Perinatal deaths preventable by intervention of the Unified Health System of Brazil. / Óbitos perinatais evitáveis por intervenções do Sistema Único de Saúde do Brasil.

OBJECTIVE: To describe the epidemiological characteristics of perinatal deaths through the actions of the Unified Health System. METHODS: This is a descriptive study of temporal analysis with a population of perinatal deaths of mothers residing in Recife, Brazil, from 2010 to 2014. A list was used to classify the preventable diseases and the variables were analysed using Epi lnfo™ version 7. RESULTS: The perinatal deaths totalled 1,756 (1,019 foetal and 737 neonatal premature) with a reduction of neonatal deaths (-15.8%) and an increase of foetal deaths (12.1%) in the study period. The main causes of death were foetus and newborn affected by the mother´s condition and asphyxia/hypoxia at birth. CONCLUSIONS: Most deaths were avoidable, especially in the group of appropriate care to mothers during pregnancy. Faults in the care provided to women at birth explain the percentage of deaths caused by asphyxia/hypoxia. The reduction of preventable perinatal mortality is associated with the increased access and quality of care, which ensures health promotion, disease prevention, treatment and specific and timely care.

Óbitos perinatais evitáveis por intervenções do Sistema Único de Saúde do Brasil / Muertes perinatales evitables por intervención del Sistema de Salud Pública / Perinatal deaths preventable by intervention of the Unified Health System of Brazil

Resumo OBJETIVO Descrever características epidemiológicas dos óbitos perinatais por ações do Sistema Público de Saúde. MÉTODOS Estudo descritivo de análise temporal, população composta por óbitos perinatais de mães residentes no Recife, 2010-2014. Utilizado Lista de causas de mortes evitáveis para classificar a evitabilidade e EpiInfo versão 7 para análise das variáveis. RESULTADOS Ocorreram 1.756 óbitos perinatais (1.019 fetais e 737 neonatais precoce), observou-se redução dos óbitos neonatais precoces (-15,8%) e aumento dos fetais (12,1%). Apresentou como principais causas: feto e recém-nascido afetado por afecção materna e asfixia/hipóxia ao nascer. CONCLUSÕES A maior parte dos óbitos foi evitável, concentrando-se no grupamento de assistência adequada dispensada à mulher na gestação. Lacunas na assistência dispensada à mulher no parto, explicam o percentual de asfixia/hipóxia. Redução da mortalidade perinatal evitável associa-se à ampliação do acesso e qualidade da assistência para garantir promoção, prevenção, tratamento, cuidados específicos e oportunos.

Resumen OBJETIVO Describir las características epidemiológicas de las muertes perinatales por acciones del Sistema de Salud Pública. MÉTODOS Estudio descriptivo del análisis temporal, población compuesta por muertes perinatales de madres residentes en Recife, 2010-2014. Lista de causas de muertes evitables para clasificar la evitación y, EpiInfo versión 7 para el análisis de variables. RESULTADOS Hubo 1.756 muertes perinatales (1.019 fetales, 737 prematuros neonatos), reducción de muertes neonatales tempranas (-15,8%) y aumento fetal (12,1%). Principales causas: feto y recién-nacido afectados por afección materna y asfixia / hipoxia al nacer. CONCLUSIONES La mayoría de las muertes fueron evitables, concentrándose en la agrupación adecuada de la atención prestada a la mujer durante el embarazo. Las fallas en el cuidado dado a la mujer al nacer explican el porcentaje de asfixia/hipoxia. La reducción de la mortalidad perinatal prevenible se asocia con un mayor acceso y calidad de atención para asegurar la promoción, prevención, tratamiento y atención específica y oportuna.

Abstract OBJECTIVE To describe the epidemiological characteristics of perinatal deaths through the actions of the Unified Health System. METHODS This is a descriptive study of temporal analysis with a population of perinatal deaths of mothers residing in Recife, Brazil, from 2010 to 2014. A list was used to classify the preventable diseases and the variables were analysed using Epi lnfo™ version 7 RESULTS The perinatal deaths totalled 1,756 (1,019 foetal and 737 neonatal premature) with a reduction of neonatal deaths (-15.8%) and an increase of foetal deaths (12.1%) in the study period. The main causes of death were foetus and newborn affected by the mother´s condition and asphyxia/hypoxia at birth. CONCLUSIONS Most deaths were avoidable, especially in the group of appropriate care to mothers during pregnancy. Faults in the care provided to women at birth explain the percentage of deaths caused by asphyxia/hypoxia. The reduction of preventable perinatal mortality is associated with the increased access and quality of care, which ensures health promotion, disease prevention, treatment and specific and timely care.

