新生儿缺氧缺血性脑病的CT诊断分析

新生儿缺氧缺血性脑病(hypoxic-ischemic encephalopathy, HIE)是由于各种因素引起的围产期脑缺氧缺血导致胎儿或新生儿的脑损伤,主要由宫内窘迫、新生儿窒息缺氧引起,少数可发生于其他原因引起的脑损害,多发生在窒息的足月儿,但也可发生在早产儿.     

血浆cTnI、CK-MBmass及CK-MBmass/CK比值在围产期窒息后的变化及其比较研究

评价血浆心肌肌钙蛋白Ⅰ(cTnI)、肌酸激酶心型同工酶质量(CK-MB-mass)、肌酸激酶心型同工酶质量/肌酸激酶活性的比值(CK-MBmass/CK)对围产期窒息后心肌损伤诊断价值,对71例围产期窒息新生儿及27例对照组新生儿生后6～48小时血浆cTnI、CK-MBmass及CK水平进行测定并计算CK-MBmass/CK比值,运用Wilcoxon秩和检验等方法进行分析.结果显示(1)新生儿窒息伴胎儿窘迫组(23例)cTnI、CK-MBmass、CK均显著高于对照组(27例);新生儿窒息伴胎儿窘迫组CK-MB-mass、CK显著高于单纯窘迫组(38例);单纯窒息组(10例)与对照组相比,仅CK-MB-mass/CK明显降低,其它指标差异无显著性.(2)围产期窒息组重度心脏损害患儿(8例)cTnI、CK-MBmass、CK均明显高于该组无重度心脏损害患儿(63例).(3)重度窒息组(17)例仅CK-MBmass、CK明显高于轻度窒息组(16例).因此,新生儿严重缺氧时,血浆cTnI、CK-MBmass、CK均明显增高,表明存在心肌损伤.cTnI虽对心肌损伤有高度特异性,但敏感性低于CK-MBmass、CK,且受胎龄影响;在判断早产儿心肌损伤时有一定的局限性.CK-MBmass/CK比值不宜作为围产期窒息后心肌损伤的生化指标.     

胎儿窘迫孕妇血及脐血一氧化氮

为了解胎儿窘迫时孕妇血及脐血中一氧化氮(NO)水平的变化及其与胎儿窘迫及新生儿窒息的关系.对42例胎儿窘迫孕妇(胎儿窘迫组)及36例正常晚孕妇女(对照组)母血、脐血中NO代谢产物亚硝酸/硝酸基(NO-2/NO-3)进行测定;以血气分析仪测定脐血pH值.结果显示胎儿窘迫组母血及脐血NO水平均较对照组明显下降(P均＜0.01),胎儿窘迫组与对照组相比脐血pH下降(P＜0.01);新生儿Apgar评分下降(P＜0.01);新生儿一分钟Apar评分≤7分的例数所占比例上升(P＜0.01).母血NO≤2.66umol/L,脐血NO≤2.03umol/L时新生儿窒息率明显上升(P＜0.01),与脐血pH值＜7.20时相比,两者新生儿窒息率无显著差异(P＞0.05).新生儿脐血pH值与脐血NO水平呈高度正相关(r=0.74,P＜0.01).结论母血及脐血NO下降与胎儿窘迫有一定关系;NO水平下降在预测新生儿窒息时与脐血pH值有同等价值;监测母血及脐血NO水平可作为诊断胎儿窘迫的指标之一.指导临床及时处理胎儿窘迫,为减少新生儿窒息的发生起很重要的作用.     

