ABSTRACT
Introducción: Recientemente se ha sugerido que la procalcitonina (PCT) tiene capacidad discriminativa en el diagnóstico de sepsis neonatal. El objetivo de este estudio prospectivo multicéntrico es evaluar la utilidad de la PCT como marcador de sepsis neonatal de origen nosocomial. Pacientes y métodos: Se incluyeron 100 neonatos con sospecha de sepsis nosocomial de entre 4 y 28 días de vida ingresados en los servicios de neonatología de 13 hospitales de tercer nivel de España durante un período de 1 año. Se midió la concentración de PCT mediante análisis inmunoluminométrico. Se calculó la eficacia diagnóstica de la PCT en el momento de la sospecha de infección, a las 12-24 h y a las 36-48 h. Resultados: Se diagnosticaron 61 casos de sepsis nosocomial. Las concentraciones de PCT fueron superiores en los casos de sepsis nosocomial frente a los neonatos con sospecha de sepsis no confirmada. Los neonatos con sepsis por estafilococos coagulasa-negativos mostraron niveles de PCT más bajos que aquellos con sepsis nosocomial por otros agentes. Los puntos de corte óptimo para la PCT de acuerdo con las curvas ROC fueron 0,59 ng/mL en el momento de la sospecha de infección (sensibilidad 81,4%, especificidad 80,6%), 1,34 ng/mLa las 12-24 h (sensibilidad 73,7%, especificidad 80,6%) y 0,69 ng/mL a las 36-48 h (sensibilidad 86,5%, especificidad 72,7%) para el diagnóstico de sepsis de origen nosocomial. Conclusiones: La PCT mostró una moderada capacidad diagnóstica para la sepsis neonatal de origen nosocomial desde el momento de la sospecha de infección. Aunque por sí sola no sería suficientemente fiable, podría ser útil como parte de un chequeo de sepsis más completo (AU)
Background: It has recently been suggested that serum procalcitonin (PCT) is of value in the diagnosis of neonatal sepsis, with varying results. The aim of this prospective multicenter study was to assess the usefulness of PCT as a marker of neonatal sepsis of nosocomial origin. Methods: One hundred infants aged between 4 and 28 days of life admitted to the Neonatology Services of 13 acutecare teaching hospitals in Spain over 1-year with clinical suspicion of neonatal sepsis of nosocomial origin were included in the study. Serum PCT concentrations were determined by a specific immunoluminometric assay. The reliability of PCT for the diagnosis of nosocomial neonatal sepsis at the time of suspicion of infection and at 12-24 h and 36-48 h after the onset of symptoms was calculated. Results: The diagnosis of nosocomial sepsis was confirmed in 61 neonates. Serum PCT concentrations were significantly higher at initial suspicion and at 1224 h and 36- 48 h after the onset of symptoms in neonates with confirmed sepsis than in neonates with clinically suspected but not confirmed sepsis. Optimal PCT thresholds according to ROC curves were 0,59 ng/mL at the time of suspicion of sepsis (sensitivity 81,4%, specificity 80,6%); 1,34 ng/mL within 12-24 h of birth (sensitivity 73,7%, specificity 80,6%), and 0,69 ng/mL within 36-48 h of birth (sensitivity 86,5%, specificity 72,7%). Conclusions: Serum PCT concentrations showed a moderate diagnostic reliability for the detection of nosocomial neonatal sepsis from the time of suspicion of infection. PCT is not sufficiently reliable to be the sole marker of sepsis, but would be useful as part of a full sepsis evaluation (AU)
Subject(s)
Male , Female , Infant, Newborn , Humans , Sepsis/complications , Sepsis/diagnosis , Cross Infection/complications , Cross Infection/diagnosis , Calcitonin , Sensitivity and Specificity , Risk Factors , Predictive Value of Tests , Prospective Studies , Polymerase Chain Reaction/methods , Polymerase Chain Reaction/trendsABSTRACT
