ABSTRACT
Introducción: La malformación congénita de las vías aéreas pulmonares (MCVAP), anteriormente denominada malformación adenomatoidea quística, es un raro trastorno del desarrollo del tracto respiratorio bajo. Los pacientes pueden estar asintomáticos durante muchos años, o bien presentar una dificultad respiratoria neonatal. Muchos casos actualmente se detectan mediante ecografía prenatal. El objetivo de este estudio era describir los casos diagnosticados en un hospital de segundo nivel durante un periodo de observación de 10 años. Casos clínicos: Encontramos 6 casos de MCVAP, tras un seguimiento desde los 7 meses a los 9 años de edad. El diagnóstico se realizó mediante ecografía prenatal. La incidencia en nuestro hospital resultó ser de 2,44 casos por 10.000 recién nacidos vivos. Conclusiones: El tratamiento quirúrgico es definitivo, y debe realizarse en un hospital con experiencia en cirugía pediátrica. En los pacientes asintomáticos, el manejo dependerá de las características asociadas al riesgo de complicaciones. Para los pacientes asintomáticos y de bajo riesgo, ambas opciones (operar o manejo conservador) son razonables, siempre tras una adecuada información a la familia
Introduction: Congenital pulmonary airway malformation, previously known as congenital cystic adenomatoid malformation, is a rare developmental anomaly of the lower respiratory tract. Affected patients may present with respiratory distress in the newborn period or may remain asymptomatic until later in life. Many cases are now detected by routine prenatal ultrasound examination. Our objective was to describe the fetal-neonatal outcome of our cases of 10 years on a second level hospital. Clinical cases: Six cases of congenital cystic adenomatoid malformation of the lung are reported. The incidence in our hospital was 2.44 per 10,000 live births. They were followed up over a period of 7 months to 9 years. Diagnosis was made by prenatal ultrasound. Conclusion: Surgical resection is the definitive treatment in a hospital with experienced pediatric surgery. In asymptomatic infants subsequent management depends on whether there are characteristics that suggest a high risk of complications. For asymptomatic infants and children with small lesions and none of the high-risk features, either elective surgical resection or conservative management with observation are reasonable options, always after a detailed discussion with the family
Subject(s)
Humans , Male , Female , Infant, Newborn , Infant , Child, Preschool , Child , Cystic Adenomatoid Malformation of Lung, Congenital/diagnostic imaging , Cystic Adenomatoid Malformation of Lung, Congenital/surgery , Follow-Up Studies , Prenatal Diagnosis , Retrospective Studies , Respiratory Distress Syndrome, Newborn/diagnosis , Bronchopulmonary Sequestration/diagnostic imaging , UltrasonographyABSTRACT
A method of identification and quantitative determination of amitriptyline and cocaine at trace levels in biological fluids is described. After the extraction of both drugs from the biological material in an alkaline medium, and posterior purification and concentration of the extract, one proceeds to unequivocal identification using the combined capillary GC/MS system with the Selected Ion Monitoring (SIM) technique. Quantitative determination is carried out by GC with a N-P detector. The precision of the method and limits of sensitivity are presented.
Subject(s)
Amitriptyline/analysis , Body Fluids/analysis , Cocaine/analysis , Chromatography, Gas , Gas Chromatography-Mass Spectrometry , HumansABSTRACT
Alkanes, alcohols, and ketones which are metabolized to a gamma-diketone can produce peripheral neuropathy in experimental animals and in man. A study was conducted to obtain information about the metabolic pathway of n-heptane and its potential neurotoxicity. Female Wistar rats were exposed to 2000 ppm n-heptane inhalation for 12 weeks. Metabolites in urine were identified by gas chromatography-mass spectrometry. Urinary metabolites were quantified following 6-hr n-heptane exposures. n-Heptane metabolites were 1-, 2-, 3-, and 4-heptanols, 2- and 3-heptanones, 2,5- and 2,6-heptanediols, 5-hydroxy-2-heptanone, 6-hydroxy-2-heptanone, 6-hydroxy-3-heptanone, 2,5- and 2,6-heptanediones, and gamma-valerolactone. The amount of urinary metabolites increased greatly after the second exposure day, achieving a steady-state concentration on subsequent exposure days over the 12 weeks of the exposure regimen. These results showed that n-heptane was metabolized mainly by hydroxylation at omega- 1 carbon atom and to a lesser extent at the omega- 2 carbon atom. 2-Heptanol, 6-hydroxy-2-heptanone, and 3-heptanol were the major metabolites and were excreted as sulfates and glucuronides. 2,5-Heptanedione, which is a neurotoxic agent, was the metabolite found in least amounts (2.4 +/- 2 micrograms/rat) in the urine. No clinical evidence of neurotoxicity was observed after n-heptane exposure. Apparently, the lack of neurotoxicity was due to a low production of 2,5-heptanedione, the toxic metabolite.
