Adult respiratory distress syndrome induced by salicylate toxicity

Noncardiogenic pulmonary edema induced by salicylate toxicity is becoming a well-recognized entity. However, the diagnosis can be easily missed early in the disease course. We report here adult respiratory distress syndrome (ARDS) in a 54-year-old man found to have salicylate toxicity one day after admission to the alcohol detoxification service at a community hospital. He had been taking one enteric-coated aspirin tablet twice a day for more than one year. He also had a 40 pack-year history of cigarette smoking. The list in any standard medical text of factors triggering ARDS is quite lengthy. Over the past few years, salicylate toxicity has been added to this list. As the case reported here illustrates, it is most important that salicylate toxicity be considered in the differential diagnosis for any patient with acute onset of pulmonary edema and normal cardiac function.     

保留自主呼吸对于重度急性呼吸窘迫综合征患者的影响：弊大于利

急性呼吸窘迫综合征（ARDS）是临床上常见的以顽固性低氧为表现的呼吸功能不全或衰竭的综合征，肺不均一性是其主要病理生理特点。传统观点认为，保留ARDS患者自主呼吸有助于改善全身氧合。但是近年来发现，对于重度ARDS患者，保留患者自主呼吸会加重肺损伤，过强的自主呼吸会导致重度ARDS患者跨肺压升高、肺内气体摆动、肺水肿加重以及人机不同步，引起患者肺内炎症加重，氧合功能恶化，最终影响患者预后，增加病死率。本文就自主呼吸对重度ARDS患者呼吸功能的影响机制展开综述。     

Three-view bedside ultrasound for the differentiation of acute respiratory distress syndrome from cardiogenic pulmonary edema

Bedside ultrasound is being increasingly used by emergency physicians (EPs) for the differentiation of acute dyspnea in critically ill patients. Lung ultrasound is emerging as a highly sensitive tool in diagnosing alveolar interstitial edema with the presence of diffuse “B-lines” arising from the pleural line. However, when used independently, lung ultrasound is unable to differentiate between cardiogenic and noncardiogenic causes of pulmonary edema. This case report describes a rapid 3-view or “triple scan” sonographic examination to differentiate acute respiratory distress syndrome (ARDS) from cardiogenic pulmonary edema.     

Acute lung injury and acute respiratory distress syndrome in pregnancy

Acute respiratory failure can be the result of a variety of clinical conditions, such as congestive heart failure, pneumonia, pulmonary embolism, exacerbation of obstructive lung diseases, and acute respiratory distress syndrome (ARDS). This article focuses on developments related to acute lung injury and ARDS and reviews epidemiology, pathogenesis and therapeutic advances with an emphasis on the obstetric population. A brief discussion of tocolytic-induced pulmonary edema, preeclampsia, venous air embolism, and aspiration-related ARDS is included. Management of pregnant women with ARDS is outlined.     

Acute respiratory distress syndrome

Acute respiratory distress syndrome is the clinical manifestation of severe, acute lung injury. It is characterized by the acute onset of diffuse, bilateral pulmonary infiltrates secondary to noncardiogenic pulmonary edema, refractory hypoxia, and decreased lung compliance. Acute respiratory distress syndrome occurs most frequently in the setting of sepsis, aspiration of gastric contents, trauma, or multiple transfusions. Its complex pathophysiology involves an inciting local or systemic event that initiates pulmonary endothelial and epithelial damage and subsequent increased permeability. Tachypnea, hypoxia, and respiratory alkalosis are typical early clinical manifestations, and they are usually followed by the appearance of diffuse pulmonary infiltrates and respiratory failure within 48 hours. Early identification and treatment of the underlying disorder, along with aggressive supportive care, are essential. Experimental therapies, including those using nitric oxide and surfactant, have not been shown to improve mortality in patients with ARDS, but new therapeutic approaches such as low-volume ventilation have been shown to decrease mortality. Many patients who survive ARDS have permanent, mild to moderate impairment of lung function. Quality of life after hospitalization with ARDS may be poorer than that in similar patients without ARDS.     

