Consultation with
the Specialist
Thrombocytopenia
Susan Murphy, MD*, Anne Nepo, MD*, and Richard Sills, MD*
Thrombocytopenia is a decrease in
platelet count more than two stan-
dard deviations below the mean of
the general population, that is, less
than 150 x 109/L (150,000/mm3) in
adults, children, and neonates. Mild
(100 to 150 x 109/L [100,000 to
150,000/mm3]) and moderate (50 to
100 x 109/L [50,000 to 100,000/
mm3]) thrombocytopenia rarely are
associated with clinical bleeding
without trauma. Bleeding without
obvious trauma can appear when the
platelet count falls to 20 to 30 x
109/L (20,000 to 30,000/mm3); seri-
ous bleeding usually does not occur
until the platelet count is less than
10 x 109/L (10,000/mm3). The risk
of bleeding may be increased by
factors other than the platelet count,
including recent surgery or trauma,
ongoing bleeding, septic shock,
other coagulation disturbances, and
drugs inhibiting platelet function.
Clinical Manifestations
The clinical manifestations of
thrombocytopenia are outlined and
contrasted with other bleeding disor-
ders in Table 1. The classic sign of
thrombocytopenia is petechiae.
Although petechiae can occur in
healthy individuals at sites of
trauma, scattered petechiae are
pathologic. Table 2 highlights
important aspects of the history and
physical examination in these
children.
*Division of Pediatric Hematology &
Oncology, Saint Barnabas Medical Center,
Livingston, NJ.
64
Downloaded from http://pedsinreview.aappublications.org/ at University of Manitoba Libraries on April 24, 2015
TABLE 1. Clinical
Manifestations of Bleeding
Disorders
Thrombocytopenia and
Qualitative Platelet
Dysfunction
● Superficial ecchymoses
(which are small and
multiple), petechiae,
mucosal bleeding (epistaxis,
gum bleeding, gastrointestinal
bleeding, menorrhagia),
occasionally hematuria.
Hematomas are rare.
● Bleeding usually is
immediate.
● Bleeding from superficial
cuts is persistent and often
profuse.
Vascular Disorders
● Palpable petechiae or
purpura, as seen with viral
infections, with
meningococcemia, or with the
typical rash of disorders such
as Henoch-Schönlein purpura.
Coagulation Disorders
● Subcutaneous, intramuscular,
or intra-articular hematomas.
Ecchymoses occur but are
large and solitary; petechiae
are rare.
● Bleeding commonly is
delayed, but bleeding from
superficial cuts is minimal.
Laboratory Evaluation
It is important to confirm that the
thrombocytopenia is not spurious.
Aggregation of platelets in the
syringe or collection tube during
sampling can consume platelets ex
Pediatrics in Review
vivo, which normal findings on a
repeat sample suggest. Antibodies
that interact with the ethylene-
diaminetetra-acetic acid (EDTA)
anticoagulant in the collection tubes
can induce platelet clumping ex
vivo; the platelet count is normal
when using citrate as an anticoagu-
lant or when a blood smear made
directly from a finger or heel punc-
ture without an anticoagulant is
examined. Platelet clumping ex vivo
also is caused by platelet cold
agglutinins or platelet satellitism
(platelets adhering to the outer
membranes of neutrophils or mono-
cytes), which is identified by the
pattern of platelet clumping on the
blood smear.
The laboratory evaluation of a
child who has true thrombocytope-
nia must include a complete blood
count and expert review of the
peripheral blood smear. A blood
smear evaluation that is reported as
part of routine laboratory analysis is
not adequate. The differential diag-
nosis includes disorders of impaired
production or enhanced destruction
ABBREVIATIONS
DIC: disseminated intravascular
coagulation
EDTA: ethylenediaminetetra-acetic
acid
HIV: human immunodeficiency
virus
HUS: hemolytic uremic syndrome
ITP: immune thrombocytopenic
purpura
IV IgG: intravenous gamma globulin
NAIT: neonatal alloimmune
thrombocytopenia
TTP: thrombotic thrombocytopenic
purpura
Vol. 20 No. 2 February 1999
 TABLE 2. History and Physical Examination in the Child Who Has Thrombocytopenia
POINT OF REVIEW COMMENT
Severity of bleeding More severe and prolonged bleeding, such as epistaxis, more likely is
associated with an underlying platelet disorder.
Previous surgery Absence of bleeding with surgery, particularly surgery with a high
risk of bleeding such as tonsillectomy or dental extractions,
decreases the likelihood of a pre-existing or congenital bleeding
disorder.
Menorrhagia A common problem with chronic or congenital bleeding disorders
that can be severe and often results in iron deficiency anemia.
Infection 50% to 75% of patients who have bacteremia and almost all who
have septic shock are thrombocytopenic. Human immunodeficiency
virus (HIV) infection is an increasingly common cause of
thrombocytopenia, which may be the presenting sign.
Exposures to toxic substances, drugs, Benzene, chloramphenicol, and sulfonamides, among others, suppress
radiation marrow. Drugs such as quinidine can cause severe drug-induced
immune thrombocytopenic purpura. Heparin-induced
thrombocytopenia can be associated with thromboses.
Exposures to agents inhibiting platelet Patients who have platelet disorders may report increased bleeding
function during drug use, particularly with aspirin.
Associated disorders Malignancies, collagen vascular disorders, immunologic deficiency.
Family history There are many forms of inherited thrombocytopenia; the type of
inheritance varies.
Congenital anomalies Congenital thrombocytopenia such as Fanconi anemia, hemangiomas
should be considered.
Lymphadenopathy/Hepatosplenomegaly Malignancy, collagen-vascular disease, storage disease, infection
should be considered.

