贵州省首例高致病性禽流感A/H5N1病毒感染患者的救治体会

目的 探讨成功救治高致病性禽流感A/H5N1病毒感染(简称人禽流感)患者的诊断流程和临床管理措施.方法 对2009年1月16日贵州省人民医院收治的1例人禽流感患者的临床表现、实验室检查、心电图、影像学改变和临床管理等资料进行总结.结果 经逆转录-聚合酶链反应(RT-PCR)方法和病毒分离确诊为人禽流感病例.患者男,29岁,平素体健,发病前有活禽市场环境暴露史,以发热、畏寒起病,尤明显流感样症状,高热时伴有肢体抽搐和意识障碍,继之出现咳嗽,咳大量粉红色泡沫样痰,病情进行性加重,先后出现呼吸困难、急性呼吸窘迫综合征和心房颤动,影像学显示双侧肺炎进行性加重,并伴双侧胸腔积液.病程第8大给予有创呼吸机治疗,并给予奥司他韦,但病情仍进一步加重.病程第10天给予高滴度A/H5N1病毒疫苗免疫血浆后,患者病情日见好转,呼吸道症状逐渐减少甚至消失,心房纤颤转为窦性心率,病程第23天肺内病灶明显吸收后好转出院.结论 人禽流感患者发病可无典型的流行病学史,病变进展为急性呼吸窘迫综合征合并心脏损害时病情危重,预后不佳;如能在2周内及时给予适当的病毒免疫血浆治疗,则可能迅速改善患者的预后.     

湖南省高致病性人禽流行性感冒一例临床分析

目的 了解高致病性H5N1人禽流行性感冒(流感)病例的临床表现、实验室检查、影像学特征、治疗及其预后.方法 对2009年1月在湖南省怀化市第一人民医院收治的1例高致病性H5N1人禽流感的临床表现、实验室检查、影像学改变和治疗等多方面的资料进行回顾总结.结果 患者经RT-PCR、实时荧光定量PCR方法确诊为高致病性H5N1人禽流感病例.患者发病前有禽流感环境暴露史,以咳嗽、咳痰起病,继而出现高热、咯血,病情进行性加重,出现呼吸困难,伴外周血WBC和淋巴细胞明显降低,肝功能和心肌酶谱明显异常.发病第6天胸部影像学可见右肺实变,继而迅速扩展至双肺,出现急性呼吸窘迫综合征(ARDS)样肺部表现.经抗病毒、抗细菌、精皮质激素、呼吸机支持和对症治疗未见好转,于发病后第12天死于多器官功能衰竭.结论 高致病性H5N1人禽流感病变进展快,出现ARDS合并多器官功能损害时,预后不佳.     

深圳市首例H5N1型人禽流感临床报告

目的探索H5N1型人禽流感病例的临床特点及诊治经验。方法一例H5N1型人禽流感患者,采用荧光定量RT-PCR评价抗病毒治疗效果,流式细胞术监测细胞免疫,即时动态的放射学检查、血气分析、生化检查监测病情变化,即时的细菌学检查监测细菌感染情况和抗生素治疗效果。采用抗病毒、禽流感恢复期血浆、机械辅助通气、糖皮质激素、免疫调节、抗生素、对症支持等综合治疗。结果患者以高热、咳嗽、呼吸困难为主要症状,临床诊断为重症病毒性肺炎,合并急性呼吸窘迫综合征(ARDS)和多脏器功能衰竭,并继发严重肺部细菌感染。联合奥司他韦和禽流感患者恢复期血浆治疗,患者体内的病毒在短期内得到有效控制和清除;机械通气、激素及其他对症支持治疗有效控制ARDS和多脏器功能衰竭;多黏菌素治疗有效控制广泛耐药的铜绿假单胞菌感染;免疫调节治疗促进患者免疫功能的恢复。结论H5N1型人禽流感病情重、进展快,严重的ARDS及多器官功能障碍综合征是主要临床特征。早期清除病毒、及时正确的对症辅助支持治疗、选择有效抗生素控制继发细菌感染是治疗成功的关键。激素和免疫调节剂的使用值得进一步探索。恢复期血浆治疗是重症禽流感治疗的有益尝试。     

