天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2010年
1期
32-35,后插2
,共5页
李冠华%张力%李月川%贾玮%张冬睿%高淑连%赵勇
李冠華%張力%李月川%賈瑋%張鼕睿%高淑連%趙勇
리관화%장력%리월천%가위%장동예%고숙련%조용
流感病毒A型%H1N1亚型%流感%人%肺炎%病毒性%危重病%重症监护病房%呼吸%人工%奥司他韦病理学%临床%肺%心脏
流感病毒A型%H1N1亞型%流感%人%肺炎%病毒性%危重病%重癥鑑護病房%呼吸%人工%奧司他韋病理學%臨床%肺%心髒
류감병독A형%H1N1아형%류감%인%폐염%병독성%위중병%중증감호병방%호흡%인공%오사타위병이학%림상%폐%심장
influenza A virus%H1N1 subtype%influenza%human%pneumonia%viral%critical illness%intensive care units%respiration%artificial%oseltamivir%pathology%clinical%lung%heart
目的:探讨危重症甲型H1N1流感病毒(甲流)肺炎患者的主要临床特点,分析其气道内分泌物及肺、心脏病理学改变与持续性低氧血症的关系.方法: 回顾性分析入住呼吸重症监护病房(RICU)的24例危、重症甲流肺炎患者的临床资料.24例均用抗病毒治疗(达菲剂量75或150 mg)每日2次,24例中20例用激素治疗,6例行气管插管机械通气治疗.结果:24例患者平均年龄(48.25±19.73)岁,孕产妇、肥胖及有慢性基础病者15例.进行性气短、咳嗽、肌肉酸痛是主要症状.双肺多发实变影22例(91.67%).入院后5例气道内分泌物中蛋白质为34.1~37.7 g/L,乳酸脱氢酶(LDH)为792~1 890 U/L.白细胞计数为(0.722~1.470)×10~9/L,中性粒细胞0.21~0.44,单核细胞为0.111~0.560,嗜酸粒细胞为0.027~0.110,嗜碱粒细胞为0.018~0.054.病理学变化有肺透明膜形成、肺泡腔塌陷、心肌细胞变性和心肌灶性坏死.气管插管机械通气支持治疗6例,死亡5例,病死率20.83%.结论:气道内分泌物LDH、蛋白质升高、炎性细胞增多是危重症甲流肺炎患者肺部病理损害的表现;机械通气支持治疗对于肺内广泛实变者效果不理想,且相关的并发症是部分患者病情加重或死亡的促发因素.
目的:探討危重癥甲型H1N1流感病毒(甲流)肺炎患者的主要臨床特點,分析其氣道內分泌物及肺、心髒病理學改變與持續性低氧血癥的關繫.方法: 迴顧性分析入住呼吸重癥鑑護病房(RICU)的24例危、重癥甲流肺炎患者的臨床資料.24例均用抗病毒治療(達菲劑量75或150 mg)每日2次,24例中20例用激素治療,6例行氣管插管機械通氣治療.結果:24例患者平均年齡(48.25±19.73)歲,孕產婦、肥胖及有慢性基礎病者15例.進行性氣短、咳嗽、肌肉痠痛是主要癥狀.雙肺多髮實變影22例(91.67%).入院後5例氣道內分泌物中蛋白質為34.1~37.7 g/L,乳痠脫氫酶(LDH)為792~1 890 U/L.白細胞計數為(0.722~1.470)×10~9/L,中性粒細胞0.21~0.44,單覈細胞為0.111~0.560,嗜痠粒細胞為0.027~0.110,嗜堿粒細胞為0.018~0.054.病理學變化有肺透明膜形成、肺泡腔塌陷、心肌細胞變性和心肌竈性壞死.氣管插管機械通氣支持治療6例,死亡5例,病死率20.83%.結論:氣道內分泌物LDH、蛋白質升高、炎性細胞增多是危重癥甲流肺炎患者肺部病理損害的錶現;機械通氣支持治療對于肺內廣汎實變者效果不理想,且相關的併髮癥是部分患者病情加重或死亡的促髮因素.
목적:탐토위중증갑형H1N1류감병독(갑류)폐염환자적주요림상특점,분석기기도내분비물급폐、심장병이학개변여지속성저양혈증적관계.방법: 회고성분석입주호흡중증감호병방(RICU)적24례위、중증갑류폐염환자적림상자료.24례균용항병독치료(체비제량75혹150 mg)매일2차,24례중20례용격소치료,6례행기관삽관궤계통기치료.결과:24례환자평균년령(48.25±19.73)세,잉산부、비반급유만성기출병자15례.진행성기단、해수、기육산통시주요증상.쌍폐다발실변영22례(91.67%).입원후5례기도내분비물중단백질위34.1~37.7 g/L,유산탈경매(LDH)위792~1 890 U/L.백세포계수위(0.722~1.470)×10~9/L,중성립세포0.21~0.44,단핵세포위0.111~0.560,기산립세포위0.027~0.110,기감립세포위0.018~0.054.병이학변화유폐투명막형성、폐포강탑함、심기세포변성화심기조성배사.기관삽관궤계통기지지치료6례,사망5례,병사솔20.83%.결론:기도내분비물LDH、단백질승고、염성세포증다시위중증갑류폐염환자폐부병리손해적표현;궤계통기지지치료대우폐내엄범실변자효과불이상,차상관적병발증시부분환자병정가중혹사망적촉발인소.
Objective:To investigate the main clinical features of critically ill patients with influenza A (H1N1) influenza virus pneumonia, and the relationship between airway secretions and cardiopulmonary pathology change with continuous hypoxemia. Methods: The retrospective analysis was made in critically ill patients with H1N1 influenza virus pneumonia admitted to a respiratory intensive care unit(RICU). Twenty-four patients were all administrated antiviral drugs (oseltamivir 75/150 mg Bid). Twenty of them were subjected to application of hormonal therapy, and 6 of them with mechanical ventilation. Results: The average age of 24 patients was (48.25±19.73) years old. Fifteen of them were pregnant women, obesity and who suffered from chronic underlying diseases. The main symptoms of them were progressive shortness of breath, cough and myalgia. It was found by X-ray that 22 patients(91.67%) had multiple lung consolidation shadow. After admission, airway secretions were collected, and the protein concentration of which was 34.1-37.7 g/L in 5 cases. The concentration of l-lactate dehydrogenase(LDH) was 792-1 890 U/L. White blood cell count was (0.722-1.470)×10~9/L, included 0.21-0.44 neutrophils, 0.111-0.560 mononuclear cells, 0.027-0.110 eosinophils, 0.018-0.054 basophils. Pathological changes of these patients were hyaline membrane formation, alveolar cavity collapse, myocardial cell degeneration and focal myocardial necrosis. Intubation and mechanical ventilation were performed in 6 cases, 5 of them dead and the mortality rate was 20.83%. Conclusion: The lung pathological damages were increased LDH and protein in airway secretions, and increased count of inflammatory cells. Effect of mechanical ventilation was not satisfied in part of patients who had diffuse lung consolidation in X-ray, and the related complications leaded to exacerbation or death in part of them.