RESUMEN
OBJECTIVE: To evaluate whether teaching mothers about neonatal jaundice will decrease the incidence of acute bilirubin encephalopathy among infants admitted for jaundice. STUDY DESIGN: This was a multicenter, before-after and cross-sectional study. Baseline incidences of encephalopathy were obtained at 4 collaborating medical centers between January 2014 and May 2015 (Phase 1). Structured jaundice instruction was then offered (May to November 2015; Phase 2) in antenatal clinics and postpartum. Descriptive statistics and logistic regression models compared 3 groups: 843 Phase 1 controls, 338 Phase 2 infants whose mothers received both antenatal and postnatal instruction (group A), and 215 Phase 2 infants whose mothers received no instruction (group B) either because the program was not offered to them or by choice. RESULTS: Acute bilirubin encephalopathy occurred in 147 of 843 (17%) Phase 1 and 85 of 659 (13%) Phase 2 admissions, which included 63 of 215 (29%) group B and 5 of 338 (1.5%) group A infants. OR for having acute bilirubin encephalopathy, comparing group A and group B infants adjusted for confounding risk factors, was 0.12 (95% CI 0.03-0.60). Delayed care-seeking (defined as an admission total bilirubin ≥18 mg/dL at age ≥48 hours) was the strongest single predictor of acute bilirubin encephalopathy (OR 11.4; 6.6-19.5). Instruction decreased delay from 49% to 17%. Other major risk factors were home births (OR 2.67; 1.69-4.22) and hemolytic disease (hematocrit ≤35% plus bilirubin ≥20 mg/dL) (OR 3.03; 1.77-5.18). The greater rate of acute bilirubin encephalopathy with home vs hospital birth disappeared if mothers received jaundice instruction. CONCLUSIONS: Providing information about jaundice to mothers was associated with a reduction in the incidence of bilirubin encephalopathy per hospital admission.
Asunto(s)
Ictericia/complicaciones , Kernicterus/epidemiología , Kernicterus/etiología , Madres/educación , Enfermedad Aguda , Estudios Transversales , Femenino , Humanos , Incidencia , Lactante , Recién Nacido , Kernicterus/prevención & control , Masculino , Nigeria/epidemiología , Aceptación de la Atención de SaludRESUMEN
INTRODUCCIÓN: La hiperbilirrubinemia es altamente prevalente en los recién nacidos, con riesgo de compromiso neurológico con bilirrubinemias mayor a 20-25 mg/dl. Esta progresión es prevenible con detección y tratamiento precoz. OBJETIVO: Describir incidencia y factores asociados en pacientes hospitalizados con hiperbilirrubinemia mayor de 20 mg/dl, y el seguimiento de casos sintomáticos durante hospitalización. PACIENTES Y MÉTODO: Estudio retrospectivo de pacientes con hiperbilirru- binemia severa, entre el 2013 y 2016. Se evaluaron factores de riesgo, estratificándose por nivel de bilirrubina, edad de ingreso y edad gestacional. Se compararon los datos con test exacto de Fisher, chi cuadrado y riesgo relativo (RR) en una base de excel, con un error alfa de un p<0.05. Los datos fueron obtenidos a través de la epicrisis electrónica y de la ficha de control a nivel secundarios. RESULTADOS: Durante el periodo, de 25.288 recién nacidos vivos (RNV), 593 se hospitalizaron por hiperbilirrubinemia mayor de 20 mg/dl, 1 por cada 42 RNV; y 59 con bilirrubinemia mayor a 25 mg/dl, 1 por cada 428 RNV. La hiperbilirrubinemia fue más frecuente en varones, con RR 1,22 (IC 95% 1,04-1,44) y en pretérminos tardíos, con un RR 2,39 (IC 95% 1,96-2,93) comparado con RN de término. En los ingresados con más de 4 días, el principal factor asociado fue la baja de peso excesiva, y en los primeros 3 días, la incompatibilidad de grupo clásico. Tres de 10 pacientes con encefalopatía aguda, persistieron con compromiso neurológico, lo que significa 11,8 por 100.000 nacidos vivos. CONCLUSIONES: Los principales factores de riesgo para desarrollar hiperbilirrubinemia severa fueron prematurez, baja de peso excesiva, incompatibilidad de grupo clásico y sexo masculino. Estos hallazgos permiten focalizar la atención en grupos de riesgo y disminuir la probabilidad de daño neurológico.
