新生儿缺氧缺血性脑病临床与神经病理的相关性研究

目的观察新生儿缺氧缺血性脑病临床与神经病理之间的相关性。方法纳入2014-05—2015-04缺氧缺血性脑病患儿90例,进行免疫组化法观察不同生存时间的原纤维性酸性蛋白(GFAP)标记的星形胶质细胞的变化;比较宫内窘迫组(慢性缺氧缺血)、出生窒息组(急性缺氧缺血)、混合性缺氧缺血组(同时存在出生窒息及宫内窘迫)的原纤维酸性蛋白(GFAP)标记的星形胶质细胞的变化。结果生后24h内死亡组GFAP标记的星形胶质细胞的增生程度显著高于生后24~72h内死亡组、生后72h~6d死亡组,差异有统计学意义(P0.05);宫内窘迫组(慢性缺氧缺血)、出生窒息组(急性缺氧缺血)、混合性缺氧缺血组(同时存在出生窒息及宫内窘迫)的原纤维酸性蛋白(GFAP)标记的星形胶质细胞的变化比较,差异有统计学意义(P0.05)。结论缺氧缺血性脑病患儿的神经病理改变与HIE的病程、病情严重程度密切相关。     

新生儿缺氧缺血性脑病的疗效观察(186例回顾性分析)

目的总结分析我科3年来新生儿缺氧缺血性脑病(HIE)的系统治疗方法及相应近期疗效和远期预后,探讨改善预后的措施。方法对186例HIE患儿在各个阶段进行全面系统治疗,对临床资料和随访结果进行回顾性分析。结果186例HIE中足月儿149例(80.1％),早产儿37例(19.9％)。病死率7.5％(重度HIE20.5％,中度5.1％,轻度0)。随访109例,后遗症发生率16.5％(重度HIE60.7％,中度6.1％,轻度0)。早产儿HIE者中度预后不良占37.0％,重度60.7％。结论重度和早产儿HIE预后较差。针对不同阶段病情特点给予综合治疗,可显著改善患儿预后。     

新生儿缺氧缺血性脑病神经病理及凋亡与临床关系的研究

目的 观察新生儿缺氧缺血性脑病(hypoxic-ischemic encephalopathy,HIE)临床与神经病理之间的联系.方法 通过对25例新生儿HIE病理标本进行组织病理研究,并通过原位末端TUNEL法观察Hl条件下神经细胞凋亡的变化,进一步综合分析其与新生儿HIE的发生、病程之间的关系.结果 25例新生儿HIE脑标本均存在不同程度的脑水肿、颅内出血及神经细胞坏变.神经细胞坏变包括肿胀、脱失、海绵状变性及层状坏死,足月儿大脑灰质锥体细胞、小脑蒲肯野细胞更易受损,早产儿小脑颗粒层细胞易受损;慢性缺氧时大脑神经细胞病变的程度重,急性缺氧延髓改变重,混合性缺氧大脑灰质及延髓改变均较重;存活时间越长者小脑蒲肯野细胞病变的程度相对越轻.所有标本均存在不同程度的神经细胞凋亡,大脑以存活24h～6d神经细胞凋亡程度重(P<0.05),小脑以存活3d之内神经细胞凋亡程度重(P<0.05);延髓以存活24h～3d神经细胞凋亡程度最重(P<0.05).结论 新生儿HIE神经病理变化及凋亡与HIE的发生、发展密切相关.     

新生儿缺氧缺血性脑病60例护理体会

新生儿缺氧缺血脑病(HIE)是围生期新生儿因缺氧引起的脑部病变,主要由宫内窘迫、新生儿窒息缺氧引起.多见于足月儿,是围生期足月儿脑损伤的最常见原因.少数可发生在其他原因引起的脑损害,轻者预后良好,严重者在新生儿早期死亡或造成不可逆的脑损害,产生永久性神经功能缺陷[1].我院2008-02～2010-02共收治HIE患儿60例,现将护理体会介绍如下.     

