新生儿缺氧的脑氧合功能变化及其与脑损伤程度的关系

目的 了解新生儿缺氧后脑氧合功能状态.方法 应用近红外光谱测定技术(NIRS)对39例有围产期缺氧史和42例无缺氧史的新生儿在安静状态下和声音刺激后脑的氧合功能进行了检测,并与脑电图和影像学检查进行了比较.结果 正常新生儿在安静状态下脑氧合状态稳定,声音刺激后脑氧合增强,然而在有缺氧史的新生儿,显示出脑活动抑制,对声音刺激所产生的脑氧合反应性变化减弱.13例病例在监测过程中出现发作性脑氧合降低.结论 在围产期缺氧性脑损伤后,脑氧合功能在一段时间内仍可能是异常的,这种变化与脑损伤程度有关.     

围产期窒息缺氧后脑氧合和脑血液动力学改变及其与心脏损害的关系

围产期窒息缺氧可致新生儿多脏器损伤 ,由于脑损伤可致神经系统后遗症而受到人们的关注。目前认为有多种机制参与脑损伤的病理过程 ,其中脑血液动力学改变与脑氧合密切相关 ,与脑损伤有直接的关系 ,而脑血流和脑血容量又受到心功能和全身血液动力学的影响。现就围产期窒息缺氧后脑氧合状态、脑血液动力学与心脏损害的关系作一综述。一、缺氧后脑氧合及脑血液动力学的变化脑组织的新陈代谢率高 ,其代谢耗能几乎全部依赖于血液供氧。脑循环取决于动脉压、静脉压、颅内压、脑血管的收缩和舒张。脑血管自动调节机制使脑的灌注和血流在一定范围内…     

NIRS监测新生儿缺氧缺血性脑病脑氧合代谢和脑血流量的临？…

目的 观察缺缺血性脑病（ＨＩＥ）的脑氧合代谢和脑血流量变化，早期判定不同程度缺氧缺血性脑病的脑功能状态。方法 采用近红外光谱仪监测２４例ＨＩＥ患儿音乐刺激（ＭＳ）前后脑前额皮质区域氧合血红蛋白（ＨｂＯ２），还原血红蛋白（Ｈｂ），总血红蛋白（ｔＨｂ）的变化，并与对照组（３０例）作比较。结果 对照组ＨｂＯ２、Ｈｂ、ｔＨｂ明显上升。ＨＩＥ组：轻度组ＨｂＯ２、ｔＨｂ变化差异无显著性（Ｐ〉０．０５），Ｈｂ明     

NIRS监测新生儿缺氧缺血性脑病脑氧合代谢和脑血流量的临床研究

目的 观察缺氧缺血性脑病(HIE)的脑氧合代谢和脑血流量变化,早期判定不同程度缺氧缺血性脑病的脑功能状态.方法 采用近红外光谱仪监测24例HIE患儿音乐刺激(MS)前后脑前额皮质区域氧合血红蛋白(HbO2),还原血红蛋白(Hb),总血红蛋白(tHb)的变化,并与对照组(30例 )作比较.结果 对照组HbO2、Hb、tHb明显上升.HIE组:轻度组HbO 2、tHb变化差异无显著性(P＞0.05),Hb明显增加[MS前:(-0.10±0.24)μmol/L, MS后(0.50±0.33)μmol/L,P＜0.05];中度组HbO2、tHb明显减少[MS前:(0.0 7±0.44)μmol/L,( 0.48±0.43)μmol/L,MS后:(-1.72±0.59)μmol/L,(-0.98±0.55)μmol/L,P＜0.05],Hb明显增加[MS前:(0.41±0.28)μmol/L,MS后:(0.74 ±0.36 μmol/L,P＜0.05],重度组三项均降低[MS前:(0.35±0.80)μmol/L,(0.22 ±0.47)μmol/L,(0.57±0.98)μmol/L,MS后:(-3.24±1.37)μmol/L,(0.15±0.51)μm ol/L,(-3.09±1.39)μmol/L,P＜0.05].将HIE的病情程度与MS前后tHb的变化差值进行直线相关分析,结果二者呈显著负相关关系(r=-0.64, P＜0.001).结论 NI RS可以早期监测HIE的脑功能,判定不同程度缺氧缺血性脑病的脑功能状态.     