Early neonatal deaths associated with perinatal asphyxia in infants ≥2500g in Brazil / Óbitos neonatais precoces associados à asfixia perinatal em neonatos ≥2500g no Brasil

Abstract Objective: To assess the annual burden of early neonatal deaths associated with perinatal asphyxia in infants weighing ≥2500 g in Brazil from 2005 to 2010. Methods: The population study enrolled all live births of infants with birth weight ≥2500 g and without malformations who died up to six days after birth with perinatal asphyxia, defined as intrauterine hypoxia, asphyxia at birth, or meconium aspiration syndrome. The cause of death was written in any field of the death certificate, according to International Classification of Diseases,10th Revision (P20.0, P21.0, and P24.0). An active search was performed in 27 Brazilian federative units. The chi-squared test for trend was applied to analyze early neonatal mortality ratios associated with perinatal asphyxia by study year. Results: A total of 10,675 infants weighing ≥2500 g without malformations died within six days after birth with perinatal asphyxia. Deaths occurred in the first 24 h after birth in 71% of the infants. Meconium aspiration syndrome was reported in 4076 (38%) of these deaths. The asphyxia-specific early neonatal mortality ratio decreased from 0.81 in 2005 to 0.65 per 1000 live births in 2010 in Brazil (p < 0.001); the meconium aspiration syndrome-specific early neonatal mortality ratio remained between 0.20 and 0.29 per 1000 live births during the study period. Conclusions: Despite the decreasing rates in Brazil from 2005 to 2010, early neonatal mortality rates associated with perinatal asphyxia in infants in the better spectrum of birth weight and without congenital malformations are still high, and meconium aspiration syndrome plays a major role.

Resumo Objetivo: Avaliar a taxa anual de óbitos neonatais precoces associados à asfixia perinatal em neonatos de peso ≥ 2.500 g no Brasil de 2005 a 2010. Métodos: A população do estudo envolveu todos os nascidos vivos de neonatos com peso ao nascer ≥ 2.500 g e sem malformações que morreram até seis dias após o nascimento por asfixia perinatal, definida como hipóxia intrauterina, asfixia no nascimento ou síndrome de aspiração de mecônio. A causa do óbito foi escrita em qualquer linha do atestado de óbito, de acordo com a Classificação Internacional de Doenças, 10a Revisão (P20.0, P21.0 e P24.0). Foi feita uma pesquisa ativa em 27 unidades federativas brasileiras. O teste qui-quadrado de tendência foi aplicado para analisar os índices de mortalidade neonatal associados a asfixia perinatal até o ano do estudo. Resultados: Morreram 10.675 neonatos com peso ≥ 2.500 g sem malformações até 0-6 dias após o nascimento por asfixia perinatal. Os óbitos ocorreram nas primeiras 24 horas após o nascimento em 71% dos neonatos. A síndrome de aspiração de mecônio foi relatada em 4.076 (38%) dos óbitos. O índice de mortalidade neonatal precoce relacionada à asfixia caiu de 0,81 em 2005 para 0,65 por 1.000 nascidos vivos em 2010 no Brasil (p < 0,001); o índice de mortalidade neonatal precoce relacionada a síndrome de aspiração de mecônio permaneceu entre 0,20-0,29 por 1.000 nascidos vivos durante o período do estudo. Conclusões: Apesar da redução nas taxas no Brasil de 2005 a 2010, as taxas de mortalidade neonatal precoce associadas à asfixia perinatal em neonatos no melhor espectro de peso ao nascer e sem malformações congênitas ainda são altas e a síndrome de aspiração de mecônio desempenha um importante papel.

Urine neutrophil gelatinase-associated lipocalin in asphyxiated neonates: a prospective cohort study.

BACKGROUND: Acute kidney injury (AKI) is the most common complication of perinatal asphyxia. Recent research indicates that urine neutrophil gelatinase-associated lipocalin (NGAL) is an early marker for AKI; yet, there is a paucity of data about its use in term neonates with perinatal asphyxia. METHODS: A prospective cohort study was conducted on 108 term babies in the new-born unit of Pumwani Maternity Hospital and Kenyatta National Hospital. Urine NGAL and serum creatinine were measured in 108 term asphyxiated neonates on days 1 and 3 of life. RESULTS: One-hundred and eight patients were recruited (male:female 1.4:1). At a cut-off of 250 ng/ml, urine NGAL had an acceptable discriminative capability of predicting AKI (area under the curve 0.724). The sensitivity, specificity, positive and negative predictive value and likelihood ratios were 88, 56, 30, 95%, 2 and 0.2 respectively. Urine NGAL levels were significantly higher in patients with AKI compared with those without AKI. An NGAL level greater than 250 ng/ml on day 1 was significantly associated with severe hypoxic ischaemic encephalopathy (HIE); odds ratio = 8.9 (95% CI 1.78-37.69) and mortality; odds ratio = 8.9 (95% CI 1.78-37.69). CONCLUSION: Urine NGAL is a good screening test for the early diagnosis of AKI. It is also a predictor of mortality and severity of HIE in asphyxiated neonates.

Claims for compensation after alleged birth asphyxia: a nationwide study covering 15 years.