(Table 3), but it is difficult to distin-
guish between these two processes
clinically. Bone marrow aspirate,
biopsy, or both may be helpful in
determining whether megakaryo-
cytes are increased or decreased. In
general, nearly all hypoproductive
thrombocytopenias are associated
with anemia and neutropenia;
destructive processes usually are
associated with isolated thrombocy-
topenia. Exceptions include dissemi-
nated intravascular coagulation
(DIC) and hemolytic-uremic syn-
drome (HUS), in which the destruc-
tive thrombocytopenia usually is
accompanied by anemia. A combi-
nation of decreased platelet produc-
tion and increased clearance also
may occur, as in Wiskott-Aldrich
syndrome, May-Hegglin anomaly,
and human immunodeficiency virus
(HIV) infection.
Examination of the peripheral
smear is critical: Fragmentation of
red cells is consistent with a throm-
botic microangiopathy (eg, DIC,
HUS), leukocytosis with toxic gran-
ulation suggests sepsis, blasts lead to
a diagnosis of leukemia, and leuko-
cyte inclusions suggest several con-
genital thrombocytopenias. Young
platelets are large, and the presence
of large platelets may indicate rapid
turnover or consumption of platelets,
as occurs in immune thrombocyto-
penic purpura (ITP). Many auto-
mated blood cell counters measure
platelet size as the mean platelet
volume; an elevated value usually
indicates a younger platelet popula-
tion. If a child appears severely ill, a
coagulation profile that includes pro-
thrombin and partial thromboplastin
times and fibrinogen is indicated to
assess concomitant coagulation
abnormalities such as those seen in
DIC. Evaluation of renal, liver, and
immunologic function as well as
HIV serology may be indicated in a
child whose clinical course is com-
plex or chronic.
Children who have classic clini-
cal signs of thrombocytopenia but
normal platelet counts may have
qualitative platelet dysfunction. The
bleeding time has been the tradi-
tional screening test for these abnor-
malities, but it has flaws as a diag-
nostic tool, particularly for small
children, and must be performed and
interpreted with care. Assays to
identify von Willebrand disease and
more specific measurements of
platelet function often are necessary.
The platelet count also is normal in
vascular disorders, which usually are
recognized on the basis of clinical
presentation.
Thrombocytopenia in
Acutely Ill Children
Children who have thrombocytope-
nia and are acutely ill frequently

Pediatrics in Review Vol. 20 No. 2 February 1999 65

Downloaded from http://pedsinreview.aappublications.org/ at University of Manitoba Libraries on April 24, 2015
 TABLE 3. Differential Diagnosis of Thrombocytopenia in Children
Acutely ill child
● Sepsis ● Thrombotic thrombocytopenic purpura
● Disseminated intravascular coagulation ● Massive transfusion or hemorrhage
● Liver disease ● Hypothermia
● Hemolytic-uremic syndrome ● Hyperthermia (eg, heat stroke)
● Malignant infiltrative marrow disease ● Cardiopulmonary bypass
● Purpura fulminans

