Outbreak of adenovirus D8 in a neonatal intensive care unit involving multiple simultaneous transmission pathways.

BACKGROUND: Adenovirus (ADV) outbreaks in neonatal intensive care units (NICU) can lead to durable transmission and serious adverse outcomes. This study describes the investigation and control of an ADV-D8 outbreak in an NICU, associated with ophthalmologic equipment used during retinopathy of prematurity (ROP) screening. Cases were observed in neonates, parents and nurses. METHODS: The outbreak investigation was performed including sampling patients, parents and health care workers as well as the environment for molecular detection of ADV DNA. The investigation was also conducted in the guest house where some parents were temporary residents. A retrospective cohort study focused on neonates hospitalized during the epidemic period to assess the risk associated with ROP examination. RESULTS: Fifteen cases were identified in neonates; all but one presented with conjunctivitis. Two healthcare workers and 18 parents acquired conjunctivitis. ADV DNA was identified on the RetCam and on the freezer shared by parents. All ADV-positive samples were typed as ADV-D8. ADV infections occurred more frequently in neonates who had ROP examinations (37.8% (14/37) vs (0.9% (1/110); P<0.001) (relative risk 41.6; (5.7-305.8)). The RetCam was disinfected between two examinations using a disinfectant that was virucidal on ADV after a 30-min contact. CONCLUSION: This outbreak was significantly associated with ROP examination with a RetCam that had a disinfection protocol ill-adapted to rapid patient turnover. In addition, nosocomial transmission via the parents to neonates and parent-to-parent transmission is likely to have played a role in the dissemination of cases. No further cases were observed after the new disinfection procedure was enforced.

Review shows that using surfactant a number of times or as a vehicle for budesonide may reduce the risk of bronchopulmonary dysplasia.

AIM: Bronchopulmonary dysplasia (BPD) remains the most common respiratory morbidity in immature infants. This review describes the diagnosis of BPD has evolved and summarises the therapeutic approaches that have made it possible to limit the incidence of BPD. METHOD: We reviewed the literature from the first definition of BPD by Northway in 1967 to the surfactant treatment policies that are currently in use, drawing on more than 50 papers up to 2017. RESULTS: Our review showed that improvements in neonatal survival have been associated with an increased risk of severe BPD, significant levels of long-term morbidity and the increased use of healthcare resources. These issues have encouraged researchers to explore potential new treatments that limit the incidence of BPD. Repeated surfactant instillation and the use of surfactant as a vehicle for budesonide are promising strategies for alleviating the burden of chronic lung disease. Ongoing research on surfactant or stem cell therapy may further improve the respiratory prognosis for prematurely born children. CONCLUSION: Considerable research has been carried out into the increase in BPD, which has resulted from improvements in neonatal survival. Key areas of research include repeated surfactant administration, using surfactant as a vehicle for budesonide and stem cell therapy.

[Oxidative stress after preterm birth: origins, biomarkers, and possible therapeutic approaches]. / Stress oxydant chez l'enfant prématuré : causes, biomarqueurs et possibilités thérapeutiques.

The survival of preterm babies has increased over the last few decades. However, disorders associated with preterm birth, known as oxygen radical diseases of neonatology, such as retinopathy, bronchopulmonary dysplasia, periventricular leukomalacia, and necrotizing enterocolitis are severe complications related to oxidative stress, which can be defined by an imbalance between oxidative reactive species production and antioxidant defenses. Oxidative stress causes lipid, protein, and DNA damage. Preterm infants have decreased antioxidant defenses in response to oxidative challenges, because the physiologic increase of antioxidant capacity occurs at the end of gestation in preparation for the transition to extrauterine life. Therefore, preterm infants are more sensitive to neonatal oxidative stress, notably when supplemental oxygen is being delivered. Furthermore, despite recent advances in the management of neonatal respiratory distress syndrome, controversies persist concerning the oxygenation saturation targets that should be used in caring for preterm babies. Identification of adequate biomarkers of oxidative stress in preterm infants such as 8-iso-prostaglandin F2α, and adduction of malondialdehyde to hemoglobin is important to promote specific therapeutic approaches. At present, no therapeutic strategy has been validated as prevention or treatment against oxidative stress. Breastfeeding should be considered as the main measure to improve the antioxidant status of preterm infants. In the last few years, melatonin has emerged as a protective molecule against oxidative stress, with antioxidant and free-radical scavenger roles, in experimental and preliminary human studies, giving hope that it can be used in preterm infants in the near future.

Developmental origins of chronic renal disease: an integrative hypothesis.