纳洛酮治疗55例新生儿缺氧缺血性脑病的疗效观察

新生儿缺血缺氧性脑病（ＨＬＥ）是围产期新生儿缺血缺氧引起的脑部改变。脑组织的主要病理改变有水肿、软化、坏死和出血。围产期足月儿脑损伤最常见。据国外报道，大多数有脑瘫的儿童为足月儿，尽管足月儿脑瘫发病率为３．３８‰，较早产儿９０‰低，但足月儿占新生儿的９２％。若不及时、恰当治疗，易导致新生儿死亡、脑功能缺陷、智力障碍及癫痫病。１临床资料１．１一般资料 我院自１９９７～１９９９年收住ＨＬＥ５５例，均符合韩玉昆诊断标准［１］，随机分两组，治疗组２８例，男１４例，女１４例，轻度９例，中度１４例，重度５例…     

脑电图检查在新生儿缺氧缺血性脑病中的价值

目的 探讨脑电图(EEG)检查在新生儿缺氧缺血性脑病中的价值.方法 对36例临床确诊的新生儿缺氧缺血性脑病(HIE)患儿进行EEG检查,并对所有患儿进行1～3次EEG复查,观察其变化情况.结果 (1)36例HIE患儿中EEG异常的35例,占97.2%;正常的1例,占3.8%.(2)临床预后均较好HIE轻度患儿EEG异常率95.2%,中、重度HIE患儿EEG异常率均为100%.(3)临床后遗症发生率:EEG轻度异常预后均较好,中度异常者为33.3%,重度异常为100%.结论 脑电图检查能客观、直接的反映脑的功能状态及损害程度,对HIE早期诊断、指导治疗及判断预后有重要价值.     

缺氧缺血性脑病中血清钠的变化

目的 观察79例缺氧缺血性脑病(HIE)中血清钠的变化及相关因素。方法 对79例于生后2d收入院的足月HIE患儿按病情轻重分作轻度纽(26例)、中度组(34例)、重度组(19例)。在开始治疗前由股静脉采血2ml,送检血清钠的含量,并选择同期于生后2d内因黄疸收入院,出生Apgar评分均为10分,无胎儿宫内窘迫史,无先心病及肾脏病史,母无妊高征的30例足月儿作对 照。对数据作t检验。结果 (1)轻度HIE患儿急性期血清钠浓度为135.21±4.71,与对照组比较有显著性差异(P<0.01);中度HIE患儿急性期血清钠浓度为133.7±3.86,与对照组比较也有显著性差异(P<0.01);重度HIE患儿急性期血清钠浓度为131.8±2.85,与对照组比较有显著性差异(P<0.01)。因此缺氧缺血性脑病患儿急性期血清钠含量明显低于正常组;(2)中度HIE患儿与轻度HIE患儿血清钠含量相比有差异(P<0.05),重度HIE患儿与中度HIE患儿血清钠含量相比有显著性差异(P<0.01),由此,缺氧缺血性脑病患儿血清钠水平与缺氧缺血性脑病程度呈正相关,缺氧缺血性脑病程度越严重,血清钠水平越低。结论 患儿缺氧缺血性脑病时,易引起低钠血症。疾病越重,则血清钠含量越低。因此,HIE患儿应注意限制液体量,适量补充钠盐,以纠正稀释性低钠血症及失钠性低钠血症,并注意其它支持疗法(血清钠浓度单位为:     

贵州省人民医院癫痫儿童流行病学调查

目的调查贵州省人民医院癫痫儿童流行病学特点。方法对贵州省人民医院确诊的14岁以内癫痫患儿860例进行临床资料采集。随访患儿1年,根据治疗后发作频率的改变来进行疗效评价。对结果进行统计学分析。结果贵州省人民医院癫痫患儿临床特点为:以1~3岁幼儿为主;男性患儿较多;新生儿窒息、胎儿窘迫是导致儿童癫痫发作的主要围产期诱因,5.26%患儿有癫痫家族史。患儿中农村患儿占57.23%,其与城市患儿存在统计学差异的相关指标为:发病年龄、生产史、生产方式、围产期发生胎儿宫内窘迫及母孕期服药史(P0.05~0.01)。治疗依从性差是影响癫痫患儿预后的危险因素(OR=0.06,95%CI:0.023~0.152,P0.01)。结论贵州省人民医院癫痫儿童以1~3岁幼儿为主,男性患儿及农村患儿较多。良好的服药依从性是影响其预后的关键因素。改善农村生产条件、加强孕期健康宣教可能减少农村儿童癫痫发生率。     