INTRODUCTION: Hyperbilirubinemia is highly prevalent in newborns, with risk of neurological invol vement with bilirubinemia higher than 20 to 25 mg/dl. This progression is preventable with early de tection and treatment. OBJECTIVE: To describe the incidence and associated factors in hospitalized pa tients with hyperbilirubinemia higher than 20 mg/dl, and the follow-up of symptomatic cases during hospitalization. OATIENTS Y METHOD: Retrospective study of patients with severe hyperbilirubine mia, between 2013 and 2016. Risk factors were evaluated, stratifying by bilirubin level, admission age, and gestational age. The data were compared with Fisher's exact test, chi-square test, and relative risk (RR) in an Excel database, with an alpha error of p <0.05. The data were obtained from the electronic discharge summary and the medical record of secondary level follow-up. RESULTS: During the studied period, out of 25,288 live newborns (NB), 593 were hospitalized due to hyperbilirubinemia higher than 20 mg/dl, one per each 42 live NB; and 59 with bilirubinemia higher than 25 mg/dl, one per each 428 live NB. Hyperbilirubinemia was more frequent in males, with RR 1.22 (95% CI 1.04-1.44), and in late preterm newborns, with RR 2.39 (95% CI 1.96-2.93) compared with term NB. In those admitted with more than four days, the main associated factor was excessive weight loss, whereas in the first three days was classic group incompatibility. Three of ten cases with acute encephalopathy persisted with neurological involvement, which means 11.8 per 100,000 live births. CONCLUSIONS: The main risk factors for developing severe hyperbilirubinemia were prematurity, excessive weight loss, classic group incompatibility, and male sex. These findings allow to focus attention on risk groups and decrease the probability of neurological damage.
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Humanos , Masculino , Femenino , Recién Nacido , Pérdida de Peso , Edad Gestacional , Hiperbilirrubinemia Neonatal/epidemiología , Índice de Severidad de la Enfermedad , Incompatibilidad de Grupos Sanguíneos , Recien Nacido Prematuro , Factores Sexuales , Incidencia , Estudios Retrospectivos , Factores de Riesgo , Hiperbilirrubinemia Neonatal/etiologíaRESUMEN
Aunque la ictericia afecta a más de la mitad de los neonatos en la primera semana de vida, sólo un grupo de ellos pueden desarrollar hiperbilirrubinemia severa y estar en riesgo de desarrollar encefalopatía bilirrubínica. La afectación neurológica puede presentarse con un cuadro agudo (la encefalopatía bilirrubínica aguda), la cual puede o no progresar a una forma crónica (Kernicterus), o con una constelación de síntomas sensoriales, motores y cognitivos, subagudos o crónicos, dependiendo de la presencia de factores de riesgo que aumentan la susceptibilidad al daño neurológico. La bilirrubina libre interactúa con citoquinas inflamatorias y es la responsable del daño neuronal y de las células de la glía en el sistema nervioso central. A pesar de las diferentes medidas de prevención de hiperbilirrubinemia severa, se siguen reportando casos de Kernicterus sobre todo en países en vías de desarrollo, en algunos de los cuales constituyen un problema de salud pública.
Although jaundice affects more than half of infants in the first week of life, only a few of them develop severe hyperbilirubinemia and are at risk of developing bilirubin encephalopathy. Neurological involvement may occur acutely (acute bilirubin encephalopathy,) which may or may not progress to a chronic form (Kernicterus), or with a constellation of sensory, motor and cognitive, subacute or chronic symptoms, depending on the presence of risk factors that increase susceptibility to neurological damage. Free bilirubin interacts with inflammatory cytokines and is responsible for neuronal and glial cell damage in the central nervous system. Despite different methods to prevent severe hyperbilirubinemia, Kernicterus cases continue to be reported, especially in developing countries, including some where this condition constitutes a public health problem.
RESUMEN
OBJECTIVE: To evaluate the ability of the bilirubin-induced neurologic dysfunction (BIND) score to predict residual neurologic and auditory disability and to document the relationship of BIND score to total serum bilirubin (TSB) concentration. STUDY DESIGN: The BIND score (assessing mental status, muscle tone, and cry patterns) was obtained serially at 6- to 8-hour intervals in 220 near-term and full-term infants with severe hyperbilirubinemia. Neurologic and/or auditory outcomes at 3-5 months of age were correlated with the highest calculated BIND score. The BIND score was also correlated with TSB. RESULTS: Follow-up neurologic and auditory examinations were performed for 145/202 (72%) surviving infants. All infants with severe acute bilirubin encephalopathy (BIND scores 7-9) either died or suffered residual neurologic and auditory impairment. Of 24 cases with moderate encephalopathy (BIND 4-6), 15 (62.5%) resolved following aggressive intervention and were normal at follow-up. Three of 73 infants with mild encephalopathy (BIND scores 1-3) but severe jaundice (TSB ranging 33.5-38 mg/dL; 573-650 µmol/L) had residual neurologic and/or auditory impairment. A BIND score ≥4 had a specificity of 87.3% and a sensitivity of 97.4% for predicting poor neurologic outcomes (receiver operating characteristic analysis). BIND scores trended higher with severe hyperbilirubinemia (r2 = 0.54, P < .005), but 5/39 (13%) infants with TSB ≥36.5 mg/dL (624 µmol/L) had BIND scores ≤3, and normal outcomes at 3-5 months. CONCLUSIONS: The BIND score can be used to evaluate the severity of acute bilirubin encephalopathy and predict residual neurologic and hearing dysfunction.