胎儿窘迫孕妇血及脐血一氧化氮及其与新生儿窒息的相关研究

为了解胎儿窘迫时孕妇血及脐血中一氧化氮 (NO)水平的变化及其与胎儿窘迫及新生儿窒息的关系。对 42例胎儿窘迫孕妇 (胎儿窘迫组 )及 36例正常晚孕妇女 (对照组 )母血、脐血中 NO代谢产物亚硝酸 /硝酸基 (NO- 2 / NO- 3 )进行测定 ;以血气分析仪测定脐血 p H值。结果显示　胎儿窘迫组母血及脐血 NO水平均较对照组明显下降 (P均 <0 .0 1 ) ,胎儿窘迫组与对照组相比 :脐血 p H下降 (P<0 .0 1 ) ;新生儿Apgar评分下降 (P<0 .0 1 ) ;新生儿一分钟 Apgar评分≤ 7分的例数所占比例上升(P<0 .0 1 )。母血 NO≤ 2 .6 6 umol/ L,脐血 NO≤ 2 .0 3umol/ L时新生儿窒息率明显上升 (P<0 .0 1 ) ,与脐血 p H值 <7.2 0时相比 ,两者新生儿窒息率无显著差异 (P>0 .0 5 )。新生儿脐血 p H值与脐血 NO水平呈高度正相关 (r=0 .74,P<0 .0 1 )。结论　母血及脐血 NO下降与胎儿窘迫有一定关系 ;NO水平下降在预测新生儿窒息时与脐血 p H值有同等价值 ;监测母血及脐血 NO水平可作为诊断胎儿窘迫的指标之一。指导临床及时处理胎儿窘迫 ,为减少新生儿窒息的发生起很重要的作用。     

2015围产期窒息、新生儿复苏和新生儿危重症诊治专题研讨会征文通知

中华医学会围产医学分会新生儿复苏学组定于2015年7月30日至8月1日在广东省深圳市召开"2015围产期窒息、新生儿复苏和新生儿危重症诊治专题研讨会",本次会议将以"围产期窒息、新生儿复苏和新生儿危重症诊治"为主题,邀请我国大陆、港台地区及国外知名专家做专题报告,欢迎围产同道踊跃参加。参会者可获得国家级Ⅰ类继续教育学分。会议征文主要内容:(1)围产期窒息:包括胎儿宫内窘迫、胎儿监护、新生儿窒息的诊断、对Apgar评分的评价等;     

新生儿缺氧缺血性脑病诊断标准

新生儿缺氧缺血性脑病(HIE)是指围产期窒息导致脑的缺氧缺血性损害,临床出现一系列中枢神经异常的表现。其诊断根据临床表现,同时具备以下4条者可确诊,第4条暂时不能确定者可作为拟诊病例:①有明确的可导致胎儿宫内窘迫的异常产科病史,以及严重的胎儿宫内窘迫表现(胎心<100次,持续5min以上;和/或羊水III度污染),或者在分娩过程中有明显窒息史;②出生时有重度窒息,指Apgar评分1min≤3分,并延续至5min时仍≤5分;或者出生时脐动脉血气pH≤7. 00;③出生后不久出现神经系统症状、并持续至24h以上;④排除电解质紊乱、颅内出血和产伤等原因引起的抽搐,以及宫内感染、遗传代谢性疾病和其他先天性疾病所引起的脑损伤。本诊断标准仅适用于足月新生儿HIE的诊断。     

胎粪吸入综合征的诊断和治疗

胎粪吸入综合征[1] (MAS)是新生儿期特有的呼吸道疾病 ,主要发生在足月儿及过期产儿 ,偶可发生在早产儿 ,发生率约为活产新生儿的 1.2 %～ 2 .2 %。其病因主要是由于胎儿发生宫内窘迫或产时窒息排出胎粪 ,吸入后发生肺部病变引起。临床上以低氧血症、高碳酸血症和酸中毒为特征 ,MAS是引起新生儿呼吸衰竭的主要原因之一。　　一、MAS的诊断1.病史 :( 1)大多数患儿有明确的宫内窘迫或出生窒息等缺氧史 ,Apgar评分常 <6分。 ( 2 )一般均有胎粪污染羊水史。羊水被胎粪污染后呈黄绿色或墨绿色 ,有时夹有胎粪颗粒或粪块 ,可自咽部或气管内吸出…     

脐血血气分析评价围生期窒息及新生儿预后的相关研究

目的通过分析脐动脉血血气与胎儿宫内窘迫、Apgar评分及新生儿窒息后并发症等因素之间的相关关系,探索脐血血气在评价围生期窒息及新生儿窒息预后中的作用。方法对2 281例新生儿生后即采集脐动脉血进行血气分析,同时将脐血pH值与出生后Apgar评分、宫内窘迫及窒息后并发症等相关因素进行对比分析。结果出生后Apgar评分与脐血pH值相关性强,评分越低,脐血pH值也越低。胎儿宫内窘迫与Apgar评分无显著相关,但与脐血pH值关系密切。低Apgar评分新生儿,如果脐血pH<7.20,尤其是pH<7.00,容易发生窒息后并发症。结论脐血血气分析比Apgar评分更客观、更直接地反映胎儿缺血、缺氧程度,并有助于判断新生儿预后。对有宫内窘迫征象及出生低Ap-gar评分的新生儿应常规做脐血血气分析。     