新生儿缺氧缺血性脑病的护理体会

新生儿缺氧缺血性脑病 (hypoxicischemicencephalopathy ,HIE)是新生儿窒息后的严重并发症 ,病情重 ,病死率高 ,并可产生永久性神经功能障碍 ,如智力低下、癫、脑性瘫痪、痉挛和共济失调等。我们根据HIE患儿的特点 ,对 60例病人采取针对性护理 ,有效地促进了患儿康复 ,取得满意的疗效 ,现报告如下。1　对象及方法1 1　对象　 60例HIE患儿系我科 2 0 0 2 0 1～ 2 0 0 4 0 8收治的病人 ,男 3 8例 ,女 2 2例 ,轻度 45例 ,中重度 15例。早产、宫内发育迟缓 3 0例 ,占 5 0 % ;窒息与产伤 12例 ,占 2 0 % ;围产期窒息 18例 ,占 3 0 %。1 2…     

新生儿缺氧缺血性脑病急性期的护理

新生儿缺氧缺血性脑病(HIE)是指围产期缺氧窒息,导致脑的缺氧缺血性损害,包括特征性的神经病理及病理生理改变,并在临床上出现一系列脑病的表现,部分病例可留有不同程度神经系统后遗症[1].我科2004-10～2006-03收治56例HIE患儿,加强急性期护理,效果满意,总结如下.     

Intracranial hemorrhage in the full-term neonate and young infant: correlation of the location and outcome

The cranial computed tomography (CT) and outcome for 13 full-term neonates and 12 young infants with intracranial hemorrhage (ICH) were studied. The full-term neonates had perinatal asphyxia or neurological signs such as seizures. All infants were breast-fed and showed bleeding diathesis. In the full-term neonates there was a high incidence of intraventricular hemorrhage (IVH) and hemorrhage around the falx. The location of the hemorrhage on CT and brain pathology suggested that the original site of IVH might be the choroid plexus vessels in the lateral ventricle or in the subependymal layer. On the other hand, the sites of ICH in infants were multifocal compared with those in full-term neonates. Subdural hemorrhage (SDH) was seen more frequently and IVH less frequently in infants than in full-term neonates. The cases with SDH frequently showed accompanying cerebral infarction followed by porencephaly. Thus, SDH with cerebral low density on CT may predict a poor prognosis.     

Vascular endothelial growth factor in neonates with perinatal asphyxia

Background: Vascular endothelial growth factor (VEGF) is a polypeptide growth factor that is activated by tissue hypoxia. The role of VEGF in perinatal asphyxia in human neonates is yet to be clarified. In infants who develop moderate to severe acute hypoxic ischemic encephalopathy (HIE) it is crucial to clearly understand physiologic and biochemical changes that accompany HIE before a novel treatment can be developed. Objectives: To assess VEGF in cord blood of infants suffering from perinatal asphyxia, and to determine whether an association exists between increased concentrations of VEGF and the risk for development of encephalopathy. Study design: We prospectively studied 40 full term infants; of them 20 infants suffered from perinatal asphyxia, and 20 control infants of comparable age and sex. We obtained cord blood samples from all subjects immediately after delivery. Neurological examination and grading of HIE were performed during the first day of life. Results: Birth weight, gestational age and gender did not differ between the control (n = 20) and asphyxia (n = 20) groups. Within the asphyxia group four infants developed HIE; one with severe encephalopathy who died shortly after birth, while the other three infants had moderate HIE. Concentrations of VEGF were increased in infants with asphyxia when compared to controls (P  0.001). Within the asphyxia group, infants with HIE had significantly increased concentrations of VEGF when compared to non-HIE asphyxiated infants (P = 0.008). In the logistic regression model, VEGF inversely correlated with pH and PO₂ in cord blood, and Apgar scores at 1 min, while it did not associate with gestational age and birth weight. Conclusions: This study indicates that VEGF is increased in cord blood of neonates following birth asphyxia, and that VEGF is specifically most increased in infants who later developed encephalopathy. Further studies are required to determine the role of VEGF in brain insult. Such studies will help determine whether a therapeutic role for VEGF or VEGF inhibitors can exist for HIE infants.     

