child should be referred to a pediatric hematologist/oncologist. n
anemia
Erythroblastopenia
DIFFERENTIAL DIAGNOSIS
When the only abnormal laboratory result indicates an erythrocyte hypoplasia, the hematologist must rule out further diagnostic possibilities. Aplastic anemia, congenital hypoplastic anemia (CHA), or Diamond-Blackfan anemia, and pure red-cell aplasia have many of the same presenting symptoms as TEC
(Table 2). Children with aplastic anemia have decreased numbers of all bone marrow elements. Children with CHA usually become symptomatic before 1 year of age, whereas pure red-cell aplasia occurs in adolescents and adults. Children with CHA also frequently have congenital anomalies, including triphalangeal thumbs, short stature, webbed neck, and mental retardation. These children also have increased levels of Hgb F (Alter, 1987; Hockenberry & Hoots, 1986; Wang & Mentzer, 1976). Another diagnostic possibility that must be considered is that the child has, or is developing, leukemia: either acute lymphoblastic leukemia (ALL), or acute nonlymphocytic leukemia (ANLL). A bone marrow aspiration must be done to determine the cause of the low hemoglobin. The primary care provider can give an age-appropriate explanation of the procedure to the child, or can help the parents to do so, before referring the family to the hematologist/oncologist. The time between learning the blood count results and learning the results of the bone marrow aspiration is characterized by the extreme anxiety of the parents. The primary health care provider may suspect the child has leukemia, and will inform the parents of his or her suspicions. Even if they are not told this, the parents’ imaginations frequently fill in
202
Volume 3, Number 4 July-August 1989
Brewin-Wilson
the details. Ongoing contact from the primary care provider can help provide continuity and support to the family during this difficult period. When the family meets members of the pediatric hematology/oncology team, the parents are often afraid that their child is dying. The child and parents require much reassurance during the following days, as further bloodwork is performed, a diagnosis is made, and treatment begins.
A
bone marrow aspiration must be done to determine the cause of the low hemoglobin.
child to be transfused. For some, no amount of reassurance about screening blood donors or donated blood may convince them. If a transfusion is medically indicated, a designated donor from the family may be used, provided there is sufficient time for the blood donation and processing to occur without compromising the child’s health status. Parents need to know that they did nothing to cause the TEC. It is not related to diet or hereditary factors. Parents may feel guilty for not noticing their child’s pallor or decreased activity level. The nurse can help by listening as they express their feelings, then reassuring them that they did nothing to cause their child’s illness. n
The hematologist will first perform another CBC and will examine a smear to determine which elements are low. A bone marrow aspiration will then be performed. Members of the hematology/oncology team will reinforce explanations given of the procedure. Depending upon the individual caregiver’s philosophy and the parents’ feelings, parents sometimes stay with their child during the procedure. Parents should be there only to emotionally support their child-not for physical restraint. In TEC, the bone marrow aspirate reveals a decreased percentage of erythroid elements, but normal percentages of other cell types (Alter, 1987; Freedman, 1983; Freedman & Saunders, 1983; Zwerdling, Finlay, & Glader, 1986). This contrasts with aplastic anemia, in which all cell types are decreased, and also with ALL, in which the lymphoblasts, and ANLL, in which the myeloblasts, crowd out other normal cell types. n
TREATING THE CHILD WITH TEC
Once the diagnosis is made, the physician determines if treatment will be needed. Children with TEC fully recover from the disorder, usually within 1 to 2 months. Some children require no treatment at all, having reached their lowest hemoglobin levels by the time they are diagnosed. Others require a transfusion of packed red blood cells, especially if evidence of cardiac compromise exists (Alter, 1987). Some patients have atypical presentations or courses and require steroids (Freedman, 1983; Zwerdling, Finlay, & Glader, 1986). The majority of children with TEC, however, do not require steroids (Alter, 1987). Parents require a great deal of information and reassurance after the diagnosis is made, especially if a blood transfusion is needed. In today’s AIDSconcerned society, parents may refuse to allow their
PLANNING
FOLLOW-UP
CARE
Parents need reassurance about the temporary nature of TEC. Most children with TEC who receive one blood transfusion will not require another. Reticulocytosis (an increase in reticulocytes) shortly occurs, and the hemoglobin returns to a normal level and sustains itself. “Rebound” levels may be seen on the complete blood count, with an increased number of reticulocytes and erythrocytes. The erythrocytes may also increase in size, so the MCV will be increased. Higher levels of fetal hemoglobin (Hgb F) may also be found during the recovery period (Alter, 1987).
