Clinical and growth outcomes after meconium-related ileus improved with Gastrografin enema in very low birth weight infants.

BACKGROUND: Meconium-related ileus in very low birth weight infants can lead to increased morbidity or mortality and prolonged hospitalization without prompt diagnosis and treatment. This study primarily aimed to identify the incidence of and factors associated with meconium-related ileus and secondarily sought to investigate clinical and growth outcomes after water-soluble contrast media (Gastrografin) enema. METHODS: We retrospectively reviewed medical records of very low birth weight infants born between February 2009 and March 2019 in the neonatal intensive care unit of a single medical center. Perinatal factors, clinical outcomes, and growth outcomes were compared between the group with meconium-related ileus that received Gastrografin enema and the control group. RESULTS: Twenty-four (6.9%) patients were diagnosed with meconium-related ileus among 347 very low birth weight infants. All achieved successful evacuation of meconium with an average of 2.8 (range: 1-8) Gastrografin enema attempts without procedure-related complications. Initiation of Gastrografin enema was performed at mean 7.0 days (range: 2-16) after birth. Incidences of moderate to severe bronchopulmonary dysplasia were higher and the duration of mechanical ventilation and need for oxygen were longer in the meconium-related ileus group (P = 0.039, 0.046, 0.048, respectively). Meconium-related ileus infants took more time to start enteral feeding and the nothing per oral time was longer (P = 0.001 and 0.018, respectively). However, time to achieve full enteral feeding and Z-scores for weight and height at 37 weeks and at 6 months corrected age did not differ between the two groups. CONCLUSIONS: Gastrografin enema in very low birth weight infants with meconium-related ileus was an effective and safe medical management. Following Gastrografin enema, very low birth weight infants with meconium-related ileus achieved similar subsequent feeding progress and similar growth levels as the control groups without meconium-related ileus.

Neonatal sepsis-causing bacterial pathogens and outcome of trends of their antimicrobial susceptibility a 20-year period at a neonatal intensive care unit.

BACKGROUND: Due to increases in the number of infants born with younger gestational age (GA) and lower birth weight, the incidence of neonatal sepsis is increasing. PURPOSE: We investigated the changes in the prevalence of bacterial pathogens, their antimicrobial susceptibility, and sepsis-related mortality during 20 years at a neonatal intensive care unit. METHODS: The study period was divided into two 10-year phases (1998-2007 vs. 2008-2017). Medical records were reviewed to gather data on demographics, causative microbial pathogens, incidence of multidrug-resistant organisms, antimicrobial susceptibility, and rates of sepsis-related mortality. RESULTS: In both study phases, the most common pathogens for neonatal sepsis were coagulase-negative Staphylococcus (CoNS) (28.6%) and Enterobacter cloacae (16.1%) for early-onset sepsis (EOS, ≤72 hours after birth) and CoNS (54.7%) and Staphylococcus aureus (12.9%) for late-onset sepsis (LOS, >72 hours after birth). CoNS and S. aureus showed 100% sensitivity to vancomycin in both phases. The susceptibility of S. aureus to oxacillin increased from 19.2% to 57.9% in phase II than phase I. K. pneumonia and E. cloacae showed increases in its susceptibility to gentamicin, cefotaxime and ceftriaxone in phase II than phase I. In both phases, the most common pathogens that caused sepsis-related death were K. pneumoniae (18.2%) and Pseudomonas aeruginosa (13.6%). Sepsis-related mortality rate was higher in infants with GA <37 weeks than those with GA over 37 weeks (P=0.016). In addition, the mortality rate of neonatal sepsis caused by gram-negative bacteria was significantly higher than that caused by gram-positive bacteria (P<0.001). CONCLUSIONS: CoNS was the most common pathogen for EOS and LOS. While we found significant changes in antimicrobial sensitivities over time. GA below 37 weeks and gram-negative organisms are associated with mortality rate.

Morbidity and Mortality of Very Low Birth Weight Infants with Congenital Heart Disease.

BACKGROUND AND OBJECTIVES: This study aimed to provide morbidity and mortality information on very low birth weight (VLBW) infants with congenital heart disease (CHD-VLBWs). METHODS: The study used a 10-year cohort of VLBW infants from a single institution. CHD was classified according to International Classification of Diseases, Version 9, Clinical Modification. Mortality and neonatal outcomes were assessed by comparing the CHD-VLBWs with gestational age- and birth weight-matched controls. RESULTS: The prevalence of CHD-VLBWs was 7.5% (79/1,050), mean gestational age was 31.1±3.2 weeks, and mean birth weight was 1,126.2±268.3 g; 50.6% of the infants were small for the gestational age. The CHD-VLBWs more commonly had bronchopulmonary dysplasia (BPD), and the longer they were exposed to oxygen, the more frequently they developed BPD. Those with cyanotic heart disease developed severe BPD more frequently. Necrotizing enterocolitis (NEC) occurred frequently in the CHD-VLBWs and was not associated with their feeding patterns. CHD-VLBWs had a higher mortality rate; prematurity-related diseases were the leading cause of death before surgery, while heart-related problems were the leading cause of death after surgery. We found no significant difference in mortality from prematurity-related disease between the CHD-VLBWs and controls. In the subgroup analysis of CHD, the cyanotic CHD group had a higher incidence of BPD and higher mortality rate than the acyanotic CHD group. CONCLUSIONS: CHD-VLBWs showed higher BPD, NEC, and mortality rates than those without CHD. There was also a higher incidence of BPD and mortality in VLBW infants with cyanotic CHD than in those with acyanotic CHD.