OBJECTIVE: To analyze compensation claims with neurological sequela or death following alleged birth asphyxia. DESIGN: A cohort study. SETTING: A nationwide study in Norway. SAMPLE: All claims made to The Norwegian System of Compensation to Patients (NPE) concerning sequela related to alleged birth asphyxia, between 1994 and 2008. A total of 315 claims of which 161 were awarded compensation. METHODS: Examination of hospital records, experts' assessments and the decisions made by the NPE, the appeal body and courts of law. MAIN OUTCOME MEASURES: Characteristics of deliveries resulting in intrapartum asphyxia and causes of substandard care categorized in eight groups. RESULTS: In the 161 compensated cases, 107 children survived (96 with neurological sequela), and 54 children died. Human error was a frequent reason of substandard care, seen as inadequate fetal monitoring (50%), lack of clinical knowledge and skills (14%), noncompliance with clinical guidelines (11%), failure in referral for senior medical help (10%) and error in drug administration (4%). System errors were registered in only 3%, seen as poor organization of the department, lack of guidelines and time conflicts. The health personnel held responsible for substandard care was an obstetrician in 49% and a midwife in 46%. CONCLUSIONS: Substandard care is common in birth asphyxia, and human error is the cause in most cases. Inadequate fetal monitoring and lack of clinical knowledge and skills are the most frequent reasons for compensation after birth asphyxia.

Asfixia perinatal associada à mortalidade neonatal precoce: estudo populacional dos óbitos evitáveis / Perinatal asphyxia associated with early neonatal mortality: populational study of avoidable deaths / Asfixia perinatal asociada a la mortalidad neonatal temprana: estudio de población de los óbitos evitables

OBJETIVO: Comparar o perfil epidemiológico dos óbitos neonatais precoces evitáveis associados à asfixia perinatal conforme a região de ocorrência do óbito no Estado de São Paulo. MÉTODOS: Coorte populacional constituída por 2.873 óbitos evitáveis até seis dias de vida associados à asfixia perinatal ocorridos entre janeiro de 2001 e dezembro de 2003. Considerou-se como asfixia perinatal a presença de hipóxia intraútero, asfixia ao nascer ou síndrome de aspiração de mecônio em qualquer linha da Declaração de Óbito original. Variáveis epidemiológicas também foram extraídas das Declarações de Nascido Vivo. RESULTADOS: No triênio, 1,71 mortes por 1.000 nascidos vivos estavam associadas à asfixia perinatal, correspondendo a 22% dos óbitos neonatais precoces. Dos 2.873 óbitos evitáveis, 761 (27%) ocorreram em São Paulo, capital; 640 (22%), na região metropolitana da capital; e 1.472 (51%), no interior do estado. Nas duas primeiras regiões predominaram as mortes em hospitais públicos, recém-nascidos com idade gestacional inferior a 37 semanas e peso abaixo de 2500g. No interior, os óbitos foram mais frequentes em entidades beneficentes, recém-nascidos a termo e com peso superior a 2500g. A maioria dos bebês nasceu durante o dia no município de residência materna e evoluiu para óbito no hospital de nascimento até 24 horas após o parto. A síndrome de aspiração de mecônio esteve presente em 18% dos óbitos. CONCLUSÕES: A asfixia perinatal é um contribuinte frequente para a morte neonatal precoce evitável no estado com o maior produto interno bruto per capita do Brasil, evidenciando a necessidade de intervenções específicas com enfoque regionalizado na assistência ao parto e ao nascimento.

OBJECTIVE: To compare the epidemiological profile of avoidable early neonatal deaths associated with perinatal asphyxia according to region of death in the State of São Paulo, Brazil. METHODS: Population-based cohort study including 2,873 avoidable deaths up to six days of life associated with perinatal asphyxia from January 2001 to December 2003. Perinatal asphyxia was considered if intrauterine hypoxia, birth asphyxia, or meconium aspiration syndrome were written in any line of the original Death Certificate. Epidemiological data were also extracted from the Birth Certificate. RESULTS: During the three years, 1.71 deaths per 1,000 live births were associated with perinatal asphyxia, which corresponded to 22% of the early neonatal deaths. From the 2,873 avoidable deaths, 761 (27%) occurred in São Paulo city; 640 (22%), in the metropolitan region of São Paulo city; and 1,472 (51%), in the countryside of the state. In the first two regions, deaths were more frequent in public hospitals, among newborns with gestational age of 36 weeks or less, and among babies weighing less than 2500g. In the countryside, mortality was more frequent in philanthropic hospitals, in term newborns and in neonates weighing over 2500g. Most of these neonates were born during daytime in their hometown and died at the same institution in which they were born within the first 24 hours after delivery. Meconium aspiration syndrome was related to 18% of the deaths. CONCLUSIONS: Perinatal asphyxia is a frequent contributor to the avoidable early neonatal death in the state with the highest gross domestic product per capita in Brazil, and it shows the need for specific interventions with regionalized focus during labor and birth care.

