甲型流感儿童病毒核酸持续时间及其影响因素

目的 分析甲型流感（甲流）患儿病毒核酸持续时间的规律和影响因素。方法 收集90例鼻咽拭子甲流病毒核酸PCR检测阳性的甲流患儿临床资料,并将其分为单纯甲流组（10例）、甲流并发肺炎组（61例）、甲流并发神经系统损害组（10例）、基础疾病合并甲流组（9例）,对其临床特点、治疗经过、病毒核酸持续时间和转归进行回顾性分析。结果 90例甲流患儿的前5位临床症状主要为发热（89/90,99%）、咳嗽（89/90,99%）、流涕（69/90,77%）、气促（26/90,29%）、肌痛（23/90,26%）。病毒核酸持续时间平均9.4±2.9 d。单纯甲流组病毒核酸持续时间短于甲流并发肺炎组、甲流并发神经系统损害组及基础疾病合并甲流组,差异均有统计学意义（P < 0.05）;甲流并发肺炎组、甲流并发神经系统损害组及基础疾病合并甲流组之间的病毒核酸持续时间的差异均无统计学意义（P > 0.05）。起病48 h内抗病毒治疗组的病毒核酸持续时间和体温恢复正常所需时间均短于48 h以后用药的患儿,差异有统计学意义（P < 0.05）。83%的体温恢复正常的甲流患儿病毒核酸仍呈阳性。结论 并发症、基础性疾病和抗病毒治疗时机是影响甲流病毒核酸持续的主要因素,体温是否恢复正常不宜作为甲流患儿是否继续抗病毒治疗的参考。     

儿童脑病：一类与各种疾病都相关的疾病

脑病是一种影响大脑结构和功能的严重且复杂的疾病，可导致严重的神经系统症状，甚至死亡，根据病程可分为急性脑病（急性脑功能障碍）和慢性脑病（慢性脑功能障碍）两类。急性脑病是一种由多种综合征组成的异质性疾病，可发生在任何年龄组，最常见于婴儿和学龄前儿童，可根据既往感染的病原体或生物学及临床病理特征分别进行分类，病因复杂多样，其中急性坏死性脑病是需要重点鉴别的脑病。儿童慢性脑病包括发育性脑病和家庭虐待所致的慢性创伤性脑病。脑病患儿可表现为认知障碍和语言发育迟缓、精神运动发育迟缓，或伴有惊厥等脑功能障碍的其他表现。遗传学检测是明确儿童慢性脑病病因的重要方法之一。文章介绍了脑病的不同病因及可能的临床症状，帮助临床医师早期识别诊断并给予及时有效的治疗。     

616例小儿热性惊厥首次发作的临床特点及危险因素分析

目的了解热性惊厥患儿首次发作的临床特点及危险因素,指导临床医师对有危险因素的患儿采取相应干预措施,降低热性惊厥的发生。方法选取我院2016年8月至2018年8月收治的616例首次热性惊厥患儿为研究对象,回顾性分析患儿的临床特征及首次发作危险因素,并随机抽取同期发热但无惊厥发作(既往也无惊厥病史)的601例患儿为对照组。结果616例热性惊厥患儿,男344例,女272例,汉族584例,蒙古族32例。1岁以下126例(20.5%),~3岁405例(65.8%),3岁以上85例(13.7%)。发作病因中以急性上呼吸道感染[53.6%(330/616)]、疱疹性咽峡炎[25.9%(160/616)]及幼儿急疹[10.5%(65/616)]居前3位。惊厥发作时体温在38.0℃及以上者570例(92.5%),16例(2.6%)患儿惊厥发作后出现发热。534例(86.7%)患儿在发热24 h内出现惊厥发作。608例(98.7%)患儿表现为全面强直阵挛性发作。惊厥持续时间<5 min 548例(89.0%)、~14 min 48例(7.8%)、~29 min 16例(2.6%)及≥30 min 4例(0.4%)。572例(92.9%)患儿在单次热程中仅1次惊厥发作。临床类型中单纯性热性惊厥占88.3%(544/616),复杂性热性惊厥占11.0%(68/616),惊厥持续状态占0.7%(4/616)。危险因素分析显示首次惊厥时年龄、低钠、低铁、低锌、剖宫产、异常出生史、抽搐前1周疫苗接种史及热性惊厥家族史在热性惊厥组和对照组中差异有统计学意义(P<0.05)。Logistic回归分析发现首次发热惊厥年龄、低铁、剖宫产、低钠及热性惊厥家族史是热性惊厥首次发作的独立危险因素(P<0.05)。结论热性惊厥首次发作多见于3岁以内婴幼儿,以单纯性热性惊厥为主,惊厥发作时体温高,易发生于发热后24 h内,病毒感染是最常见病因。引起热性惊厥首次发作的危险因素依次为首次发作年龄、低铁、剖宫产、低钠及热性惊厥家族史,针对危险因素采取相应的干预措施可降低热性惊厥的发生。     