选择性头部亚低温治疗新生儿缺氧缺血性脑损伤对脑血流和氧合代谢的影响

目的探讨新生儿缺氧缺血性脑损伤(hypoxic-ischemicbraindamage,HIBD)选择性头部亚低温治疗期间脑血流和脑氧合代谢的变化。方法38例中、重度HIBD新生儿随机分为常温组和低温组;7例相对正常的新生儿作为对照组。生后6h以内开始治疗,常温组维持体温在36℃,低温组维持鼻咽温度在34℃,低温持续72h,然后自然复温,其它治疗方法两组相同。三组均持续观察84h。三组患儿分别在生后6、12、24、48、72和84h,采用经颅多普勒血流诊断仪测定大脑中动脉的血流速率的变化,采用近红外光谱分析技术测定细胞色素aa3(cytochromeaa3,Cytaa3)的变化。结果低温组新生儿生后6h内收缩期血流速率(Vs)[(250．5±7．69)cm／s],平均血流速率(Vs)[(15．67±5．97)cm／s]、舒张末期血流速率(Vd)[(7．27±5．06)cm／s]和△Cytaa3均较对照组降低,阻力指数(RI)(0．81±0．15)较对照组(0．67±0．09)增加(P均<0．05);低温组Vs和Vm在生后12-48h较常温组增加(P均<0．05),RI降低(P<0．05),且与对照组无差别。与常温组比较,低温组△Cytaa3在生后36-60h显著增加(P<0．05或0．01)。结论中重度新生儿HIBD脑血速率明显降低,存在明显的脑氧合障碍;选择性头部亚低温治疗新生儿HIBD可以改善脑血流动力学和脑氧合代谢状态。     

脑蛋白水解物防治新生儿病理性黄疸临床研究

目的:探讨脑蛋白水解物在防治新生儿病理性黄疸中的作用。方法:将180例高危新生儿、新生儿吸入性肺炎、新生儿窒息随机分成治疗组与对照组各90例,对照组常规给予保暖、防治感染、支持、指脉氧饱和度≤85%给予吸氧,达到光疗指标给予间断光疗。治疗组在常规治疗基础上加用脑蛋白水解物注射液(长春富春制药有限公司)2ml/d.观察黄疸出现时间、黄疸严重程度、黄疸持续时间。结果:脑蛋白水解物有防治新生儿病理性黄疸作用。     

早发型子痫前期合并GDM患者血脂及游离脂肪酸含量与新生儿乳酸及心肌酶水平的探讨

目的:探讨早发型子痫前期(EOPE)合并妊娠期糖尿病(GDM)患者血脂和游离脂肪酸(FFA)水平与新生儿出生后早期动脉血气、乳酸(LAC)及心肌酶水平的变化。方法:110例EOPE患者根据IADPSG标准被分为EOPE合并GDM组(EOPE+GDM组)49例和糖代谢正常的EOPE组(单纯EOPE组)61例。测定并比较两组孕母体质量指数(BMI)、糖脂代谢指标[血脂、FFA、糖化血红蛋白(Hb A1c)等]及血液常规及血液生化指标,比较两组新生儿出生后1小时内外周动脉血血气分析、LAC、心肌酶[肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)]水平,采用Pearson相关分析探讨EOPE患者糖脂代谢指标及新生儿出生情况对新生儿LAC、CK-MB水平的影响,逐步多元线性回归分析影响EOPE患者新生儿CK-MB水平的独立性相关因子。结果:1EOPE+GDM组孕妇具有较高的BMI、Hb A1c、血脂(TC、TG、LDL、VLDL)、FFA、Fbg、HCT水平,两组比较差异有统计学意义(P0.05)。2EOPE+GDM组新生儿1分钟Apgar评分较低、新生儿外周动脉血p H值降低、碱剩余(BE)增加,LAC水平、心肌酶(CK、CK-MB、LDH)水平升高,两组比较,差异均有统计学意义(P0.05)。3Pearson相关分析示:EOPE患者新生儿CK-MB水平与LAC呈正相关(P0.05),LAC、CK-MB均与新生儿的胎龄、出生体质量、Apgar评分、动脉血p H值呈负相关(P0.05),而与孕妇Hb A1c、FFA、TC、TG水平呈正相关(P0.05)。逐步多元回归显示:EOPE患者的Hb A1c、FFA及胎龄、新生儿LAC水平是新生儿心肌酶CK-MB水平的独立相关因子。结论:EOPE合并GDM患者常存在更为显著的糖脂代谢异常,可进一步干扰围生儿物质代谢,引起新生儿体内LAC水平升高和潜在心肌损伤。     

