南宁市新生儿窒息257例临床分析

1991年6月至1994年6月在南宁市妇幼保健院产科分娩活产新生儿3697例,其中轻度窒息86例.重度窒息171例,共计257例.发生率6.95%,通过对257例新生儿窒息进行分析.认为窒息与孕周、体重、分娩方式密切相关,与性别无关.过期产对缺氧耐受力差.低体重儿体内糖原储备少,巨大儿难产率高.分娩方式以臀牵引、胎吸产明显高于顺产、剖腹产,差异有显著意义.     

盐酸钠洛酮治疗新生儿重度窒息的临床分析

新生儿窒息可危及新生儿的生命，且影响预后。其抢救治疗必须及时、有效、分秒必争。我科于1992年5月-1994年12月用盐酸钠洛酮抢救重度窒息儿21例。取得了满意效果。现总结如下。     

围生期窒息新生儿血氧灌注指数监测的临床价值

目的:观察围生期窒息新生儿脉搏血氧灌注指数(PI)变化及其临床价值。方法:将77例足月窒息新生儿分为休克组和非休克组,均采用脉搏血氧灌注仪连续检测其出生时、治疗24h和72h后的PI值,并与正常对照组对比分析。结果:围生期窒息新生儿出生时PI值明显低于正常对照组(P<0.01);休克组出生时及治疗24h后PI值均低于非休克组(P<0.01);休克组患儿治疗72h后PI值较出生时明显升高(P<0.01)。结论:PI值对判断窒息新生儿病情程度、观察干预治疗效果有重要临床指导意义。     

新生儿窒息165例临床分析

新生儿窒息１６５例临床分析东北电业中心医院妇产科（沈阳，１１００１５）王学平本文对１９９１年１月至１９９３年１２月发生的１６５例新生儿窒息的原因及引起新生儿窒息的诸多因素中的几项主要因素进行分析研究，并与同时分娩的无新生儿窒息者进行对照，现报告如下。...     

新生儿窒息151例临床分析

新生儿窒息１５１例临床分析海军４０１医院妇产科（青岛，２６６０７１）王秀清新生儿窒息是产科临床中最常见的新生儿危象，是新生儿死亡及致残的主要原因，为了探讨其预防措施，现将我院１９８５年１月至１９９１年１２月１５１例新生儿窒息进行回顾性分析。临床资料一...     

足月新生儿窒息后阴离子间隙状态分析

酸碱平衡紊乱，严重损害机体代谢和生理功能，甚至威胁生命。新生儿由于酸碱平衡的调节功能低下，更易发生紊乱，而阴离子间隙（ＡＧ）在判断酸碱紊乱中有重要意义。本文就足月新生儿窒息复苏后ＡＧ状态作一分析。资料与方法１．患儿娩出后作１分钟Ａｐｇａｒ评分，≤３分...     

新生儿窒息心肌酶谱临床分析

目的；通过检测窒息新生儿心肌酶谱值，探讨临床意义，指导治疗及预防。方法：应用化学分析对27例窒息新生儿，25例正常新生儿的血清心肌酶谱进行检测和对比分析。结果：窒息新生儿心肌酶谱值明显高于对照组。结论：新生儿窒息可导致心肌酶谱升高，对心肌有损害，建议应用抗氧化剂治疗新生儿窒息。     

围生期窒息新生儿脑血流检测及意义

目的探索经颅多普勒检测脑血流对窒息新生儿脑损伤的临床意义.方法采用RIMED TRANS-LINK9000第四代彩色经颅多普勒超声仪对79例围生期窒息新生儿进行脑血流检测.结果 79例窒息新生儿有75例生后第一天脑血流速度下降(94.94%),且以大脑前、中动脉血流下降为著,与对照组比较有显著差异.结论经颅多普勒检测脑血流可早期诊断新生儿缺氧缺血性脑病,且较颅脑CT敏感性高,并可指导临床治疗.     