江西省首例高致病性H5N1人禽流感临床特点分析

目的了解高致病性H5N1人禽流感病例的临床表现、实验室检查、影像学特征、治疗及其预后。方法对2005年12月在江西省遂川县人民医院收治的1例高致病性H5N1人禽流感的临床表现、实验室检查、心电图、影像学改变、病理变化和治疗等多方面的资料进行总结。结果患者经逆转录-聚合酶链反应（RT-PCR）、实时荧光定量PCR（real-time PCR）方法和病毒分离确诊为高致病性H5N1人禽流感病例。患者发病前有禽流感环境暴露史，以发热、畏寒起病，伴流感样症状，继之出现咳嗽、咳脓痰和脓血痰，病情进行性加重，出现腹泻和呼吸困难，伴外周血白细胞和淋巴细胞明显降低、大量尿蛋白、肝功能和心肌酶谱明显异常及血清白蛋白明显降低。发病第6天后痰培养多次发现耐苯唑西林肺炎球菌，在病情明显加重后，痰培养出现其他细菌和真菌。发病初期（第5天）胸部影像学可见右肺中下高密度病灶，继之迅速发展至双肺，出现急性呼吸窘迫综合征（ARDS）样肺部表现。经抗病毒、抗细菌、抗真菌、糖皮质激素和对症治疗未见好转，于发病后第27天死于感染性休克和多器官功能衰竭。病理表现为双肺弥漫性肺泡损伤合并感染，继发弥漫性血管内凝血（DIC）；淋巴组织中淋巴细胞明显减少，组织细胞增生；心肌水肿、空泡变性；肾小管广泛坏死。结论高致病性H5N1人禽流感患者病变进展为ARDS合并多器官功能损害时。预后不佳。     

福建省高致病性禽流感A/H5N1病毒感染并支气管胸膜瘘患者的救治体会

目的 总结重症高致病性禽流感A/H5N1病毒感染(简称人禽流感)患者的临床特点、治疗经验以及合并支气管胸膜瘘的处理方法.方法 对2007年2月福建省建瓯市立医院成功救治的1例重症人禽流感并发右侧支气管胸膜瘘患者的临床资料和诊治过程进行回顾性分析.结果 患者女,44岁,发病前3 d有病死鸡接触史,以发热、气促为主要症状,经呼吸道分泌物检测A/H5N1病毒核酸阳性确诊.患者住院第7天发展为急性呼吸窘迫综合征,病情重、进展快,病程中出现呼吸机相关肺炎、双侧气胸、右侧支气管胸膜瘘等多种并发症.经奥司他韦抗病毒、糖皮质激素抗炎、输注康复期血浆、机械通气、抗感染等治疗,病情有所缓解,但支气管胸膜瘘持续存在并形成脓胸,导致脱机困难.经纤维支气管镜下气囊探查加选择性支气管封堵术、经纤维支气管镜右侧支气管胸膜瘘OB胶粘堵术等介入治疗,患者痊愈,发病第99天出院.结论 人禽流感并发难治性支气管胸膜瘘患者在采取抗病毒、抗感染、机械通气支持、输注康复期血浆等综合治疗的基础上结合介入治疗是可行的.     

浅谈人感染H7N9禽流感病毒肺炎救治体会

自2013年3月,我国上海和安徽报告3例人感染H7N9禽流感病毒肺炎以来,截至2017年2月24日,中国向WHO报告的总发病例数为1 258例.确诊病例中,绝大多数有活禽接触史,重症肺炎ARDS常见,总体病死率高达41%[1].近几个月,我国11省出现散发病例,病例数与死亡人数明显增加.实际上已经开始经历H7N9禽流感第5个流行季.因此,呼吸与危重症同道必须密切关注疫情进展并指导当地患者救治.下面就H7N9人禽流感重症肺炎救治等问题谈谈经验教训.     