近红外光谱技术产时监测宫内缺氧性脑损伤的价值

目的 探讨近红外光谱技术产时监测宫内缺氧性脑损伤的价值,为临床评价脑损伤提供客观、量化依据.方法 63例宫内窘迫胎儿根据出生后是否合并新生儿缺氧缺血性脑病(hypoxic-ischemic encephalopathy,HIE)分为HIE组(34例)及无HIE组(29例);35例无宫内窘迫的正常新生儿为对照组.应用近红外光谱技术测定3组新生儿胎头拨露时和生后5 min时脑组织氧饱和度(regional oxygen saturation,rSO2),受试者工作特性曲线评价脑rSO2对HIE的诊断价值.结果 HIE组患儿产程中胎头拨露及生后5 min时脑rSO2分别为(36.6±5.0)%和(52.0±4.2)%,均明显低于对照组[分别为(45.9±4.6)%和(59.6±4.4)%]及宫内窘迫但无HIE组[分别为(44.1±3.1)%和(57.6±3.5)%](P<0.01).对照组、宫内窘迫但无HIE组、HIE组产程中胎头拨露时脑rSO2与脐动脉血气pH值间均呈正相关性(r=0.463,P<0.01;r=0.619,P<0.01;r=0.688,P<0.01),与脐动脉血气血氧饱和度间亦呈正相关性(r=0.709,P<0.01;r=0.736,P<0.01;r=0.516,P<0.01).以胎头拨露时脑rSO2<39.5%为界值,rSO2评判宫内窘迫新生儿发生HIE的敏感性及特异性分别为67%及93%;以生后5 min脑rSO2<53.5%为界值,rSO2评判宫内窘迫新生儿发生HIE的敏感性及特异性分别为70%及86%.结论 近红外光谱技术测定脑rSO2能客观评价宫内窘迫新生儿脑氧合状态,可提示新生儿HIE的存在.     

早产猪呼吸窘迫综合征模型的建立与治疗

目的建立早产猪呼吸窘迫综合征(respiratory distress syndrome,RDS)模型并探讨猪肺表面活性物质(pul monary surfactant,PS)制剂的治疗效果。方法选择相当于足月孕期85%(94~97d)的早产猪作RDS模型,随机分成4组(C组:对照组;C50组:PS50mg/kg;C100组:PS100mg/kg;N组:自主呼吸组)。除N组外,其余早产猪气管切开插管,压力控制模式通气,吸入高浓度氧和标准潮气量通气。分别在治疗0~6h测血气与呼吸力学参数,6h后处死动物留取肺组织和肺泡灌洗液(bronchoalveolar lavage,BALF)进行形态学与生化分析。结果RDS动物BALF中总磷脂约10mg/kg;电子显微镜下板层小体仅零星可见;光学显微镜下可见肺泡基本处于萎陷状态。C100组PaO2/Fi O2由(92±37)上升到(235±137)mm Hg,肺顺应性由(0.48±0.08)上升到(0.76±0.29)ml/(cm H2O.kg),肺泡扩张均匀,少见损伤;C50组肺氧合及呼吸力学改善不明显。结论早产猪RDS模型用于研究新生儿呼吸系统疾病具有一定价值,100mg/kg的PS对肺氧合、呼吸力学及形态学的改善具有明显作用。     

新生儿窒息的肾血流动力学改变及影响因素的研究

目的 探索窒息后新生儿肾血流动力学的变化规律.方法 应用彩色超声血流显像技术,对窒息后新生儿的肾动脉血流参数及心输出量进行动态监测.结果 1.窒息后新生儿第1天肾动脉血流速度和血流量较正常对照组低下,阻力增加,这种改变随窒息程度加重而加重.窒息轻度组3天内可恢复,重度组完全恢复常需1周以上.2.正常新生儿肾血流量与心输出量的比值(RFV/Co)较稳定,为15.6%±0.51%.RFV/Co的降低能相对反映窒息后肾缺血程度.3.心输出量的大小、血液粘滞度及是否合并代谢性酸中毒将对肾血流动力学改变有直接影响.4.与临床化验指标相比,能早期、敏感地反映窒息后肾损伤.结论 超声多普勒监测窒息后新生儿肾血流动力学变化安全、可靠、方便、无创,并可动态观察,有利于窒息后肾损伤的早期诊断和指导治疗.     

