小儿高热惊厥80例临床分析

1资料与方法1.1一般资料80例患儿中男54例,女26例。6个月～1岁27例,>1～3岁43例,>3～6岁10例。惊厥时测体温<38.5℃10例,38.5℃～39.0℃32例,39.0℃～40.0℃23例,>40.0℃15例。1.2方法1.2.1保持呼吸道通畅:将患儿头偏向一侧,及时清理口腔分泌物及吸痰;牙关紧闭者应放置牙垫,防止舌咬伤;放置床     

小儿高热惊厥40例护理体会

高热惊厥是小儿常见的急症之一 ,发病率约为成人的 5～10倍 ,发病年龄 6个月～ 3岁多见。临床表现为突然起病 ,意识丧失 ,眼球固定、上翻或斜视 ,口吐白沫 ,牙关紧闭 ,面部四肢肌肉呈强直性或阵挛性抽搐 ,伴大小便失禁。惊厥发作时间过长未及抢救或反复发作可导致脑严重缺氧发生脑水肿 ,严重者可导致中枢性呼吸衰竭死亡。我科自 2 0 0 3 -0 3～ 2 0 0 4-0 7共收高热惊厥患儿 40例 ,通过及时抢救全部治愈出院。1　临床资料本组患儿 40例 ,男 2 1例 ,女 19例 ;6个月～ 3岁 3 5例 ,4～ 7岁 5例。2　护理体会2 1　保持呼吸道通畅　惊厥发作时即…     

小儿高热惊厥120例临床分析

目的：探讨小儿高热惊厥发生的相关因素,分析最理想的治疗方案。方法选择我院2009-06-2013-06收治的120例高热惊厥患儿,其中简单型56例,复杂型64例。分析患儿发病情况、体温、惊厥类型及脑电图等相关情况。结果简单型患儿体温达38·5～39·5℃时导致惊厥现象,持续时间短,脑电图在体温恢复后2周表现正常;复杂型发生惊厥时体温＜38·5℃,伴随持续抽搐,且复发性高,24 h 内均有发作,而脑电图在体温恢复后2周仍有异常。结论早期预防及第一时间正确处理小儿高热惊厥的症状至关重要。     

32例小儿高热惊厥的护理体会

高热惊厥是指在小儿发育的某一时期,单纯由发热诱发的四肢、躯干与颜面骨骼肌突然发生不自主收缩,并伴意识障碍,常见于6个月~6岁儿童。发作时病情危急,体温常升高至38.5℃~40℃,70%以上的高热惊厥与上呼吸道感染有关[1]。发作时间常数秒至几分钟,若得不到及时救治,惊     

高热惊厥80例急救及护理体会

惊厥是儿科较常见的急症,发病率很高,约为成人的10~15倍[1],其临床表现多为突然发作、意识丧失,全身或局部肌群强直性或痉挛性抽动,呼吸节律不整或暂停。可伴面部青紫、牙关紧闭、口吐白沫、两眼球固定或上翻、凝视或斜视,有时可伴大、小便失禁。惊厥发生时间短则几秒钟,长至几     

Seasonal variation of febrile convulsion in Japan

The 6-year incidence rates of febrile convulsions in all 3-year-old children in Fuchu (covering 95% of children, number examined 17,044) was 8.2%. The incidence was higher in boys than in girls (9.0%: 7.5%, P less than 0.001). The incidence rates varied with the month and year of birth, but the variations observed were slight. Two peak appearances of seasonal variation of the first febrile convulsion were found in November-January and in June-August. The former could be interpreted as a tendency to winter virus infection of the upper respiratory tract in children. The other peak in summer could be explained as a tendency to gastrointestinal infection. Liability to febrile convulsion was influenced by the age of children and by the seasonal variations of febrile illness, but not by the season of birth.     

Role of apolipoprotein E in febrile convulsion

Apolipoprotein E is consistently associated with the progression of some common human neurodegenerative diseases, e.g., epilepsy. We hypothesized that genetic variations in the apolipoprotein E gene have implications for susceptibility to, and prognoses in, febrile convulsion, which plays an apparent role in the development of epilepsy. We used the polymerase chain reaction and restriction enzyme digestion to characterize variations of the apolipoprotein E gene. Sixty-nine patients with febrile convulsion (simple/complex) and a corresponding cohort of healthy patients (n = 75) were used. There was no significant difference in genotypic distribution and allelic frequencies of the apolipoprotein E gene between the febrile convulsion and control groups. Comparing subpopulations of the febrile convulsion group (patients with simple and complex febrile convulsion), we noted that no patients with the epsilon3/epsilon4 genotype had complex febrile convulsions. The apolipoprotein E epsilon3/epsilon4 genotype was more frequently seen in the simple febrile than in the complicated febrile convulsion group (9 versus 0 patients, respectively). The data indicate an association with the epsilon3/epsilon4 genotype of the apolipoprotein E gene with a milder phenotype. Although apolipoprotein E4 is not a vulnerability factor regarding febrile convulsions, it seems effective in regard to prognoses.     