湖南省首例成人高致病性禽流感A/H5N1病毒感染患者的救治体会

目的 探讨高致病性禽流感A/H5N1病毒感染(简称人禽流感)患者的临床特点及治疗经验.方法 总结2009年1月中南大学湘雅医院成功救治的1例确诊的人禽流感患者的临床表现、实验室检查、影像学改变和诊治过程中的成功经验.结果 患者经逆转录-聚合酶链反应(RT-PCR)方法确诊为人禽流感病例.患者女,21岁.以发热、咳嗽、呼吸困难为主要症状,肺部病灶进展快,并伴有多器官功能障碍.经早期奥司他韦抗病毒治疗及加强器官功能维护,患者康复出院.结论 早发现、早诊断、早期合理使用抗病毒治疗,积极维护脏器功能,防治多器官功能衰竭可挽救患者的生命.     

中国高致病性禽流感A/H5N1病毒感染病例临床管理专家共识(草案)

自2003年末起,在家禽与鸟类中广泛传播的高致病性禽流感A/H5 N1病毒(简称A/H5 N1病毒)感染几乎覆盖了全球大部分地庆,导致A/H5 N1病毒感染病例(简称人禽流感)不时出现,流感大流行的危险性日益增加.     

如何早期甄别高致病性禽流感A/H5N1病毒感染病例

高致病性禽流感A/H5N1病毒感染(简称人禽流感)是近几年来新发的一种呼吸道传染病,对人类首例禽流感A/H5N1病毒感染病例的确诊,标志着禽流感A/H5N1病毒已冲破种属的界线,成功实现了向人类的"跳跃式"感染.截止到2009年2月27日,全球人禽流感病例共408例,死亡256例,病死率约为63%[1].     

9例重症人感染H7N9禽流感的临床特征分析

目的分析重症人感染H7N9禽流感病例的临床特征,为临床诊断和治疗提供依据。方法回顾性分析2017年我院收治的9例人感染H7N9禽流感重症病例的流行病学特征、临床症状、实验室检查及治疗转归。结果 9例重症患者均以发热、咳嗽、气促等症状起病,部分患者呈持续性高热,热程第3-10天进展为急性呼吸窘迫综合征(ARDS)。胸部CT提示双肺感染病灶广泛,以实变为主,进展迅速;实验室检查显示:白细胞计数正常或者降低,可伴血小板下降,乳酸脱氢酶、超敏C反应蛋白升高,CD_4~+T淋巴细胞计数下降,部分危重病例降钙素原、1-3-β葡聚糖水平升高。流行病学调查显示:9例患者均有禽类接触史。最终治愈6例,死亡3例。结论人感染H7N9禽流感肺部病变进展迅速,死亡率高,高龄、高血压、糖尿病、慢阻肺等基础疾病是死亡高危因素,因此早发现、早诊断、早治疗是关键。在冬春季节应高度重视不明原因肺炎,特别是合并心血管、肺部基础疾病患者更需加强重视。     

新型甲型H1N1流感重症患者肺部影像学变化及临床特点

目的 探讨新型甲型H1N1流感(简称甲型流感)危重病例肺部影像学的变化及其临床特点. 方法 山西省太原市第四人民医院2009年10月20日至11月22日收治的10例重症甲型流感确诊患者,男6例,女4例,年龄5～41岁,平均19.3岁.采用常规技术检测血常规、血气指标、肝肾功能及心肌酶学变化,并行胸部X线及CT检查;给予奥司他韦、吸氧、呼吸支持、抗感染及对症支持等综合治疗. 结果 患者均以发热、咳嗽、呼吸困难为主要症状,肺部病灶表现多种多样,表现为磨玻璃影及实变影、肺不张、液气胸及胸腔积液等征象,进展快,同时存在急性肺炎和急性间质性肺炎的影像学改变,10例中5例发展为急性肺损伤,3例发展为ARDS;奥司他韦、呼吸支持及抗感染治疗有效. 结论 甲型流感危重病例的影像学表现为急性肺炎和急性间质性肺炎改变,临床表现为病情重、进展快,可发展为ARDS.     