Histologic and biochemical study of the brain, heart, kidney, and liver in asphyxia caused by occlusion of the umbilical cord in near-term fetal lambs

OBJECTIVE: We sought to determine the relationship between the degree of histologic changes in the brain, heart, kidney, and liver in fetal lambs after severe asphyxia and to analyze the role of oxidative stress in the pathogenesis of fetal multiple organ failure. STUDY DESIGN: Eight chronically instrumented near-term fetal lambs were asphyxiated by partial umbilical cord occlusion for approximately 60 minutes until the fetal arterial pH reached <6.9 and the base excess reached <-20 mEq/L. An additional 6 fetuses were used as sham-asphyxiated controls. Fetal heart rates, blood pressure, fetal breathing movements, and arterial blood gases and acid-base states were serially monitored. The brain, heart, kidney, and liver were collected 72 hours after asphyxia, processed, and histologically examined after hematoxylin and eosin staining. Fetal brain histologic features were classified into 5 grades, with 5 being the most severe damage. The other organs were examined histologically by pathologists who were blinded to the treatment. Each organ was assayed for tissue concentrations of thiobarbituric acid-reactive substances, superoxide dismutase, glutathione, lactate, and glucose. RESULTS: Myocardial changes of necrosis, phagocytosis, and contraction bands occurred in only 2 of the most severely (grade 5) brain-damaged fetuses. The same 2 cases showed fatty changes and congestion in the liver. In the kidney all asphyxiated cases showed tubular necrosis, but glomeruli were generally spared. Of the measures of oxidative stress, only liver tissue levels of thiobarbituric acid-reactive substances and superoxide dismutase were significantly higher in the asphyxiated group than in the control group, but there was no correlation with the degree of damage. Lactate level was higher only in the heart in the asphyxiated fetuses. CONCLUSION: Renal tubular damage was seen with all degrees of asphyxia, despite variable brain damage. Histologic changes in the myocardium and liver were seen only with the most severe brain damage. Oxidative stress appears to play a role in the pathogenesis of liver damage.     

宫内窘迫新生儿脐动脉血超氧化物歧化酶及丙二醛检测的临床意义

目的　探讨脂质过氧化与胎儿窘迫,以及与新生儿缺血缺氧性脑病(HIE)的关系。方法　将产程中发生宫内窘迫的新生儿60例作为研究对象其中出生后无窒息者39例为检测Ⅰ组,有窒息者21例为检测Ⅱ组;取同期正常新生儿30例为对照组。检测各组新生儿脐动脉血超氧化物歧化酶(SOD)、丙二醛水平,观察各组新生儿HIE发生情况;分析宫内窘迫持续不同时间的新生儿SOD、丙二醛的变化及HIE发生情况。结果　(1)SOD水平检测:检测Ⅰ组为(12 896±247)U/gHb,检测Ⅱ组为(9846±268)U/gHb,对照组为(17 282±134)U/gHb。检测Ⅰ、Ⅱ组SOD水平分别与对照组比较,均显著降低,差异有统计学意义(P<0 01)。检测Ⅰ、Ⅱ组共发生HIE9例(HIE组),SOD水平为(7486±245)U/gHb,未发生HIE51例(非HIE组),SOD水平为(13 878±257)U/gHb,两组比较,差异有统计学意义(P<0 01)。检测Ⅰ、Ⅱ组宫内窘迫持续时间≤30min共19例,SOD水平为(17 411±324)U/gHb,持续时间31~120min共26例,SOD水平为(12 076±230)U/gHb,持续时间≥121min共15例,SOD水平为(9786±249)U/gHb。(2)丙二醛水平检测:检测Ⅰ组为(6 3±0 4)μmol/L,检测Ⅱ组为(8 6±1 5)μmol/L,对照组为(4 1±0 5)μmol/L,检测Ⅰ、Ⅱ组丙二醛水平显著高于对照组,两者比较,差异有统计学意义(P<0 01)。HIE组为     