Cardiovascular diseases are one of the leading causes of mortality. Hypertension (HT) is one of the principal risk factors associated with death. Chronic kidney disease (CKD), which is probably underestimated, increases the risk and the severity of adverse cardiovascular events. It is now recognized that low birth weight is a risk factor for these diseases, and this relationship is amplified by a rapid catch-up growth or overfeeding during infancy or childhood. The pathophysiological and molecular mechanisms involved in the "early programming" of CKD are multiple and partially understood. It has been proposed that the developmental programming of arterial hypertension and chronic kidney disease is related to a reduced nephron endowment. However, this mechanism is still discussed. This review discusses the complex relationship between birth weight and nephron endowment and how early growth and nutrition influence long term HT and CKD. We hypothesize that fetal environment reduces moderately the nephron number which appears insufficient by itself to induce long term diseases. Reduced nephron number constitutes a "factor of vulnerability" when additional factors, in particular a rapid postnatal growth or overfeeding, promote the early onset of diseases through a complex combination of various pathophysiological pathways.

The neonatal kidney: implications for drug metabolism and elimination.

The kidney is a major organ for drug elimination. The function of the neonatal kidney is markedly immature with a reduction of renal blood flow, of glomerular filtration and of active tubular secretion, even in healthy, term infants. Maturation of renal function in particular of glomerular filtration rate is gestational age and postnatal age-dependant. Moreover, many neonatal pathological conditions such as preterm birth, sepsis or perinatal asphyxia can also affect renal function. These developmental changes have a major impact on drug metabolism and elimination. Alterations in renal clearance can influence significantly both drugs efficacy and toxicity. Moreover, nephrogenesis is a still ongoing process in a number of premature infants before 36 wks postconceptional age. Drugs and toxic factors that may alter the constitution of the congenital nephron number endowment during this period may have long term consequences on arterial pressure and renal function at adulthood.

[Restrictive cardiomyopathy due to myofibrillar myopathy]. / Une cardiomyopathie restrictive révélatrice d'une myopathie myofibrillaire.

UNLABELLED: Early and severe cardiomyopathy may be related to myofibrillar myopathy. CASE REPORT: We report a one-year-old child with early and severe restrictive cardiomyopathy. The diagnosis of myofibrillar myopathy was obtained on skeletal muscle and endomyocardial biopsies. The patient died despite inotropic support and mechanical ventilation. CONCLUSION: Myofibrillar myopathy must be considered when exploring the etiology of a restrictive cardiomyopathy in children. The diagnosis relies on examination of endomyocardial or skeletal muscle biopsy samples.

[Outcome of infants with hypoplastic left heart syndrome diagnosed in utero]. / Devenir des enfants atteints d'une hypoplasie du coeur gauche diagnostiquée in utero.

The authors report the results of prenatal diagnosis of the hypoplastic left heart syndrome since 1998 in the University Hospitals of Marseille and Montpellier. Twenty-four prenatal diagnoses of this condition were made in mothers with a mean age of 29 (18 to 40 years) and after a mean term of 22 (18.5 to 33) weeks of amenorrhea. Seventeen therapeutic abortions were carried out and 7 neonates born after a mean term of 39 (28 to 40) weeks, were admitted to the paediatric intensive care unit. Two patients required ventilatory assistance with one early death. The other patients were stable after surgery. A Norwood (first stage) procedure was carried out in 6 neonates at a mean age of 5 (1 to 6) days. There was only one survivor (17%). Prenatal diagnosis of the hypoplastic left heart syndrome allows cardiac and extracardiac evaluation of foetuses with this condition. Therapeutic abortions may be proposed and was the commonest choice of the parents in this study. On the other hand, despite better management of neonates with this prenatal diagnosis, the poor prognosis of the Norwood first stage procedure is unchanged. A systematic search for a restriction of the foramen ovale on foetal echocardiography could optimise neonatal management of this problem.

[Dextrocardia with situ solitus, ventricular loop, double outlet hypoplastic right ventricle and L-malposition of the great arteries. Description and surgical treatment of a rare and complex cardiopathy]. / Dextrocardie avec situs solitus, coeur croisé, ventricule droit hypoplasique à double issue et L-malposition des gros vaisseaux. Description et traitement chirurgical d'une cardiopathie rare et complexe.

Despite the cardiac surgery improvements allowing the correction of the majority of congenital heart diseases with ventricle-great vessels discontinuity, some abnormalities increase the risk of bi-ventricular reparation. We herein report the case of a patient presenting a rare form of double outlet right ventricle with a ventricular loop, with moderate right ventricle hypoplasia. L-malposition of great vessels and pulmonary artery stenosis, and for whom we opted for a palliative surgical treatment including a systemic-pulmonary anastomosis followed by a upper right bi-directional cavo-pulmonary derivation. The last surgery was followed by recurrent right pleural effusions disappearing after the embolization of the systemic-pulmonary anastomosis by catheterism as it probably obstructed the draining of the cavo-pulmonary anastomosis. The relevance of this clinical case reported is, firstly the description of this ventricle loop resulted from a marked ventricular malposition which is a rare heart disease, and secondly the discussion about the surgical treatment, especially about the choice between palliative and curative surgery. Only comparative studies on long term morbidity and mortality between the bi-ventricular reparation and mono-ventricular palliation will allow the selection of the most appropriate surgical treatment.