新型甲型H1N1流感重症患者肺部影像学变化及临床特点

目的 探讨新型甲型H1N1流感(简称甲型流感)危重病例肺部影像学的变化及其临床特点. 方法 山西省太原市第四人民医院2009年10月20日至11月22日收治的10例重症甲型流感确诊患者,男6例,女4例,年龄5～41岁,平均19.3岁.采用常规技术检测血常规、血气指标、肝肾功能及心肌酶学变化,并行胸部X线及CT检查;给予奥司他韦、吸氧、呼吸支持、抗感染及对症支持等综合治疗. 结果 患者均以发热、咳嗽、呼吸困难为主要症状,肺部病灶表现多种多样,表现为磨玻璃影及实变影、肺不张、液气胸及胸腔积液等征象,进展快,同时存在急性肺炎和急性间质性肺炎的影像学改变,10例中5例发展为急性肺损伤,3例发展为ARDS;奥司他韦、呼吸支持及抗感染治疗有效. 结论 甲型流感危重病例的影像学表现为急性肺炎和急性间质性肺炎改变,临床表现为病情重、进展快,可发展为ARDS.     

A case of acute respiratory distress syndrome induced by fulminant influenza A (H3 N2) pneumonia]

We report a rare case of acute respiratory distress syndrome (ARDS) induced by Influenza A (H3 N2) without secondary microbiological infection. A 69-year-old woman was admitted to our hospital because of cough and severe dyspnea. We diagnosed ARDS, because of the severe respiratory failure resistant to high-dose oxygen, the diffuse bilateral infiltrates without cardiomegaly on chest radiography, and the normal pulmonary artery wedge pressure. This patient was treated with high doses of methylprednisolone, antibiotics, globulins, urinastatin, neutrophilic elastase inhibitor, nitric oxide inhalation, and extracorporeal membrane oxygenation, but died on the thirteenth hospital day. Our final diagnosis was ARDS induced by fulminant influenza (A/Hong Kong/68 (H3 N2)) virus pneumonia, because the antibody titers of H3 N2 influenza of paired sera showed a 128-fold increase.     

新型甲型H1N1流感重症患者肺部影像学变化及临床特点

目的 探讨新型甲型H1N1流感(简称甲型流感)危重病例肺部影像学的变化及其临床特点. 方法 山西省太原市第四人民医院2009年10月20日至11月22日收治的10例重症甲型流感确诊患者,男6例,女4例,年龄5～41岁,平均19.3岁.采用常规技术检测血常规、血气指标、肝肾功能及心肌酶学变化,并行胸部X线及CT检查;给予奥司他韦、吸氧、呼吸支持、抗感染及对症支持等综合治疗. 结果 患者均以发热、咳嗽、呼吸困难为主要症状,肺部病灶表现多种多样,表现为磨玻璃影及实变影、肺不张、液气胸及胸腔积液等征象,进展快,同时存在急性肺炎和急性间质性肺炎的影像学改变,10例中5例发展为急性肺损伤,3例发展为ARDS;奥司他韦、呼吸支持及抗感染治疗有效. 结论 甲型流感危重病例的影像学表现为急性肺炎和急性间质性肺炎改变,临床表现为病情重、进展快,可发展为ARDS.     

Review of clinical symptoms and spectrum in humans with influenza A/H5N1 infection

Abstract:   Influenza A/H5N1 infection has become the major emerging infectious disease of global concern again since late 2003. A history of exposure to dead or sick poultry or wild birds occurs in over 60% of cases of human H5N1 infection. The incubation period of avian-to-human transmission is generally between 2 and 5 days and the median duration of symptoms before hospitalization is about 4.5 days. The clinical spectrum has ranged from asymptomatic infection or mild influenza-like illness to severe pneumonia and multi-organ failure. Fever > 38°C, cough and dyspnoea are the major symptoms on presentation, whereas gastrointestinal symptoms such as watery diarrhoea, vomiting and abdominal pain are common early in the course of the disease. In contrast, upper respiratory tract symptoms are less prominent in human H5N1 infection when compared to seasonal influenza. Laboratory features of human H5N1 infection include leucopoenia, especially lymphopenia, elevated amino-transaminases, thrombocytopenia, prolonged prothrombin time and activated partial thromboplastin time, increased D-Dimer, increased serum lactate dehydrogenase and creatinine phospho-kinase, and hypoalbuminemia. A low absolute lymphocyte count on admission is associated with more severe disease and death. Radiographic abnormalities include multi-focal airspace consolidation, interstitial infiltrates, patchy or lobar involvement, with rapid progression to bilateral and diffuse ground-glass opacities consistent with ARDS. However, none of the clinical, laboratory and radiographic features are specific to H5N1 infection. A detailed exposure history needs to be elicited, including any close contact with sick or dead poultry, wild birds, other severely ill persons, travel to an area with A/H5N1 activity or work in laboratory handling samples possibly containing A/H5N1 virus.     

