RESUMO

Resumen Las crisis convulsivas tienen una alta incidencia en la etapa neonatal, representando la principal manifes tación de disfunción neurológica. Ciertas condiciones fisiológicas del cerebro neonatal facilitan su aparición. Su diagnóstico puede ser un reto debido a que su semio logía no es tan clara comparado con niños mayores, y además, es necesario la confirmación por medio de EEG continuo o aEEG. Su reconocimiento oportuno es muy importante para un adecuado tratamiento y así evitar un impacto negative en el pronóstico a largo plazo. En la siguiente revisión, recapitulamos la fisiopatología, las causas y la clasificación de las crisis convulsivas neo natales, además de su correcto abordaje y las mejores opciones terapéuticas para su tratamiento dependiendo de la causa.

Abstract Seizures have a high incidence in the neonatal stage, being the main manifestation of neurological dysfunc tion. Certain physiological conditions of the neonatal brain facilitate its appearance. Its diagnosis can be a challenging because its semiology is not as clear as in older children, furthermore, confirmation by either EEG or aEEG is necessary. Its timely recognition is very im portant for adequate treatment and thus avoid a nega tive impact on the long-term outcome. In the following review, we recapitulate the pathophysiology, causes, and classification of neonatal seizures, as well as their correct approach and the best therapeutic options for their treatment depending on the cause.

RESUMO

Seizures have a high incidence in the neonatal stage, being the main manifestation of neurological dysfunction. Certain physiological conditions of the neonatal brain facilitate its appearance. Its diagnosis can be a challenging because its semiology is not as clear as in older children, furthermore, confirmation by either EEG or aEEG is necessary. Its timely recognition is very important for adequate treatment and thus avoid a negative impact on the long-term outcome. In the following review, we recapitulate the pathophysiology, causes, and classification of neonatal seizures, as well as their correct approach and the best therapeutic options for their treatment depending on the cause.

Las crisis convulsivas tienen una alta incidencia en la etapa neonatal, representando la principal manifestación de disfunción neurológica. Ciertas condiciones fisiológicas del cerebro neonatal facilitan su aparición. Su diagnóstico puede ser un reto debido a que su semiología no es tan clara comparado con niños mayores, y además, es necesario la confirmación por medio de EEG continuo o aEEG. Su reconocimiento oportuno es muy importante para un adecuado tratamiento y así evitar un impacto negative en el pronóstico a largo plazo. En la siguiente revisión, recapitulamos la fisiopatología, las causas y la clasificación de las crisis convulsivas neonatales, además de su correcto abordaje y las mejores opciones terapéuticas para su tratamiento dependiendo de la causa.

Assuntos

RESUMO

OBJECTIVE: To examine the frequency of placental abnormalities in a multicenter cohort of newborn infants with hypoxic-ischemic encephalopathy (HIE) and to determine the association between acuity of placental abnormalities and clinical characteristics of HIE. STUDY DESIGN: Infants born at ≥36 weeks of gestation (n = 500) with moderate or severe HIE were enrolled in the High-dose Erythropoietin for Asphyxia and Encephalopathy Trial. A placental pathologist blinded to clinical information reviewed clinical pathology reports to determine the presence of acute and chronic placental abnormalities using a standard classification system. RESULTS: Complete placental pathologic examination was available for 321 of 500 (64%) trial participants. Placental abnormalities were identified in 273 of 321 (85%) and were more common in infants ≥40 weeks of gestation (93% vs 81%, P = .01). A combination of acute and chronic placental abnormalities (43%) was more common than either acute (20%) or chronic (21%) abnormalities alone. Acute abnormalities included meconium staining of the placenta (41%) and histologic chorioamnionitis (39%). Chronic abnormalities included maternal vascular malperfusion (25%), villitis of unknown etiology (8%), and fetal vascular malperfusion (6%). Infants with chronic placental abnormalities exhibited a greater mean base deficit at birth (-15.9 vs -14.3, P = .049) than those without such abnormalities. Patients with HIE and acute placental lesions had older mean gestational ages (39.1 vs 38.0, P < .001) and greater rates of clinically diagnosed chorioamnionitis (25% vs 2%, P < .001) than those without acute abnormalities. CONCLUSIONS: Combined acute and chronic placental abnormalities were common in this cohort of infants with HIE, underscoring the complex causal pathways of HIE. TRIAL REGISTRATION: ClinicalTrials.gov: NCT02811263.