Cerebral Blood Flow and Metabolism in Ovine Fetuses During Asphyxia Resulting in Seizures

Severe fetal asphyxia can cause neurologic damage, but little is known about cerebral oxidative metabolism under these conditions. This study was designed to measure cerebral blood flow and oxygen consumption during severe global asphyxia in fetal sheep, asphyxiated to the point at which seizure activity subsequently occurred. Six sheep were chronically instrumented with fetal electrodes, fetal and maternal vascular catheters, and an adjustable occluder on the maternal common hypogastric artery. Measurements were made of fetal arterial blood gases, blood pressure, heart rate electrocorticogram (ECoG), nuchal muscle electromyogram (EMG), and regional blood flow (radioactive microspheres) during control, and at 30 and 60 min after complete occlusion of the maternal hypogastric artery. The ECoG became isoelectric, and the fetuses developed a marked respiratory and metabolic acidosis, the pH falling to 6.99 ± 0.03, the pCO₂ rising to 73 ± 11 mm Hg, and base excess falling to ?16 ± 1 mEq/L at 60 min of occlusion. Control fetal arterial blood pressure was 52 ± 9 mm Hg and did not change significantly with asphyxia at 60 min. Cerebral cortical blood flow was 127 ± 54 ml/100 g/min at control, and 204 ± 130 ml/100 g/min at 60 min of asphyxia. Cerebral oxygen consumption was 201 ± 50 μM/100 g/min at control, and 76 ± 57 μM/100 g/min at 60 min of asphyxia (P < 0.05), i.e., 45% of control. All 6 fetuses had episodic seizure activity based on ECoG and nuchal EMG activity, beginning 50 ± 47 min after release of the occluder. This seizure activity continued for 24-36 h. This study shows that 60 min of asphyxia associated with suppressed ECoG activity and severe acidosis induced neuronal damage, manifesting as seizure activity, and that this occurred when cerebral oxidative metabolism was reduced to ≤50% of control.     

Mortality and morbidity after intrapartum asphyxia in the preterm fetus.

This matched cohort study examined the significance of intrapartum fetal asphyxia determined biochemically in the preterm newborn in regard to outcome during the first year. Thirty preterm newborns with metabolic acidosis at delivery were compared with 60 preterm newborns, matched for birth weight, with normal blood gas measures. Deaths during the first year were reviewed. Assessment of the surviving children at 1 year corrected age included neurologic examination, Bayley scales, and Uzgiris and Hunt scale to define motor and cognitive development. Seven asphyxiated infants (23%) died during the first year compared with two nonasphyxiated infants (3%), a statistically significant difference (P less than .006). Among the surviving children, the incidence of minor motor and/or cognitive deficits was the same in the two groups. The incidence of major motor and/or cognitive deficits in the group with asphyxia (eight of 30) was significantly greater than in the control group (eight of 60) (P less than .03). These results indicate that intrapartum fetal asphyxia in the preterm newborn is a contributing factor to the mortality and morbidity observed in these children.     

Hypoxanthine: a marker for asphyxia

It has been hypothesized that hypoxanthine concentrations in the blood of newborn infants are a marker of asphyxia. To test this hypothesis, we measured serum hypoxanthine levels in relationship to perinatal and neonatal asphyxia, and compared arterial hypoxanthine levels with arterial pH and base deficit. We also compared hypoxanthine levels of survivors with those of asphyxiated non-survivors. Forty-two newborns were classified as asphyxiated by either of two methods: 1) Infants from whom umbilical cord hypoxanthine levels were taken were classified as asphyxiated if they had an Apgar score of 6 or less at 1 or 5 minutes, fetal heart rate below 100 beats per minute, or meconium-stained amniotic fluid; and 2) infants from whom peripheral arterial hypoxanthine samples were taken were classified by clinical assessment, whereby one author, blinded to the infants' hypoxanthine levels, prospectively assessed each patient's condition for evidence of asphyxia. Hypoxanthine levels correlated with increased base deficit (P less than .001; r = 0.8) and with decreased pH (P less than .001; r = -0.5). By both of our asphyxia classification methods, hypoxanthine levels were significantly higher (P less than .002) in the asphyxiated groups. We also noted a higher hypoxanthine level in asphyxiated non-survivors as compared with all survivors (P less than .02). We propose that serum hypoxanthine levels may help define asphyxia. Because hypoxanthine, when metabolized by xanthine oxidase, generates oxygen radicals that are highly destructive to tissue, hypoxanthine levels may have important therapeutic implications for asphyxiated patients.     