儿童2009甲型H1N1流感相关神经系统并发症报道

报道儿童2009甲流H1N1流感相关神经系统并发症的临床特征。方法　对深圳市儿童医院2009 - 11 - 04 - 2010 - 01 - 19因2009甲型H1N1流感住院,并发神经系统并发症的21例患儿进行前瞻性调研,对其临床特征及转归进行总结。结果　在150例儿童危重症2009甲型H1N1流感住院患儿中,神经系统并发症的发生率为14.0%（21/150）,其中脑病18例（85.7%）,惊厥2例（9.5%）,脑炎1例（4.7%）。男14例,女7例;年龄中位数为5岁。12例（57%）入住ICU监护,6例（28.5%）接受气管插管及机械通气。17例80.9%）痊愈出院,1例仍在住院,3例（14%）死于脑病。结论　2009甲型H1N1流感相关神经系统并发症发生率高,严重脑病患儿可以导致死亡。随着2009甲型H1N1流感的流行,这一结果应该引起广泛关注。     

以神经系统症状起病的儿童血管迷走性晕厥或体位性心动过速综合征88例临床分析

目的 探讨以神经系统症状起病的儿童血管迷走性晕厥（VVS）及体位性心动过速综合征（POTS）的临床特点，为该类疾病早期识别提供依据。方法 回顾性分析88例以一过性意识丧失、头晕、头痛及抽搐等神经系统症状为首发症状，最终确诊为VVS或POTS的患儿的临床资料。结果 88例患儿中，男性35例（40%），女性53例（60%），年龄4~15岁，发病高峰年龄10~13岁。88例患儿皆以一过性意识丧失、头晕、头痛及抽搐为首发症状，经脑电图、脑脊液及头颅磁共振等检查，排除了神经系统疾病，经直立倾斜试验（HUTT）最终确诊为VVS 53例（60%），POTS 35例（40%）。有5例以一过性意识丧失为首发症状的患儿被误诊为癫痫。59例（67%）患儿发病前可追溯到诱因，常见诱因依次为长时间站立、体位变化及剧烈运动。66例（75%）有发作先兆症状，常见的先兆症状依次为胸闷、消化道症状（恶心、呕吐及腹痛）及面色苍白。88例患儿均接受了健康教育、自主神经功能锻炼，53例VVS患儿予口服补液盐治疗，35例POTS患儿予口服补液盐联合美托洛尔治疗。对88例患儿进行为期18个月的随访，随访3、6、12、18个月时的治疗有效率分别为87%、93%、93%、90%。结论 以一过性意识丧失、头晕、头痛及抽搐为首发症状的患儿除了考虑神经系统疾病外，需警惕VVS及POTS等功能性心血管疾病，进一步HUTT检查可明确诊断；明确诊断后早期治疗可取得较好的疗效。     