Chronically ill child

● Human immunodeficiency virus ● Hypersplenism
● Systemic lupus erythematosus or other connective tissue disease ● Prosthetic heart valve
● Liver disease ● Cyanotic heart disease
● Chemotherapy/radiotherapy ● Nutritional deficiencies
(eg, iron, folate, B12)
Well-appearing child
● Destructive thrombocytopenia

● Immune

— Immune thrombocytopenic purpura (ITP)

— Drug-induced thrombocytopenia
— Systemic lupus erythematosus or other mixed connective tissue disease
— Posttransfusion purpura
— Allergy and anaphylaxis
● Nonimmune

— Hypersplenism
— Kasabach-Merritt syndrome
— Catheters, vascular prostheses, artificial heart valves
— Congenital or acquired heart disease
● Decreased or impaired production

— Aplastic anemia — Fanconi anemia

— May-Hegglin anomaly — Mediterranean thrombocytopenia
— Bernard-Soulier syndrome — Wiskott-Aldrich syndrome
— Congenital megakaryocytic thrombocytopenia — Other rare familial syndromes

have life-threatening conditions.
They require urgent evaluation and
treatment for conditions such as bac-
terial sepsis, DIC due to septic or
other types of shock, HUS, throm-
botic thrombocytopenic purpura
(TTP), liver disease, and malignan-
cies. If a child presents with fever,
lethargy, petechial rash, or hemody-
namic instability, sepsis and con-
comitant DIC must be the initial
consideration. Supportive laboratory
evidence includes leukocytosis or
leukopenia, anemia and red cell
fragmentation, prolongation of the
prothrombin time and partial throm-
boplastin time, and low fibrinogen
level. Red cell, platelet, and fresh
frozen plasma transfusions are
administered as needed to control
anemia and prevent or treat bleed-
ing. Children who have a history of
gastroenteritis or upper respiratory
tract infection, acute renal disease,
and microangiopathic hemolytic ane-
mia may have HUS. Treatment is
supportive, including red cell trans-
fusions as needed. TTP must be
considered in the child who has
microangiopathic hemolytic anemia,
neurologic disturbances (including
seizures), and renal involvement.
The treatment of choice in TTP is
plasmapheresis and plasma infu-
sions. Platelet transfusions can exac-
erbate the disease and usually are
given only for life-threatening
bleeding.
Thrombocytopenia in
Otherwise Well Children
Thrombocytopenia most commonly
presents in children who, except for
petechiae and purpura, appear well;
more than 95% of these children
have ITP. Therefore, an otherwise
healthy child who has isolated
thrombocytopenia and an examina-
tion notable only for petechiae and
purpura almost can be assumed to
have ITP. A preceding viral illness
1 to 3 weeks earlier is common, and
epistaxis and mucosal and gastroin-
testinal bleeding can occur. The
blood count and peripheral smear
reveal isolated thrombocytopenia,
usually with large platelets. Marrow
examination is not required for chil-
dren who have typical clinical find-
ings and do not require treatment or
who are treated with intravenous
gamma globulin. Marrow usually
has been examined before cortico-
steroids are administered to avoid
masking a leukemic process. The
marrow must be examined in chil-
dren who exhibit atypical findings
and in those in whom therapy does
not increase the platelet count.
Children who have ITP do well;
80% who present between the ages
of 2 and 10 years recover com-
pletely within 6 months. Treatment