Investigation of cerebral energy metabolism in newborn infants by phosphorus nuclear magnetic resonance spectroscopy

31P NMR spectroscopy can be safely and successfully used to study cerebral energy metabolism in sick newborn infants, provided a suitable life support and monitoring system is available. Studies of normal infants have shown characteristic spectral peaks assigned to adenosine triphosphate, phosphocreatine, phosphodiesters plus phospholipids, inorganic orthophosphate, and a large peak at the phosphomonoester resonance frequency that is attributable mainly to phosphoethanolamine, a precursor of membrane phospholipids. Both the PCr/Pi and PCr/ATP ratios were lower in normal newborn infants than reported in studies using invasive techniques in adult animals. Tissue hypoxia-ischemia was associated with a fall in PCr levels and a rise in Pi. The PCr/Pi ratio, which is an index of cerebral energy status, was normal during the first day of life in infants who had suffered severe birth asphyxia, but subsequently fell to levels well below the normal range. The presence of this latent period raises the possibility of effective early treatment following birth asphyxia, before irreversible impairment of cellular energy metabolism occurs. Low PCr/Pi ratios have also been demonstrated in infants with idiopathic cerebral infarction, periventricular leukomalacia and inborn errors of metabolism. Preliminary experience suggests that ratios below 0.8 are associated with irrecoverable failure of energy metabolism and cellular necrosis. 31P NMRS and other spectroscopic NMR techniques utilizing, for instance, 1H and 13C nuclei, have exciting potential for exploring the mechanisms and methods of prevention of various forms of cerebral damage in the newborn period.     

宫内窒息后新生鼠的状态与脑损伤关系的研究

目的 探讨宫内窒息后的新生鼠脑病理变化。并与生后的状况相联系。方法 制备宫内不同程度缺血缺氧（15，30，45及60min)及再灌注（缺血缺氧15min后再灌注1，4，8，15及24h)模型。观察剖宫产后新生鼠的一般状况并进行光，电镜下的脑病理观察。结果 轻度的宫内缺血缺氧可引起神经元的变化，但生后的一般状态无明显改变；严重的宫内缺血缺氧当时即可引起胎死宫内，此时神经元表现为坏死，宫内轻度窒息的新生鼠，出生时一般状态尚可，但再灌注后状态越来越差，与神经元再灌注后呈现的进行性凋亡过程相平行。结论 急性宫内缺血缺氧可以引起胎死宫内，神经元表现为坏死，在坏死之前再灌注将引起凋亡。再灌注后进行性凋亡过程是某些宫内窒息新生儿在出生后状态越来越差的主要原因。新生儿缺氧缺血性脑病的病理变化可能在宫内已经开始发生。     

Does glucose administration affect the cerebral response to fetal asphyxia?

This study was designed to test whether the fetal brain has an increased resistance towards asphyxia at high levels of blood-glucose, compared with low levels. 35 fetal sheep were exteriorized and investigated under general anesthesia. Cerebral blood flow (CBF) was estimated with the 133Xenon-washout method. Cerebral uptake of oxygen, glucose, and lactate was measured. Somatosensory evoked potentials (SEP) were recorded. The fetuses were subjected to controlled asphyxia by ventilating the ewes with gas mixtures low in oxygen. The blood sugar levels of the fetuses were varied over a four-fold range. During normal oxygenation of the fetus variations in the blood glucose concentration induced considerable changes in the cerebral glucose uptake, whereas CBF and oxygen uptake were unaffected. During asphyxia, hyperglycemia was associated with rapid development of acidosis and reduction in cerebral oxygen consumption together with deterioration of the neurophysiological characteristics of the brain. Far from being beneficial during asphyxia, fetal hyperglycemia appeared to reduce the tolerance of the fetal brain towards asphyxia. This report together with other evidence provides support for the view that extra glucose might be disadvantageous for the asphyxiated fetus.     

Do concepts of causes and prevention of cerebral palsy require revision?