Assuntos

RESUMO

Perinatal asphyxia (PA) is a relevant cause of death at the time of labour, and when survival is stabilised, associated with short- and long-term developmental disabilities, requiring inordinate care by health systems and families. Its prevalence is high (1 to 10/1000 live births) worldwide. At present, there are few therapeutic options, apart from hypothermia, that regrettably provides only limited protection if applied shortly after the insult.PA implies a primary and a secondary insult. The primary insult relates to the lack of oxygen, and the secondary one to the oxidative stress triggered by re-oxygenation, formation of reactive oxygen (ROS) and reactive nitrogen (RNS) species, and overactivation of glutamate receptors and mitochondrial deficiencies. PA induces overactivation of a number of sentinel proteins, including hypoxia-induced factor-1α (HIF-1α) and the genome-protecting poly(ADP-ribose) polymerase-1 (PARP-1). Upon activation, PARP-1 consumes high amounts of ATP at a time when this metabolite is scarce, worsening in turn the energy crisis elicited by asphyxia. The energy crisis also impairs ATP-dependent transport, including glutamate re-uptake by astroglia. Nicotinamide, a PARP-1 inhibitor, protects against the metabolic cascade elicited by the primary stage, avoiding NAD+ exhaustion and the energetic crisis. Upon re-oxygenation, however, oxidative stress leads to nuclear translocation of the NF-κB subunit p65, overexpression of the pro-inflammatory cytokines IL-1ß and TNF-α, and glutamate-excitotoxicity, due to impairment of glial-glutamate transport, extracellular glutamate overflow, and overactivation of NMDA receptors, mainly of the extrasynaptic type. This leads to calcium influx, mitochondrial impairment, and inactivation of antioxidant enzymes, increasing further the activity of pro-oxidant enzymes, thereby making the surviving neonate vulnerable to recurrent metabolic insults whenever oxidative stress is involved. Here, we discuss evidence showing that (i) inhibition of PARP-1 overactivation by nicotinamide and (ii) inhibition of extrasynaptic NMDA receptor overactivation by memantine can prevent the short- and long-term consequences of PA. These hypotheses have been evaluated in a rat preclinical model of PA, aiming to identify the metabolic cascades responsible for the long-term consequences induced by the insult, also assessing postnatal vulnerability to recurrent oxidative insults. Thus, we present and discuss evidence demonstrating that PA induces long-term changes in metabolic pathways related to energy and oxidative stress, priming vulnerability of cells with both the neuronal and the glial phenotype. The effects induced by PA are region dependent, the substantia nigra being particularly prone to cell death. The issue of short- and long-term consequences of PA provides a framework for addressing a fundamental issue referred to plasticity of the CNS, since the perinatal insult triggers a domino-like sequence of events making the developing individual vulnerable to recurrent adverse conditions, decreasing his/her coping repertoire because of a relevant insult occurring at birth.

