Pediatric Clinics of North America - CIPERJ

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VENOUS THROMBOEMBOLISM IN CHILDREN 309 childhood), a flank mass that often is palpable on examination. RVT in older children often is associated with nephrotic syndrome (a risk factor for VTE in general) and, hence, may present with associated stigmata of peripheral and periorbital edema when diagnosed at presentation of nephrosis [11]. Thrombocytopenia may be a presenting manifestation not only of RVT but also of an intracardiac (eg, right atrial) thrombus, especially as in cases of CRT associated with sepsis and DIC. Portal vein thrombosis characteristically presents with splenomegaly and is associated with thrombocytopenia and, often, anemia; gastrointestinal bleeding at presentation typically signals the presence of gastroesophageal varices as a result of portal hypertension. Internal jugular vein thrombosis may manifest with neck pain or swelling and, in the Lemierre syndrome, also is associated classically with fever, trismus, and a palpable mass in the lateral triangle of the neck. Isolated intracardiac thrombosis in association with cardiac surgery or central venous catheter placement most often is asymptomatic. Chronic VTE may be diagnosed incidentally without signs or symptoms (as sometimes occurs for CSVT during unrelated brain imaging) or, alternatively, may present with signs and symptoms of chronic venous obstruction or post-thrombotic syndrome (PTS) secondary to central venous or extremity thrombosis, including limb pain and edema, dilated superficial collateral veins, venous stasis dermatitis, or frank ulceration of the skin. Diagnostic evaluation Radiologic imaging Historically, venography has been the gold standard for diagnosis of venous thrombosis but limited by its invasiveness. In recent years, this modality has experienced a diminishing role with the development of effective noninvasive or minimally invasive radiologic imaging techniques. Radiologic imaging is used not only to confirm the clinical diagnosis of VTE but also to define the extent and occlusiveness of thrombosis. For suspected DVT of the distal or proximal lower extremity, compression ultrasonography with Doppler imaging typically is used for objective confirmation. When the thrombus may affect or extend into deep pelvic or abdominal veins, CT or MRI often is required. In suspected DVT of the upper extremity, compression ultrasound with Doppler effectively evaluates the limb, but other modalities (eg, echocardiography, CT, and MRI) are needed to disclose involvement of more central vasculature (eg, right atrial thrombosis and SVC thrombosis). In the case of asymptomatic nonocclusive extremity DVT, conventional venography may be used as an alternative to CT or MRI. To establish a diagnosis of DVT of the jugular venous system (such as in suspected cases of the Lemierre syndrome) [12], compression ultrasound with Doppler imaging typically is used. PE in children commonly is disclosed by spiral CT or, alternatively, ventilation-perfusion scan, the latter generally is suboptimal in cases wherein
310 GOLDENBERG & BERNARD other lung pathology exists and at centers wherein availability of (and expertise with) this modality is limited. CSVT typically is diagnosed by standard CT or CT venography or, alternatively, MRI or MR venography. The diagnosis of RVT most often is made clinically in neonates and supported by Doppler ultrasound findings of intrarenal vascular resistive indices; however, in some cases a discrete thrombus may be suggested by Doppler ultrasound (especially when extending into the inferior vena cava [IVC]) or disclosed further via MR venography. When RVT occurs in older children, Doppler ultrasound or CT often is diagnostic. Similarly, portal vein thrombosis typically is visualized by Doppler ultrasound or CT. When new-onset venous thrombosis is evaluated in patients in areas of anatomic abnormality of the venous system (eg, extensive collateral venous circulation due to a prior VTE episode, May-Thurner anomaly, or atretic IVC with azygous continuation), more sensitive methods, such as CT venography or magnetic resonance (MR) venography, often are required to delineate the vascular anatomy adequately and the presence, extent, and occlusiveness of thrombosis. In some cases, conventional venography may be required. MR venography is more expensive than CT venography, typically requires sedation in children less than 8 years of age or those who are developmentally delayed or very anxious, and its feasibility during acute VTE evaluation may be limited by availability of MR-trained technologists. MR venography offers a significant advantage over CT venography, however, in that it provides diagnostic sensitivity at least as great as CT venography, without engendering the significant radiation exposure of the latter modality. Laboratory evaluation Diagnostic laboratory evaluation for pediatric acute VTE includes a complete blood count, comprehensive thrombophilia evaluation (discussed previously), and beta-hCG testing in postmenarchal women. Additional laboratory studies may be warranted depending on associated medical conditions and VTE involvement of specific organ systems. Table 2 summarizes a panel of thrombophilia traits and markers identified as risk factors for VTE in pediatric studies and recommended by the Scientific and Standardization Committee Subcommitee on Perinatal and Pediatric Haemostasis of the International Society on Thrombosis and Haemostasis for the diagnostic laboratory evaluation of acute VTE in children [13]. The panel is comprised of testing for states of anticoagulant (eg, protein C, protein S, and antithrombin) deficiency and procoagulant (eg, factor VIII) excess, mediators of hypercoagulablity or endothelial damage (eg, APAs, lipoprotein(a), and homocysteine), and markers of coagulation activation (eg, D-dimer). Treatment A summary of conventional antithrombotic agents and corresponding target anticoagulant levels, based on recent pediatric recommendations