分娩方式对产妇初乳及新生儿胃肠激素的影响

围产期新生儿体内胃肠激素对新生儿生后胃肠功能的成熟与调节具有重要作用,且与许多围产期新生儿疾病的病理生理密切相关。为探讨阴道分娩与择期剖宫产对产妇初乳及新生儿血中胃肠激素水平的影响。我们应用放射免疫法对36例阴道分娩、23例择期剖宫产的产妇初乳及新生儿血中生长抑素(SS)、胃泌素(GAS)和胃动素(MTL)水平进行了测定。资料与方法一、对象2005年1月至2005年12月在我院出生的胎龄37~42周、出生日龄<3d、除外胎儿宫内窘迫、新生儿窒息、感染、溶血、遗传代谢性疾病等因素,出生体重2500~4000g的正常新生儿共59例作为研究对象,产…     

16例窒息新生儿血脂肪酸观察

围产期窒息缺氧可引起新生儿出生时血糖的改变,产生高血糖或低血糖,有关文献报道较多,但窒息缺氧对新生儿血脂代谢的影响,文献报道尚不多,为了观察窒息对新生儿血脂的影响,本文测定了一些新生儿在窒息时及窒息恢复后血脂肪酸的情况,现报告如下。     

Perinatal events and neonatal morbidity: An analysis of 5380 cases

The associations between perinatal events and neonatal morbidity were examined in a regional population of 5 380 newborns weighing 500 g or more. Perinatal mortality was 6.9%0, and neonatal mortality was 3.0%0. The low birth weight (< 2500 g) rate was 3.8%. The incidence of prematurity (gestational age < 37 weeks) was 6.6%. Respiratory distress syndrome was found in 0.9%, nonhaemolytic hyperbilirubinaemia in 16.5%, hypoglycaemia in 0.5%, septic infection in 0.8%, asphyxia in 4.0%, intracerebral haemorrhage in 0.3%, and cerebral symptoms in 0.7%. Maternal toxaemia, multiple pregnancy and maternal short stature were associated with spontaneous prematurity and a birthweight below the 10th percentile. Prematurity was associated with respiratory distress syndrome, hyperbilirubinaemia, hypoglycaemia, infection, low Apgar scores, asphyxia and intracerebral haemorrhage. Placental complications were associated with spontaneous prematurity, low Apgar scores and asphyxia. Premature rupture of the membranes was associated with spontaneous prematurity, infection, low Apgar scores and asphyxia.     

头颅CT影像在判断新生儿缺氧性脑损伤时的作用

目的：围生期缺氧可致新生儿脑损伤。该文探讨头颅CT对新生儿缺氧后脑损伤程度判断的作用。方法：收集有缺氧过程的足月新生儿114例,分为HIE组、窒息组、窘迫组;取同期正常新生儿20例为对照组,于生后2~7d做头部CT检测及NBNA评分。结果：HIE组、窒息组、窘迫组、对照组NBNA评分异常率及组间NBNA评分分值比较差异有显著性(均P<0.05)。4组间CT异常率比较及HIE组与其他3组CT异常率比较差异有显著性(均P<0.01),对照组、窘迫组、窒息组之间两两比较CT异常率没有差异(均P>0.05)。HIE组25例患儿中,临床分度为轻度HIE15例,中度HIE6例,重度HIE4例。CT分度为正常3例,轻度10例,中度7例、重度5例。HIE的CT分度与临床分度不完全吻合。CT对于轻、中、重度HIE诊断的灵敏度分别为47%,33%,50%,特异度为70%,74%,86%,准确度为48%,64%,80%。结论：头颅CT对HIE临床分度的判断存在不确定性,对宫内窘迫、窒息所致轻微脑损伤的判断更无把握。     

Clinical Evaluation of the Pathogenesis of Neonatal Asphyxia

The perinatal mortality rate in Japan decreased from 16.8 per 1000 live-births in 1964 to 4.5. in 1980, and the early neonatal mortality rate from 8.1 in 1964 to 1.1 in 1980. These decreases are mainly due to the improvement in prognosis of premature infants. The incidence of neonatal asphyxia in mature infants also decreased from 8.8% in 1967–68 to 5.1% in 1979–80. Fetal distress, breech delivery and Caesarean section were the major causes of neonatal asphyxia. Early detection of fetal distress and appropriate care decreased both the incidence of neonatal asphyxia and the neurological signs even in severely asphyxiated infants.     