63例围生期新生儿死因分析

目的:探讨围生期新生儿死亡原因,为降低围生期新生儿死亡率而制定措施。方法:回顾分析近5年围生期新生儿死亡 63例临床资料。结果:63例围生期新生儿中死亡原因依次为:窒息、极低体重儿、败血症、出生缺陷、新生儿肺透明膜病、ASO溶血症、新生儿捂热综合征。结论:加强围生期保健,采取适宜分娩方式,预防窒息与早产的发生是降低围生期新生儿死亡率的关键。     

肌酸激酶同工酶对围产期窒息程度和短期预后的预测价值

目的评估血清肌酸激酶同工酶（CK-MB）的变化与围产期窒息程度及短期预后的相关性。方法采用前瞻性序贯试验研究方案,随机选择245例足月新生儿为研究对象,比较142例窒息新生儿和103例正常新生儿血清CK-MB水平差异,评估CK-MB与围产期窒息严重度指标1min Apgar评分、脐动脉血pH及其短期预后的相关性。结果窒息组CK-MB水平显著高于正常对照组,差异比较有统计学意义（P〈0.001）。CK-MB与围产期窒息严重度指标1min Ap-gar评分和脐动脉血pH呈负相关（P〈0.001）,与围产期窒息短期不利预后呈正相关（P〈0.001）。结论血清CK-MB有助于早期预测围产期窒息程度和短期预后。     

Prevalence and outcomes of acute kidney injury in term neonates with perinatal asphyxia

Background

The kidney is the most damaged organ in asphyxiated full-term infants. The severity of its damage is correlated with the severity of neurological damage. We determined the prevalence of perinatal asphyxia-associated acute kidney injury (AKI).

Methods

We conducted a prospective cohort study including 60 full-term neonates admitted at the Kenyatta National Hospital newborn unit (NBU) in Nairobi with hypoxic ischaemic encephalopathy (HIE) from June 2012 to November 2012. Renal function was assessed by measuring serum creatinine on day 3 of life. AKI was defined by a level of creatinine above 133 µmol/l. The degree of neurological impairment was determined daily until patient discharge, death or day 7 of life.

Results

Of the 60 infants 36.6% had HIE I, 51.6% HIE II and 11.8% HIE III. The prevalence of AKI was 11.7 %. There was a 15 fold increase risk of developing AKI in HIE III versus HIE I, p=0.034. Mortality rate in perinatal asphyxia associated AKI was 71.4 % with a 24 fold increase risk of death in neonates with AKI, p=0.001.

Conclusions

AKI is common and associated with poorer outcomes in perinatal asphyxia. Larger studies need to be done to correlate maternal factors and perinatal asphyxia-associated AKI.     

Delayed neuronal death following perinatal asphyxia in rat

 The consequences of perinatal asphyxia on the rat brain were studied 80 min to 8 days after birth with hematoxylin-eosin and in situ DNA double-strand-breaks labeling histochemistry. Asphyxia was induced by immersing fetus-containing uterus horns, removed from ready-to-deliver Sprague-Dawley rats, in a water bath at 37°C for various time periods (0–22 min). Spontaneous- and cesarean-delivered pups were used as controls. Perinatal asphyxia led to a decrease in the rate of survival, depending upon the length of the insult. No gross morphological changes could be seen in the brain of either control or asphyctic pups at any of the studied time points after delivery. However, in all groups, nuclear chromatin fragmentation, corresponding to in situ detection of DNA fragmentation, was observed at different stages. Nuclear fragmentation in control pups showed a specific distribution that appeared to be related to brain maturation, thus indicating programmed cell death. A progressive and delayed increase in nuclear fragmentation was found in asphyctic pups, which was dependent upon the length of the perinatal insult. The most evident effect was seen in frontal cortex, striatum, and cerebellum at postnatal day 8, although changes were also found in ventral-posterior thalamus, at days 1 and 2. Thus, nuclear chromatin fragmentation in asphyctic pups indicates a delayed post-asphyctic neuronal death. The absence of signs of inflammation or necrosis suggests that delayed neuronal cell death following perinatal asphyxia is an active, apoptosis-like phenomenon. Received: 16 August 1996 / Accepted: 6 December 1996     