Introducción. La asfixia perinatal es una causa potencialde daño cerebral y puede dar lugar a alteraciones en el desarrolloneurológico posterior del niño. Durante los últimos años,numerosas investigaciones se han centrado en la fisiopatología dela asfixia intraparto; no obstante, la correlación de la asfixia con eldesarrollo posterior de una lesión cerebral irreversible sigue estandomal definida. Pacientes y métodos. Se realiza un estudio descriptivoretrospectivo sobre todos los recién nacidos asfícticos nacidosen el Hospital General de Segovia durante un período de inclusiónde 10 años (1992-2001). Se revisaron las historias clínicasde estos niños y se recogieron datos tanto de la gestación como delparto, del período neonatal y del período de seguimiento en consultasexternas. Resultados. Durante el período de estudio se diagnosticaron703 casos de asfixia perinatal, lo que supone una incidenciaen nuestra población de 7,2 casos por cada 100 recién nacidos.Sólo se siguió a 116 de estos niños en consultas externas deneurología pediátrica de nuestro hospital por un período mínimode dos años al cumplir criterios de riesgo. De estos 116 casos, el45% (53 casos) presentó manifestaciones neurológicas en el períodoneonatal. A lo largo de los dos años de seguimiento se observaronsecuelas en 42 de los niños expuestos (36%); la más frecuentefue el retraso psicomotor. Conclusión. Para una adecuada interpretaciónde la relación entre asfixia perinatal y los trastornos neurológicospresentes posteriormente en los niños que la han sufrido esnecesario realizar un análisis riguroso del conjunto de datos perinatalesy descartar otras posibles etiologías y mecanismos patogénicos
Introduction. Perinatal asphyxia is a potential cause of brain injury that can produce some alterations on theneurologic development of the newborn. On the last years most part of the investigation have been focused on the physiopathologyof the perinatal asphyxia, but correlation between asphyxia and brain damage is not well defined. Patients andmethods. A retrospective study was made of the patients with the diagnosis of perinatal asphyxia born at the General Hospitalof Segovia during a period of ten years (1992-2001). We took data about gestation, birth, neonatal period and follow-up periodfrom their clinical histories. Results. Over this period of ten years 703 cases of perinatal asphyxia have been diagnosed,supposing this an incidence of 7,2 cases of each 100 newborns. 116 of these newborns present risk factors of brain damage andwere followed at least two years. 53 of the 116 newborns (45%) present evidence of hypoxic-ischemic encephalopathy onneonatal period. During the period of two years, 42 of the asphyxiated infants follow up (36%) present neurologic sequelae,being psychomotor retardation the most common. Conclusion. For a correct interpretation of the relationship betweenperinatal asphyxia and neurologic sequelae we have to analyze all of the perinatal data and discard any other possibleaetiology or pathogenic mechanism
Subject(s)
Male , Female , Pregnancy , Infant, Newborn , Humans , Asphyxia Neonatorum/complications , Asphyxia Neonatorum/diagnosis , Asphyxia Neonatorum/physiopathology , Nervous System Diseases/etiology , Nervous System Diseases/physiopathology , Brain Injury, Chronic/etiology , Brain Injury, Chronic/physiopathology , Follow-Up Studies , Retrospective Studies , Risk Factors , Health Statistics , Epidemiology, Descriptive , Apgar Score , SpainABSTRACT
INTRODUCTION: Perinatal asphyxia is a potential cause of brain injury that can produce some alterations on the neurologic development of the newborn. On the last years most part of the investigation have been focused on the physiopathology of the perinatal asphyxia, but correlation between asphyxia and brain damage is not well defined. PATIENTS AND METHODS: A retrospective study was made of the patients with the diagnosis of perinatal asphyxia born at the General Hospital of Segovia during a period of ten years (1992-2001). We took data about gestation, birth, neonatal period and follow-up period from their clinical histories. RESULTS: Over this period of ten years 703 cases of perinatal asphyxia have been diagnosed, supposing this an incidence of 7,2 cases of each 100 newborns. 116 of these newborns present risk factors of brain damage and were followed at least two years. 53 of the 116 newborns (45%) present evidence of hypoxic-ischemic encephalopathy on neonatal period. During the period of two years, 42 of the asphyxiated infants follow up (36%) present neurologic sequelae, being psychomotor retardation the most common. CONCLUSION: For a correct interpretation of the relationship between perinatal asphyxia and neurologic sequelae we have to analyze all of the perinatal data and discard any other possible aetiology or pathogenic mechanism.