OBJETIVO: Comparar el perfil epidemiológico de los óbitos neonatales tempranos evitables asociados a la asfixia perinatal conforme a la región de ocurrencia del óbito en la provincia de São Paulo (Brasil). MÉTODOS: Cohorte de población constituida por 2.873 óbitos evitables hasta seis días de vida asociados a la asfixia perinatal ocurridos entre enero de 2001 y diciembre de 2003. Se consideró como asfixia perinatal la presencia de hipoxia intraútero, asfixia al nacer o síndrome de aspiración de meconio en cualquier línea de la Declaración de Óbito original. Variables epidemiológicas también fueron extraídas de las Declaraciones de Nacido Vivo. RESULTADOS: En el trienio, 1,71 muertes por 1.000 nacidos vivos estaban asociadas a la asfixia perinatal, correspondiendo al 22% de los óbitos neonatales tempranos. De los 2.873 óbitos evitables, 761 (27%) tuvieron lugar en São Paulo, capital; 640 (22%), en la región metropolitana de la capital; y 1.472 (51%) en el interior de la provincia. En las dos primeras regiones predominaron las muertes en hospitales públicos, recién nacidos con edad gestacional inferior a 37 semanas y peso inferior a 2.500g. En el interior, los óbitos fueron más frecuentes en entidades benéficas, recién nacidos a término y con peso superior a 2.500g. La mayoría de los bebés nació durante el día en el municipio de residencia materna y evolucionó a óbito en el hospital de nacimiento hasta 24 horas después del parto. El síndrome de aspiración de meconio estuvo presente en el 18% de los óbitos. CONCLUSIONES: La asfixia perinatal es un contribuyente frecuente a la muerte neonatal temprana evitable en la provincia con el más grande producto interno bruto per capita de Brasil, lo que evidencia la necesidad de intervenciones específicas con enfoque regionalizado en la asistencia al parto y al nacimiento.

Apgar score and neonatal mortality in a hospital located in the southern area of São Paulo City, Brazil / Escore de Apgar e mortalidade neonatal em um hospital localizado na zona sul do município de São Paulo

Objective: To correlate the Apgar score, and neonatal mortality and its causes at a hospital located in the southern area of São Paulo City. Methods: A retrospective study performed by analysis of medical charts (n=7,094) of all live newborns during the period of 2005 to 2009, with data up to 28 days of life in reference to weight, Apgar score, survival and cause of mortality. Cases were analyzed by the X² test (p < 0.05). Results: In 7,094 births, there were 139 deaths, 58.3% during the first week, and 3.6% of them with Apgar < 4 in the 1st minute. A positive association was found between mortality and this variable, with significantly declining values up to 2,000 g in weight. In the group with weight < 1,000 g, the association with Apgar < 4 in the 1st minute with mortality was three-fold greater than in the 1,000-1,500 g weight group, and 35-fold greater than in the ? 3,000 g group. Among newborns with Apgar 8-10, the rate of mortality and low weight was two times greater than in those with weight > 2,499 g. Fetal distress and prematurity were associated with early neonatal death; malformations and fetal distress to late mortality. The predictive value of death with Apgar < 4 varied, according to weight, from 62.74% in the < 1,000 g group to 5.5%, in the > 3,000 g group. Conclusions: The Apgar score proved linked to factors both epidemiological and related to attention given to the birth and neonatal mortality, and was associated with extremely low birth weight.

Objetivo: Correlacionar o escore de Apgar e a mortalidade neonatal e suas causas em um hospital localizado na zona Sul do município de São Paulo. Métodos: Estudo retrospectivo por análise de prontuário (n=7.094), de todos os recém-nascidos vivos, no período de 2005 a 2009, com dados referentes até os 28 dias de vida, quanto a peso, escore de Apgar, sobrevida e causa de mortalidade. Os casos foram analisados pelo teste do X² (p < 0,05). Resultados: Nos 7.094 nascimentos, houve 139 óbitos, 58,3% na primeira semana, 3,6% com Apgar < 4 no 1º minuto. Foi encontrada associação positiva entre mortalidade e essa variável, com valores decrescentes significantemente até o peso de 2.000 g. No grupo de peso < 1.000 g, a associação do Apgar < 4 no 1º minuto com mortalidade foi três vezes maior do que no grupo 1.000 a 1.500 g e 35 vezes maior do que no grupo ? 3.000 g. Entre os recém-nascidos com Apgar de 8 a 10, a mortalidade entre baixo peso foi duas vezes maior do que nos de peso > 2.499 g. O sofrimento fetal e a prematuridade se associaram a óbito neonatal precoce; malformações e o sofrimento fetal à mortalidade tardia. O valor preditivo de morrer quando o Apgar < 4 variou, conforme o peso, entre 62,74% no grupo < 1.000 g a 5,5% no grupo > 3.000 g. Conclusões: O escore de Apgar se mostrou ligado a fatores epidemiológicos e de atenção ao parto, à mortalidade neonatal e se associou a extremo baixo peso.

Mortalidad neonatal: enfrentando el futuro / Neonatal mortality: confronting the future