Comparative clinical study of preterm and full-term newborn neonatal seizures

OBJECTIVE: To compare the characteristics of neonatal seizures between preterm and full-term infants in intensive care unit. METHOD: A prospective study was developed with 104 high-risk newborn, 30 preterm and 74 full-term infants, with clinical seizures. The dependent variable was gestational age. Statistical analyses: Fisher's exact test, odds-ratio and Mann Whitney U test. RESULTS: There were significant differences (p<0.05): i) Premature neonates develop neonatal seizures later, probably related to the etiologies of the seizures; ii) Etiologically, there is a predominance of peri-intraventricular hemorrhage in preterm and of asphyxia in full term neonates; iii) Clonic seizures are most frequent in preterm and subtle seizures in full term neonates. CONCLUSION: Although the study had a clinical basis, it was possible to identify differences when the dependent variable was gestational age.     

A case of cardiac arrest encephalopathy in athetotic cerebral palsy]

A 25-year-old woman with cerebral palsy of spastic quadriplegia and athetosis showed typical cardiac arrest encephalopathy on neuropathology. The etiology of cerebral palsy was perinatal origin including prematurity, asphyxia and hyperbilirubinemia. Ventricular premature beats had developed since about 20 years of age. Muscle tone also increased with aging and symptoms of vago-vagal reflex were occasionally observed after eating. At 25 years, cardiac arrest occurred and cardiopulmonary resucitation was done immediately. She remained unconscious with absent corneal reflex and irregular respiration. EEG or auditory brain stem response showed flat activity. She died of respiratory failure 53 days after the episode of cardiac arrest. Neuropathology showed bilaterally symmetrical necrosis in the superior colliculi, gracilis nuclei, cuneate nuclei and spinotrigeminal nuclei accompanied with severe necrosis in the cerebrum and cerebellum. These findings in this adult case of total asphyxia were compatible with those observed in total plus partial asphyxia in the neonates. This discrepancy may be due to difference in cerebral maturity. Children or young adults with athetotic type cerebral palsy have a high risk of sudden death. Sudden cardiac arrest seems to play an important role in sudden death of these patients.     

新生儿行为神经测定对足月窒息儿预后的评价

目的 探讨新生儿行为神经测定(NBNA)对新生儿重症监护室(Mcu)足月窒息儿预后的预测意义.方法 对NICU住院治疗的326例足月窒息儿分别在12～14d龄、25～28d龄行NBNA测定,并随访至24月龄,行婴幼儿智能发育测定(CDCC)评估.结果 12～14d龄、25～28d龄NBNA评分异常(≤35分)组患儿在24月龄时行CDCC发育评估,智力发育落后[智力发育指数(MDI)≤69]发生率分别为61.54%、75.81%;运动发育落后[精神运动发育指数(PDI)≤69]发生率分别为65.38%、79.03%,与NBNA评分>35分组相比,差异均有统计学意义(P<0.05).且行为能力中的视听定向项目以及主动肌张力是NBNA的敏感指标.结论 NBNA评分对足月窒息儿的预后有较好的预测意义,对于12～14d龄后NBNA≤35分患儿,特别是视听定向及主动肌张力反应差的患儿需特别注意,要尽早对这些患儿行早期干预治疗.     

Damage of thalamus and basal ganglia in asphyxiated full-term neonates

Thalamic-striatal damage of symmetric bilateral distribution was found in four severely asphyxiated neonates born at term. Two patients showed evidence of bilateral thalamic-striatal necrosis and two showed hemorrhage of the same distribution. The four patients had a common history of prolonged asphyxia in the neonatal period combined with severe acidosis and respiratory insufficiency. The outcome was lethal in all children. Three patients survived for some time and showed additional evidence of generalized brain damage including cortical necrosis and subcortical leucomalacia and one patient was found to have intravital calcification of the putamen at 14 days of age. The appearance of thalamic-striatal damage in US, CCT and NMR imaging is discussed. Thalamic-striatal damage may not be detectable by US until several days after the initial insult. US does not permit a distinction between necrosis and hemorrhage, but CCT and NMR imaging may be successful. Only five infants with a comparable pattern of brain damage due to asphyxia have been described so far. Our own studies seem to indicate that thalamic-striatal damage is the hallmark of more widespread brain damage, and that it will be found more frequently if carefully looked for in asphyxiated neonates born at term.     

