The Acute Respiratory Distress Syndrome: Myths and Controversies

摘要

The term Adult Respiratory Distress Syndrome (ARDS), was first introduced by Ashbaugh and Petty more than two decades ago. Since then, our understanding of this clinicopathological entity has increased significantly. However, little therapeutic progress has been achieved and the mortality remains high. ARDS is characterized by diffuse pulmonary microvascular injury resulting in increased permeability and, thus, non-cardiogenic pulmonary edema. Ventilation-perfusion lung studies have demonstrated that the predominant pathogenesis of hypoxemia in ARDS is related to intrapulmonary shunts. Common symptoms include dyspnea, tachypnea, dry cough, retrosternal discomfort, and moderate to severe respiratory distress. In most cases the diagnosis of ARDS is that of exclusion. The mainstay of therapy for this syndrome is the management of the underlying disorder causing it. To date, there are no specific pharmacological interventions of proven value for the treatment of ARDS. Once the potentially treatable sources have been found and their therapy started, the main treatment for ARDS is supportive. Ashbaugh and coworkers, in 1967, described a syndrome characterized by refractory hypoxemia, diffuse lung infiltrates on chest radiograph, and decreased lung compliance in a group of 12 patients suffering from severe respiratory failure.1 In addition, these patients had different underlying diseases (e.g. pancreatitis, pneumonia, trauma). Originally, this condition was named by the authors as the Acute Respiratory Distress Syndrome of Adults. However, in 1971 the same authors renamed the syndrome to what we now know as the Adult Respiratory Distress Syndrome or Acute Respiratory Distress Syndrome (ARDS).2 Since then, our understanding of this clinicopathological syndrome has increased significantly. Although the vast majority of patients with ARDS are ultimately managed in intensive care units (ICU), the purpose of this article is to present to emergency physicians, intensivists, surgeons, and other health care providers a review of the pathophysiology, early clinical features, diagnosis, acute management and prognosis as well as some of the common myths and controversies of this devastating syndrome. Definition The definition of ARDS has changed over time. In the early 1960s Burke and coworkers utilized the term High Output Respiratory Failure to describe a type of respiratory failure characterized by the inability to provide adequate oxygenation and carbon dioxide excretion.3 Terms frequently used when referring to this syndrome include: adult hyaline-membrane disease, adult respiratory insufficiency syndrome, congestive atelectasis, hemorrhagic lung syndrome, Da Nang lung, stiff-lung syndrome, shock lung, white lung and, wet lung among others.4 Although there are currently diverse opinions regarding the proper use of the term “ARDS”, all definitions of this syndrome include patients who meet the following criteria:5,6 Clinical evidence of respiratory distress. Chest radiograph revealing diffuse bilateral airspace disease (“pulmonary edema”). Hypoxemia that is difficult to correct with oxygen supplementation. Hemodynamic evidence of a pulmonary artery occlusion (wedge) pressure < 18 mm Hg. Thoracic static compliance less than 40 mL/cm of water. Incidence The incidence of ARDS varies depending on the diagnostic criteria used for its definition, as well as the underlying diseases that are acting as risk factors. The estimated incidence of ARDS in the USA in recent years has been calculated to be close to 150,000 new cases each year.7,8 In a study by Fowler and coworkers, the incidence varied from 2% (e.g. in patients post coronary-artery bypass grafts or burns) to 36% (e.g. gastric bronchoaspiration).9 In a similar cohort, Pepe et. al., found that the incidence of ARDS ranged from 8% (in patients with multiple fractures) to 38% (in patients with sepsis).10 Etiology The major risk factors for the development of ARDS are depicted in Table 1. Amon