66 Pediatrics in Review Vol. 20 No. 2 February 1999

Downloaded from http://pedsinreview.aappublications.org/ at University of Manitoba Libraries on April 24, 2015
is aimed primarily at preventing cat-
astrophic intracranial hemorrhage,
which occurs in fewer than 1% of
patients. Although a platelet count
of 20 x 109/L (20,000/mm3) has
been the traditional threshold for
treatment, it probably is best to base
therapy decisions on the clinical
manifestations of bleeding. Those
who have few or no petechiae and
minimal purpura may not require
treatment. Those who exhibit wide-
spread petechiae and purpura, and
especially mucosal bleeding, are at
greatest risk and always should be
treated. Intravenous gamma globulin
(IV IgG) and corticosteroids are
both effective; IV IgG is associated
with a slightly faster response but is
much more expensive, and intrave-
nous methylprednisolone may be as
effective. These treatments do not
alter the long-term course of the
disease; they are employed simply
to prevent dangerous bleeding until
improvement occurs spontaneously.
Platelet transfusions have no role in
the treatment of acute ITP unless the
patient is having a life-threatening
hemorrhage. The management of
chronic ITP, which is defined as
persisting for 6 months or more, is
more complex and beyond the scope
of this review.
Thrombocytopenia in the
Neonate
The evaluation of the neonate who
has thrombocytopenia requires the
consideration of several other factors
and diagnoses (Tables 4 and 5).
Thrombocytopenia is very common
in preterm or sick neonates; more
than one third of newborns in inten-
sive care nurseries have thrombocy-
topenia. As with older children,
thrombocytopenia in acutely ill neo-
nates is associated with high mor-
bidity and mortality. Critically ill
hypoxemic neonates frequently
develop isolated thrombocytopenia
or DIC. Bacterial sepsis always
should be considered in neonates
who have thrombocytopenia, which
necessitates appropriate cultures and
antibiotic therapy. Necrotizing
enterocolitis, polycythemia, and
thromboses also should be consid-
ered. Other neonates who are not
acutely ill may have anomalies asso-
ciated with thrombocytopenia, such
as Kasabach-Merritt syndrome
(hemangiomas and thrombocytope-
nia) or a trisomy. Because of the
higher risk of hemorrhage (espe-
cially intracranial), neonates who
have thrombocytopenia are treated at
comparatively higher platelet counts
than are older children. Maintaining
a platelet count of at least 30 x
109/L (30,000/mm3) during the first
48 hours of life is recommended.
The differential diagnosis for an
otherwise healthy neonate who has
isolated thrombocytopenia includes
neonatal alloimmune thrombocyto-
penia (NAIT), maternal ITP, mater-
nal lupus, or inherited causes. NAIT
accounts for 10% to 20% of cases
of neonatal thrombocytopenia. This
is of great concern because as many
as 10% to 25% of these infants have
intracranial hemorrhages, which
often occur prenatally. NAIT results
from the development of maternal
IgG antibodies directed against fetal
platelet antigens inherited from the
father. These antibodies cross the
placenta and destroy fetal platelets.
Mothers of these infants are well
and do not have thrombocytopenia.
First-born infants can be affected,
but the severity of disease tends to
increase in subsequent affected sib-
lings. Establishing a diagnosis is
critical to prevent or treat neonatal
hemorrhage. Affected neonates
should undergo ultrasonographic
examination to determine whether
an intracranial hemorrhage is
present. An otherwise healthy infant
who has a platelet count of less than
30 x 109/L (30,000/mm3) should be
presumed to have NAIT and be
evaluated and treated accordingly.
Random donor platelets generally
fail to increase the platelet count for
more than a few hours, but concen-
trated washed maternal platelets
(which are negative for the involved
platelet antigen) provide a dramatic
and more sustained rise in the neo-
natal platelet count. The infant also
should receive IV IgG, 1 g/kg per
day for up to 3 days; corticosteroids
are less effective and never should
be used as the sole treatment. The
thrombocytopenia is transient,
resolving in 3 weeks or less. The
diagnosis ultimately must be con-

TABLE 4. Differential Diagnosis of Thrombocytopenia in the Neonate

Acutely ill infant
● Sepsis ● Erythroblastosis fetalis
● Hypoxia ● Postexchange transfusion
● Disseminated intravascular coagulation ● Congenital leukemia or neuroblastoma
● Necrotizing enterocolitis ● Metabolic disorders (eg, methylmalonic aciduria)
● Thrombosis ● Heparin-induced thrombocytopenia
● Persistent pulmonary hypertension

Infants who have congenital malformations

● Congenital infections ● Thrombocytopenia-absent radii syndrome
● Trisomy 21, 13, or 18 ● Fanconi anemia
● Kasabach-Merritt syndrome

Well-appearing infant
● Neonatal alloimmune thrombocytopenia ● Polycythemia
● Maternal immune thrombocytopenic purpura or lupus ● Hereditary thrombocytopenias
● Congenital infections

