ABSTRACT
Background: The sudden infant's death syndrome (SD) is the leading cause of death in children under one year. Despite advances in its study, the pathogenesis has not been yet fully elucidated. Aim: To assess the prevalence of SD in Chilean infants and its changes in recent years. Material and Methods: Review of birth and death databases of the Ministry of Health from 1997 to 2009. All cases diagnosed as SD, according to the lnternational Classification of Diseases, 10th edition, were selected. A demographic analysis was performed and mortality rates for each year were calculated. Results: We identified 1442 cases of SD (847 males, 517 deaths at home). The median age of death was 2 months (0 to 11.0 months). Ninety six percent of deaths occurred in children aged <6 months. Mortality rate for SD was 0.45/1000 live births. There was a 23% reduction between 1997 and 2009. When analyzing geographic distribution, more cases were found in the Southern latitudes of the country. Conclusions: The overall rate of SD in Chile is higher than in European countries and in North America. The observed decrease in cases over the years is still far from optimal.
Subject(s)
Female , Humans , Infant , Infant, Newborn , Male , Sudden Infant Death/epidemiology , Chile/epidemiology , Prevalence , Retrospective Studies , Risk FactorsABSTRACT
Difficult airway is a life-threatening situation which compromises the permeability of the upper airway and thus adequate ventilation and oxygenation. Multiple factors, acute and chronic such as: infectious, neoplastic and trauma have been associated with critical airway. Morbidity and mortality related to a difficult airway management remains as a significant problem in children, so is essential for the pediatric health team to be trained to recognize and anticipate situations that in clinical practice might determine a critical airway. The aim of this review is to provide concepts and guidance to assess patients with potentially difficult airway.
Una vía aérea difícil condiciona una situación con riesgo vital, ya que pone en peligro la permeabilidad de la vía aérea superior y con esto la capacidad de mantener una adecuada ventilación y oxigenación. Múltiples factores, tanto agudos como crónicos, entre ellos factores anatómicos propios del niño/a, complicaciones infecciosas, neoplásicas y/o traumáticas se han asociado con una vía aérea crítica. La morbilidad y mortalidad asociada al manejo inadecuado de esta condición continua siendo un problema significativo en la edad pediátrica; siendo fundamental que el equipo de salud se encuentre entrenado en reconocer y anticipar situaciones que en la práctica clínica podrían asociarse con una vía aérea difícil o crítica. El objetivo de la presente revisión es otorgar conceptos y una orientación en el enfrentamiento de los pacientes con una vía aérea potencialmente difícil.
Subject(s)
Humans , Child , Respiratory Insufficiency/etiology , Respiratory Insufficiency/therapy , Airway Management/methods , Airway Obstruction/etiology , Airway Obstruction/therapy , Craniofacial Abnormalities/complications , Respiratory Insufficiency/classification , Respiratory Insufficiency/pathology , Airway Obstruction/classification , Airway Obstruction/pathologyABSTRACT
Background: Long term use of ganciclovir (GCV) is associated with acquired resistance to it. Ninety percent of the responsible mutations occur in cytomegalovirus (CMV) UL 97 gene. Aim: To search for these mutations, comparing nucleotide sequences of CMV-positive samples from post transplant and immunocompromised patients receiving GCV, with sequences of CMV isolates obtained from subjects not exposed to the drug. Patients and Methods: Codons 440 to 465 of gene UL 97, in-cluding the most common mutations causing resistance to GCV, were amplifed in 33 plasma samples from patients exposed to GCV and in 15 urine samples of newborns. Both populations and their nucleotide sequences were compared with the prototype strain CMV AD169. Results: Samples of exposed patients had multiple mutations but only one had a mutation associated with clinical resistance (M460I). Eight subjects had the D605E mutation, whose role in resistance is controversial. The remaining 150 mutations were silent mutations. Conclusions: A low frequency of mutations associated with CMV resistance to GCV was found in these exposed and unexposed samples. These mutations may refect coexistence of multiple genetic variants of CMV. The absence of clinical expression of resistance, even with these mutations, can be explained by the use of GCV for a shorter lapse than that associated with the appearance of resistance.