El objetivo fue estudiar la mortalidad neonatal de los años 2005 a 2008, conocer su ocurrencia, determinar características maternas, condiciones obstétricas y factores relacionados. Es un estudio observacional analítico de 164 neonatos. Para el lapso hubo 10180 recién nacidos vivos en el Departamento de Obstetricia y Ginecología. Departamento Clínico Integral de la Costa. Universidad de Carabobo. Hospital Dr. Adolfo Prince Lara, Puerto Cabello, Estado Carabobo. La mortalidad neonatal fue 16.11 por mil recién nacidos vivos o una muerte cada 62 nacidos vivos. Hubo predominio de madres de 24 años y menos (55,56%), en antecedentes familiares destacó la hipertensión arterial (30,86%) y diabetes (4,3%), en antecedentes personales la prematurez (16,1%). El diagnóstico de ingreso fue amenaza de parto prematuro 21,61%, trabajo de parto pre-término 19,14% y rotura prematura de membrana 19,75%. No realizaron control prenatal 64,2%; eran multigestas 63,6%, con edad de embarazo menor igual 36 a semanas 72,22% y resultado en parto normal 71,61%. Predominaron los fetos masculinos (53,66%), con peso menor igual 2.500 g (78,66%) y talla menor igual 49 cm (88,4%), el índice Apgar de 7 y menos (84,75%). El factor de muerte directo conocido prevaleciente en 164 casos fue la insuficiencia repiratoria (53,66%), seguida de sepsis (21,95%) y asfixia perinatal (19,51%).

El objetive was to study the neonatal mortality of the years 2005-2008, knowing its impact, determine the material characteristics, obstetric conditions and related factors. It is a observational and analytical study of 164 neonatal death. For the period there were 10.180 live births in the Department of Obstetrics and Gynecology, Hospital "Dr. Adolfo Prince Lara", Puerto Cabello, Estado Carabobo. The neonatal mortality was 16,11 per thousand live births, or one death every 62 births. There were more mothers 24 years or less (55.56%), in personal prematurity (16.1%). The initial diagnosis was premature labor 21.61%, labor preterm 19.14% and pre-term premature rupture of membranes 19.75%. No prenatal care 64.2%, were multiparous 63.6%, with gestational age minor igual 36 weeks 72.22%, and ended in normal delivery 71.61%. A predominance of male fetuses (53,66%) with weight minor igual 2500 g (78.66%) and height minor igual 49 cm (88.4%), Apgar Index of 7 or less (84.75%). Factor prevalent direct death in 164 cases was respiratory failure (53.66%), followed by sepsis (21.95%) and perinatal asphyxia (19.51%).

Genetic factors that influence short-term neurodevelopmental outcome in term hypoxic-ischaemic encephalopathic neonates.

It is difficult to predict outcome in neonates that experience perinatal hypoxic ischaemia. Morbidity and mortality may be affected by genetic factors that augment inflammatory and coagulative responses. This prospective study analysed the effects of proinflammatory cytokine gene polymorphisms (tumour necrosis factor-α [TNFA] 308G>A and interleukin-6 [IL6] 174G>C) and prothrombotic factor gene mutations (prothrombin G20210A, factor V Leiden G1691A and methylenetetra hydrofolate reductase [MTHFR] C677T) on the early neurological prognosis in 40 term hypoxic ischaemic encephalopathic neonates. There were significant relationships for Sarnat and Sarnat staging with electroencephalographic findings, transfontanelle ultrasound (US) results, early neonatal outcome and neurological morbidity. Genetic mutations in the prothrombotic proteins, the TNFA 308G>A polymorphism and the cerebrospinal fluid levels of TNF-α protein were not related to clinical stage, electroencephalography, transfontanelle US or neurological status at discharge or at postnatal months 6 and 12. The IL6 174GC genotype demonstrated a protective role, being significantly correlated with normal electroencephalography, transfontanelle US and normal neurological findings at discharge. In conclusion, the IL6 174GC gene polymorphism seems to play a role in determining the risk and/or severity of perinatal cerebral injury.

Placental pathology in asphyxiated newborns meeting the criteria for therapeutic hypothermia.

OBJECTIVE: We sought to describe placental findings in asphyxiated term newborns meeting therapeutic hypothermia criteria and to assess whether histopathologic correlation exists between these placental lesions and the severity of later brain injury. STUDY DESIGN: We conducted a prospective cohort study of the placentas of asphyxiated newborns, in whom later brain injury was defined by magnetic resonance imaging. RESULTS: A total of 23 newborns were enrolled. Eighty-seven percent of their placentas had an abnormality on the fetal side of the placenta, including umbilical cord lesions (39%), chorioamnionitis (35%) with fetal vasculitis (22%), chorionic plate meconium (30%), and fetal thrombotic vasculopathy (26%). A total of 48% displayed placental growth restriction. Chorioamnionitis with fetal vasculitis and chorionic plate meconium were significantly associated with brain injury (P = .03). Placental growth restriction appears to significantly offer protection against the development of these injuries (P = .03). CONCLUSION: Therapeutic hypothermia may not be effective in asphyxiated newborns whose placentas show evidence of chorioamnionitis with fetal vasculitis and chorionic plate meconium.

Acute kidney failure in neonatal period.

