Rehabilitation Protocols for Children with Dysfunctional Voiding

Dysfunctional voiding is a functional voiding disorder characterized by an intermittent uroflow rate due to involuntary intermittent contractions of the striated muscle of the external urethral sphincter or pelvic floor muscles (PFMs) during voiding in neurologically normal children. Symptoms include voiding difficulties as well as urgency, voiding frequency and, in some instances, urinary incontinence and/or nocturnal enuresis. Recurrent urinary tract infections, chronic constipation and/or fecal incontinence and vesicoureteral reflux (VUR) contribute to this condition. Urotherapy is the mainstay of the treatment. It starts with education and demystification and simple behavioral modifications. Specific measures include PFM exercises with various forms of biofeedback concentrating at the recognition of PFM function and their relaxation. However, the PFMs are part of the abdominal capsule and they act in coordination with lower abdominal muscles. These muscles need to be relaxed during voiding. Diaphragmatic breathing exercises were introduced to teach children abdominal muscle relaxation. Easy to learn exercises do not require any specific equipment and can be performed at all health care levels. Children from five years of age could benefit from these exercises. In children resistant to standard treatment, botulinum toxin type A application, intermittent catheterization and surgery in children with VUR are recommended

Racial differences in systemic sclerosis disease presentation: a European Scleroderma Trials and Research group study

Objectives. Racial factors play a significant role in SSc. We evaluated differences in SSc presentations between white patients (WP), Asian patients (AP) and black patients (BP) and analysed the effects of geographical locations.Methods. SSc characteristics of patients from the EUSTAR cohort were cross-sectionally compared across racial groups using survival and multiple logistic regression analyses.Results. The study included 9162 WP, 341 AP and 181 BP. AP developed the first non-RP feature faster than WP but slower than BP. AP were less frequently anti-centromere (ACA; odds ratio (OR) = 0.4, P < 0.001) and more frequently anti-topoisomerase-I autoantibodies (ATA) positive (OR = 1.2, P = 0.068), while BP were less likely to be ACA and ATA positive than were WP [OR(ACA) = 0.3, P < 0.001; OR(ATA) = 0.5, P = 0.020]. AP had less often (OR = 0.7, P = 0.06) and BP more often (OR = 2.7, P < 0.001) diffuse skin involvement than had WP.AP and BP were more likely to have pulmonary hypertension [OR(AP) = 2.6, P < 0.001; OR(BP) = 2.7, P = 0.03 vs WP] and a reduced forced vital capacity [OR(AP) = 2.5, P < 0.001; OR(BP) = 2.4, P < 0.004] than were WP. AP more often had an impaired diffusing capacity of the lung than had BP and WP [OR(AP vs BP) = 1.9, P = 0.038; OR(AP vs WP) = 2.4, P < 0.001]. After RP onset, AP and BP had a higher hazard to die than had WP [hazard ratio (HR) (AP) = 1.6, P = 0.011; HR(BP) = 2.1, P < 0.001].Conclusion. Compared with WP, and mostly independent of geographical location, AP have a faster and earlier disease onset with high prevalences of ATA, pulmonary hypertension and forced vital capacity impairment and higher mortality. BP had the fastest disease onset, a high prevalence of diffuse skin involvement and nominally the highest mortality