窒息新生儿免疫功能变化及其临床意义的研究

目的观察窒息新生儿免疫功能的动态变化.方法选择40例窒息新生儿作为观察对象,同时选择30例健康新生儿作为对照组,于生后第1d和第10d两次采血,分别检测CD23、IgG、IgA、IgM、CD3、CD4、CD8等免疫指标.结果治疗前窒息新生儿与对照组相比细胞免疫和体液免疫功能明显抑制,且与窒息程度成正比.治疗后第10天重新检测各免疫指标,重度窒息组细胞免疫和体液免疫功能虽较治疗前好转,但仍低于对照组.轻度窒息组各免疫指标和对照组相比无明显差异.结论窒息新生儿免疫功能明显抑制,且与窒息程度成正比,重度窒息患儿免疫功能恢复较慢.     

514例新生儿窒息病因分析

新生儿窒息是新生儿缺氧缺血性脑病的主要原因，也是造成永久性中枢神经后遗症的首要因素［１］。本文通过５１４例新生儿窒息的临床分析，探讨该病的主要病因为脐带因素与过期妊娠，其中以脐带脱垂、脐带绕颈三周者本症发病最高。从而对新生儿窒息的预防提供一些参考资料。     

新生儿窒息对血糖的影响

目的探讨新生儿窒息引起的血糖变化,并分析窒息程度与血糖变化的关系。方法对窒息组及对照组新生儿进行血糖测定,并对结果进行比较分析。结果新生儿轻度窒息存在低血糖,而重度窒息时血糖升高。结论注意监测血糖,保持血糖稳定,减轻脑损伤。     

Plasticity of basal ganglia neurocircuitries following perinatal asphyxia: effect of nicotinamide

The potential neuroprotection of nicotinamide on the consequences of perinatal asphyxia was investigated with triple organotypic cultures. Perinatal asphyxia was induced in vivo by immersing foetuses-containing uterine horns removed from ready-to-deliver rats into a water bath for 20 min. Sibling caesarean-delivered pups were used as controls. Three days later tissue from substantia nigra, neostriatum and neocortex was dissected and placed on a coverslip. After a month, the cultures were processed for immunocytochemistry and phenotyped with markers against the NMDA receptor subunit NR1, tyrosine hydroxylase (TH), or neuronal nitric oxide synthase (nNOS). Some cultures were analysed for cell viability. Nicotinamide (0.8 mmol/kg, i.p.) or saline was administered to asphyxia-exposed and caesarean-delivered control pups 24, 48 and 72 h after birth. Perinatal asphyxia produced a decrease of cell viability in substantia nigra, but not in neostriatum or neocortex. Immunocytochemistry confirmed the vulnerability of the substantia nigra, demonstrating that there was a significant decrease in the number of NR1 and TH-positive (+) cells/mm², as well as a decrease in the length of TH⁺ processes, suggesting neurite atrophy. In control cultures, many nNOS⁺ cells were seen, with different features, regional distribution and cell body sizes. Following perinatal asphyxia, there was an increase in the number of nNOS⁺ cells/mm² in substantia nigra, versus a decrease in neostriatum including reduced neurite length, and no apparent changes in neocortex. The main effect of nicotinamide was seen in the neostriatum, preventing the asphyxia-induced decrease in the number of nNOS⁺ cells and neurite length. Nicotinamide also prevented the effect of perinatal asphyxia on TH-positive neurite length. The present results support the idea that nicotinamide can prevent the effects produced by a sustained energy-failure condition, as occurring during perinatal asphyxia. The contribution of VK and PM has been equally relevant.     