EEG and long-term outcome of term infants with neonatal hypoxic-ischemic encephalopathy.

OBJECTIVE: The prognostic value of a burst suppression pattern (BSP) on the electroencephalograph (EEG) in the prediction of long-term outcome for full term newborns with hypoxic-ischemic encephalopathy (HIE) is well established. The purpose of our study was to compare the patterns of burst suppression on EEG with long-term neurological outcome in term infants with HIE. METHODS: We retrospectively analyzed all records of all full-term newborn infants born at the University of Alberta Hospital between January 1, 1991 and December 31, 1992, who had clinical evidence of HIE and had at least one EEG during the first week of life. The EEGs were reviewed and blindly subclassified into a BSP, or if the pattern was not continuous or was incomplete, a modified burst suppression pattern (MBSP), based on specified electrophysiological criteria. The long-term neurological outcome was then correlated with the EEG pattern. RESULTS: Twenty-three full-term infants were studied. Fifteen had a BSP on EEG and 8 had a MBSP. Six of 15 infants with a BSP died. Of the 9 survivors with a BSP, 7 are disabled and two are normal. Of the 8 infants in the MBSP group, one infant died, two are disabled and 5 are normal. In the BSP group, 6/7 disabled infants developed cerebral palsy while in the MBSP group, only one developed cerebral palsy. CONCLUSION: The results are suggestive of a better outcome for infants with neonatal HIE and MBSP on EEG compared with those with a BSP. Subclassification of the EEG changes of neonatal HIE into BSP and MBSP may give a more accurate prediction of outcome in perinatal asphyxia and assist in discussion with parents about prognosis.     

Evaluation of the Cerebral Function Monitor as a tool for neurophysiological surveillance in neonatal intensive care patients

BACKGROUND: Cerebral function in critically ill infants is difficult to assess and would certainly require continuous monitoring. Therefore, this study was performed to evaluate the Cerebral Function Monitor (CFM) as a tool for continuous neurophysiological surveillance in the Neonatal Intensive Care Unit (NICU). PATIENTS: A total of 40 neurological risk neonates were included in the study. They were classified on the basis of their primary diagnoses as infants with clinically manifest seizures, suspected seizure activity, intracranial hemorrhage (ICH) and hypoxic-ischemic encephalopathy (HIE). A group of 20 neurologically normal (preterm and full-term) infants served as controls. RESULTS AND CONCLUSION: All patients with seizures showed pathologic patterns in both the CFM and the conventional EEG tracings. The patients with ICH showed depressed amplitudes, an increase in discontinuous activity, and a high incidence of seizure activity. The patients with HIE were characterized by depressed activities correlating with the severity of the pathology. Our results indicate that the CFM is a very helpful tool for neurophysiological surveillance in high-risk neonates.     

Evaluation of etiologic and prognostic factors in neonatal convulsions

This study evaluated etiologic and risk factors affecting long-term prognoses of neurologic outcomes in newborns with neonatal seizures. We enrolled patients at chronologic ages of 23-44 months, referred to the Department of Pediatric Neurology, Istanbul Medical Faculty, from January 1, 2007-December 31, 2009, after manifesting seizures in their first postnatal 28 days. Of 112 newborns, 41 were female, 71 were male, 33 were preterm, and 79 were full-term. Perinatal asphyxia (28.6%) and intracranial hemorrhage (17%) were the most common causes of neonatal seizures. Cerebral palsy developed in 27.6% of patients during follow-up. The incidence of epilepsy was 35.7%. Almost 50% of patients manifested developmental delay in one or more areas. Global developmental delay was the most common (50.8%) neurologic disorder. The correlation between gestational age or birth weight and adverse outcomes was nonsignificant. Etiology, Apgar score, need for resuscitation at birth, background electroencephalogram, neonatal status epilepticus, cranial imaging findings, type/duration of antiepileptic treatment, and response to acute treatment were all strong prognostic factors in neurologic outcomes. Neonatal seizures pose a threat of neurologic sequelae for preterm and full-term infants. Although the number of recognized etiologic factors in neonatal seizures has increased because of improvements in neonatology and diagnostic methods, perinatal asphyxia remains the most common factor.