Pediatrics in Review Vol. 20 No. 2 February 1999 67

Downloaded from http://pedsinreview.aappublications.org/ at University of Manitoba Libraries on April 24, 2015
 TABLE 5. Factors Associated with Neonatal Thrombocytopenia
FACTOR COMMENT
Maternal thrombocytopenia or Neonatal thrombocytopenia due to transplacental transfer of
lupus antiplatelet antibodies.
Obstetric complications Maternal pre-eclampsia/eclampsia, abruptio placentae, amniotic fluid
embolism, dead twin fetus.
Congenital malformations Fanconi anemia; thrombocytopenia-absent radii syndrome; trisomy
21, 18, or 13; Kasabach-Merritt syndrome.
Congenital or acquired infections Bacterial sepsis, congenital infections (cytomegalovirus, rubella,
toxoplasmosis, syphilis, herpes, human immunodeficiency virus).
Maternal drug ingestion Hydralazine, sulfonamides, quinidine.
Parental consanguinity Increased risk for inherited thrombocytopenia.
Family history of thrombocytopenia Increased risk for inherited disorders such as May-Hegglin. Sibling
or bleeding who had neonatal thrombocytopenia suggests neonatal alloimmune
thrombocytopenia, maternal immune thrombocytopenic purpura, or
maternal lupus.
Severe alloimmune hemolytic Can be associated with thrombocytopenia on presentation or
anemia (eg, Rh incompatibility) following exchange transfusion.

firmed by studying both parents to Consultation with a NAIT should be evaluated by a

demonstrate platelet antigen incom-
patibility and the presence of mater-
nal antibody against the father’s
platelets. The risk of antenatal intra-
cranial hemorrhage in future siblings
is as high as 25%; it is critical to be
aware of this risk to counsel the
parents about the management of
future pregnancies in an attempt to
prevent this devastating
complication.
Neonates of mothers who have
ITP or systemic lupus erythematosus
may develop thrombocytopenia
because of transplacental transfer of
the mother’s platelet autoantibody.
This autoantibody is active against
all platelets. Transfused platelets,
regardless of the donor source, are
destroyed. Only 10% to 15% of
these infants will have a platelet
count less than 50 x 109/L (50,000/
mm3), but it is impossible to predict
noninvasively which infants will be
affected. Fortunately, the risk of
life-threatening bleeding is much
less than that associated with NAIT.
IV IgG and corticosteroids are used
to manage more severe thrombocy-
topenia or symptomatic disease;
platelet transfusions are used for
life-threatening bleeding or very
severe thrombocytopenia.
Pediatric Hematologist/
Oncologist
The complex question of when to
undertake a consultation must be
individualized for each patient and
pediatrician. If the thrombocytopenia
is a manifestation of a systemic dis-
ease (eg, sepsis, shock, liver disease,
the mild-to-moderate thrombocyto-
penia seen so commonly in the criti-
cally ill neonate), consultation with a
pediatric hematologist often is not
necessary. Consultation may be help-
ful if the platelet count or bleeding
symptoms are not responding to con-
ventional management for the under-
lying problem. The pediatric hematol-
ogist provides not only an experienced
overview of diagnosis and manage-
ment, but also is best qualified to
evaluate the peripheral blood smear.
Consultation is particularly critical if
anemia, leukopenia, or both accom-
pany the thrombocytopenia.
The child in whom ITP is sus-
pected should be seen by a consultant
when the diagnosis is in question,
when bone marrow examination is
indicated, and when treatment is nec-
essary. All children who have chronic
ITP should be evaluated by a pediatric
hematologist/oncologist.
All neonates who possibly have
pediatric hematologist. The diagno-
sis and management of this serious
disorder are complex and evolving
rapidly. Accurate diagnosis and fam-
ily counseling are required because
of the high risk of prenatal compli-
cations in future siblings. Neonatal
thrombocytopenia resulting from
maternal ITP merits consultation
when the platelet count falls below
50 x 109/L (50,000/mm3) and the
risk of bleeding increases.
SUGGESTED READING
Beardsley DS. Platelet abnormalities in
infancy and childhood. In: Nathan DG,
Oski FA, eds. Hematology of Infancy and
Childhood. 4th ed. Philadelphia, Penn: WB
Saunders; 1993:1561–1504
Bussel JB, Corrigan JJ. Platelet and vascular
disorders. In: Miller DR, ed. Blood Dis-
eases in Infancy and Childhood. 7th ed.
St. Louis, Mo: CV Mosby; 1995:877–904
Hoffman R, Benz EJ Jr, Shattil SJ, Furie B,
Cohen HJ, Silberstein LE, eds. Hematol-
ogy: Basic Principles and Practice. 2nd
ed. New York, NY: Churchill Livingstone;
1995:1849 –1909
Homans A. Thrombocytopenia in the neonate.
Pediatr Clin North Am. 1996;43:737–756
Medeiros D, Buchanan GR. Current contro-
versies in the management of idiopathic
thrombocytopenic purpura during child-
hood. Pediatr Clin North Am. 1996;43:
757–772