Asunto(s)
Bilirrubina/sangre , Discapacidades del Desarrollo/fisiopatología , Ictericia Neonatal/diagnóstico , Kernicterus/diagnóstico , Enfermedad Aguda , Estudios de Cohortes , Discapacidades del Desarrollo/epidemiología , Femenino , Estudios de Seguimiento , Edad Gestacional , Humanos , Incidencia , Lactante , Recién Nacido , Recien Nacido Prematuro , Ictericia Neonatal/epidemiología , Kernicterus/epidemiología , Masculino , Examen Neurológico , Valor Predictivo de las Pruebas , Curva ROC , Estudios Retrospectivos , Medición de Riesgo , Sensibilidad y Especificidad , Índice de Severidad de la Enfermedad , Factores de TiempoRESUMEN
El síndrome de Crigler Najjar II aparece por un déficit en la conjugación de la bilirrubina debido a la deficiencia parcial de la enzima uridindifosfato-glucuronil transferasa. Por lo general, tiene un curso benigno, a diferencia del Crigler Najjar de tipo I, donde el déficit enzimático es total y los afectados mueren a edades tempranas. Se presenta el caso de una adolescente de16 años con hiperbilirrubinemia indirecta, síndrome convulsivante y parálisis cerebral. Una correcta historia clínica con estudio genealógico y pruebas funcionales apropiadas, permitieron determinar el diagnóstico definitivo. Esta enfermedad genética se transmite de forma autosómica recesiva, tiene una prevalencia muy baja a nivel mundial y constituye, en general, un reto diagnóstico para los médico.(AU)
Crigler Najjar syndrome type II is related to a defect of bilirubin conjugation due to partial deficiency of the enzyme uridine diphosphate-glucuronyl transferase. Usually has a benign course, unlike Crigler Najjar type I, where the enzyme deficiencyis total and the affected patients usually die at early ages. We present the case of a teenager with indirect hyperbilirubinemia, seizures and cerebral palsy. A good clinical historywith pedigree and appropriate functional tests allowed us to determine the definitive diagnosis. This is an autosomal recessive disorder, has a very low prevalence worldwide, and is adiagnostic challenge for physicians in general.(AU)
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Humanos , Adolescente , Femenino , Hiperbilirrubinemia Hereditaria/complicaciones , Síndrome de Crigler-Najjar/diagnóstico , Síndrome de Crigler-Najjar/etiología , KernicterusRESUMEN
El síndrome de Crigler Najjar II aparece por un déficit en la conjugación de la bilirrubina debido a la deficiencia parcial de la enzima uridindifosfato-glucuronil transferasa. Por lo general, tiene un curso benigno, a diferencia del Crigler Najjar de tipo I, donde el déficit enzimático es total y los afectados mueren a edades tempranas. Se presenta el caso de una adolescente de16 años con hiperbilirrubinemia indirecta, síndrome convulsivante y parálisis cerebral. Una correcta historia clínica con estudio genealógico y pruebas funcionales apropiadas, permitieron determinar el diagnóstico definitivo. Esta enfermedad genética se transmite de forma autosómica recesiva, tiene una prevalencia muy baja a nivel mundial y constituye, en general, un reto diagnóstico para los médico.
Crigler Najjar syndrome type II is related to a defect of bilirubin conjugation due to partial deficiency of the enzyme uridine diphosphate-glucuronyl transferase. Usually has a benign course, unlike Crigler Najjar type I, where the enzyme deficiencyis total and the affected patients usually die at early ages. We present the case of a teenager with indirect hyperbilirubinemia, seizures and cerebral palsy. A good clinical historywith pedigree and appropriate functional tests allowed us to determine the definitive diagnosis. This is an autosomal recessive disorder, has a very low prevalence worldwide, and is adiagnostic challenge for physicians in general.