Objective: My purpose was to explore the criteria of The American College of Obstetricians and Gynecologists (Technical Bulletin No. 163) for perinatal asphyxia to be linked to subsequent cerebral palsy.Study design: Analysis of four cases of intrapartum fetal insults with subsequent cerebral palsy and a literature review are presented.Results: All of the four cerebral palsy cases had sufficient intrapartum causes of cerebral palsy, yet none fulfilled The American College of Obstetricians and Gyneclogists' linkage criteria. Complications in the cerebral palsy cases were as follows: maternal intrapartum cardiac arrest, fetal skull fracture with brain infarct, intrapartum fetal stoke, and a newborn delivered after uterine rupture with only central nervous system defects. There are no well-done laboratory or clinical studies that unequivocally support the “criteria” that umbilical artery pH must be < 7.00 or the requirements of Apgar score < 3, hypoxic-ischemic encephalopathy, and multiple organ dysfunction. Apparent exceptions to these criteria occur.Conclusions: The American College of Obstetricians and Gynecologists Technical Bulletin's criteria for cerebral palsy linkage and the role of parturition in cerebral palsy should be reevaluated. A rebirth of obstetric enthusiasm for cerebral palsy research, teaching, and treatment needs to occur.     

Prevention of cerebral palsy during labour: role of foetal lactate

OBJECTIVES: Intrapartum foetal monitoring goal is to prevent foetal asphyxia and its most severe consequence: cerebral palsy (CP). In this paper we describe the detection methods and the criteria needed to assess asphyxia during labour for preventing CP. Foetal cerebral damage assessment is considered from the medical-legal point of view. CP represents the most frequent pathology of childhood related to pregnancy and childbirth with an incidence of 0.2% in children born alive. It is clinically regarded as the result of a spectrum of diseases due to damage or to faded development of the nervous system which generally appears at the time of the first stage of intra-uterine growth or depends on problems arising at birth. The goal of our analysis is to recall the various moments in which this event can take place and, if possible, the moment and the degree of the event of asphyxia and its effect on foetal conditions, in order to control and treat it. STUDY DESIGN: One hundred and eighty-eight fetuses were evaluated by means of Apgar score, intrapartum cardiotocography, observation of the presence of meconium stained amniotic fluid, and clinical features of distress at birth. Lactate concentrations were measured during labour and at delivery in blood samples obtained from the foetal presenting part (foetal scalp) and from the umbilical cord with the use of a rapid electrochemical technique. RESULTS: Evidence of clinical foetal distress was not related to the severity of asphyxia. An increased lactate level was found in asphyctic infants and a clear correlation between lactic acidosis and foetal distress was documented. Low Apgar scores were observed in infants with moderate or severe asphyxia at delivery. Scalp lactate correlated significantly with umbilical artery lactate (P = 0.49, 0.01), but with neither Apgar score at 1 min (R = -0.21, ns) nor at 5 min (R = -0.11, ns). Lactate concentration was higher in case of instrumental delivery compared to spontaneous delivery (P = 0.0001). No perfect correlation was found between lactate level and neonatal outcome, but there were not a significant number of neonates with immediate complications. The rate of instrumental delivery in the distress group was significantly higher than in that of the healthy fetuses (P < 0.01), so spontaneous labour was less frequently associated with foetal distress than instrumental delivery (P < 0.01). In the distress group, severe variable decelerations were generally recorded in the second stage of labour. The incidence of neonatal Apgar score /=45 min, compared with a shorter active second stage, and acidaemia at birth implied larger arterial-venous lactate differences (P < 0.001). The presence of foetal lactate at crowning was also significantly associated with the level of umbilical arterial-venous lactate difference (P = 0.03). CONCLUSIONS: Analysis of the fetus should start with the assessment of lactates and acid-base balance. The method which revolutionized the techniques of foetal monitoring is undoubtedly represented by cardiotocography. However, likely most of neurological outcomes are not correlated with a perinatal event or with peripartum asphyxia. Approximately 10% of cases of CP would actually be due to perinatal asphyxia, and this percentage approaches approximately to 15% if we consider only newborns at term. This again confirms the weak association of a causal relationship between asphyxia and CP. In addition, available foetal suffering markers are vague and allow to identify only less than half of the effective cases of newborns which will develop CP.