Long-term follow-up of a febrile convulsion cohort

Determining the clinical prognosis a 16-year follow-up study of a clinic-based FC cohort was made. The cohort comprises 528 FC children under 5 years of age at first clinic visit. Thirty-nine patients (7.4%) were found to have developing non-febrile seizures (FCC). Discrimination formula was applied; differences in actual cumulative FCC rates differed: a) whether the discriminant score was plus or minus (15%, 31/208 and 2.5% 8/320, respectively; p less than 0.001); b) whether the discriminant score was plus or minus in the group with no medication (47%, 22/47 and 3%, 6/229; p less than 0.001); and c) whether the treatment was applied or not in the group with plus value (6%, 9/161 and 47%, 22/47; p less than 0.001). No difference was detected whether the treatment was introduced or not in the group with a minus discriminant score (2%, 2/91 and 3%, 6/229, ns). The effective prediction and prevention for the FCC development were thus proved. Correlation between the number of predictive eight-risk factors and rates of FCC development are analyzed.     

Vasopressin: Its role in antipyresis and febrile convulsion

When pyrogenic substances are injected intravenously into experimental animals, a sequence of events is set in motion which involves the hypothalamus and perhaps other portions of the diencephalon to produce a febrile response. We now present evidence that the brain produces its own endogenous antipyretic which may serve as a means of controlling the extent of the fever. When arginine vasopressin is perfused through the lateral septal area of the hypothalamus of the sheep, fever is suppressed. Vasopressin alone does not lower normal body temperature when perfused through this region of the brain. In addition, evidence is provided to indicate that vasopressin is released within the lateral septal area during the febrile response. It is concluded that, in fever, arginine vasopressin may be released in the lateral septal area of the brain and serve as an endogenous antipyretic. Results indicate that, following an initial application of vasopressin into the brain itself, a subsequent similar administration of vasopressin produces seizure-like activity. Therefore, it is suggested that this release of arginine vasopressin may contribute to the production of febrile convulsion.     

小儿热性惊厥复发的危险因素分析

目的探讨儿童首次热性惊厥(febrile convulsion,FC)后复发的危险因素,为临床决策提供理论依据.方法对213例首次FC的患儿进行跟踪、随访,应用Logistic回归分析对所得数据进行处理.结果首次发作时惊厥次数超过2次、发病前已有中枢神经系统异常、惊厥为部分性或左右不对称性是FC复发的相关危险因素.并建立了FC复发的预测模型.结论临床工作中对于首次FC发作的患儿,如存在上述危险因素,可预防性使用抗惊厥药.     

Maternal smoking, alcohol drinking, and febrile convulsion.

BACKGROUND: Previous studies have suggested that maternal cigarette smoking and alcohol drinking during pregnancy may increase risk for febrile convulsion during childhood. We evaluated the relationship of maternal smoking, alcohol drinking, and their interaction on febrile convulsion. METHOD: Pregnant women (n=10,108) enrolled in the Child Health and Development Studies in California between 1959 and 1966 were interviewed about their habits during pregnancy and febrile convulsions of the child were ascertained soon after an event. RESULTS: Febrile convulsions were reported in 2.9% of children of mothers who both smoked and drank alcohol, 2.0% for children of mothers who smoked but did not drink, 1.5% for children of mothers who drank but did not smoke and 2.1% of children of mothers who neither smoked nor drank. After adjusting for covariates, children of smokers who did not drink and children of drinkers who did not smoke did not have a significant hazard for febrile convulsion, compared to children of non-smokers non-drinkers. However, children of smokers who drank had a 30% increased hazard of febrile convulsion (95% CI=1.0, 1.9). The interaction term for smoking and alcohol drinking was significant in the multivariable model (p=0.02). CONCLUSION: These results suggest that children of mothers who both smoke and drink alcohol during pregnancy may have a higher risk for febrile convulsions.     

龙胆碱对高热惊厥大鼠海马神经元的保护

Gentianine has been shown to have a protective effect on hippocampal CA1 neurons in rats subjected to recurrent febrile convulsion(FC).The present study sought to explore the possible mechanism of gentianine by intraperitoneally injecting gentianine into rats with warm water-induced FC.The results revealed that neuronal organelle injury was slightly ameliorated in the hippocampal CA1 region.The level of glutamate was decreased,but the level of γ-aminobutyric acid was increased,as detected by ninhydrin staining.In addition,glutamate acid decarboxylase expression in hippocampal CA1 was increased,as determined by immunohistochemistry.The results demonstrated that gentianine can ameliorate FC-induced neuronal injury by enhancing glutamate acid decarboxylase activity,decreasing glutamate levels and increasing γ-aminobutyric acid levels.