肺表面活性物质联合N—CPAP治疗呼吸窘迫综合征患儿的疗效及护理

目的探讨呼吸窘迫综合征患儿的有效治疗及护理方法.方法将28例患呼吸窘迫综合征早产的患儿随机分为治疗组(15例)及对照组(13例).治疗组于生后30min至2h即从气管插管内滴入肺表面活性物质(PS)100mg/kg,用药后应用鼻塞持续气道正压(N-CPAP)装置辅助呼吸;对照组单纯应用持续气道正压辅助呼吸.结果治疗组辅助呼吸、机械通气、住院时间明显缩短,与对照组比较,差异有显著性意义(均P＜0.05);72 h胸部X线摄片正常率高于对照组(P＜0.05).结论 PS联合N-CPAP治疗早产儿呼吸窘迫综合征,可减轻病情,缩短氧疗时间.     

肺泡表面活性物质辅助治疗新生儿持续肺动脉高压的疗效观察

目的观察肺表面活性物质（PS）联合呼吸机机械通气治疗新生儿持续肺动脉高压（PPHN）的疗效。方法将40例达到机械通气标准的PPHN患儿分成2组。治疗组18例在常规机械通气基础上、采用从气管插管内滴入PS治疗,对照组22例给予常规机械通气治疗,其余治疗相同。比较分析两组肺动脉压、平均气道压、吸入氧浓度、血气分析、机械通气时间、氧疗时间、住院时间。结果治疗组与对照组在肺动脉压、平均气道压、吸入氧浓度、血气分析、机械通气时间、氧疗时间、住院时间方面均有显著性差异（P均〈0.05）。结论 PS联合呼吸机机械通气治疗PPHN能迅速缓解临床症状,缩短氧疗时间及住院时间。     

联合应用肺表面活性物质和保护性机械通气策略治疗婴幼儿体外循环后急性肺损伤

目的　探讨联合应用外源性肺表面活性物质 (PS)和保护性肺通气策略对体外循环后急性肺损伤 (ALI) /急性呼吸窘迫综合征 (ARDS)的治疗效应。方法　婴幼儿体外循环术后ALI/ARDS患者 16例 ,随机分为A和B两组 ,A组 9例采用保护性肺机械通气治疗 ;B组 7例在保护性肺通气治疗基础上经气管插管联合应用外源性PS(15 0mg/kg体重 )。观察两组患儿的临床转归 ,并监测 48h内肺动态顺应性 (Cdyn)、氧合指数 (OI)、血浆肿瘤坏死因子 (TNF α)的水平。结果与以往同类病例的治疗结果相比 ,本组患儿死亡率 (6.2 5 % )和并发症显著降低。在治疗后 48h内的各个时点 ,B组Cdyn显著高于A组 (P <0 .0 5 ) ,OI和TNF α的水平显著低于A组 (P <0 .0 5～0 .0 1)。结论　外源性PS与保护性肺通气具有协同作用 ,二者联合应用可明显提高体外循环后ALI/ARDS的治疗效应     

新生儿气胸40例临床分析

目的:探讨新生儿气胸发生的原因及治疗。方法:回顾性分析2008年1月～2012年6月共40例新生儿气胸的临床资料。结果:40例气胸中,吸入综合征28例(包括羊水吸入21例及胎粪吸入7例),呼吸窘迫综合征(RDS)7例,新生儿肺炎3例,新生儿湿肺1例,自发性气胸1例,其中有经鼻持续气道正压通气(NCPAP)应用史13例。经保守治疗,胸腔穿刺抽气,闭式引流,肺表面活性物质的应用及机械通气等治疗,36例治愈,3例好转后自动出院,1例死亡。结论:气胸的原因主要有吸入综合征,NCPAP的使用,呼吸窘迫综合征。在积极治疗原发病的基础上,选择适当的治疗手段、合理应用呼吸机、恰当的时候应用肺表面活性物质是新生儿气胸治疗的关键。     

