Pediatric Clinics of North America - CIPERJ

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PEDIATRIC ARTERIAL ISCHEMIC STROKE 329 tend to have multiple deficits and alteration of consciousness. As discussed previously, a history of head or neck trauma, recent varicella infection, and the presence of sickle cell disease or cardiac disease may aid in understanding the underlying etiology. A recent single-center retrospective series of AIS in non-neonatal children found that a nonabrupt pattern of neurologic symptoms or signs (including those in whom the maximum severity of symptoms or signs developed more than 30 minutes from the time of symptom onset, the presentation of symptoms or signs was waxing and waning, or the presentation was preceded by recurrent transient symptoms or signs with intercurrent resolution) often was associated with findings of arteriopathy on diagnostic neuroimaging [40]. Strokes of metabolic etiology frequently manifest a progressive course of stroke-like episodes. Often, there is a family history of early-onset strokes, early-onset dementia, or severe migraines. A classic example of a metabolic stroke occurs in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). MELAS is caused by mitochondrial DNA defects encoding tRNA involved in the generation of ATP and the majority of cases (80%) have the mt3243 mutation [41]. In addition to a maternal history of migraine and stroke, there often is a history of short stature, diabetes, hearing loss, occipital lobe seizures, and optic atrophy [41]. The presentation often is characterized by stroke-like episodes with complete resolution of neurologic function. Over time, however, neurologic deficits persist, often in the form of hemianopia [42]. Acute lesions observed by MRI can be distinguished from typical AIS by virtue of their paradoxic bright appearance on apparent diffusion coefficient (ADC) maps. In cases of a family history of cryptogenic stroke or atypical presentation of stroke, other inherited disorders (eg, non-MELAS mitochondrial DNA defects, organic acidemias, lysosomal diseases, severe congenital thrombophilias, and cerebral autosomal dominant arteriopathy with subcortical infarctions and leukoencephalopathy [CADASIL]), should be considered [41]. Diagnostic evaluation Diagnostic evaluation of pediatric AIS is more extensive than in adult stroke because of the broad differential diagnosis at presentation and the higher incidence of ateriopathies in childhood AIS. In a child presenting with an acute focal neurologic deficit, multiple alternative etiologies must be considered, including hypoglycemia, prolonged focal seizures, prolonged postictal paresis (Todd’s paralysis), acute disseminated encephalomyelitis, meningitis, encephalitis, and brain abscess [43]. For this reason, MRI brain with diffusion-weighted images is becoming the radiographic modality of choice in most cases of childhood AIS. Acutely, CT can rule out hemorrhage, tumor, and abscess and may be an appropriate first-line evaluation in some cases. Typically, this needs to be followed by an MRI with
330 BERNARD & GOLDENBERG diffusion-weighted images to assess for cytotoxic edema, the hallmark of acute ischemia (see Fig. 1). The use of perfusion-weighted imaging largely is experimental in children [44] but as acute interventions become more available in childhood AIS, this modality likely will be used increasingly as a means by which to identify potentially preservable territories of atrisk functioning brain. Furthermore, the pattern of infarction also may be suggestive of etiology. For example, a case of multiple infarctions in separate arterial distributions likely is thromboembolic, findings of occipital and parietal strokes that cross vascular territories may suggest MELAS, a distribution between vascular territories is consistent with watershed infarction suggestive of a hypotensive etiology, and a pattern of small multifocal lesions at the gray-white junction is suspicious for vasculitis. Although routine CT and MRI evaluate for ischemia, hemorrhage, mass/ mass effect, and other non-AIS pathologies, vascular imaging (magnetic resonance angiography [MRA], CT angiography [CTA], or conventional angiography) can demonstrate arteriopathy, including dissection, stenosis, irregular contour, or intra-arterial thrombosis of the head and neck. Typically, MRA or CTA is the modality used as first-line arterial imaging, unless MRI reveals a pattern consistent with small vessel vasculitis, in which case conventional angiography is indicated. If MRA or CTA suggests moyamoya or atypical vasculature, conventional angiography is warranted, as MRA or CTA may underestimate or overestimate the degree of disease [45]. An additional important component of diagnostic imaging in pediatric AIS is echocardiography with peripheral venous saline injection. In addition to disclosing a septal defect and other congenital cardiac anomalies, echocardiography with saline injection may disclose a small lesion, including a PFO that otherwise may not be detected by conventional transthoracic echocardiography. The prevalence of PFO in patients who have cryptogenic stroke is 40% to 50% compared with 10% to 27% in the general population [9,10]. The use of Doppler imaging during echocardiography assists in determining the direction of shunt through a lesion, although the prognostic significance of the direction of shunt is not well established in pediatric stroke. At a minimum, diagnostic laboratory evaluation in pediatric acute AIS involves a complete blood count, toxicology screen, complete metabolic panel, erythrocyte sedimentation rate/C-reactive protein (ESR/CRP) to assess for biochemical evidence of systemic inflammation that may suggest vasculitis or infection in the etiology of AIS, b-hCG testing in postmenarchal women, fasting lipid profile, and a comprehensive thrombophilia panel (Box 1). Further investigation into metabolic, genetic, infectious, or rheumatologic diseases should be considered in cases of atypical presentation. In the setting of arteritis, arthritis, or elevated ESR/CRP, rheumatologic evaluation should be considered and include testing of antinuclear antibodies and rheumatoid factor. In childhood AIS with encephalopathy of unclear etiology, nonarterial distribution, or other multisystem disorders of unclear etiology (eg, hearing loss, myopathy, or endocrinopathy), testing should
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Page 6 and 7: DECISION ANALYSIS IN PEDIATRIC HEMA
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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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406 BLANCHETTE & BOLTON-MAGGS findi
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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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