INTRODUCTION: Acute kidney failure (AKF) is a common clinical problem in neonatal intensive care units and is usually associated with a contributing condition such as sepsis, asphyxia, and heart failure. The aim of this study was to determine the types, frequency of associated contributing conditions, and short-term outcome of neonatal AKF. MATERIALS AND METHODS: Medical records of neonates with a diagnosis of AKF from March 2003 to September 2006 were studied in a tertiary care children's hospital in Tabriz, Iran. RESULTS: Of 6042 hospitalized neonates, 151 with documented AKF (100 boys and 51 girls) were reviewed in the study. Ninety-one patients (60.3%) had been referred from other cities. Fifty-seven patients (37.7%) developed AKF following a surgery. Causes of AKF were intrinsic kidney failure in 52.3%, prerenal in 42.4%, and postrenal in 5.3%. Oliguria was observed in 72.2% of the patients. Perinatal asphyxia was present in 29.8% of the neonates, sepsis in 28.5%, respiratory distress syndrome in 25.2%, dehydration in 24.2%, and heart failure in 21.2%. Most patients (85.4%) had more than 1 associated contributing condition. Mortality rate was 20.5%. Most patients (76.2%) were discharged with normal kidney function and 3.3% with diminished kidney function. Initial admission to NICU, female sex, septicemia, and the need for mechanical ventilation were associated with a higher mortality rate. CONCLUSIONS: The frequency of associated contributing conditions and short-term outcome of neonatal AKF in our institution is comparable with other studies; however, intrinsic kidney failure comprises the most common form of AKF in our patients.

Pulmonary dysfunction and therapeutic hypothermia in asphyxiated newborns: whole body versus selective head cooling.

Compared with whole body cooling (WBC), selective head cooling (SHC) of asphyxiated newborns presumably allows effective brain cooling with less systemic hypothermia and potentially fewer systemic adverse effects. It is not known if pulmonary dysfunction, one of the potential adverse systemic effects of therapeutic hypothermic neuroprotection, differs with the method of cooling. We sought to investigate if pulmonary mechanics and gas exchange during therapeutic hypothermia differ between WBC and SHC. The severity of pulmonary dysfunction was determined in 59 asphyxiated newborns receiving therapeutic hypothermic neuroprotection by either SHC ( N = 31) or WBC ( N = 28). Ventilatory parameters and simultaneous alveolar-arterial oxygen gradient (A-a DO (2)) and partial pressure of carbon dioxide, arterial (PaCO (2)) were measured before the start of cooling (baseline), and at 4, 8, 12, 24, 48, and 72 hours of cooling. The diagnosis of persistent pulmonary hypertension of the newborn (PPHN) was established by echocardiography. Clinical monitoring and treatment during cooling, whether SHC or WBC, were similar. All (96%) but two infants (from the SHC group) required mechanical ventilation of varying duration during cooling, and nine infants (15%) developed PPHN. The baseline ventilator pressures requirement, and A-a DO (2) were similar among the 48 ventilated infants without PPHN (WBC 23, SHC 25) at the start of cooling. Ventilatory requirements remained modest and did not differ with the method of cooling. Similar numbers of infants without PPHN were able to be extubated after improvement in respiratory status while being cooled (WBC 42.8% versus SHC 37.9%, P = 0.79, odds ratio [OR] 1.2, 95% confidence interval [CI] 0.4 to 3.5). Nine infants (WBC 5, SHC 4) developed PPHN. Six of the nine (WBC 4, SHC 2) required inhaled nitric oxide therapy, and one infant from the WBC group subsequently required extracorporeal membrane oxygenation. The incidence of PPHN was similar in both the WBC and SHC groups (17.8% versus 12.9%, P = 0.72, OR 1.5, 95% CI 0.3 to 6.1). Pulmonary dysfunction is common but not severe in asphyxiated infants during therapeutic hypothermia. Pulmonary mechanics and gas exchange do not differ with the method of achieving hypothermia.

Consequences of neonatal resuscitation with supplemental oxygen.

There has been considerable controversy surrounding the optimal inspired oxygen concentration for resuscitation of term and preterm infants. We have developed a rat pup model to quantify both physiologic and biochemical parameters associated with normoxic vs. hyperoxic resuscitation. We have confirmed existing human data that hyperoxic resuscitation of rat pups is associated with a significant delay in onset of spontaneous respiratory efforts. Both 40% and 100% inspired oxygen delayed onset of respiratory activity when compared to 21% oxygen. We have also documented, in the rat pup model, that hyperoxic resuscitation is associated with reduced levels of glutathione at 24 hours post resuscitation. The implications of these and other findings for human infants are that term asphyxiated babies can be safely resuscitated in 21% oxygen and that supplementary oxygen can be reserved for non-responders. In contrast, resuscitation of extremely low gestational age infants does appear to require an initial low inspired oxygen concentration (eg, 30%) with subsequent pulse oximetry titration to optimize oxygenation status.

Asfixia neonatal / Neonatal asphyxia

La asfixia neonatal sigue siendo un problema importante de mortalidad y morbilidad a largo plazo en las unidades de neonatología, a pesar de las mejorasen estudio y monitoreo perinatal. Su principal expresión clínica usada como sinónimo es la encefalopatía hipóxico isquemica. La presente revisión tiene el fin de recordar la etiopatogenia, fisiopatología, expresión clínica y actualizar el manejo y tratamiento establecido como experimental.