轻度胃肠炎伴婴幼儿良性惊厥在婴幼儿急性腹泻伴惊厥疾病谱中的地位及意义

目的探讨轻度胃肠炎伴婴幼儿良性惊厥(BICE)在婴幼儿急性腹泻伴惊厥疾病谱中的地位及意义。方法对2009-2011年收治的急性腹泻并有惊厥症状患儿的住院资料进行回顾性分析。结果 184例急性腹泻伴惊厥的病例中,轻度胃肠炎伴婴幼儿良性惊厥58例、热性惊厥49例、癫癎43例、病毒性脑炎19例、低钠性脑病6例、高钠性脑病5例、中毒性脑病2例、低钙惊厥2例。BICE患儿年龄为(17.47±7.90)个月,全身症状轻,脱水轻或无,惊厥多呈全面性强直或强直阵挛发作,发作持续时间短,多发生在病程前2 d;轮状病毒阳性率为65.52%;血常规、生化、脑脊液、CT/MRI、脑电图等无明显异常。BICE患儿入院后予补液治疗,在首次惊厥后给予肌注苯巴比妥,住院过程惊厥再发者立即静脉注射地西泮,均住院2～5 d治愈出院。结论 BICE为婴幼儿急性腹泻伴惊厥中的常见疾病,临床应以对症治疗为主,应避免不必要的检查和过度药物治疗。     

发热诱导的儿童难治性癫痫性脑病的救治及预后分析

目的：探讨发热诱导的儿童难治性癫痫性脑病的合理救治及预后。方法回顾性分析3例发热诱导的儿童难治性癫痫性脑病的临床表现、抢救措施,并对预后进行分析。结果3例患儿既往正常,急性起病,病初有高热、抽搐、意识障碍,头颅 CT 正常,脑脊液正常,脑电图提示慢波增多,按照病毒性脑炎治疗病情不能缓解,常见病原学检验均为阴性。急性期主要是维持生命体征的稳定,积极控制惊厥发作。3例患儿经过抢救后生命体征稳定,但1例遗留明显神经系统后遗症,认知功能障碍,语言交流困难,面部肌肉痉挛,流涎。结论对于发热诱导的儿童难治性癫痫性脑病急性期的早期诊断,确认患儿处于癫痫持续状态时及时联合抗癫痫药物以抗惊厥、保护脑组织为主的综合治疗,有可能减轻患儿的神经系统后遗症。     

儿童中央-颞区放电的良性癫癎与热性惊厥的关系

目的 研究中央—颞区放电的小儿良性癫痫(BCECT)和热性惊厥的关系，探讨BCECT和热性惊厥的关系。方法 通过问卷对26例BCECT患儿的家族史及热性惊厥家族史进行调查。并做VEEG、头颅CT或MRI。同时选择26例年龄相当的正常儿童做对照。结果 26例BCECT患儿的头颅CT或MRI均未发现异常，仅2例既往有热性惊厥史，与人群中热性惊厥发病率相比无差异。26例BCECT患儿的癫痫家族史和对照组相比无显著差异(P＞0.05)，但其热性惊厥家族史的发生率却明显高于对照组(0．0l＜P＜0．05)。结论 证BCECT和热性惊厥有密切关系，二者在发生学上可能有同源性。     

小儿热性惊厥86例回顾性分析

目的总结小儿热性惊厥的临床特点,为防治提供依据。方法对86例小儿热性惊厥患儿的临床资料进行回顾性分析。结果发作仅1次54例,反复发作2次以上32例,1 d内发作2次8例。全身强直阵挛或阵挛性发作78例,失张力发作2例,限局性发作6例。结论小儿热性惊厥发作时需尽快治疗,防止抽搐时间过长对神经系统造成损伤。对于反复发作2次以上、低热发作、有癫痫家族史的患儿可以预防性应用镇静药。     

