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題名 | 急性呼吸窘迫症候群之歷史回顧、個人經驗與爭論點=ARDS-History, Experience and Debate |
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作者姓名(中文) | 紀崑山; | 書刊名 | 中華民國重症醫學雜誌 |
卷期 | 6:2 民93 |
頁次 | 頁141-158 |
分類號 | 415.47 |
關鍵詞 | 成人呼吸窘迫症候群; 急性呼吸窘迫症候群; 呼吸器; Adult respiratory distress syndrome; Acute respiratory distress syndrome; Ventilator; |
語文 | 中文(Chinese) |
中文摘要 | 成人或急性呼吸窘迫症候群(adult or acute respiratory distress syndrome, ARDS)是非心因性肺水腫(non-cardiognic pulmonary edema)之一,在西元1967年Asbaugh DG等報導之前其實並非從未發生過,只是未被重視。由於ARDS屬於疾病症候群,其診斷之確定與否符合所設定之條件有關,在西元1988-1994年以前ADRS設定之診斷條件非常混亂,西元1994年北美洲與歐洲共識聯合研討會(North American-European Consensus Conference)提出之急性肺損傷(acute lung injury)及急性呼吸窘迫症候群(acute respiratory distress syndrome, ARDS)之定義才解決定義上之紛爭。陽壓機械過氣術與吐氣末陽壓(PEEP)是肺臟支持治療之主要手段,但是ARDS死亡之主要原因是敗血症與多器功能衰竭,僅10-15%死於頑固性動脈血氧不足。雖然最近20年來吾等對於ARDS致病機制之瞭解有突破性進展,但是針對ARDS肺病變之藥治療卻仍然沒有太大地突破。雖然嚴謹之ARDS治療性臨床研究之結果大多數無法獲得正面結論,但流行病學研究顯示;從1990年代開始ARDS之死亡率有逐年下降之趨勢。其原因為:(1)呼吸器導致肺損傷(ventilator-induced lung injury)之觀念逐漸被接受,而採用保護肺之通氣策略(lung-protective ventilatory strategy); (2)重症整合支持性照護之技術大有改善。SARS (severe acute respiratory distress)之引用與急性或成人呼吸窘迫症候群(acute or adult respiratory distress syndrome, ARDS)之流行病學有關,但是美國疾病管制暨預防中心(CDC)與國際衛生組織(WHO)等公共衛生與流行病專家卻偏好使用SARS以取代ARDS有其歷史背景。 |
英文摘要 | Acute respiratory distress syndrome is one of the non-cardiogenic pulmonary edema with increased pulmonary vascular permeability and consists of a constellation of symptoms and signs. ARDS presented itself in the medical literatures with different name and drew little public attention until the Lancert’s publication of Asbaugh’s article in 1967. the definitions of ARDS were diversified until the North American-European Consensus Conference in 1994. Positive pressure mechanical ventilation and positive end-expiratory pressure (PEEP)are the cornerstones of supportive measures for the respiratory system, but only 10-15% of ARDS died of refractory hypoxemia, most of mortality cases died of severe sepsis and multiple organ dysfunction syndrome. Many clinicians are concerned that it may exacerbate lung injury in patients with acute respiratory failure. Further, ongoing inflammation in the lung from mechanical ventilation may contribute to multiple organ failure. Numerous animal studies suggest that mechanical ventilation can cause damage to normal lungs or increase damage to injured lungs. This ventilation-derived lung injury is functionally and histologically similar to ARDS. Injury may occur from increased airway pressure with regional overdistension of alveoli or the repeated opening and closing of small airways with resultant shear forces, Gattinoni et al suggests the ARDS lung may be separated into thirds: one third is consolidated and does not participate in ventilation, one third is overdistended forming bullae, and the last third has a relatively normal ventilation-perfusion relationship. Thus, the lung is not uniformly stiff in ARDS; rather, there is a reduced amount of normal lung tissue, referred to as a “baby lung.” Ventilation with high airway pressures or volumes favors delivery of a disproportionate share of tidal volume to the ventilated small lung, resulting in overdistension and damage. In spite of tremendous advances in our understanding of the pathophysiology of ARDS, pharmacolotical manipulation of the ARDS targeted at the disease lung shows little breakthrough. There was epidemiological evidence that the ARDS mortality rate improves since 1990, which may be attributable to the adaptation of sophisticated multidisciplinary supportive care and lung-protective entilatory strategy based on the concept of ventilator-induced lung injury. The CDC of USA and WHO use severe acute respiratory syndrome (SARS) instead of ARDS to draw medical attentions and report disease outbreaks to the medical authorities, which could be traced back to Hantavirus pulmonary syndrome. |
本系統之摘要資訊系依該期刊論文摘要之資訊為主。