Thirty-day readmissions in children with complex chronic conditions.

INTRODUCTION: The rate of hospital readmission within 30 days of discharge is a quality indicator in health care. Paediatric patients with complex chronic conditions have high readmission rates. Failure in the transition between hospital and home care could explain this phenomenon. OBJECTIVES: To estimate the incidence rate of 30-day hospital readmission in paediatric patients with complex chronic conditions, estimate how many are potentially preventable and explore factors associated with readmission. MATERIALS AND METHOD: Cohort study including hospitalised patients with complex chronic conditions aged 1 month to 18 years. Patients with cancer or with congenital heart disease requiring surgical correction were excluded. The outcomes assessed were 30-day readmission rate and potentially preventable readmissions. We analysed sociodemographic, geographic, clinical and transition to home care characteristics as factors potentially associated with readmission. RESULTS: The study included 171 hospitalizations, and 28 patients were readmitted within 30 days (16.4%; 95% CI, 11.6%-22.7%). Of the 28 readmissions, 23 were potentially preventable (82.1%; 95% CI, 64.4%-92.1%). Respiratory disease was associated with a higher probability of readmission. There was no association between 30-day readmission and the characteristics of the transition to home care. CONCLUSIONS: The 30-day readmission rate in patients with complex chronic disease was 16.4%, and 82.1% of readmissions were potentially preventable. Respiratory disease was the only identified risk factor for 30-day readmission.

Hypothermia prevents gliosis and angiogenesis development in an experimental model of ischemic proliferative retinopathy.

PURPOSE: To develop a time course study of vascularization and glial response to perinatal asphyxia in hypoxic-ischemic animals, and to evaluate hypothermia as possible protective treatment. METHODS: We used retinas of 7-, 15-, 21-, and 30-day-old male Sprague-Dawley rats that were exposed to perinatal asphyxia at either 37°C (PA) or 15°C (HYP). Born to term animals were used as controls (CTL). We evaluated the thickness of the most inner layers of the retina (IR), including internal limiting membrane, the retinal nerve fiber layer, and the ganglion cell layer; and studied glial development, neovascularization, adrenomedullin (AM), and VEGF by immunohistochemistry, immunofluorescence, and Western blot. RESULTS: A significant increment in IR thickness was observed in the PA group from postnatal day (PND) 15 on. This alteration was concordant with an increased number of new vessels and increased GFAP expression. The immunolocalization of GFAP in the internal limiting membrane and perivascular glia of the IR and in the inner processes of Müller cells was coexpressed with AM, which was also significantly increased from PND7 in PA animals. In addition, VEGF expression was immunolocalized in cells of the ganglion cell layer of the IR and this expression significantly increased in the PA group from PND15 on. The retinas of the HYP group did not show differences when compared with CTL at any age. CONCLUSIONS: This work demonstrates that aberrant angiogenesis and exacerbated gliosis seem to be responsible for the increased thickness of the inner retina as a consequence of perinatal asphyxia, and that hypothermia is able to prevent these alterations.

Hypothermia prevents nitric oxide system changes in retina induced by severe perinatal asphyxia.

One-third of asphyctic neonates develop long-term neurological injuries, including several degrees of ischemic proliferative retinopathy (IPR) such as retinopathy of prematurity (ROP). Given that the retina is altered by perinatal asphyxia, our aim was to study the effects of nitric oxide (NO) in the retina in order to analyze its impact on the retinal injury. Application of hypothermia was evaluated as preventive treatment. Sprague-Dawley rats were subjected to perinatal asphyxia [either at 37°C (PA group) or at 15°C (HYP group)]. Full-term rats were used as controls (CTL). A significantly increased activity of both constitutive NO synthase (nNOS, Ca(2+)-dependent) and inducible NO synthase (iNOS, Ca(2+)-independent) was observed in PA retinas from 21 days old up to 60 days old with respect to age-matched CTL, with a significant increase along the time course in the PA. nNOS was immunolocalized at amacrine, horizontal, and ganglion cells of the PA group, with a significant increase in relative optical density (R.O.D.), cellular area, and number of cells. iNOS immunoreactivity was observed in the inner nuclear layer and in the internal Müller cell processes of PA, with a significant increase in R.O.D. and colocalizing with GFAP in the 60-day-old PA group. Six nitrated protein species were increased in retinas from PA rats. Nitrotyrosine immunoreactivity showed a localization similar to that of iNOS, with increased R.O.D. in the PA group and colocalization with GFAP in 60-day-old animals. HYP prevented all the changes observed in PA rats. Although the NO system displays changes induced by hypoxia-ischemia, hypothermia application shows a strong protective effect.

Hypothermia prevents the development of ischemic proliferative retinopathy induced by severe perinatal asphyxia.

Obstetric complications, such as perinatal asphyxia, may cause retinal injuries as retinopathy of prematurity (ROP), a type of ischemic proliferative retinopathy. Up to date there are no appropriate experimental models for studying the long-term sequels of this disease. In the present work, we present an experimental model of perinatal asphyxia which shows structural and ultrastructural retinal alterations at the most inner layers of the retina, such as neurodegeneration, development of neoformed vessels and glial reaction, which are compatible with the histopathological description of ROP. Besides, the application of hypothermia during perinatal asphyxia showed effective results preventing cellular and morphological alterations. This study may contribute to the development of therapies in order to either ameliorate or prevent retinal damage. In this manner, hypothermia may improve life quality and decrease medical, family and social costs of these avoidable causes of blindness.