甲型流感相关急性坏死性脑病2例影像特征及诊治体会

正甲型流感于2009年3月爆发于墨西哥并迅速蔓延到全球,年龄2岁患儿易发生严重并发症,约10%儿童流感患者出现神经系统并发症如脑炎、急性坏死性脑病(acute necrotizing encephalopathy,ANE)、出血性休克脑病综合征、肌炎等[1],约20%为ANE[2]。ANE是一种爆发性的临床综合征,以快速进展的脑病、顽固性惊厥发作及极差的预后为特征,有较高病死率,幸存者中大部分遗留严重神经系统后遗症。现将昆明市儿童医院诊断的2例甲型流感相关ANE患儿临床与影像学特征及诊治体会进行分析。     

Neurological complications of pandemic influenza A H1N1 2009 infection: European case series and review

Neurological manifestations and outcomes of children with the 2009 H1N1 virus infection have been reported in three American series and from smaller cohorts and case reports worldwide. Of the 83 children admitted between April 2009 and March 2010 with H1N1 virus infection to a tertiary children’s hospital in a European setting, five children aged between 2 and 10 years had neurological symptoms. Four patients had seizures and encephalopathy at presentation. One patient presented with ataxia; one developed neuropsychiatric manifestations, and two developed movement disorders during the disease course. Early neuroimaging showed evidence of acute necrotising encephalopathy (ANE) in one case and non-specific white matter changes in another. Initial neuroimaging was normal for the other three, but interval MRI showed increased signal in bilateral periventricular distribution in one and significant cerebral volume loss in the other. Clinical outcomes varied: two recovered fully while three had residual seizures and/or significant cognitive deficits. Conclusion An analysis of our patients along with all reported cases reveal that seizures and encephalopathy were common neurological presentations associated with pandemic 2009 H1N1 influenza virus infection in children requiring hospital admission. Neuroimaging suggestive of ANE, basal ganglia involvement and volume loss appears to be associated with worse neurological outcome.     

2009甲型H1N1流感住院患儿多中心临床研究

目的 了解2009年全国多中心2009甲型H1N1流感住院患儿的临床特征,探讨危重症的高危因素和死亡原因.方法 对2009年秋冬季全国17家医院的810例2009甲型H1N1流感住院患儿的临床表现、实验室检查结果以及治疗和转归进行回顾性总结和分析.结果 810例住院患儿中,男508例,女302例,年龄中位数为43个月,其中＜5岁550例(67.9%),合并基础疾病148例(18.5%).常见的表现及例数为:发热780例(96.3%),流涕294例(36.3%),鼻塞192例(23.7%),咽痛147例(18.1%),咳嗽759例(93.7%),咯痰347例(42.8%),喘息219例(27.0%),呼吸困难163例(20.1%),呕吐130例(16.0%),腹泻66例(8.1%),烦躁79例(9.8%),嗜睡64例(7.9%),惊厥32例(4.0%).常见的实验室异常为:外周血白细胞计数增高或降低377例(46.5%),乳酸脱氢酶增高346例(42.7%),C反应蛋白增高306例(37.8%),天冬氨酸转氨酶增高257例(31.7%),肌酸激酶增高174例(21.5%).586例(72.3%)合并肺炎,49例(6.0%)合并脑炎/脑病,30例(3.7%)合并心肌炎.危重症患儿183例,其基础疾病、外周血白细胞计数增高、中性粒细胞比率增高、淋巴细胞比率降低和C反应蛋白增高的发生率明显高于非危重症患儿.19例死亡,占危重患儿的10.4%,8例死于脑炎/脑病,10例主要死于严重肺炎和急性呼吸窘迫综合征,其中5例同时伴有脑炎/脑病,1例死于继发性真菌性脑膜炎.结论 2009甲型H1N1流感容易引起全身多脏器损害.有基础疾病、外周血白细胞计数增高、中性粒细胞比率增高、淋巴细胞比率降低和C反应蛋白增高可能是发生危重症病例的高危因素.合并严重肺炎和急性呼吸窘迫综合征,以及脑炎/脑病是导致死亡的主要因素.     

Clinical and MRI features of neurological complications after influenza A (H1N1) infection in critically ill children

Background

Influenza A (H1N1) can cause severe neurological complications.