C hildren
with TEC fully recover from the disorder, usually within 1 to 2 months.
Although most children with TEC have had a viral illness in their recent past, the role that plays in the development of TEC is not clear. It may not be related at all, because viral illnesses frequently develop in most toddlers, especially if they are in group care situations. Nevertheless, some physicians may recommend that complete blood counts be obtained whenever the child has a viral illness. Recurrent erythroblastopenia has been reported (Alter, 1987; Freedman, 1983). Once discharged from the care of the pediatric hematologist/oncologist, the child can return to the primary health care provider. The hemoglobin will be periodically followed until it returns to normal. Routine follow-up should include checking for resolution of any cardiovascular compromise, as well as determining how the illness and treatment experience have affected the family. The primary health care
lournal of Pediatric Health
Care
provider has an excellent opportunity to reassure parents that their child is healthy once more. Case Study
A 23-month-old white child was admitted to the hospital by his pediatrician with a hemoglobin of 3.1 gm/dl and a reticulocyte count of 0.1%. The patient’s medical history was negative except for an upper respiratory tract infection the week before his hospital admission. The physical examination was normal, except for pallor and a grade II/VI systolic ejection murmur. A bone marrow aspiration revealed decreased erythroid cells but was otherwise normocellular.
M
ost children with TEC who receive one blood transfusion will not require another.
The child received a total of 250 ml of packed red blood cells in two aliquots, thus exposing him to only one blood donor. His hemoglobin rose from 3.1 gm/dl to 9.4 gm/dl. During his hospital stay, his mother met the mother of a child with ALL who was receiving chemotherapy. The patient’s mother became visibly distraught after the meeting, crying and tightly holding her son. She required reassurance from the members of the pediatric hematology/oncology team that her son did not have leukemia. He recovered fully, with no residual problems related to his once-compromised cardiac status. n
DISCUSSION
The case study emphasizes several points about the child with TEC and the nurse’s role. The pediatric
Transient
Erythroblastopenia
of Childhood
203
nurse practitioner, whether the primary care provider or one involved through a referral, has an excellent opportunity to assist the family by providing information about the disorder, its diagnosis, and its treatment. The PNP can reassure parents about the temporary nature of the disorder, and can also provide necessary follow-up care for the child. TEC is not a common disorder. Its onset is so gradual that one wonders how many children may develop the disorder and spontaneously recover. Perhaps there are degrees of severity of TEC, and only the more severely affected children are identified and treated. Research on this disorder continues, and perhaps these questions will be answered in the future. n I wish to acknowledge sistance in the preparation
Cindy Steele, MD, for her asof this manuscript.
REFERENCES Alter, B. P. (1987). The bone marrow failure syndromes. In D. G. Nathan & F. A. Oski (Eds.), Hematology o$%jzq and Childhood, ThirdEd. (pp. 159-241). Philadelphia: W.B. Saunders Company. Freedman, M. H. (1983). ‘Recurrent’ erythroblastopenia of childhood: An @M-mediated BBC aplasia. Amricm Jout-n.~ of Dkemes in Childhood, 137, 458-460. Freedman, M. H. & Saunders, E. F. (1983). Transient erythroblastopenia of childhoocl varied pathogenesis. Am&an JOUYml OfHemutol~g, 14, 247-254. Hockenbeny, M. J. & Hoots, W. K. (1986). Childhood anemia. In M. J Hockenbeny and D. K. Goody (Eds.), Pediakc Oncology and Hema~olo~: Perspectives on Care (pp. 172-214). St. Louis: The C.V. Mosby Company. Koenig, H. M., Lightsey, A. L., Nelson, D. P., & Diamond, L. K. (1979). Immune suppression of erythropoiesis in transient erythroblastopenia of childhood. Blood, 54, 742-746. Wang, W. C. & Mentzer, W. C. (1976). Differentiation of transient erythroblastopenia of childhood from congenital hypoplastic anemia. The Jaurnul of Pediatrb, 88, 784-789. Zwerdling, T., Finlay, J., & Glader, B. E. (1986). Transient erythroblastopenia of adolescence. Clinical Pediuti, 25, 563-565.