新生儿经鼻持续正压通气管道固定方法的改进

经鼻持续呼吸道正压通气(NCPAP)是临床常用的治疗新生儿呼吸衰竭的无创辅助通气方式,广泛用于新生儿呼吸窘迫综合征(NRDS)、湿肺、新生儿肺炎、呼吸暂停、拔管撤离呼吸机后的过渡等[1]。传统的帽式固定法,利用帽子上的系带     

成人呼吸窘迫综合征机械通气期间呼吸道的管理

目的:探讨成人呼吸窘迫综合征机械通气期间呼吸道的管理.方法:对36例ARDS患者机械通气治疗采用肺保护性通气策略,主要措施为应用呼气末正压(PEEP)使呼气末肺容量增加,萎陷的小气道和肺泡再开放,减轻肺泡水肿,增加功能残气量和肺顺应性,从而改善通气和氧合,减少肺内分流.小潮气量,防止肺泡过度充气,允许性高碳酸血症.做好呼吸道的管理.结果:成人呼吸窘迫综合征机械通气期间通过呼吸道的管理可明显提高机械通气的治疗效果.结论:成人呼吸窘迫综合征机械通气期间通过加强呼吸道的管理,降低身心刺激,促进病人康复.     

影响经面罩机械通气治疗慢性阻塞性肺病呼吸衰竭的因素分析

目的:探讨影响经面罩机械通气治疗慢性阻塞性肺病呼吸衰竭发生急性呼吸窘迫综合征的因素。方法:选择慢性阻塞性肺病呼吸衰竭患者120例,都采用影响经面罩机械通气治疗,观察急性呼吸窘迫综合征发生情况与影响因素。结果:治疗中与治疗后发生呼吸窘迫综合征12例,发生率为8.0%。单因素分析显示pH值、严重感染、呼衰指数、肺顺应性是导致急性呼吸窘迫综合征的危险因素(P<0.05)。多因素分析显示严重感染、pH值、肺顺应性为主要的危险因素(P<0.05)。结论:经面罩机械通气治疗慢性阻塞性肺病呼吸衰竭有很好的效果,但是容易出现急性呼吸窘迫综合征,为此要对应加强预防处理。     

不同月龄先天性心脏病婴儿术后急性呼吸窘迫综合征应用肺表面活性物质治疗的临床研究

目的评价肺表面活性物质(pulmonary surfactant,PS)对不同月龄先天性心脏病(先心病)婴儿术后呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)治疗效果。方法采用PS治疗先心病患儿术后ARDS,其中2012年1月至2017年6月符合入选标准的患者共43例。分为小婴儿组(3个月,12例)、婴儿组(3个月至1岁,31例),比较两组患儿用药前后氧合和换气指标的变化情况。结果小婴儿组体重更低,两组患儿体外循环时间、主动脉阻断时间、机械通气时间、住ICU时间差异无统计学意义,两组患儿在用药前动脉血氧分压(PaO2)、氧吸入浓度(FiO2)、氧合指数(PaO2/FiO2,P/F)及肺泡动脉氧压比(a/A)差异无统计学意义(P0.05)。用药治疗24 h后,两组患儿与用药前比较,PaO2、P/F及a/A均显著升高;FiO2明显降低,差异有统计学意义(P0.05),用药24 h后,小婴儿组PaO2、P/F及a/A显著高于婴儿组,小婴儿组FiO2显著低于对照组。结论 PS治疗对小月龄先心病患儿术后ARDS者有更好的氧合通气改善作用。     

BiPAP联合PS治疗早产儿呼吸窘迫综合征的护理

目的 提高早产儿呼吸窘迫综合征（RDS）的治疗效果.方法 对42例RDS早产儿,采取气管插管内滴入肺表面活性物质（PS）,给药后拔除气管插管,立即给予BiPAP正压通气;同时做好滴入PS前后及应用BiPAP的护理,维持SpO2 0.85～0.93.结果 38例RDS早产儿3～12 d成功脱离BiPAP,改为空氧混合吸氧后逐渐脱氧;3例病情加重转为机械通气;1例放弃治疗.结论 BiPAP联合PS应用能改善RDS早产儿的症状和体征;精心的综合护理有利于减少并发症、预防感染,提高疗效.     