Assuntos

RESUMO

Patient identification matching problems are a major contributor to data integrity issues within electronic health records. These issues impede the improvement of healthcare quality through health information exchange and care coordination, and contribute to deaths resulting from medical errors. Despite best practices in the area of patient access and medical record management to avoid duplicating patient records, duplicate records continue to be a significant problem in healthcare. This study examined the underlying causes of duplicate records using a multisite data set of 398,939 patient records with confirmed duplicates and analyzed multiple reasons for data discrepancies between those record matches. The field that had the greatest proportion of mismatches (nondefault values) was the middle name, accounting for 58.30 percent of mismatches. The Social Security number was the second most frequent mismatch, occurring in 53.54 percent of the duplicate pairs. The majority of the mismatches in the name fields were the result of misspellings (53.14 percent in first name and 33.62 percent in last name) or swapped last name/first name, first name/middle name, or last name/middle name pairs. The use of more sophisticated technologies is critical to improving patient matching. However, no amount of advanced technology or increased data capture will completely eliminate human errors. Thus, the establishment of policies and procedures (such as standard naming conventions or search routines) for front-end and back-end staff to follow is foundational for the overall data integrity process. Training staff on standard policies and procedures will result in fewer duplicates created on the front end and more accurate duplicate record matching and merging on the back end. Furthermore, monitoring, analyzing trends, and identifying errors that occur are proactive ways to identify data integrity issues.

Assuntos

RESUMO

OBJECTIVE: to test the clinical utility of an early amplitude-integrated electroencephalography (aEEG) to predict short-term neurological outcome in term newborns at risk of neurology injury. METHODS: this was a prospective, descriptive study. The inclusion criteria were neonatal encephalopathy, neurologic disturbances, and severe respiratory distress syndrome. Sensitivity, specificity, positive and negative predictive values, and likelihood ratio (LR) were calculated. Clinical and demographic data were analyzed. Neurological outcome was defined as the sum of clinical, electroimaging, and neuroimaging findings. RESULTS: ten of the 21 monitored infants (48%) presented altered short-term neurologic outcome. The aEEG had 90% sensitivity, 82% specificity, 82% positive predictive value, and 90% negative predictive value. The positive LR was 4.95, and the negative LR was 0.12. In three of 12 (25%) encephalopathic infants, the aEEG allowed for a better definition of the severity of their condition. Seizures were detected in eight infants (38%), all subclinical at baseline, and none had a normal aEEG background pattern. The status of three infants (43%) evolved and required two or more drugs for treatment. CONCLUSIONS: in infants with encephalopathy or other severe illness, aEEG disturbances occur frequently. aEEG provided a better classification of the severity of encephalopathy, detected early subclinical seizures, and allowed for monitoring of the response to treatment. aEEG was a useful tool at the neonatal intensive care unit for predicting poor short-term neurological outcomes for all sick newborn. .

OBJETIVO: testar a utilidade clínica do aEEG precoce em recém-nascidos a termo com risco delesão neurológica, para prever resultados neurológicos de curto prazo. MÉTODOS: estudo prospectivo e descritivo. Os critérios de inclusão foram encefalopatia neonatal, distúrbios neurológicos e bebês com SARA grave. Sensibilidade, especificidade, valor preditivo positivo e negativo e razão de verossimilhança foram calculados. Dados clínicos edemográficos foram analisados. O resultado neurológico foi definido como a soma de conclusões clínicas, de eletro e de neuroimagem. RESULTADOS: dentre os 21 neonatos monitorados, dez (48%) apresentaram resultado neurológico de curto prazo alterado. O aEEG apresentou sensibilidade de 90%, especificidade de 82%, valor preditivo positivo de 82% e valor preditivo negativo de 90%. A VR positiva foi de 4,95, e a RV negativa de 0,12. Em três dos 12 (25%) neonatos com encefalopatia foi possível definir melhora gravidade de sua condição pelo aEEG. Foram detectadas convulsões em oito neonatos (38%), todas subclínicas no início do estudo, e nenhum apresentou um padrão histórico normal no aEEG. O estado de três neonatos (43%) evoluiu e exigiu dois ou mais medicamentos para tratamento. CONCLUSÕES: em neonatos com encefalopatia ou outra doença grave, os distúrbios no aEEGocorrem com mais frequência. O aEEG forneceu uma classificação melhor da gravidade da encefalopatia, detectou convulsões subclínicas precoces e permitiu que fosse feito o monitoramento da resposta ao tratamento. O aEEG é uma ferramenta útil para prever resultados neurológicos de curto prazo em todos os bebês doentes na UTIN. .