Objective

The purpose of this study was to analyze clinical and MRI features of neurological complications after H1N1 infection in critically ill children.

Materials and methods

We retrospectively analyzed clinical and neuroimaging findings in 17 children who were hospitalized in an intensive care unit with severe neurological complications after H1N1 infection in South China between September 2009 and December 2011. All children underwent pre- and post-contrast-enhanced brain MRI. Postmortem studies were performed in two children.

Results

Six children died, five because of acute necrotizing encephalopathy (ANE) and one because of intracranial fungal infection. Eleven recovered; their manifestations of H1N1 were meningitis (3), encephalitis (1) and influenza encephalopathy (7). MRI features of ANE included multiple symmetrical brain lesions demonstrating prolonged T1 and T2 signal in the thalami, internal capsule, lenticular nucleus and pontine tegmentum. Postmortem MRI in two children with acute necrotizing encephalopathy showed diffuse prolonged T1 and T2 signal in the bilateral thalami, brainstem deformation and tonsillar herniation.

Conclusion

Fatal neurological complications in children after H1N1 infection include ANE and opportunistic fungal infection. MRI is essential for identification of neurological complications and for clinical evaluation.     

A case of acute necrotizing encephalopathy associated with parainfluenza virus infection

Acute necrotizing encephalopathy (ANE) may be suspected when a young child presents with abrupt onset of altered mental status, seizures, or both. Definitive clinical diagnosis is based on magnetic resonance imaging (MRI) results. ANE is associated with influenza virus infections. Preliminary data suggests that up to 25% of ANE patients die, and up to 25% of ANE survivors develop substantial neurologic sequelae. Here, we describe a case of a comatose 22-month-old girl who was admitted to our hospital because of febrile illness and seizures. On day 13 of her illness, she died from ANE associated with infection from parainfluenza virus. Brain MRI results indicated diffuse bilateral symmetric signal changes in both basal ganglia, thalami, periventricular white matter, pons, and cerebral white matter, as well as generalized swelling of the brain.     

The correlation between neurological evaluations and neurological outcome in acute encephalitis: a hospital-based study.

Acute encephalitis is a common CNS infectious disease in children. However, there are limited studies concerning about the correlation between the clinical evaluations and neurological outcome. To investigate the value of neurological evaluations, and the correlation between these evaluations and neurological outcomes of acute encephalitis, in the present study we retrospectively evaluated the neurological outcome of 0- to 16-year-old children with encephalitis or meningoencephalitis between 1999 and 2000. Of 101 children enrolled, 4 died and 25 had other neurological sequelae, including epilepsy, headache, developmental delay, and emotional or behavioral changes during the 5 years of follow-up. The causative organisms in patients with neurological sequelae were herpes virus (HSV) 2/2 (100%), influenza 2/3 (67%), mycoplasma 5/12 (42%), and enterovirus 71 2/7 (29%). The important predictors for adverse outcomes were focal neurological signs, multiple seizures or status epilepticus on admission, leukopenia, focal slow waves or continuous generalized delta waves in electroencephalography (EEG), and focal cortical parenchymal hyperintensity in the magnetic resonance imaging (MRI) (p<0.05). Patients with initial presentations of focal neurological signs, papilledema, myoclonic jerks, and status epilepticus tended to have higher incidence of abnormal findings in brain MRI, although not achieving statistic significances. In addition, children with focal spikes or continuous generalized delta waves in EEG also had higher incidence of MRI abnormalities. We conclude that brain MRI studies may be indicated in patients with focal neurological signs, intractable seizure, and focal spikes, focal delta waves, or continuous generalized delta waves in EEG. For those with MRI examinations, focal cortical hyperintensity suggests poorer neurological outcomes.     

