Intravenous methylprednisolone versus intravenous methylprednisolone combined with inhaled budesonide in acute severe pediatric asthma.

INTRODUCTION: Corticosteroids are important part of acute severe asthma (ASA) management in pediatric intensive care units. Few studies look at the efficacy of inhaled corticosteroids (ICS) in critical care settings. We aimed to investigate the potential beneficial effects of ICS when added to intravenous corticosteroids in pediatric patients with ASA admitted to the pediatric intensive care unit (PICU). METHODS: This was a randomized controlled trial involving pediatric patients aged 1-21 years admitted to PICU with ASA. Patients were randomized into 2 groups using block randomization. Patients in Group A received intravenous methylprednisolone (2 mg/kg/day) alone and patients in Group B received intravenous methylprednisolone (2 mg/kg/day) plus budesonide nebulization (0.5 mg every 12 h). Main outcomes were duration of continuous albuterol treatment, PICU and hospital length of stay (LOS), and need and duration of respiratory support. Kruskal-Wallis and Chi-square tests were used for statistical analysis, in which a p-value < 0.05 was considered statistically significant. RESULTS: Duration of continuous albuterol treatment was not different between the 2 groups median/(QR), 30/(18-51) vs. 25/(14-49). (p = 0.38) PICU and hospital LOS between the 2 groups was similar, median/(QR), 44/(30-64) vs. 46/(30-62), (p = 0.75) and 78/(65-95) vs.72/(58-92), (p = 0.19). Number of patients requiring respiratory support was 22(58%) in Group A and 25(64%) in Group B (p = 0.19). CONCLUSIONS: In critically ill children with ASA, intravenous methylprednisolone combined with inhaled budesonide did not shorten the duration of continuous albuterol inhalation treatment, the PICU and hospital LOS, and the need for respiratory support.

You Cannot Hit Snooze on OSA: Sequelae of Pediatric Obstructive Sleep Apnea.

Pediatric obstructive sleep apnea (OSA) has been shown to not only affect the quality of sleep, but also overall health in general. Untreated or inadequately treated OSA can lead to long-term sequelae involving cardiovascular, endothelial, metabolic, endocrine, neurocognitive, and psychological consequences. The physiological effects of pediatric OSA eventually become pathological. As the complex effects of pediatric OSA are discovered, they must be identified early so that healthcare providers can be better equipped to treat and even prevent them. Ultimately, adequate management of OSA improves overall quality of life.

Much Ado about Sleep: Current Concepts on Mechanisms and Predisposition to Pediatric Obstructive Sleep Apnea.

Obstructive Sleep Apnea (OSA) is a form of sleep-disordered breathing characterized by upper airway collapse during sleep resulting in recurring arousals and desaturations. However, many aspects of this syndrome in children remain unclear. Understanding underlying pathogenic mechanisms of OSA is critical for the development of therapeutic strategies. In this article, we review current concepts surrounding the mechanism, pathogenesis, and predisposing factors of pediatric OSA. Specifically, we discuss the biomechanical properties of the upper airway that contribute to its primary role in OSA pathogenesis and examine the anatomical and neuromuscular factors that predispose to upper airway narrowing and collapsibility.

Pneumoperitoneum without Intestinal Perforation in a Neonate: Case Report and Literature Review.

Pneumoperitoneum in a preterm neonate usually indicates perforation of the intestine and is considered a surgical emergency. However, there are cases of pneumoperitoneum with no evidence of rupture of the intestine reported in the literature. We report a case of pneumoperitoneum with no intestinal perforation in a preterm neonate with respiratory distress syndrome who was on high frequency oscillatory ventilation (HFOV). He developed bilateral pulmonary interstitial emphysema with localized cystic lesion, likely localized pulmonary interstitial emphysema, and recurrent pneumothoraces. He was treated with dexamethasone to wean from the ventilator. Pneumoperitoneum developed in association with left sided pneumothorax following mechanical ventilation and cardiopulmonary resuscitation. Pneumoperitoneum resolved after the pneumothorax was resolved with chest tube drainage. He died from acute cardiorespiratory failure. At autopsy, there was no evidence of intestinal perforation. This case highlights the fact that pneumoperitoneum can develop secondary to pneumothorax and does not always indicate intestinal perforation or require exploratory laparotomy.