RESUMO
BACKGROUND: COVID-19 pandemic caused huge decrease of pediatric admissions to Emergency Department (ED), arising concerns about possible delays in diagnosis and treatment of severe disorders. METHODS: Impact of COVID-19 on Pediatric Emergency Room (ICOPER) was a retrospective multicentre observational study including 23 Italian EDs.All the children <18 years admitted, between March 9th and May 3rd 2020 stratified by age, priority code, cause of admission and outcome have been included and compared to those admitted in the same period of 2019.Our objectives were to assess the characteristics of pediatric admissions to EDs since COVID-19 outbreak until the end of lockdown, and to describe the features of critical children. FINDINGS: 16,426 children were admitted in 2020, compared to 55,643 in 2019 (-70·48%). Higher reduction was reported in hospitals without Pediatric Intensive Care Unit (PICU) (-73·38%) than in those with PICU (-64·08%) (P<0·0001). Admissions with low priority decreased more than critical ones (-82·77% vs. 44·17% respectively; P<0·0001). Reduction of discharged patients was observed both in hospitals with (-66·50%) and without PICU (-74·65%) (P<0·0001). No difference in the duration of symptoms before admission was reported between 2019 and 2020, with the majority of children accessing within 24 h (55·08% vs. 57·28% respectively; P = 0·2344). INTERPRETATION: Admissions with low priority decreased significantly more than those with high priority; we suppose that the fear of being infected in hospital maybe overcame the concerns of caregivers. Compared to 2019, no significant referral delay by caregivers was reported. Our data suggest the need of adaptation of EDs and primary care services to different needs of children during COVID-9 pandemic.
RESUMO
Medium chain acyl CoA dehydrogenase deficiency (MCAD) is the most common inborn error of fatty acid oxidation. This condition may lead to cellular energy shortage and cause severe clinical events such as hypoketotic hypoglycemia, Reye syndrome and sudden death. MCAD deficiency usually presents around three to six months of life, following catabolic stress as intercurrent infections or prolonged fasting, whilst neonatal-onset of the disease is quite rare. We report the case of an apparently healthy newborn who suddenly died at the third day of life, in which the diagnosis of MCAD deficiency was possible through peri-mortem blood-spot acylcarnitine analysis that showed very high concentrations of octanoylcarnitine. Genetic analysis at the ACADM locus confirmed the biochemical findings by demonstrating the presence in homozygosity of the frame-shift c.244dup1 (p.Trp82LeufsX23) mutation, a severe genotype that may explain the unusual and very early fatal outcome in this newborn. This report confirms that inborn errors of fatty acid oxidation represent one of the genetic causes of sudden unexpected deaths in infancy (SUDI) and underlines the importance to include systematically specific metabolic screening in any neonatal unexpected death.