Brain white matter lesions correlated to newborns death and lethality

OBJECTIVES: to describe hospital lethality rates and factors correlated to death in neonates with brain white matter lesions. METHODS: a retrospective study was performed from January 1994 to December 2001. Neonates with white brain matter lesions were divided into survival and death groups and their medical files reviewed through the single blind method to determine evolution. Death certificates provided the cause of death. The groups were compared through correlation coefficients. Hospital lethality rate was calculated. RESULTS: ninety three cases of white brain matter lesions and seven deaths were determined. Hospital lethality rate was of 8.2. percent (95 percentCI: 2.4-14.0) independently from lesion occurrence time, and of 10.3 percent (95 percentCI: 3.3-17.3) for deaths occurred during prenatal and perinatal periods. Death was correlated to: Apgar score, non-cephalic presentation, gestational age, hyperglicemia, hypercalcemia, convulsion, respiratory insufficiency and atelectasy. CONCLUSIONS: hospital lethality was of 10.3 percent generating the following hypothesis: perinatal asphyxia must be the principal direct and indirect etiologic factor (aggravating the expression of prematurity and infection diseases), of prenatal and perinatal mortality among newborns with white brain matter lesions; and <7 Apgar score in the 5th minute associated to brain white matter lesions, are markers for perinatal asphyxia diagnosis.

OBJETIVOS: descrever a taxa de letalidade hospitalar e fatores correlacionados com o óbito em crianças com lesão da substância branca cerebral (LSB). MÉTODOS: estudo retrospectivo realizado de janeiro de 1994 a dezembro de 2001. Os neonatos com LSB foram divididos em sobreviventes ou óbito, e seus prontuários revisados de forma cega para a evolução. Dos atestados de óbito, a causa de morte. Os grupos foram comparados por coeficientes de correlação. Calculada a taxa de letalidade hospitalar. RESULTADOS: foram encontrados 93 casos de LSB e sete óbitos. A taxa de letalidade hospitalar foi de 8,2 por cento, (IC95 por cento: 2,4-14,0), independentemente da época de instalação da lesão, e de 10,3 por cento (IC95 por cento: 3,3-17,3) para aqueles de ocorrência pré/perinatal. O óbito correlacionou-se com: escore de Apgar, apresentação não-cefálica, idade gestacional, hiperglicemia, hipercalcemia, convulsão, insuficiência respiratória e atelectasia. CONCLUSÕES: a letalidade hospitalar foi de 10,3 por cento e as seguintes hipóteses foram geradas: a asfixia perinatal deve ser o principal fator etiológico, direto e indireto (agravando a expressão das doenças da prematuridade e da infecção), da mortalidade pré/perinatal entre neonatos com LSB; e o escore de Apgar do 5o minuto <7, associado à LSB, são marcadores para o diagnóstico de asfixia perinatal.

Neonatal mortality and morbidity in vertex-vertex second twins according to mode of delivery and birth weight.

OBJECTIVE: To assess the risk of neonatal mortality and morbidity in vertex-vertex second twins according to mode of delivery and birth weight. STUDY DESIGN: Data from a historical cohort study based on a twin registry in the US (1995-1997) were used. Multivariate logistic regression was used to control for maternal age, race, marital status, cigarette smoking during pregnancy, parity, medical complications, gestational age, and other confounders. RESULTS: A total of 86 041 vertex-vertex second twins were classified into two groups: second twins delivered by cesarean section after cesarean delivery of first twin (C-C) (43.0%), second twins whose co-twins delivered vaginally (V-X) (57.0%). In infants of birth weight>or=2500 g group, the risks of noncongenital anomaly-related death (adjusted odds ratio (aOR): 4.64, 95% confidence interval (95% CI): 1.90, 13.92), low Apgar score (aOR: 2.39, 95% CI: 1.43, 4.14), and ventilation use (aOR: 1.31, 95% CI: 1.18, 1.47) were higher in the V-X group compared with the C-C group. No asphyxia-related neonatal deaths occurred in C-C group, whereas the incidence of this death was 0.04% in the V-X group. CONCLUSION: The risks of neonatal mortality and morbidity are increased in vertex-vertex second twins with birth weight>or=2500 g whose co-twins delivered vaginally compared with second twins delivered by cesarean section after cesarean delivery of first twin.

Thrombopoietin level is increased in the serum of asphyxiated neonates: a prospective controlled study.

BACKGROUND: Thrombopoietin (TPO) is a growth factor that controls platelet production. Despite the known association of chronic hypoxia and acute asphyxia with hematologic changes, TPO had not been studied in neonatal asphyxia. OBJECTIVE: To assess TPO concentrations in the serum of asphyxiated and nonasphyxiated neonates, and examine any correlation with the severity of asphyxia. DESIGN/METHODS: This prospective study was carried out on 32 asphyxiated neonates and 30 control subjects admitted at Cairo University Medical Center. Asphyxia was defined if two of the following were found: (1) Apgar score /=-10 and (3) clinical evidence of perinatal asphyxia. Encephalopathy was classified clinically according to Sarnat's stages during the first day of life. Platelet count and TPO level (pg/ml) were measured at 1st, 3rd and 7th day of life. RESULTS: : TPO measured on the first day of life did not differ between cases and controls (900.2+/-526.4 vs 726.6+/-441.9 pg/ml, p=0.2). It increased on the 3rd day of life and was significantly higher in asphyxiated infants compared to controls (1291.4+/-627.9 vs 885.5+/-400.3 pg/ml, respectively; p=0.004). This difference remained significant in a logistic regression model controlling for birth weight, sex and mode of delivery (regression coefficient=476.9+/-146.8; p=0.002). In asphyxiated infants (n=32), encephalopathy was classified as mild (n=17), moderate (n=10) and severe (n=5). TPO correlated with the degree of clinical severity on the 7th day of life (r=0.59, p=0.003). TPO did not differ between survivors (n=24) and nonsurvivors (n=8) within the asphyxia group (1197.1+/-596.8 vs 1613.1+/-605.9 pg/ml; p=0.09). Platelet counts correlated negatively with TPO measured on day 1 (r=-0.415; p=0.02), day 3 (r=-0.64; p=0.001) and day 7 (r=-0.562; p=0.007). CONCLUSIONS: TPO increased and correlated with severity of asphyxia at 3 and 7 days of life. It correlated negatively with the platelet count at all times.