Report of the American-European consensus conference on ARDS: Definitions,mechanisms, relevant outcomes and clinical trial coordination

The acute respiratory distress syndrome (ARDS), a process of non-hydrostatic pulmonary edema and hypoxemia associated with a variety of etiologies carries a high morbidity, mortality (10–90%) and financial cost. The reported annual incidence in the United States is 150000 cases, but this figure has been challenged and may be different in Europe. Part of the reason for these uncertainties is the heterogeneity of diseases underlying ARDS and the lack of uniform definitions for ARDS. Thus, those whose wish to know the true incidence and outcome on this clinical syndrome are stymied. The European American Consensus Committee on ARDS was formed to focus on these issues and on the pathophysiologic mechanisms of the process. It was felt that international coordination between North America and Europe in clinical studies of ARDS was becoming increasingly important in order to address the recent plethora of potential therapeutic agents for the prevention and treatment of ARDS.     

Use of corticosteroids in the adult respiratory distress syndrome: A clinical review

Adult respiratory distress syndrome (ARDS) is a major cause of morbidity and mortality in critically ill patients. This form of acute respiratory failure represents a stereotypic response of the lung to many injurious mediators. Adult respiratory distress syndrome is characterized by pulmonary infiltrates, severe hypoxemia, and reduced lung compliance, and expresses clinically as an increased-permeability pulmonary edema. Despite modern treatment modalities, the high mortality rate (>50%) from ARDS has not appreciably decreased over the last 20 years. A major issue of controversy in the therapy of ARDS is the use of corticosteroids (CS) for the prophylaxis and treatment of this syndrome. In this report, current concepts of the pathophysiology of ARDS are discussed, while focusing on potential areas of benefit of CS. Experience with steroids is then reviewed, considering human studies of CS in established ARDS and pulmonary fibrosis, and the prevention of ARDS in high risk patients. After considering available data, it is concluded that the use of CS cannot be recommended for the prevention or therapy of ARDS.     

The acute respiratory distress syndrome

The acute respiratory distress syndrome (ARDS) is an important cause of acute respiratory failure that is often associated with multiple organ failure. Several clinical disorders can precipitate ARDS, including pneumonia, sepsis, aspiration of gastric contents, and major trauma. Physiologically, ARDS is characterized by increased permeability pulmonary edema, severe arterial hypoxemia, and impaired carbon dioxide excretion. Based on both experimental and clinical studies, progress has been made in understanding the mechanisms responsible for the pathogenesis and the resolution of lung injury, including the contribution of environmental and genetic factors. Improved survival has been achieved with the use of lung-protective ventilation. Future progress will depend on developing novel therapeutics that can facilitate and enhance lung repair.     

Ehrlichiosis with severe pulmonary manifestations despite early treatment

It is generally thought that if patients with ehrlichiosis are treated promptly, life-threatening illness can be avoided. We report a patient who sought medical attention 1 day after the onset of symptoms, was immediately given doxycycline, and still had serious illness with generalized edema, pulmonary infiltrates, acute respiratory distress syndrome, and noncardiogenic pulmonary edema, while receiving replacement intravenous fluids. This case alerts physicians to the serious end of the disease spectrum that can occur even though patients are given prompt, appropriate drug treatment at the onset of illness. Further studies are needed to clearly define the mechanisms involved in pulmonary complications and generalized edema, including noncardiogenic pulmonary edema, in patients with ehrlichiosis.     

The adult respiratory distress syndrome

The adult respiratory distress syndrome (ARDS) is an extreme form of noncardiogenic pulmonary edema associated with alveolar-capillary damage. Clinical features include acute respiratory distress, dyspnea and tachypnea, severe hypoxemia refractory to oxygen therapy, and diffuse bilateral pulmonary infiltrates. Any number of serious disorders can cause ARDS, but the processes leading to the alveolar permeability defect are not understood. Therefore, therapy remains nonspecific and supportive. Treatment includes positive end-expiratory pressure, careful fluid management, steroid therapy, and adequate nutrition. Unfortunately, even with the most sophisticated intensive care, the mortality of ARDS is still greater than 50%.     

