Abstract:Pulmonary oedema due to transient myocardial dysfunction can be a rare cause in the differential diagnosis of respiratory distress of the newborn. Myocardial impairment after probable hypoxia can be present without concomitant encephalopathy.
BackgroundTo provide recommendations for the care of infants with stage 5 chronic kidney disease (CKD5).SettingEuropean Paediatric Dialysis Working Group.Data SourcesLiterature on clinical studies involving infants with CKD5 (end stage renal failure) and consensus discussions within the group.RecommendationsThere has been an important change in attitudes towards offering RRT (renal replacement therapy) to both newborns and infants as data have accumulated on their improved survival and long-term outcomes. The management of this challenging group of patients differs in a number of ways from that of older children. The authors have summarised the basic recommendations for treating infants with CKD5 in order to support the multidisciplinary teams who endeavour on this difficult task.
BackgroundTo provide recommendations for the care of infants with stage 5 chronic kidney disease (CKD5).SettingEuropean Paediatric Dialysis Working Group.Data SourcesLiterature on clinical studies involving infants with CKD5 (end stage renal failure) and consensus discussions within the group.RecommendationsThere has been an important change in attitudes towards offering RRT (renal replacement therapy) to both newborns and infants as data have accumulated on their improved survival and long-term outcomes. The management of this challenging group of patients differs in a number of ways from that of older children. The authors have summarised the basic recommendations for treating infants with CKD5 in order to support the multidisciplinary teams who endeavour on this difficult task.
“…However, the pathogenesis of TTN is largely unknown. Mild degree of pulmonary immaturity (3), slight and transient surfactant deficiency (4) or myocardial left‐heart failure due to asphyxia, resulting in pulmonal interstitial edema (5) are discussed to be underlying pathophysiological factors in the etiology of TTN. Surfactant‐associated protein B (SP‐B) was demonstrated to be an important component of the pulmonal surfactant system for the immediate postnatal pulmonary adaptation (6).…”
“…A further hypothesis is TTN to result from a slight and transient surfactant deficiency in affected infants [20]. Myocardial leftheart failure due to asphyxia resulting in pulmonanary interstitial edema is discussed as pathological mechanism in the cause of TTN [22].…”
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