Effects of perinatal asphyxia on the mesostriatal/mesolimbic dopamine system of neonatal and 4-week-old male rats

The present study was undertaken in order to study the effects of perinatal asphyxia on tyrosine hydroxylase (TH) activity, dopamine levels and turnover, and dopamine metabolites (3,4-dihydroxyphenylacetic acid, DOPAC, homovanillic acid, HVA, and 3-methoxytyramine, 3-MT, analyzed by high-performance liquid chromatography, HPLC) measured in the basal ganglia of the 20- to 40-min-old newborn and 4-week-old male rat. Asphyxia was induced in pups by placing the fetuses, still in their uterus horns removed by hysterectomy from pregnant rats at full term, in a 37°C water bath for 15–16 min or 19–20 min. Following asphyxia, the uterus horns were opened, and the pups were removed and stimulated to breathe. A 100% and 50–80% pup survival was obtained following 15–16 min and 19–20 min of asphyxia, respectively. Acute changes were studied in brains from newborn pups 20–40 min after delivery, and long-term changes were studied in brains from 4-week-old rats. No changes in TH-activity could be observed in the substantia nigra/ventral tegmental area (SN/VTA), the striatum, or the accumbens nucleus/olfactory tubercle (ACC/TUB), in the newborn or the 4-week-old rat. In the newborn rat, 19–20 min of asphyxia increased (as compared to controls) dopamine levels in the SN/VTA to 136±14% and in the ACC/TUB to 160±10%, indicating an increased synthesis and/or release of dopamine. DOPAC levels were increased in the SN/VTA to 150±14% and in the ACC/TUB to 151±10%, and HVA levels were increased to 152±16% in the striatum and to 117±4% in the ACC/TUB. Following 15–16 min of asphyxia, dopamine levels were increased to 130±12% in the ACC/TUB, and DOPAC levels were increased to 135±6% and 130±12% in the SN/VTA and the ACC/TUB, respectively. This suggests that the increased dopamine levels may preferably reflect an increased release of dopamine following perinatal asphyxia. In the 4-week-old rat, dopamine levels were decreased in the SN/VTA to 71±4%, in the striatum to 52±8%, and in the ACC/TUB to 53±7%, following 19–20 min of perinatal asphyxia as compared to controls. No changes were observed in DOPAC, HVA, or 3-MT levels, indicating that the reduced dopamine levels reflect a reduced dopamine synthesis following perinatal asphyxia. A decrease in dopamine utilization was observed in the striatum to 15±8% and in the ACC/TUB to 9±13% following 19–20 min of perinatal asphyxia as compared to controls. This indicates that perinatal asphyxia produced long-lasting reductions in activity in the mesostriatal/mesolimbic dopamine systems in the 4-week-old rat.     

抚触对足月小样儿早期生长发育影响的临床研究

目的探讨抚触对足月小样儿生长发育的影响。方法将89例符合诊断标准的足月小样儿随机分成抚触组和对照组,比较2组患儿1w内体重的变化和28天内新生儿神经测定等发育指标。结果抚触组1w内生理性体重恢复速率快于对照组;新生儿神经行为评分高于对照组（P〈0.05）。结论抚触对足月小样儿早期体格和神经系统发育有明显的促进作用。     

新生儿窒息后心肌酶检测的临床价值探讨

目的探讨心肌酶在新生儿窒息后引起的缺氧性心肌损伤中的变化及临床价值。方法选择新生儿科86例窒息新生儿,按窒息程度分为轻度窒息、重度窒息两组,于24h内及治疗七天后抽血检测天冬氨酸氨基移换酶（AST）、乳酸脱氢酶（LDH）、肌酸激酶（CK）、肌酸激酶同工酶MB（CK-MB）、α-羟丁酸脱氢酶（α-HBDH）,并选择同期出生的正常新生儿30例作为对照组进行分析比较。结果新生儿轻、重度窒息组血清AST、LDH、CK、CK-MB、HBDH明显高于对照组,而重度窒息组又明显高于轻度窒息组,经统计学处理有非常显著意义（P〈0.01）。结论新生儿窒息早期即有心肌酶活性升高,升高水平与新生儿窒息程度呈正相关;心肌酶谱检测可作为新生儿窒息后提示心肌损害的早期、灵敏的重要指标,临床上有重要实用价值。