Chronic Placental Inflammation as a Risk Factor of Severe Retinopathy of Prematurity.

BACKGROUND: Chronic placental inflammation (CPI) has been implicated in the pathogenesis of diseases in premature infants, whereas retinopathy of prematurity (ROP) is a major complication primarily affecting preterm and very low-birth-weight (VLBW) infants. This study aims to investigate the association between CPI and ROP in VLBW infants. METHODS: We performed a retrospective review of clinical records of VLBW infants born between 2013 and 2016. Placental pathology findings including CPI cases were analyzed using logistic regression to study infants' morbidities and other clinical characteristics. RESULTS: A total of 402 infants with a mean (standard deviation) gestational age of 28.5 (2.8) weeks and birth weight of 1,027.2 (304.4) g were included. The incidence of ROP was 24.1%. CPI was found in 90 infants (22.4%), among which 28.9% (26 of 90) developed ROP, and 21.1% (19 of 90) underwent laser photocoagulation. Lower gestational age, lower birth weight, longer duration of oxygen supply, and presence of CPI were associated with the development of ROP. After adjustment for gestational age, birth weight, sex, duration of oxygen supply, and other overlapping placental pathology, CPI was associated with the odds for type 1 ROP that required laser photocoagulation (adjusted odds ratio, 2.739; 95% confidence interval, 1.112 to 6.749; p = .029). CONCLUSIONS: CPI was associated with severe ROP requiring treatment with laser photocoagulation in VLBW infants.

Parotid sialolithiasis in a two-year-old boy.

Sialolithiasis is caused by the obstruction of a salivary gland or its excretory duct by the formation of calcareous concretions or sialoliths; this results in salivary ectasia and provokes subsequent dilation of the salivary gland. Sialolithiasis is relatively common, accounting for 30% of salivary diseases; however, it is rarely observed in childhood. This case report describes a 2-year-old male patient who complained of a painful swelling over the right cheek, and presented with palpable stones and pus discharge from the orifice of the right Stensen's duct. Computerized tomography of the neck confirmed the diagnosis, and the patient received intravenous empiric antibiotics combined with intraoral sialolithotomy. We also provide a review of the spectrum of concepts regarding the pathogenesis, diagnosis, and treatment of sialolithiasis.

Cytotoxicity of diacetoxyscirpenol is associated with apoptosis by activation of caspase-8 and interruption of cell cycle progression by down-regulation of cdk4 and cyclin B1 in human Jurkat T cells.

To understand the mechanism underlying T-cell toxicity of diacetoxyscirpenol (DAS) from Fusarium sambucinum, its apoptogenic as well as growth retardation activity was investigated in human Jurkat T cells. Exposure to DAS (0.01-0.15 microM) caused apoptotic DNA fragmentation along with caspase-8 activation, Bid cleavage, mitochondrial cytochrome c release, activation of caspase-9 and caspase-3, and PARP degradation, without any alteration in the levels of Fas or FasL. Under these conditions, necrosis was not accompanied. The cytotoxicity of DAS was not blocked by the anti-Fas neutralizing antibody ZB-4. Although the DAS-induced apoptotic events were completely prevented by overexpression of Bcl-xL, the cells overexpressing Bcl-xL were unable to divide in the presence of DAS, resulting from the failure of cell cycle progression possibly due to down-regulation in the protein levels of cdk4 and cyclin B1. The DAS-mediated apoptosis and activation of caspase-8, -9, and -3 were abrogated by either pan-caspase inhibitor (z-VAD-fmk) or caspase-8 inhibitor (z-IETD-fmk). While the DAS-mediated apoptosis and activation of caspase-9 and caspase-3 were slightly suppressed by the mitochondrial permeability transition pore inhibitor (CsA), both caspase-8 activation and Bid cleavage were not affected by CsA. The activated normal peripheral T cells possessed a similar susceptibility to the cytotoxicity of DAS. These results demonstrate that the T-cell toxicity of DAS is attributable to not only apoptosis initiated by caspase-8 activation and subsequent mitochondrion-dependent or -independent activation of caspase cascades, which can be regulated by Bcl-xL, but also interruption of cell cycle progression caused by down-regulation of cdk4 and cyclin B1 proteins.