Assuntos

RESUMO

OBJECTIVE: to test the clinical utility of an early amplitude-integrated electroencephalography (aEEG) to predict short-term neurological outcome in term newborns at risk of neurology injury. METHODS: this was a prospective, descriptive study. The inclusion criteria were neonatal encephalopathy, neurologic disturbances, and severe respiratory distress syndrome. Sensitivity, specificity, positive and negative predictive values, and likelihood ratio (LR) were calculated. Clinical and demographic data were analyzed. Neurological outcome was defined as the sum of clinical, electroimaging, and neuroimaging findings. RESULTS: ten of the 21 monitored infants (48%) presented altered short-term neurologic outcome. The aEEG had 90% sensitivity, 82% specificity, 82% positive predictive value, and 90% negative predictive value. The positive LR was 4.95, and the negative LR was 0.12. In three of 12 (25%) encephalopathic infants, the aEEG allowed for a better definition of the severity of their condition. Seizures were detected in eight infants (38%), all subclinical at baseline, and none had a normal aEEG background pattern. The status of three infants (43%) evolved and required two or more drugs for treatment. CONCLUSIONS: in infants with encephalopathy or other severe illness, aEEG disturbances occur frequently. aEEG provided a better classification of the severity of encephalopathy, detected early subclinical seizures, and allowed for monitoring of the response to treatment. aEEG was a useful tool at the neonatal intensive care unit for predicting poor short-term neurological outcomes for all sick newborn.

Assuntos

Assuntos

RESUMO

OBJECTIVE: To determine whether early hyperoxemia in neonates with severe perinatal acidemia is associated with the development of hypoxic-ischemic encephalopathy (HIE). STUDY DESIGN: We identified 120 infants at ≥ 36 weeks gestational age with perinatal acidosis born at Parkland Hospital who qualified for a screening neurologic exam for cooling therapy. Based on a PaO2 measurement during the first hour of life, the cohort was divided into infants with hyperoxemia (PaO2 >100 mmHg) and those without hyperoxemia (PaO2 ≤ 100 mmHg). The rate of moderate-severe encephalopathy was compared between the groups using χ(2) analysis, as well as multiple logistic regression, taking into account baseline characteristics and confounding variables. RESULTS: Thirty-six infants (30%) had an initial PaO2 >100 mmHg. Infants with and without hyperoxemia had similar baseline maternal and infant characteristics. Infants with hyperoxemia had a higher incidence of HIE than those without hyperoxemia (58% vs 27%; P = .003). Admission hyperoxemia was associated with a higher risk of HIE (OR, 4; 95% CI, 1.4-10.5; adjusted P = .01). Among the neonates with moderate-severe HIE during the first 6 hours of life, those with hyperoxemia had a higher incidence of abnormal brain magnetic resonance imaging results, consistent with hypoxic ischemic injury, compared with those without hyperoxemia (79% vs 33%; P = .015). CONCLUSION: In neonates with perinatal acidemia, admission hyperoxemia is associated with a higher incidence of HIE. Among neonates with HIE, admission hyperoxemia is associated with abnormal brain magnetic resonance imaging findings. The judicious use of oxygen during and after resuscitation is warranted.