Morbidity estimates of conditions originating in the perinatal period: United States, 1986 through 1987

Morbidity estimates of conditions originating in the perinatal period have not been reported in the United States. Conditions originating in the perinatal period were identified according to the International Classification of Diseases. The National Hospital Discharge Survey provided a weighted, nationally representative sample of newborns discharged each year from short-stay, nonfederal hospitals. From 1986 through 1987, 33.7% of all newborns had at least one nonteratologic perinatal condition. However, 6.8% of all newborns had physiologic jaundice as their only discharge diagnosis. Nonphysiologic jaundice was diagnosed in 4.4%, maternal causes of perinatal morbidity in 3.1%, birth trauma in 2.5%, fetal distress in 2.3%, birth asphyxia in 2.1%, and infections specific to the perinatal period in 2.0% of all newborn discharges. The average hospital stay for all newborns was 3.5 days, but it was 5.3 days for newborns with at least one nonteratologic perinatal condition and 2.6 for newborns discharged without a morbid condition. This study provides nationally representative estimates of perinatal morbidity useful for comparisons with smaller hospital-based samples. In addition, the study provides estimates of the public health impact of these conditions in terms of hospital stay days.     

Glucose transporters, hexokinase, and phosphofructokinase in brain of rats with perinatal asphyxia

Transport by glucose transporters from blood to the brain during hypoxic-ischemic conditions is well studied. However, the recent availability of a clinically related animal model of perinatal asphyxia and the fact that no concomitant determination of glucose transporters, parameters for glucose utilization, brain glucose, and cerebral blood flow (CBF) have been reported and the early phase of perinatal asphyxia has never been studied led us to perform the following study. Cesarean section was performed on full-term pregnant rats. The obtained pups within patent uterus horns were placed into a water bath at 37 degrees C from which they were subsequently removed after 5-20 min of graded asphyxia. Brain pH, brain tissue glucose, CBF, mRNA and activity of hexokinase and phosphofructokinase, and mRNA and protein of the glucose transporters GLUTI and GLUT3 were determined. Brain pH decreased and brain tissue glucose and CBF increased with the length of the asphyctic period; hexokinase and phosphofructokinase mRNA and activity were unchanged during the observation period. The mRNA and protein of both glucose transporters were comparable between normoxic and asphyctic groups. We show that glucose transport and utilization are unchanged in the early phase of perinatal asphyxia at a time point when CBF and brain glucose are already significantly increased and severe acidosis is present.     

Kinetics of serum S100B in newborns with intracranial lesions.

BACKGROUND: The purpose of the present study was to evaluate the usefulness of serum S100B as a clinical marker of intracranial lesions in newborns. METHODS: The study involved 22 normal and 40 diseased newborns. Serum S100B level was measured on days 1 and 6 in normal newborns. Diseased newborns were classified into four groups: birth asphyxia with hypoxic-ischemic encephalopathy (HIE); birth asphyxia without HIE; intracranial hemorrhage (mainly subarachnoid); and brain malformation. In each group the serum S100B level was measured on days 1, 2 and 6. Development was also assessed to investigate the relation between serum S100B level and prognosis at 18 months after birth. RESULTS: In normal newborns, serum S100B level was significantly higher in those with liquor to meconium stain than in those without. In diseased newborns, serum S100B level on day 1 was significantly higher in the HIE group than in all other groups (P < 0.05). There was no significant difference in serum S100B level between control and intracranial hemorrhage, or brain malformation. In newborns with birth asphyxia, serum S100B level was significantly higher in severe birth asphyxia than in mild or moderate birth asphyxia; two newborns with serum S100B level > or =10 microg/L on days 1 and 2 developed cerebral palsy, others with no increase of S100B were all developing normally. CONCLUSIONS: Serum S100B level is a useful marker of acute perinatal brain damage, and is particularly valuable for fetal distress. In newborns with birth asphyxia, serum S100B levels serve as a biochemical marker of HIE.     

How much of neonatal encephalopathy is due to birth asphyxia?