分化综合征合并急性呼吸窘迫综合征患者的护理

对6例分化综合征合并急性呼吸窘迫综合征患者转重症医学科抢救治疗,均给予经口气管插管、呼吸机辅助呼吸,采取肺保护性通气策略,3例好转,3例死亡。紧急配合各项抢救措施到位,严密观察生命体征及白血病相关颅内并发症的发生,做好机械通气的管理及感染预防等是有效救治的基础。     

Surfactant analysis and replacement therapy: a future tool of the lung transplant surgeon?

From 1965 to 1974 extensive research was carried out concerning the effects of experimental lung reimplantation and allografting on the surface tension properties of pulmonary surfactant. Since then, surfactant has been more rigorously examined in terms of its composition and function, and the potential roles of three surfactant-associated proteins have been established. Furthermore, surfactant replacement therapy for neonatal respiratory distress syndrome has come of age. The efficacy of surfactant treatment for adult respiratory distress syndrome is currently under clinical scrutiny, and experimental work on alterations in surfactant after lung transplantation has resumed after a 15-year hiatus. This article reviews current knowledge of the pulmonary surfactant system, as well as previous studies of the changes in surfactant after experimental lung transplantation. The experience in surfactant replacement therapy for the neonatal and adult respiratory distress syndromes is briefly described. Suggestions are made concerning the potential experimental and clinical applications of surfactant analysis and replacement therapy in lung transplantation.     

Surfactant replacement in neonatal and adult respiratory distress syndrome

Animal experiments and clinical trials have shown that the neonatal respiratory distress syndrome (RDS) can be treated effectively by surfactant replacement via the airways. This treatment facilitates the resorption of fetal pulmonary fluid, promotes uniform air expansion of the lungs, enhances gas exchange, reduces the protein leak across the alveolar epithelium, and prevents the development of bronchiolar epithelial lesions during artificial ventilation. Data from recent animal experiments indicate that surfactant replacement prevents epithelial lung lesions also during high frequency ventilation. Surfactant replacement restores blood gases to normal in adult experimental animals with severe respiratory insufficiency induced by repeated lung lavage, suggesting that this type of treatment might be effective in clinical adult RDS.     

Diagnosis and treatment of the respiratory distress syndrome during surgery in children under artificial circulation

The authors examined 152 children with congenital heart diseases complicated by pulmonary hypertension. 109 patients were operated on under conditions of hypothermic perfusion and 43--under deep hypothermia with extracorporeal circulation. Combination of disturbed mechanics of respiration and gas exchange was determined as the respiratory distress syndrome. The initial value of lung expansibility was found to be in inverse proportion to the degree of pulmonary hypertension. With the increase of pulmonary hypertension lung expansibility reduced before extracorporeal circulation and gas exchange became worse. Hypothermic perfusion at volumetric rates of 1.7-2.55 l/min/m2 led to diminished lung expansibility in the early postperfusion period of the operation, the mechanics and gas exchange grew worse. In patients who underwent operation under conditions of deep hypothermia the values of lung expansibility and gas exchange were stable. The incidence of the respiratory distress syndrome was 56.3% after hypothermic perfusion and 7.2% after deep hypothermia.     

