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(1) Background: Acinetobacter baumannii has emerged as a leading cause of nosocomial infections as they are capable of evolving resistance to various classes of antibiotics. The ability of A. baumannii to form biofilm might also be associated with increased antibiotic resistance and hence treatment failure. This study was carried to associate the biofilm formation with the drug resistance pattern of A. baumannii and to detect blaOXA-23, blaOXA-24, and blaOXA-51 from carbapenem resistance isolates. (2) Methods: Among different clinical samples, a total of 19 Acinetobacter spp. were identified with conventional microbiological procedures. The biofilm production was determined by a quantitative adherence assay. The antimicrobial susceptibility test was carried out by the Kirby-Bauer disc diffusion method, carbapenemase production detection was confirmed by Modified Hodge Test, and target resistant genes were detected by polymerase chain reaction. (3) Results: Out of 90 clinical specimens, 64.44% (58/90) showed bacterial growth, whereas 32.75% (19/58) isolates were identified as A. baumannii. Among all A. baumannii isolates, 84.21% (16/19) were multidrug-resistance and 63.16% (12/19) carbapenem resistance phenotypically. blaOXA-51 was detected in all the isolates and blaOXA-23 was detected only in 63.16% (12/19) isolates. However, blaOXA-24 was not detected in any of the isolates. Among A. baumannii, 89.47% (17/19) isolates produced biofilm with 47.37% (9/19) strong biofilm producers. (4) Conclusions: In the majority of MDR A. baumannii, blaOXA-51 and blaOXA-23 were detected as the determinant factor for carbapenem resistance having a direct relation with biofilm formation. This study provided a valuable clue for the management of A. baumannii infections in clinical settings.

Tracheobronchial compression due to cardiovascular disease is a rare cause of respiratory distress in children, and common causes include vascular slings and rings, abnormal origin of major vessels, and left atrial enlargement. Intrathoracic airway compression due to pericardial effusion is a rare cause of respiratory distress in children. Here, we present a 6-month-old male child who presented with respiratory distress due to extraluminal compression of the left main bronchus by large pericardial effusion leading to left lung collapse, which improved after pericardiocentesis. [ABSTRACT FROM AUTHOR]

Mechanical ventilation is one of the common lifesaving interventions used in the care of critically ill children admitted to the pediatric intensive care unit. However, it may induce lung inflammation that can cause or aggravates lung injury. Ventilator-induced lung injury (VILI) is defined as acute lung injury inflicted or aggravated by mechanical ventilation. In the presence of preexisting lung disease (pneumonia and acute respiratory distress syndrome), the immune system hyper-reactivity may lead to cascading lung injury due to mechanical ventilation. The possible mechanisms postulated are too high tidal volume (volutrauma), excessive pressure (barotrauma), repetitive opening and closure of alveoli (atelectotrauma), inflammation (biotrauma), oxygen toxicity, adverse heart-lung interactions, deflation-related injuries, effort-related injuries, and genetic variation in expression of inflammatory mediators. Prevention is the most important strategy for VILI by using lung-protective mechanical ventilation strategies to prevent volutrauma, barotrauma, and atelectotrauma. Low tidal volume ventilation, optimal positive end-expiratory pressure and FiO2, limiting plateau pressure, neuromuscular blockers, and prone positioning are some of the important strategies to prevent and treat VILI. VILI has the potential to cause significant morbidity, mortality, and long-term pulmonary sequelae. The clinical relevance of VILI is poorly understood in critically ill children due to lack of pediatric literature, and most of the information are derived from the adult literature. In this review, we will elucidate the epidemiology, etiopathogenesis, clinical evaluation, management, and measures to attenuate or prevent VILI. [ABSTRACT FROM AUTHOR]

Background Staphylococcus aureus co-infection is seldom reported in children with severe dengue. Methodology In this retrospective study, we reported five children with severe dengue and S. aureus  co-infection admitted to pediatric intensive care unit (PICU) during July–December 2021. Results All children had prolonged fever, persistence of bilateral pleural effusion beyond the critical phase, thrombocytopenia and raised inflammatory markers [C-reactive protein (CRP) and procalcitonin]. S. aureus  was isolated from pleural fluid (n  = 2, 40%), blood (n  = 2, 40%) and endotracheal aspirate (n  = 1, 20%). Four children (80%) grew methicillin-sensitive S. aureus , while 1 (20%) had methicillin-resistant S. aureus. Two children (40%) had septic thromboemboli in skin, and 1 (20%) had limb cellulitis. One child required anterior thoracotomy, pericardiectomy and bilateral pleural decortication, while all other children required intercostal chest tube drainage. All children required prolonged targeted antibiotics, invasive mechanical ventilation and had prolong stay in PICU and all of them survived. Conclusion In children with severe dengue, persistence of fever, persistence of pleural effusion beyond critical phase and raised CRP and procalcitonin should raise suspicion of bacterial/ S. aureus co-infection. [ABSTRACT FROM AUTHOR]

A preterm neonate born at 27 weeks, with a birth weight of 555 g, was on continuous positive airway pressure (CPAP ) for apnoea of prematurity and initially received total parenteral nutrition (TPN) through the umbilical venous catheter. Peripherally inserted central catheter (PICC) was inserted in the left basilica vein on day 8 to continue TPN. The baby developed respiratory distress with persistent hypoxia after TPN was initiated through the PICC line. The baby required mechanical ventilation due to worsening of respiratory distress, and chest X-ray, as well as ultrasound conducted 12 hours, postinfusion of TPN revealed right-sided pleural effusion. On careful observation, we could trace the PICC in the right lung area. The PICC line was removed immediately and the baby improved over the next 18 hours and was extubated to CPAP within the next 48 hours. We report this case of contralateral pleural effusion secondary to malposition of PICC line in an extremely preterm neonate. [ABSTRACT FROM AUTHOR]

Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Competing Interests: There are no conflicts of interest.