In the literature on neonatal encephalopathy, the pervasive assumption is that once infants with major malformations or infections have been excluded, most of the remaining cases are due to birth asphyxia. Assessing the proportion of neonatal encephalopathy that is due to asphyxia during birth is difficult because of problems in defining asphyxia and neonatal encephalopathy and in recognizing the cause of neonatal neurologic illness. Available evidence indicates that neonatal neurologic signs are not strongly related to obstetric complications, signs of fetal distress, or biochemical markers usually considered to indicate perinatal asphyxia. Most studies that have sought positive evidence of independent markers of intrapartum asphyxia have found them to be absent in a large majority of neurologically symptomatic neonates. We conclude that the proportion of neonatal encephalopathy that is asphyxial in origin is not known but warrants examination, especially in view of the probable need in the near future to identify, on the basis of evidence available in the first hour or so of life, suitable candidates for clinical trials of powerful but risky treatments of birth asphyxia.     

Cerebral blood flow and O2 metabolism after asphyxia in neonatal lambs

A neonatal lamb model has been developed to examine the regulation of cerebral blood flow (CBF) and oxygen metabolism during the critical period after an asphyxial insult. Nine newborn lambs had control measurements and timed measurements after asphyxia of CBF (radioactive microsphere technique), arterial and cerebral venous (sagittal sinus) blood gases and oxygen contents performed. Immediately after resuscitation from asphyxia, there was a marked increase in CBF compared to control (239 +/- 22 versus 82 +/- 7 ml X 100 g-1 X min-1, mean +/- SEM; p less than 0.01). Cerebral oxygen delivery (CBF X arterial O2 content) increased from 12.87 +/- 1.20 to 37.40 +/- 3.40 ml X 100 g-1 X min-1 (p less than 0.01), while cerebral O2 consumption was significantly decreased compared to control (4.75 +/- 0.42 to 3.42 +/- 0.46 ml X 100 g-1 X min-1, p less than 0.05). Cerebral fractional O2 extraction, the relationship between oxygen uptake and delivery fell from 0.38 +/- 0.03 to 0.09 +/- 0.02; p less than 0.01. This reactive hyperemia was followed in all animals by a period of hypoperfusion. CBF (52 +/- 4 ml X 100 g-1 X min-1), O2 delivery (7.94 +/- 0.50 ml X 100 g-1 X min-1), and cerebral O2 consumption (3.34 +/- 0.24 ml X 100 g-1 X min-1) were all significantly depressed when compared to control. These data demonstrate important changes in CBF and O2 metabolism after neonatal asphyxia that may be important to the pathogenesis of brain injury.     

Cerebral blood flow velocity in term newborns following intrapartum fetal asphyxia

Twenty-six term newborns with intrapartum fetal asphyxia, determined biochemically (umbilical artery base deficit < 12mmol/1), were compared with 59 normal newborns to determine the effect of intrapartum fetal asphyxia on newborn blood pressure and cerebral blood flow velocity following delivery. Cerebral blood flow velocity observations with concurrent measures of blood pressure and heart rate were obtained during the 24 h after delivery and after 24 h. After delivery, diastolic blood pressure in the newborns of the asphyxia group was significantly greater than that of the newborns of the normal group and this difference persisted after 24 h. Cerebral blood flow velocity in the newborns of the asphyxia group was of the same order as that of the newborns of the normal group during the 24 h after delivery. However, there was a significant increase in both peak systolic and end-diastolic blood flow velocity after 24 h. The duration of metabolic acidosis may be a factor in the occurrence of this delayed cerebral blood flow velocity response. Observations of cerebral blood flow velocity should be continued for more than 24 h following delivery to determine the effect of intrapartum fetal asphyxia.     

Respiratory distress in a special care baby unit in Nigeria

Although respiratory distress is common among African newborn infants in special care, respiratory distress syndrome, which is the commonest cause of respiratory distress in other races, has been reported as uncommon among African infants. A prospective study of 312 consecutive newborn Nigerian infants admitted to a special care unit revealed 103 (33%) with respiratory distress. In 100 cases studied there was transient tachypnoea of the newborn ( TTN ) in 40% while specific diseases such as pneumonia and septicaemia, severe aspiration syndromes and respiratory distress syndrome (RDS) accounted for 25%, 19% and 12%, respectively. TTN and RDS occurred mostly among preterm infants with moderate perinatal asphyxia while severe aspiration syndrome was found among term infants with severe birth asphyxia. The study suggests that prevention and/or improved management of perinatal asphyxia and infections should reduce the incidence and mortality associated with neonatal respiratory distress.