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Page 6 and 7: DECISION ANALYSIS IN PEDIATRIC HEMA
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Table 1 Clotting factor concentrate
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Table 1 (continued ) Factor VIII (o
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364 RODRIGUEZ & HOOTS was administe
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366 RODRIGUEZ & HOOTS Antifibrinoly
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368 RODRIGUEZ & HOOTS infections an
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370 RODRIGUEZ & HOOTS Fig. 3. Schem
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372 RODRIGUEZ & HOOTS protein is no
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374 RODRIGUEZ & HOOTS [2] Berntorp
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376 RODRIGUEZ & HOOTS [42] Carcao M
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378 ROBERTSON et al von Willebrand
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380 ROBERTSON et al Fig. 2. A propo
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382 ROBERTSON et al a heterogenous
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384 ROBERTSON et al of considering
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386 ROBERTSON et al Type 2M Type 2M
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388 ROBERTSON et al Desmopressin is
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390 ROBERTSON et al References [1]
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392 ROBERTSON et al [46] Nesbitt IM
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394 BLANCHETTE & BOLTON-MAGGS A key
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396 BLANCHETTE & BOLTON-MAGGS recep
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398 BLANCHETTE & BOLTON-MAGGS and p
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400 BLANCHETTE & BOLTON-MAGGS Fig.
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402 BLANCHETTE & BOLTON-MAGGS in di
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404 BLANCHETTE & BOLTON-MAGGS the s
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408 BLANCHETTE & BOLTON-MAGGS as a
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410 BLANCHETTE & BOLTON-MAGGS splen
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412 BLANCHETTE & BOLTON-MAGGS with
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414 BLANCHETTE & BOLTON-MAGGS react
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416 BLANCHETTE & BOLTON-MAGGS [16]
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422 FASANO & LUBAN of storage and t
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424 FASANO & LUBAN Leukocyte reduct
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426 FASANO & LUBAN RBCs is decrease
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Table 1 Blood component characteris
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430 FASANO & LUBAN Alloimmunization
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432 FASANO & LUBAN of individual un
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434 FASANO & LUBAN patients have an
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436 FASANO & LUBAN adults; therefor
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438 FASANO & LUBAN [21]. Meta-analy
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440 FASANO & LUBAN Pretransfusion m
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442 FASANO & LUBAN [55,56]. This is
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444 FASANO & LUBAN [20] Roseff SD,
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Pediatr Clin N Am 55 (2008) 447-460
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THALASSEMIA UPDATE 449 hypochromia
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THALASSEMIA UPDATE 451 Fig. 1. Chan
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THALASSEMIA UPDATE 453 delivery of
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THALASSEMIA UPDATE 455 thromboses i
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THALASSEMIA UPDATE 457 On the basis
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THALASSEMIA UPDATE 459 [31] Kan YW,
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ORAL IRON CHELATORS 463 large iron-
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ORAL IRON CHELATORS 465 of 50 child
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ORAL IRON CHELATORS 467 Table 2 Com
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ORAL IRON CHELATORS 469 use in Nort
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ORAL IRON CHELATORS 471 needed to d
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ORAL IRON CHELATORS 473 in liver fi
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ORAL IRON CHELATORS 475 in the lowe
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ORAL IRON CHELATORS 477 Other oral
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ORAL IRON CHELATORS 479 [12] Borgna
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ORAL IRON CHELATORS 481 [55] Wonke
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HYDROXYUREA FOR CHILDREN WITH SICKL
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Fig. 1. Guideline for initiating, m
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504 TRACY & RICE congenital spheroc
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506 TRACY & RICE and antibodies aga
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508 TRACY & RICE limited splenic vo
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510 TRACY & RICE constitutes the pi
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512 TRACY & RICE German experience
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514 TRACY & RICE Table 1 Effect of
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516 TRACY & RICE decreased bilirubi
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518 TRACY & RICE [13] Bader-Meunier
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