Erhaltene spontane Atemtätigkeit während partieller Flüssigkeitsbeatmung

Controlled mechanical ventilation (CMV) may contribute to impaired hemodynamics in patients with respiratory failure. It is rational to assume that hybrid modalities of mechanical ventilation have fewer hemodynamic side-effects when spontaneous respiratory activity is allowed during the application of positive airway pressure. Partial liquid ventilation (PLV) has been shown to improve gas exchange in subjects with severe alveolar lung disease. We have shown that spontaneous respiratory efforts during proportional assist ventilation (PAV) is possible in experimental animals without lung disease whose lungs are partially filled with perfluorocarbons. In another series of experiments we demonstrated that PLV improves oxygenation and lung compliance in adult rabbits with severe surfactant deficiency, and in rabbits with meconium aspiration. In animals with meconium aspiration mortality, work of breathing and the degree of lung injury, as assessed by histological analysis, were reduced. In another two series of animals with and without surfactant deficiency spontaneous breathing supported by PAV was associated with increased cardiac output, stroke volume and oxygen transport, as compared to CMV after pharmacologically induced muscle paralysis. An increased arterial and venous pH in animals with surfactant deficiency during spontaneous breathing supported by PAV suggests improved tissue perfusion. Furthermore, gas exchange was improved during spontaneous breathing supported by PAV as compared to CMV and muscle paralysis.     

Peritoneal ventilation in rabbits: augmentation of gas exchange with cisapride.

BACKGROUND: Peritoneal ventilation has been shown to be effective in achieving extrapulmonary oxygenation and carbon dioxide elimination in an animal model of severe adult respiratory distress syndrome (ARDS). Cisapride is a "prokinetic" agent (increases gastric emptying), that may increase the splanchnic circulation and thus favourably affect gas exchange in peritoneal ventilation. METHODS: Using Doppler ultrasound the effect of cisapride on the portal venous circulation was examined in eight spontaneously breathing rabbits and the effect of cisapride on gas exchange in five rabbits spontaneously breathing room air was compared with that of a control group who did not receive cisapride. Its effect on gas exchange in five rabbits with ARDS being treated with mechanical lung and peritoneal ventilation was compared with that of a control group, and its effect on gas exchange in five rabbits with ARDS treated with conventional ventilation was also compared with that of a control group. RESULTS: Enteral administration of cisapride increased portal venous blood velocity, as measured ultrasonographically, by a mean of 188% one hour after receiving the drug. In rabbits with ARDS being treated with both peritoneal ventilation and mechanical ventilation to the lungs, those receiving cisapride had arterial oxygen tensions 1.5-3 times that of controls. Cisapride had no effect on arterial blood gas tensions in rabbits who were spontaneously breathing room air, nor in rabbits with ARDS who received only conventional mechanical lung ventilation. CONCLUSIONS: Cisapride increases arterial oxygenation in rabbits with severe ARDS treated with peritoneal ventilation, probably due to its ability to increase splanchnic circulation. It should be considered as an adjuvant medication to peritoneal ventilation.     

Intratracheal surfactant administration restores gas exchange in experimental adult respiratory distress syndrome associated with viral pneumonia.

The effect of intratracheal surfactant administration was studied in rats with adult respiratory distress syndrome associated with infection with nebulized Sendai virus. Thirty-six hours after infection, animals (n = 7) showed severely impaired gas exchange and acidosis during artificial ventilation (PaO2 = 152.2 +/- 18.7, PaCO2 = 65.3 +/- 19.2, pH = 7.26 +/- 0.11) with a pressure-controlled mode, standard frequency of 35/min, peak airway pressure of 15 cm H2O (15/0), inspiratory/expiratory ratio of 1:2, and F1O2 = 1. Gas exchange improved (P = 0.02) with increased ventilator pressures with PEEP (25/4). Forty-eight hours after infection, blood gas tensions could no longer be significantly improved by these same ventilator settings (PaO2 = 123.8 +/- 31.0, PaCO2 = 95.1 +/- 43.6, pH = 7.12 +/- 0.16, n = 9). At this time, surfactant replacement dramatically increased arterial oxygenation within 5 min (PaO2 = 389.4 +/- 79.9) and resulted in a fourfold increase in PaO2 within 2 h. It is concluded that intratracheal surfactant administration is a promising approach in the treatment of respiratory failure during adult respiratory distress syndrome associated with viral pneumonia.     