Acute respiratory distress syndrome induced by avian influenza A (H5N1) virus in mice

RATIONALE AND OBJECTIVE: The acute respiratory distress syndrome (ARDS) caused by avian influenza H5N1 viral infection has been reported in many humans since this virus was found to infect humans in Hong Kong in 1997, but no studies regarding an animal model of ARDS with H5N1 viral infection have been found in the literature. Here we present a mouse model of ARDS induced by H5N1 virus. METHODS: Six- to 8-wk-old BALB/c mice were inoculated intranasally (50 micro l) with 1 x 10(2) 50% mouse infectious doses of A/Chicken/Hebei/108/2002 (H5N1) virus. Lung injury was assessed by observation of lung water content and histopathology. Arterial blood gas, white blood cell count in bronchial alveolar lavage fluid, and tumor necrosis factor-alpha and interleukin-6 in bronchoalveolar lavage fluid and serum were measured at the indicated time points. RESULTS: Our data showed that H5N1 viral infection in mice resulted in typical ARDS, which was characterized by the following features: (1) about 80% of mice (13 of 16) dead on Days 6 to 8 postinoculation; (2) highly edematous lungs and dramatically increased lung wet:dry weight ratios and lung wet weight:body weight ratios; (3) inflammatory cellular infiltration, alveolar and interstitial edema, and hemorrhage in lungs; (4) progressive and severe hypoxemia; and (5) significant increase in neutrophils, tumor necrosis factor-alpha, and interleukin-6 in BALF. CONCLUSION: These results suggested that we successfully established a mouse model of ARDS with H5N1 viral infection, which may benefit further investigation into the pathogenesis of human ARDS induced by H5N1 virus.     

Increased hydrogen peroxide in the expired breath of patients with acute hypoxemic respiratory failure

Acute hypoxemic respiratory failure (AHRF) can result from diverse lung insults. Toxic oxygen metabolites have been implicated in this clinical condition and in animal models of pulmonary edema. Hydrogen peroxide (H2O2), an oxygen metabolite, mediates tissue injury. We measured H2O2 levels by a spectrophotometric technique in the breath condensate of 68 mechanically ventilated patients; 13 patients with normal lungs undergoing elective surgery had no such detectable levels of H2O2. Fifty-five patients in the ICU meeting criteria for the adult respiratory distress syndrome (ARDS) had a higher concentration of H2O2 in the expired breath condensate than ICU patients without pulmonary infiltrates (2.34 +/- 1.15 vs 0.99 +/- 0.72 mumol/L, p less than 0.005). This marker had a sensitivity of 87.5 percent and a specificity of 81.3 percent in separating the two patient populations. Patients with AHRF and focal pulmonary infiltrates who did not meet criteria for ARDS also had higher concentrations of H2O2 (2.45 +/- 1.55 mumol/L) than patients without pulmonary infiltrates (p less than 0.001). No difference was observed between the expired H2O2 concentrations of patients with ARDS or patients with focal pulmonary infiltrates. Patients with brain injury or sepsis tended to have higher levels of H2O2 regardless of lung pathology. Increased levels of H2O2 are detected in the expired breath of ICU patients with focal lung infiltrates and in ARDS patients, which is consistent with the hypothesis that oxygen metabolites participate in the pathogenesis of ARDS and other forms of AHRF.