Type A2 influenza viral infections in children

We retrospectively reviewed the manifestations of influenza A2 in 83 hospitalized young children. Our purpose was to define the spectrum of clinical illness in this age group. Findings included fever (91%), vomiting or diarrhea (49%), pharyngitis (34%), pneumonitis (29%), otitis media (24%), conjunctivitis (13%), croup (13%), and bronchiolitis (6%). Neuromuscular manifestations occurred in 16 patients (19%) and included seizures, apnea, opisthotonos, and myositis. Three children had cerebrospinal fluid pleocytosis. Children younger than 3 months of age had fever less often and gastrointestinal symptoms more often than older children. Threee children died of progressive pneumonitis. We conclude that influenza A2 may cause a wide range of respiratory and neurologic findings in infancy and early childhood.     

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目的探讨甲型H1N1流感患儿的临床特点及治疗。方法对2009-11-04—2009-12-24桂林市人民医院收治的12例甲型H1N1流感重症患儿的临床资料进行回顾性分析。结果12例患儿均有发热,其中10例以呼吸道症状起病,如咽痛、咳嗽、咳痰等流感样症状;1例以消化系统症状(腹泻)起病;1例以神经系统症状起病;2例伴明显喘憋、呼吸困难;3例双肺闻及痰鸣音、湿啰音,2例闻及喘鸣音。12例患儿白细胞计数增高4例,降低3例;中性粒细胞比例增高4例,降低4例;淋巴细胞比例增高4例,降低2例;血小板计数降低1例,增高1例。6例丙氨酸转移酶(ALT)增高,7例天冬氨酸转移酶(AST)增高,7例乳酸脱氢酶(LDH)增高,7例肌酸激酶(CK)增高,3例肌酸激酶同工酶(CK-MB)增高。随着患儿病情好转,白细胞、肝功、心肌酶恢复正常。结论甲型H1N1流感重症患儿多以呼吸道症状发病,主要靶器官是肺,常合并细菌、支原体感染,出现各种并发症累及多脏器功能。以神经系统症状起病患儿进展迅速、病情凶险。     

儿童重症和危重症2009甲型H1N1流感临床特征

目的 报道儿童2009甲型H1N1流感重症与危重症的临床特征.方法 对150例经咽拭子实时荧光定量PCR检测确诊为2009甲型H1N1流感重症与危重症患儿的临床资料进行分析.结果 150例患儿中,男103例,女47例,年龄中位数为5岁;≥5岁81例,合并基础疾病21例.常见的表现依次为发热142例(95%),咳嗽133例(89%),呕吐35例(23%),喘息29例(19%),腹痛24例(16%),嗜睡11例(7%),惊厥9例(6%),肌痛9例(6%)和腹泻9例(6%).常见的检验异常为外周血白细胞计数异常60例(40%),C反应蛋白增高49例(33%),乳酸脱氢酶增高4.4例(29%),肌酸激酶增高38例(25%)和天冬氨酸转氨酶增高29例(19%).并发症主要为肺炎97例(65%),脑病18例(12%)和心肌炎7例(5%).使用奥司他韦治疗109例(73%),使用糖皮质激素治疗35例(23%).32例(21%)入住ICU,13例接受气管插管机械通气,14例接受支气管镜检查及冲洗.145例(97%)患儿治愈出院,5例死亡,其中3例死于脑病,1例死于急性呼吸窘迫综合征,1例死于继发性真菌性脑膜炎.结论 重症和危重症2009甲型H1N1流感主要发生在没有基础疾病的年长儿,其表现及检验异常比较广泛.神经系统并发症发生率较高,严重的脑病可引起死亡.早期行支气管镜检查及冲洗有可能减少肺部并发症引起的死亡.     