Surfactant inactivation and surfactant replacement in experimental models of ARDS

Lung structure and function, and the effect of surfactant replacement, were studied in three animal models of adult respiratory distress syndrome (ARDS): surfactant depletion by repeated lung lavage, proteinaceous pulmonary edema induced by prolonged exposure to hyperoxia, and inoculation with hybridoma making an antibody to the hydrophobic surfactant-associated protein, SP-B. Surfactant replacement therapy restored normal gas exchange in respiratory failure induced by repeated lung lavage but was ineffective in animals with severe lung parenchymal lesions induced by hyperoxia or antibody to SP-B. Lung edema fluid from animals exposed to hyperoxia inhibited surfactant function in a concentration-dependent manner. These observations indicate that, in experimental ARDS, the effect of surfactant replacement depends on the type of animal model and, especially, on the degree of lung injury present at the time of therapy.     

Complement and the severity of pulmonary failure

Complement-induced granulocyte aggregation is suspected as a cause of the adult respiratory distress syndrome. Quantifying the lung damage in these patients is difficult, and complement levels combined with clinical parameters of oxygenation might help define the severity of pulmonary deterioration. Forty-five high-risk patients, selected by arterial blood gas criteria, had their pulmonary insult related to C3a and C5a levels. Patients were stratified by pulmonary shunt, alveolar-arterial oxygen gradient, and radiographic findings into two categories of severity: pulmonary dysfunction, a milder insult, and ARDS, a major aberration in pulmonary function. The clinical assignment of a diagnostic category required at least 96 hours of monitoring. During this 96-hour period, multiple complement levels were obtained. These complement levels were then compared in pulmonary dysfunction and ARDS patients. ARDS patients had significantly higher C3a and C5a values after the patients were selected as high risk. These results suggest that the amount of complement activated in patients with incipient respiratory failure correlates with the severity of eventual pulmonary insult. The use of arterial blood gases and C3a and C5a levels should allow better and earlier definition of patients at risk for ARDS.     

Tumour necrosis factor in the bronchoalveolar secretions of infants with the respiratory distress syndrome and the effect of dexamethasone treatment.

BACKGROUND: Tumour necrosis factor alpha may contribute to the lung damage that occurs in the adult respiratory distress syndrome. Whether it occurs in the lungs of preterm infants with respiratory distress syndrome is unknown. METHODS: Tumour necrosis factor alpha concentrations in the bronchopulmonary secretions of 28 ventilated preterm infants were determined by the enzyme linked immunosorbent assay. RESULTS: Concentrations were low in the first three days of life, being undetectable in nine of the 20 infants whose bronchopulmonary secretions were sampled. From day 4 concentrations were increased and detectable in all but two of 14 infants. Similar concentrations were found in samples taken on days 8-20 and 21-40. Greater mean concentrations occurred in those infants requiring oxygen for a long time. In six infants who received dexamethasone treatment for prolonged ventilator dependency treatment was associated with a reduction in tumour necrosis factor alpha concentrations. CONCLUSIONS: Tumour necrosis factor may contribute to the neonatal respiratory distress syndrome, as suggested for the adult respiratory distress syndrome. The therapeutic effects of dexamethasone treatment in neonatal respiratory distress syndrome may be mediated, at least in part, by reduced production of pulmonary tumour necrosis factor.     

Pharmacologic strategies in acute respiratory distress syndrome

Treatment of the acute respiratory distress syndrome includes both supportive measures and correction of the underlying cause. Various pharmacological interventions have been proposed to limit the severity of lung injury and enhance the healing process, including exogenous surfactant, inhaled vasodilators (mainly nitric oxide), corticosteroids, prostaglandin E1, antioxidants (N-acetylcysteine), ketoconazole and other substances. Some of these interventions are administered via the airways, for example inhaled nitric oxide or liquid ventilation with perfluorocarbons. Some have beneficial effects on surrogate end-points such as pulmonary gas exchange. However, in large prospective trials none of these pharmacological approaches have resulted in significantly improved survival in acute respiratory distress syndrome patients.