Subject(s)
Asphyxia Neonatorum , Brain Damage, Chronic , Nervous System Diseases , Apgar Score , Asphyxia Neonatorum/complications , Asphyxia Neonatorum/diagnosis , Asphyxia Neonatorum/physiopathology , Brain Damage, Chronic/etiology , Brain Damage, Chronic/physiopathology , Female , Follow-Up Studies , Humans , Infant, Newborn , Nervous System Diseases/etiology , Nervous System Diseases/physiopathology , Pregnancy , Retrospective Studies , Risk Factors , Spain , Statistics as TopicSubject(s)
Pigmentation Disorders/diagnosis , Child , Extremities , Humans , Male , Purpura/etiologyABSTRACT
No disponible
Subject(s)
Male , Child , Humans , Pigmentation Disorders/diagnosis , Extremities , Purpura/etiologyABSTRACT
No disponible
Subject(s)
Infant, Newborn , Humans , Neonatal Screening/methods , Hypothyroidism/congenital , Hypothyroidism/diagnosis , Phenylketonurias/diagnosis , Hearing Loss/congenital , Hearing Loss/diagnosis , Hip Dislocation, Congenital/diagnosisABSTRACT
Methylmalonic aciduria and homocystinuria is a very rare inborn error of cellular cobalamin (Cbl) metabolism. We describe the biochemical evolution and clinical course of a boy with neonatal onset CblC mutant defect.Born after a normal pregnancy, the patient developed general hypotonia and severe feeding difficulties at 5 days of life. Diagnosis of methylmalonic aciduria and homocystinuria was established by amino-acid and organic acid analysis and was confirmed by enzyme and genetic studies. The patient was initially treated with parenteral hydroxocobalamin (1 mg/day), oral carnitine (100 mg/kg/day) and a restricted protein diet. This treatment returned methylmalonic acid levels to normal. Despite the parenteral hydroxocobalamin therapy, the patient showed no improvement in neurological dysfunction, hypotonia or developmental delay. Oral betaine supplementation (3 g/day) from months 3-15 reduced plasma total homocysteine and homocystinuria. The patient showed clinical improvement in neurological and growth development. We conclude that early betaine therapy was safe and effective in our patient with neonatal onset methylmalonic aciduria and homocystinuria type CblC.
Subject(s)
Betaine/therapeutic use , Gastrointestinal Agents/therapeutic use , Homocystinuria/drug therapy , Methylmalonic Acid/urine , Administration, Oral , Age Factors , Betaine/administration & dosage , Gastrointestinal Agents/administration & dosage , Homocystinuria/diagnosis , Homocystinuria/genetics , Humans , Infant , Infant, Newborn , Male , Time FactorsABSTRACT
La aciduria metilmalónica con homocistinuria es un infrecuente error del metabolismo celular de la cobalamina (cbl). Se describe la evolución bioquímica y el curso clínico de un paciente con la mutación cblC de comienzo neonatal. Nacido tras una gestación normal, desarrolló una hipotonía general y graves dificultades de alimentación a los 5 días. El diagnóstico de aciduria metilmalónica con homocistinuria fue establecido basándose en los análisis de los aminoácidos y de los ácidos orgánicos, y confirmado mediante estudios enzimáticos y genéticos. El paciente fue tratado inicialmente con hidroxicobalamina parenteral (1 mg diario), carnitina oral (100 mg/kg/ día) y dieta hipoproteica. Este tratamiento normalizó los niveles de ácido metilmalónico. A pesar del tratamiento con hidroxicobalamina parenteral, la disfunción neurológica, la hipotonía y el retraso del desarrollo no experimentaron ninguna mejoría. La suplementación con betaína oral (3 g diarios) desde el 3.º al 15.º mes produjo una disminución de la homocisteína total y de la homocistinuria. El paciente presentó mejoría clínicamente de su desarrollo neurológico y somatométrico. Se concluye que el tratamiento precoz con betaína fue seguro y efectivo en nuestro paciente con aciduria metilmalónica con homocistinuria tipo cblC de inicio neonatal (AU)
Subject(s)
Male , Infant, Newborn , Infant , Humans , Time Factors , Betaine , Administration, Oral , Age Factors , Homocystinuria , Gastrointestinal Agents , Methylmalonic AcidABSTRACT
La intoxicación por mercurio es un hecho muy infrecuente en el período neonatal, en particular la debida a ingestión de merbromina. Se describe el caso de un recién nacido de 10 días de vida al que se le administró mercurocromo por vía oral durante 7 días, debido a un mal entendimiento de las indicaciones médicas. Los síntomas iniciales incluyeron pérdida de apetito y escasa ganancia ponderal. Se encontraron valores de mercurio elevados en sangre. Se inició terapia quelante con dimercaprol y la evolución del paciente fue buena. Se comenta la toxicidad potencial provocada por el mercurio. Se desea poner énfasis en la importancia de la transmisión de la información por parte de los médicos, sobre todo a la población inmigrante (AU)
Subject(s)
Male , Infant, Newborn , Infant , Humans , Ubiquinone , Time Factors , Mitochondrial Myopathies , Merbromin , Mercury , Reye Syndrome , Anti-Infective Agents, Local , Chelating Agents , Dimercaprol , Administration, Oral , AccidentsABSTRACT
Neonatal mercury poisoning, especially that due to merbromin ingestion, is uncommon. We describe the case of a 10 day old newborn infant who was given mercurochrome orally for 7 days due to misunderstanding of medical instructions. Initial symptoms included loss of appetite and low weight increase. Elevated blood mercury concentrations were found. Chelating therapy with dimercaprol was initiated and the patient's evolution was good. We discuss the potential toxicity of mercury and emphasise the importance of the transmission of information by physicians, especially to the immigrant population.