Assuntos

RESUMO

OBJECTIVES: To assess whether exergaming can induce measurable changes in heart rate (HR), energy expenditure (EE), and flow-mediated dilation (FMD) arterial function in healthy children. STUDY DESIGN: Fifteen children (8 males, 10.1 ± 0.7 years, body mass index 17.9 ± 2.4 kg.m(-2)) undertook a graded exercise test and 2 × 15 minute exergaming sessions (Xbox 360-Kinect); high intensity exergaming (HiE, Kinect Sports-200 m Hurdles) and low intensity exergaming (LoE, Kinect Sports-Ten Pin Bowling). Brachial artery FMD, a measure of endothelial function and arterial health, was measured before and immediately after each exergaming intervention. Actihearts were used to measure EE and HR during game play and a physical activity enjoyment scale assessed enjoyment. RESULTS: Average HR during HiE (146 ± 11 beats per minute) was greater than during LoE (104 ± 11 beats per minute, P < .05), a pattern reinforced by EE data (HiE 294.6 ± 75.2 J.min(-1).kg(-1), LoE 73.7 ± 44.0 J.min(-1).kg(-1), P < .05). FMD decreased after HiE (P < .05), whereas no change was observed following LoE. Subjects reported no differences in enjoyment between LoE and HiE. CONCLUSION: HiE, but not LoE, induced large HR and EE responses that were associated with effects on vascular function. This study suggests that an acute bout of HiE exergaming may provide a substrate for beneficial arterial adaptations in children.

Assuntos

RESUMO

OBJECTIVES: To determine the long-term neurodevelopmental outcome for children after hypoxic-ischemic encephalopathy (HIE) without major disability, and to examine neonatal injury patterns detected on cerebral magnetic resonance imaging (MRI) in relation to later deficits. STUDY DESIGN: Prospectively enrolled children with HIE and neonatal cerebral MRI data (n = 68) were examined at a mean age of 11.2 years (range, 8.2-15.7 years). Eleven children had a major disability (ie, cerebral palsy or mental retardation). Brain injury was scored according to the region and extent of injury. RESULTS: Children without major disability (n = 57) had lower full-scale and performance IQ scores compared with norms (P = .02 and .01, respectively), and the proportion of children with an IQ <85 was higher than expected (P = .04). Motor performance on the Zurich Neuromotor Assessment was affected in the pure motor, adaptive fine motor, and gross motor domains, as well as in the movement quality domain (all P < .001). Watershed injury pattern on neonatal MRI correlated with full-scale and verbal IQ scores (P = .006 and <.001, respectively), but neonatal MRI pattern did not correlate with motor performance in children without major disability. CONCLUSION: Children who sustained neonatal HIE without major disability are at increased risk for long-term intellectual, verbal, and motor deficits. The severity of watershed injury is correlated with later intellectual performance. Long-term follow-up examinations are necessary for early detection of neurodevelopmental impairment and early initiation of adequate therapies.

Assuntos

RESUMO

OBJECTIVE: To evaluate the electrographic seizure burden in neonates with hypoxic ischemic encephalopathy (HIE) treated with or without therapeutic hypothermia and stratified results by severity of HIE and severity of injury as assessed by magnetic resonance imaging (MRI). STUDY DESIGN: Between 2007 and 2011, video-electroencephalography (EEG) monitoring was initiated in neonates with moderate to severe HIE. Seizure burden (in seconds) was calculated, and brain MRI scans were quantitatively scored. Data were analyzed by ANOVA, the Student t test, and the χ(2) test. RESULTS: Sixty-nine neonates with moderate or severe HIE were prospectively enrolled, including 51 who received therapeutic hypothermia and 18 who did not. The mean duration of video-EEG monitoring was longer in the therapeutic hypothermia group (72 ± 34 hours vs 48 ± 34 hours; P = .01). The therapeutic hypothermia group had a lower electrographic seizure burden (log units) after controlling for injury, as assessed by MRI (2.9 ± 0.6 vs 6.2 ± 0.9; P = .003). A reduction in seizure burden was seen in neonates with moderate HIE (P = .0001), but not in those with severe HIE (P = .80). Among neonates with injury assessed by MRI, seizure burden was lower in those with mild (P = .0004) and moderate (P = .02) injury, but not in those with severe injury (P = .90). CONCLUSION: Therapeutic hypothermia was associated with reduced electrographic seizure burden in neonatal HIE. This effect was detected on video-EEG in infants with moderate HIE, but not in those with severe HIE. When stratified by injury as assessed by MRI, therapeutic hypothermia was associated with a reduced seizure burden in infants with mild and moderate injury, but not in those with severe injury.

Assuntos