68 Pediatrics in Review Vol. 20 No. 2 February 1999

Downloaded from http://pedsinreview.aappublications.org/ at University of Manitoba Libraries on April 24, 2015
 PIR QUIZ
Quiz also available online at
www.pedsinreview.org.
10. Of the following, the clinical mani-
festation most characteristic of
thrombocytopenia is:
A. Hemarthrosis.
B. Large solitary ecchymosis.
C. Muscle hematoma.
D. Retinal hemorrhages.
E. Scattered petechiae.
11. Of the following, the laboratory
finding most likely to be associated
with immune thrombocytopenia is:
A. Decreased megakaryocytes in the
bone marrow.
B. Fragmented red blood cells on a
peripheral smear.
C. Increased mean platelet volume.
D. Normocytic normochromic
anemia.
E. Prolonged prothrombin time.
Earning CME Credit–Completing the PIR Quiz
The American Academy of Pediatrics
(AAP) is accredited by the Accreditation
Council for Continuing Medical Educa-
tion (ACCME) to sponsor continuing
medical education for physicians. Pediat-
rics in Review (PIR) was planned and
produced in accordance with the
ACCME Essentials.
The AAP designates this activity for
up to 38 hours in Category 1 of the Phy-
sician’s Recognition Award of the Amer-
ican Medical Association (3 hours per
completed print issue of PIR and 2 hours
per completed compact disc issue of
PIR). Each physician should claim only
those hours of credit that he/she actually
spent in the educational activity.
PIR Quiz: A short quiz can be found
at the end of each article in PIR. You
may complete the quiz by recording your
answers on the PIR Quiz Card (bound
into the January issue) or by going
online at www.pedsinreview.org. Each
question has a single best answer. The
answers to the questions ap-
pear on the inside front cover of each
print issue and under the op- tions in the
online version.
1999 Credit Deadline: February 28,
2000. If you want to receive CME credit
in 1999, a completed PIR Quiz Card
must be received in the PREP Office by
February 28, 2000. Credit reply material
re-
ceived after February 28, 2000, will be
applied to the following year. Your
CME certificate will be mailed within 1
Pediatrics in Review Vol. 20 No. 1 January 1999
Downloaded from http://pedsinreview.aappublications.org/ at University of Manitoba Libraries on April 24, 2015
12. Neonatal alloimmune thrombocyto-
penia most likely is caused by:
A. Fetal platelet autoantibodies.
B. Intrauterine viral infection.
C. Maternal antibodies against fetal
platelet antigens inherited from
the father.
D. Maternal systemic lupus
erythematosus.
E. Transplacental transfer of platelet
antibodies from a mother who
has immune thrombocytopenia.
13. Which of the following causes of
neonatal thrombocytopenia carries
the greatest risk of intracranial
hemorrhage?
A. Congenital rubella.
B. Down syndrome.
C. Maternal immune thrombocyto-
penia.
D. Maternal systemic lupus
erythematosus.
E. Neonatal alloimmune
thrombocytopenia.
month after your credit reply material is
received. If you test online, all quizzes
must be completed by February 28,
2000.
Expiration of Credit: December 31,
2001. Credit for completing the 1999
PIR will be awarded for up to 2 years.
Credits will be posted to the year in
which they are submitted.
Verification of Credit will be mailed
by: April 30, 2000. You will receive a
complimentary transcript by April 30,
2000, contain-
ing a summary of CME credits earned in
1998 through AAP programs. If you
require a transcript at any other time of
the year, there will be a $25 processing
fee.
Mail form to: American Academy of
Pediatrics - PREP Office, 141 Northwest
Point Boulevard,
PO Box 927, Elk Grove Village, IL
60009-0927
PREP Education Award: The AAP
PREP Education Award re-
cognizes Academy Fellows who earn a
minimum of 150 AAP-approved CME
credits over 3 consecutive years. The
Award will automatically be mailed in
the
summer of 2000 to all individuals who
qualify. To qualify for the PREP Educa-
tion Award, an Academy Fellow must:
● Earn a minimum of 75 credit hours
through participation in PREP or
PREP The Course, and
● Earn the remaining credit hours (75
14. A 4-year-old child has had scattered
petechiae on the trunk and extremi-
ties for 2 days. Other findings on
physical examination are unremark-
able, and the child otherwise appears
well. Complete blood count reveals:
hemoglobin, 2.02 mmol/L (13 g/dL);
white blood cell count, 7.8 x 1012/L
(7,800/mm3) with a normal differen-
tial; and platelet count, 38 x 109/L
(38,000/mm3). The most appropriate
management is:
A. Intravenous administration of
gamma globulin.
B. Observation and follow-up with
head injury precautions.
C. Oral corticosteroid therapy.
D. Plasmapheresis.
E. Platelet transfusion.
hours) through other Academy-
sponsored or -approved CME activi-
ties, including AAP Spring Session or
Annual Meeting; AAP CME courses;
ACQIP; AAP-PT, Pediatric UPDATE
Audiocassette Program; or other AAP-
approved courses.
Other Organizations Granting
Credit: PIR has been approved for
credit as follows:
● American Academy of Pediatrics
(AAP); up to 38 hours of credit
toward the AAP PREP Education
Award
● American Osteopathic Associa-
tion (AOA); up to 12 hours, Cat-
egory 2-B
● National Association of Pediatric
Nurse Associates and Practitioners
(NAPNAP); up to 38 con-
tact hours
● Canadian Paediatric Society has
approved PREP as one method
for pediatricians to demonstrate main-
tenance of competence (MOCOMP)
● American Academy of Physician Assis-
tants accepts AMA Cate-
gory 1 credit for the PRA from organi-
zations accredited by the
ACCME.
● PREP has been reviewed and accepted
by the American Academy of Family
Physicians (AAFP) for up to 38 Pre-
scribed Hours. Term of approval
begins January 1999. Enduring materi-
als are approved for 1 year with the
option to request renewal.
69
 Consultation with the Specialist: Thrombocytopenia
Susan Murphy, Anne Nepo and Richard Sills
Pediatrics in Review 1999;20;64
DOI: 10.1542/pir.20-2-64