北京季节性甲型流感与2009甲型H1N1流感住院患儿的临床比较

目的 比较因甲型流感病毒(季节性和2009甲型H1N1)感染而住院儿童的流行病学及临床特征.方法 总结回顾分析首都儿科研究所附属儿童医院2003年1月至2010年1月有明确病原学证据的季节性甲型流感组(季节甲流组)和2009甲型H1N1流感组(新型甲流组)感染患儿331例的临床表现、实验室检查等资料.结果 (1)2003年至2008年每年季节甲流组患儿住院的高峰时间在冬季,新型甲流组住院患儿集中在2009年11月至2010年1月.(2)季节甲流组患儿发病年龄中位数为35(22～63)个月,新型甲流组年龄为48(36～67)个月,两组患儿发病年龄有显著差异(Z=-6.702,P＜0.01).(3)季节甲流组和新型甲流组患儿均以发热、咳嗽等流感样症状为主要表现,季节甲流组发热天数5(3～7)d,新型甲流组发热天数6(4～7)d,有显著差异(秩和检验,Z=-7.173,P＜0.01).(4)新型甲流组出现血小板减少,CRP、ALT、CK-MB的升高,以及心电图异常的人数高于季节甲流组.(5)新型甲流组有基础病变患儿60例,其比例高于季节甲流组的25例()(2=12.553,P＜0.01).(6)季节甲流组患肺炎者75例(49.3%),新型甲流组患肺炎者117例(65.4%),后者肺炎患儿人数高于前者(x2=8.661,P＜0.01),重症病例人数明显高于季节甲流组(X2=10.595,P＜0.01),有更高的ICU住院比例(x2=12.873,P＜0.01)和住院天数(Z=-2.764,P＜0.01).结论 2009甲型H1N1流感病毒作为一种新型变异病毒,致病力更强,有基础疾病的患儿更容易被感染,出现肺部、神经及心脏系统的并发症,住院时间长,病死率高.

Abstract：

Objective The novel influenza A (H1N1)virus firstly detected in April 2009 in Mexico rapidly spread to many countries including the United States and Canada where humans were infected with the H1N1 virus and deaths were reported. The pandemic virus strain had never been detected in specimen of human beings and swine. It was so highly contagious and widely spread that threatened life of humans globally. This study aimed to analyze clinical data of hospitalized children patients with 2009 novel H1N1 influenza A virus infection confirmed by etiologic tests, and compared with that of seasonal influenza A. Method Clinical manifestations,laboratory and therapy data from the hospitalized children were collected by designed case report form and analyzed. All patients were enrolled from Capital Institute of Pediatrics from January 2003 to 2010.There were 152 cases in seasonal influenza A group, which was composed of 100 boys and 52 girls. Other 93 boys and 86 girls formed 2009 novel influenza A group.Result Influenza A was dominate from 2003 to 2008 and the peak season was December and January,while the peak hospitalized time of 2009 novel H1N1 influenza was from November 2009 to January 2010. The median age of seasonal influenza group was 35 months,which was lower than that of novel influenza group (Z=-6.702,P＜0.01).Besides,80.9% of the patients in seasonal influenza group were infants,while the novel influenza A group was mainly composed of infants and pre-school children(x2 =40.725,P＜0.01). The cases of both groups had influenza-like symptoms at onset and the most common presentations were fever and cough.The duration of fever was much longer in 2009 novel influenza group(Z=-7.173,P＜0.01). Patients in two groups nearly had the same symptoms except cough was more frequently presented by novel influenza A group cases(x=4.109,P＜0.05).In laboratory examination,the novel influenza group had more cases with abnormality in blood platelet,CRP, ALT, and CK-MB than that of seasonal influenza group (x2=7.562,17.245,4.398,6.217,P＜0.01).Patients in novel influenza A group had more changes in electrocardiogram(x2=24.461,P＜0.01).More patients had common underlying medical condition in novel influenza groups than those in seasonal influenza group(x2=12.553,P＜0.01).Furthermore, the groups had different age distribution in underlying medical diseases(x2=7.231,P＜0.05).Children with 2009 novel H1N1 virus infection tended to catch pneumonia (x2=8.661,P＜0.01)and became the severe cases (x2=10.595,P＜0.01).They had much higher ICU admission rate (x2=12.873,P＜0.01)and longer hospital stay(Z=-2.764,P＜0.01).Conclusion As a new variant of influenza virus A, 2009 novel H1N1 influenza A had stronger pathogenicity. Children with underlying medical conditions had the high risk to be infected and developed severe manifestations.