Pulmonary endothelium in acute lung injury: from basic science to the critically ill

Background Pulmonary endothelium is an active organ possessing numerous physiological, immunological, and metabolic functions. These functions may be altered early in acute lung injury (ALI) and further contribute to the development of acute respiratory distress syndrome (ARDS). Pulmonary endothelium is strategically located to filter the entire blood before it enters the systemic circulation; consequently its integrity is essential for the maintenance of adequate homeostasis in both the pulmonary and systemic circulations. Noxious agents that affect pulmonary endothelium induce alterations in hemodynamics and hemofluidity, promote interactions with circulating blood cells, and lead to increased vascular permeability and pulmonary edema formation.Objective We highlight pathogenic mechanisms of pulmonary endothelial injury and their clinical implications in ALI/ARDS patients.     

Report of the American-European Consensus Conference on acute respiratory distress syndrome: Definitions,mechanisms, relevant outcomes,and clinical trial coordination

The acute respiratory distress syndrome (ARDS), a process of nonhydrostatic pulmonary edema and hypoxemia associated with a variety of etiologies, carries a high morbidity rate, mortality rate (10% to 90%), and financial cost. The reported annual incidence in the United States is 150,000 cases, but this figure has been challenged and may be different in Europe. Part of the reason for these uncertainties is the heterogeneity of diseases underlying ARDS and the lack of uniform definitions for ARDS. Thus, those who wish to know the true incidence and outcome of this clinical syndrome are stymied. The European American Consensus Committee on ARDS was formed to focus on these issues and on the pathophysiologic mechanisms of the process. It was felt that international coordination between North America and Europe in clinical studies of ARDS was becoming increasingly important to address the recent plethora of potential therapeutic agents for the prevention and treatment of ARDS.     

肾移植术后肺部感染致急性呼吸窘迫综合征的护理

目的探讨肾移植术后重症肺部感染致急性呼吸窘迫综合征（ARDS）的护理措施。方法回顾性分析24例肾移植术后重症肺部感染致ARDS患者的临床护理措施。结果本组24例患者,15例痊愈出院,2例放弃治疗,7例抢救无效死亡。结论肾移植术后肺部感染致ARDS患者应密切观察病情,严格执行消毒隔离制度,及早提供呼吸支持,加强心理护理、基础护理及营养支持,这些对提高抢救成功率极为关键。     

Fatal pulmonary failure attributable to viral pneumonia with human herpes virus 6 (HHV6) in a young immunocompetent woman

Adult respiratory distress syndrome (ARDS) attributable to viral pneumonia is described mainly in immunodeficient persons. ARDS caused by human herpes virus 6 (HHV6) is extremely rare, and to our knowledge only 1 case has been reported in the literature. We present the case of a young woman who developed fatal pulmonary failure most probably attributable to HHV6 pneumonia.     

Quel monitorage hémodynamique pour le patient atteint de syndrome de détresse respiratoire aiguë ?

Acute respiratory distress syndrome (ARDS) is due to the increase in permeability of the capillary alveolar membrane leading to non-cardiogenic pulmonary edema and hypoxia. Because ARDS is often associated with shock, its mortality rate remains high. One of the difficulties in ARDS is the management of fluid and volume expansion. During shock, volume expansion may lead to increase in oxygen transport related to increase in cardiac output, thus improving the patient’s outcome. However, in case of ARDS, pulmonary capillary leakage could raise hypoxia and lead to decrease in oxygen transport during volume expansion. Therefore, hemodynamic monitoring is mandatory in ARDS. Monitoring allows analyzing the right ventricular function and pulmonary capillary leakage, helping to predict fluid responsiveness and risk of increased pulmonary edema. In ARDS, monitoring should be based on oxygen transport that would take into account all hemodynamic and respiratory parameters.     

Does noninvasive ventilation work in ARDS? A case report and review of the current literature

The role of noninvasive positive pressure ventilation (NIPPV) in adult respiratory distress syndrome (ARDS) is controversial, in contrast to its well established benefits in other types of respiratory failure, especially acute exacerbations of chronic obstructive pulmonary disease and cardiogenic pulmonary oedema. We report a case of ARDS caused by Mycoplasma pneumoniae in a 70 year old man, treated with NIPPV in addition to standard medical therapy and analyse current evidence regarding the role of NIPPV in patients with ARDS.     