Subject(s)
Anti-Infective Agents, Local/poisoning , Merbromin/poisoning , Accidents , Administration, Oral , Anti-Infective Agents, Local/administration & dosage , Chelating Agents/therapeutic use , Dimercaprol/therapeutic use , Humans , Infant, Newborn , Male , Merbromin/administration & dosage , Mercury/blood , Time FactorsABSTRACT
La malformación adenomatoidea quística (MAQ) es una enfermedad infrecuente. Consiste en una proliferación anormal de elementos mesenquimales pulmonares secundaria a un fallo madurativo de estructuras bronquiolares. Presenta una serie de rasgos anatomopatológicos comunes y otros diferenciadores en los cuales se basa su clasificación. Se asocia, en ocasiones, a otras malformaciones y puede manifestarse clínicamente como: hydrops fetalis, distrés respiratorio neonatal y, en ocasiones, mantenerse silente, incluso durante largo tiempo. Es posible su diagnóstico prenatal aunque la confirmación requerirá el estudio anatomopatológico de la lesión. El tratamiento es quirúrgico. Presentamos dos casos de MAQ con dos formas diferentes de presentación (AU)
Subject(s)
Female , Infant , Male , Humans , Infant, Newborn , Cystic Adenomatoid Malformation of Lung, Congenital/diagnosis , Cystic Adenomatoid Malformation of Lung, Congenital/surgery , Cystic Adenomatoid Malformation of Lung, CongenitalABSTRACT
Authors report two cases of Crohn's disease in a brother and a sister. Female showed first manifestation at 8 years of age. Male started at 12 years. Onset was acute in the girl with ileo-cecal and colonic involvement and extraintestinal manifestations. The boy had an insidious onset with ileal involvement and striking rectal and perianal symptoms. In both cases, clinical course was chronic and relapsing. HLA A and B phenotypes were studied in both patients and their parents. Different factors concerning origin of disease, as well as relationship to other diseases among relatives are discussed.
Subject(s)
Crohn Disease/genetics , Adolescent , Child , Crohn Disease/complications , Female , HLA Antigens , Humans , Male , Pedigree , Rectal Fistula/etiologyABSTRACT
Authors report case histories of four siblings with Munchausen syndrome by proxy. The diagnosis was made in the third daughter after six years. Two siblings had died as result of sudden unexplained death at two years old and twelve month old respectively. The mother had typical features outlined in some report. She denied the provocation of any episode and refused further psychiatric help but she accepted medical supervision. A review of the literature: warning signals, plan of action in order to assess the diagnosis and management of this problem are outlined, establishing a discussion about the repercussion of this syndrome.
Subject(s)
Battered Child Syndrome , Child Abuse , Munchausen Syndrome/genetics , Female , Hospitalization , Humans , Infant , Male , Munchausen Syndrome/diagnosis , Time FactorsABSTRACT
Clinical, hemodynamic and pathologic findings of three patients with total anomalous pulmonary venous drainage to the portal vein system are presented. Some of the findings are emphasized because of its rarity in previous reports. These are: 1) Cyanosis was mild. 2) There was some obstruction of the foramen ovale, besides the obstruction at the portal system level. In two patients gastrointestinal bleeding and analitical evidence of renal failure, were found, both findings not previously reported to our knowledge.
