Pediatric emergency medicine trisk 558

drugs that interfere with platelet function such as aspirin and NSAIDs, as well as
activities that increase the risk of head injury.
TABLE 93.8
BUCHANAN AND ADIX BLEEDING SEVERITY FOR CHILDREN WITH ITP
Overall bleeding severity
Score

Description

0

None

Definitely no new hemorrhage of any kind

1

Minor

Few petechiae (≤100 total) and/or ≤5 small bruises (≤3 cm
diameter)

2

Mild

Many petechiae (>100 total) and/or >5 large bruises (>3 cm
diameter); no/minimal mucosal bleeding

3

Moderate

4

5

Overt mucosal bleeding (epistaxis, gum bleeding,
oropharyngeal blood blisters, menorrhagia,
gastrointestinal bleeding, etc.) that does not require
immediate medical attention or intervention
Severe
Mucosal bleeding or suspected internal hemorrhage (in the
brain, lung, muscle, joint, etc.) that requires immediate
medical attention or intervention
Life threatening Documented intracranial hemorrhage or life-threatening or
fatal hemorrhage in any site

Reproduced with permission from Buchanan GR, Adix L. Grading of hemorrhage in children with idiopathic
thrombocytopenic purpura. J Pediatr 2002;141:683–688.

Adjuvant therapies to control bleeding for the patient with ITP, as outlined in Table
93.2 , may be of use until specific ITP treatments are effective. Nasal packing and
topical phenylephrine are useful for persistent epistaxis. Excessive menstrual bleeding
may require hormonal therapy. Antifibrinolytics may be useful in decreasing
mucocutaneous bleeding. Intractable symptoms warrant hematology consultation for
consideration of second-line or extraordinary measures.
Management of Head Trauma
Intracranial hemorrhage in the setting of ITP is rare, but it is also the major cause of
mortality in ITP and therefore requires immediate recognition and intervention. Figure
93.4 provides an algorithm for managing head trauma in the setting of ITP. No

universally accepted guideline for the evaluation and management of head trauma in
ITP patients exists. Carefully consider each case and manage in conjunction with
hematology.


Clinical Indications for Discharge or Admission
Many patients with ITP can be managed on an outpatient basis. Consider age,
developmental level, parental comfort, and distance from the hospital when identifying
patients who are safe for discharge with close outpatient follow-up.
TABLE 93.9
TREATMENT REGIMENS FOR ACUTE ITP
Treatment
Corticosteroids IVIG

Rho (D) immune globulin
(WinRho)

Treatment
regimen

Prednisone or
1 g/kg IV × 1–2 doses
prednisolone
2 mg/kg BID ×
5 days OR
2 mg/kg/day ×
10 days
Max dose: 40
mg BID

50 mcg/kg IV initial dose,
subsequent doses based
on response and
hemoglobin level

Benefits

• Enteral
• Outpatient
therapy
• Inexpensive
• Emotional
instability
• Hyperphagia
• Hyperactivity
• If diagnosis
incorrect,
potential to
partially treat
ALL

• Fastest rise of platelet
count
• Steroid sparing

• Short infusion time
• Steroid sparing

• Hypersensitivity
reaction

• Severe headache
• Aseptic meningitis
• Fever/chills
• Immune mediated
• Hemolysis
• Long infusion time
• Expensive

• Only for Rh+ patients
• Black box warning: lifethreatening
acute/subacute immunemediated intravascular
hemolysis
• Fever/chills

Risks/side
effects


FIGURE 93.4 ITP with head trauma or concern for CNS bleed.

OTHER DISORDERS ASSOCIATED WITH THROMBOCYTOPENIA
Neonatal Thrombocytopenia
Thrombocytopenia can arise in neonates from a number of different etiologies: immune
mediated, perinatal asphyxia, inherited thrombocytopenias, drug/medication toxicity,
and infection. Careful assessment of the clinical status of the neonate as well as the
timing of the thrombocytopenia can help narrow the differential diagnosis. The two
most common immune-mediated causes are neonatal alloimmune thrombocytopenia
(NAIT) and autoimmune neonatal thrombocytopenia.
NAIT can emerge in an otherwise healthy neonate and can lead to significant
morbidity and mortality if unrecognized. NAIT develops when a fetus expresses a

paternally inherited antigen on its platelets that the mother does not. Maternal exposure
to these fetal platelets generates an IgG antibody that can cross the placenta and cause
destruction of fetal platelets and megakaryocytes. This can occur with a first pregnancy
and often more severely with subsequent pregnancies. When recognized, it is an
indication for future high-risk obstetrical care. Severe thrombocytopenia leads to
increased risk of intracranial hemorrhage. Maintaining the platelet count greater than
30,000/μL during the first week of life and greater than 20,000/μL subsequently is
appropriate in nonbleeding infants. Greater than 50,000/μL is the goal in the setting of
bleeding. Random donor platelet transfusion may be ineffective if those platelets carry


the offending antigen, so monitor platelet counts after transfusion. If available, platelet
products negative for the causative antigen or maternal platelets may be more effective.
IVIG administration may also help to boost the platelet count. Consider corticosteroids
for neonates who are refractory to therapy with bleeding symptoms.
Autoimmune neonatal thrombocytopenia can occur in infants whose mothers have
primary ITP or ITP secondary to an autoimmune condition such as SLE. This condition
tends to result in less severe thrombocytopenia compared to NAIT. Fortunately,
significant bleeding episodes such as intracranial hemorrhage are rare. Monitor the
platelet count and provide therapy for neonates with platelet counts less than 30 to 50 ×
103/μL. Survival of donor platelets (platelet transfusion) is significantly shortened due
to the presence of antibody. Treatment with IVIG improves the platelet count in most
patients. Both NAIT and maternal autoantibody–mediated neonatal thrombocytopenia
are self-limited as the maternal IgG antibody wanes over the course of weeks to months.

Heparin-Induced Thrombocytopenia
Children treated with heparin are at risk for developing heparin-induced
thrombocytopenia (HIT). The incidence has increased over recent years likely due to
increased recognition of this entity in pediatric patients. In the right clinical context, HIT
is an important diagnosis to consider because it is associated with an increased risk of

thrombosis and can threaten life and limb if undiagnosed. The degree of
thrombocytopenia, timing of the fall in platelet count relative to heparin exposure,
presence of thrombosis, and other potential causes of thrombocytopenia are all
important considerations when risk stratifying for the likelihood of HIT. Table 93.10
presents a scheme for estimating a patient’s pretest probability of HIT.