促红细胞生成素在急性肺损伤与急性呼吸窘迫综合征中作用的研究进展

急性肺损伤（ALI）或急性呼吸窘迫综合征（ARDS）是临床常见急危重症。各种病因包括严重感染、创伤、休克、急性胰腺炎、肺炎等肺内或肺外因素均可导致ALI/ARDS,发病机制主要包括炎症反应、细胞凋亡、氧化应激和肺泡毛细血管膜的损害等,目前尚无特殊有效的治疗方法,临床上也无修复肺损伤的有效药物。促红细胞生成素（EPO）作为一种多功能的内源性调节因子对各种组织损伤有一定的细胞保护作用,尤其是肺组织〔1〕,成为治疗ALI/ARDS的研究热点,     

急性呼吸窘迫综合征肺容积减少的机制与肺开放策略的选择

急性呼吸窘迫综合征(ARDS)是各种肺内外病因引起的肺毛细血管内皮细胞和肺泡上皮细胞损伤,由此导致的急性非心源性低氧性呼吸衰竭。肺容积减少是ARDS最重要的病理生理改变之一,也是当前ARDS机械通气治疗的主要着眼点和难点。肺组织自身重量增加导致肺泡塌陷,肺泡水肿,心脏和腹腔导致的压迫性肺不张是ARDS患者肺容积减少的原因。肺容积减少机制导向性的肺开放策略有助于达到改善氧合和减少呼吸机相关肺损伤的最佳平衡。     

Acetyl glyceryl ether phosphorylcholine-stimulated human platelets cause pulmonary hypertension and edema in isolated rabbit lungs. Role of thromboxane A2.

Macrophages, neutrophils, and platelets may play a role in acute edematous lung injury, such as that seen in the adult respiratory distress syndrome (ARDS), but their potential actions and interactions are unclear. Because stimulated human macrophages and neutrophils can release acetyl glyceryl ether phosphorylcholine (AGEPC), a potent platelet activator, we hypothesized that in ARDS, leukocyte release of AGEPC might stimulate platelets to release thromboxane A2 (TXA2), which then produces pulmonary hypertension and lung edema. In support of this premise, we found that pulmonary hypertension and edema occurred in isolated rabbit lungs perfused with human platelets and AGEPC, but not with platelets or AGEPC alone. Infusion of a vasodilator (nitroglycerin) to maintain base-line pulmonary artery pressures in lungs perfused with platelets and AGEPC prevented the development of lung edema suggesting that platelet and AGEPC-induced edema was hydrostatic in nature. Additional experiments suggested that the increased pressure was a result of TXA2 release from platelets stimulated by AGEPC. Specifically, preincubation of platelets with imidazole, a thromboxane synthetase blocker, prior to infusion with AGEPC significantly diminished pulmonary hypertension and prevented lung edema. Furthermore, pretreating lung preparations with 13-azaprostanoic acid, a TXA2 antagonist, before infusion of AGEPC and untreated platelets also reduced the pulmonary hypertension and blocked the lung edema. The role of TXA2 was further suggested when perfusates from lungs infused with platelets and AGEPC developed high levels of TXA2, whereas perfusates from controls did not. These results suggest that platelet aggregation induced by AGEPC may contribute to ARDS by releasing TXA2, which raises microvascular pressure and increases edema formation, especially when an underlying permeability defect is present.     

Adult respiratory distress syndrome from sulfuric acid fume inhalation

A 23-year-old man had adult respiratory distress syndrome (ARDS) caused by acute exposure to sulfuric acid fumes. The patient survived the initial hospitalization to be readmitted later with a lung abscess. After therapy, his chest roentgenogram and pulmonary function tests revealed no abnormalities except a marginally decreased DLCO, and he was without functional deficit. Noncardiogenic pulmonary edema probably resulted from direct alveolar injury caused by sulfuric acid.