Updated Information &
Services
Subspecialty Collections
Permissions & Licensing
Reprints
including high resolution figures, can be found at:
http://pedsinreview.aappublications.org/content/20/2/64
This article, along with others on similar topics, appears in the
following collection(s):
Fetus/Newborn Infant
http://pedsinreview.aappublications.org/cgi/collection/fetus:newborn_
infant_sub
Hematology/Oncology
http://pedsinreview.aappublications.org/cgi/collection/hematology:on
cology_sub
Blood Disorders
http://pedsinreview.aappublications.org/cgi/collection/blood_disorder
s_sub
Information about reproducing this article in parts (figures, tables) or
in its entirety can be found online at:
http://pedsinreview.aappublications.org/site/misc/Permissions.xhtml
Information about ordering reprints can be found online:
http://pedsinreview.aappublications.org/site/misc/reprints.xhtml

Downloaded from http://pedsinreview.aappublications.org/ at University of Manitoba Libraries on April 24, 2015

 Consultation with the Specialist: Thrombocytopenia
Susan Murphy, Anne Nepo and Richard Sills
Pediatrics in Review 1999;20;64
DOI: 10.1542/pir.20-2-64

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://pedsinreview.aappublications.org/content/20/2/64

Pediatrics in Review is the official journal of the American Academy of Pediatrics. A monthly
publication, it has been published continuously since 1979. Pediatrics in Review is owned,
published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point
Boulevard, Elk Grove Village, Illinois, 60007. Copyright © 1999 by the American Academy of
Pediatrics. All rights reserved. Print ISSN: 0191-9601.

Downloaded from http://pedsinreview.aappublications.org/ at University of Manitoba Libraries on April 24, 2015