Brain damage and axonal injury in a Scottish cohort of neonatal deaths.

Despite the clinical and medicolegal significance attached to perinatal asphyxia, the neuropathological basis of this condition remains obscure. There are very few studies in the literature which correlate the pathological findings in neonatal brains with detailed epidemiological data, and none which are population based. In a Scotland-wide study of neonatal deaths, 70 brains have been examined. On the basis of glial and macrophage reactions, we previously identified infants with putative antepartum brain damage in this cohort and have related these reactions to signs of birth asphyxia. The present study explores the extent of neuronal/axonal injury in these infants since this is likely to be the basis for neurological deficits in surviving infants. We have also investigated these brains for beta-amyloid precursor protein (betaAPP) positivity to determine whether this is a useful marker of neuronal injury in neonates. Neuronal eosinophilia and karyorrhexes were detected in 43% and 27% of the cohort, respectively; maximally in the subiculum and ventral pons, but often present elsewhere. White matter damage was detected in 24% of cases but without classic cystic lesions of periventricular leucomalacia. betaAPP positivity was present in neuronal soma in 52% of cases and, in axons, in 27% of cases, and was seen from as early as 25-weeks gestation. Axonal bulbs were clearly delineated by betaAPP positivity and were usually located in the cerebral white matter and internal capsule, and infrequently in the brain stem. Although white matter damage and betaAPP axonal positivity were often detected in the same cases (P = 0.034), these features also occurred independently of each other. Both neuronal karyorrhexes and white matter betaAPP positivity were significantly correlated with the features of birth asphyxia, particularly a history of seizures. Immunocytochemistry for both betaAPP and glial fibrillary acidic protein proved useful in detecting neuropathological features which escaped detection on routine examination, particularly in preterm infants. The presence together of recent and older damage in individual brains suggests that there is an ongoing neuronal response to cerebral insults. We find that betaAPP is a useful marker of white matter damage in the neonatal brain. Immunopositivity for betaAPP in these circumstances is not attributable to inflicted or accidental trauma. While birth-related trauma cannot be ruled out, hypoxia/ischaemia is a likely cause in these infants. However, the exact pathogenesis of neuronal/axonal injury in the neonatal brain remains unclear.

Postmortem findings in term neonates.

Neonatal deaths in infants born at term are relatively rare in the USA, occurring in 0.9/1000 live births. Congenital malformations, perinatal asphyxia, infections and inborn errors of metabolism are the leading causes. Chromosomal malformation syndromes, congenital heart disease, pulmonary hypoplasia and severe neural tube defects comprise the majority of lethal malformations. Several skeletal dysplasias are lethal in the newborn infant. Group B Streptococcus still plays a major role in neonatal mortality while deaths due to other infectious agents have decreased. Hypoxic ischaemic encephalopathy is a significant cause of neonatal death. Inborn errors of metabolism have variable presentations but some, such as the fatty acid oxidation disorders, may present in neonates and cause sudden death.

Serum and urinary insulin-like growth factor-1 and tumor necrosis factor in neonates with and without acute renal failure.

Acute renal failure (ARF) in neonates may occur after renal ischemia. Growth factors participate in the tubular regeneration process. Insulin-like growth factor-1 (IGF-1) is produced in the kidney during the recovery phase of ARF. Tumor necrosis factor-alpha (TNFalpha) may play a role in renal apoptosis. We examined serum and urinary IGF-1 and TNFalpha in neonates with or without ARF after asphyxia, in order to assess their possible use as markers of renal damage and recovery. We studied 20 full-term asphyxiated neonates, 10 with ARF and 10 without ARF, and compared them with 13 normal newborns for 7 days after birth. Blood urea, creatinine, pH, base deficit, and serum and urine IGF-1 and TNFalpha were assessed. Neonates with ARF had more-severe acidosis than patients without ARF. All patients had lower serum IGF-1 values immediately after birth than control children. Serum IGF-1 remained low in the ARF patients. The initial urinary IGF-1 was higher in all patients compared with control newborns, and remained elevated for the rest of the study only in the ARF neonates. Serum and urinary TNFalpha concentrations were similar for all healthy and diseased neonates. Measurement of serum and urinary IGF-1 levels in ARF neonates might be of additional value for clinical assessment of ARF.