Pediatric Clinics of North America - CIPERJ

316 GOLDENBERG & BERNARD
significant antithrombin deficiency prevents the achievement of therapeutic
anti-Xa levels (ie, heparin ‘‘resistance’’). This may be the case in nephrotic
syndrome–associated VTE. Additionally, neonates who have clinical conditions
complicated by antithrombin consumption in particular are predisposed
to such heparin ‘‘resistance’’ because of a physiologic relative
deficiency of this key intrinsic thrombin inhibitor.
The use of vena caval filters should be considered in children of appropriate
size in whom recurrent VTE (especially PE) occurrs on therapeutic anticoagulation
in the presence of a persistent prothrombotic risk factor. In
addition, temporary vena caval filters may be considered during times of especially
heightened risk for PE. With regard to long-standing vena caval filters,
although a case series has suggested that these devices are effective
when used with concomitant therapeutic anticoagluation for primary and
secondary prevention of PE in teens [37], the impact of such nonretrievable
devices on the vena cava of developing children is not well studied, and experience
with surgical removal of permanent vena caval filters is limited.
Consequently, the use of nonretrievable vena caval filters in pediatrics
should be undertaken with great caution.
Outcomes
Complications of VTEs can occur acutely and over the long term. Shortterm
adverse outcomes include major hemorrhagic complications of
antithrombotic interventions and of the thrombotic event itself (eg, postthrombotic
hemorrhage in the brain, testis, or adrenal gland); early recurrent
VTE (including DVT and PE); SVC syndrome in DVT of the upper
venous system; acute renal insufficiency in RVT; catheter-related sepsis,
PE, and catheter malfunction (sometimes necessitating surgical replacement)
in CRT; severe acute venous insufficiency leading to venous infarction
with limb gangrene in rare cases of occlusive DVT involving the extremities;
and death from hemodynamic instability in extensive intracardiac thrombosis
or proximal PE. Given the long-term risks for recurrence, disease
sequelae, and functional impairment, however, VTE arguably is best considered
a chronic disorder in children. Long-term adverse outcomes in pediatric
VTE recently have been reviewed [38] and include recurrent VTE; chronic
hypertension and renal insufficiency in RVT; variceal hemorrhage in portal
vein thrombosis; chronic SVC syndrome in CRT involving SVC occlusion;
loss of availability for venous access in recurrent or extensive CRT of the
upper venous system; and development of the PTS, a condition of chronic
venous insufficiency after DVT. The manifestations of PTS may include
edema, visibly dilated superficial collateral veins (Fig. 2A), venous stasis dermatitis
(see Fig. 2B), and (in the most severe cases) venous stasis ulcers.
Registry [1,4,39] and cohort study [5] data in pediatric VTE of all types
indicate that children seem to have a lower risk for recurrent thrombembolism
than adults (cumulative incidences at 1 to 2 years of 6% to 11% versus