INTRODUCTION — A distinct type of hypoxemic respiratory failure characterized by acute abnormality of both lungs was first recognized during the 1960s. Military clinicians working in surgical hospitals in Vietnam called it shock lung, while civilian clinicians referred to it as adult respiratory distress syndrome [1]. Subsequent recognition that individuals of any age could be afflicted led to the current term, acute respiratory distress syndrome (ARDS).
The epidemiology, pathophysiology, pathologic stages, and etiologies of ARDS will be reviewed here. Other issues related to ARDS are discussed separately. (See "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults" and "Acute respiratory distress syndrome: Prognosis and outcomes in adults" and "Ventilator management strategies for adults with acute respiratory distress syndrome" and "Acute respiratory distress syndrome: Supportive care and oxygenation in adults" and "Acute respiratory distress syndrome: Investigational or ineffective therapies in adults".)
DEFINITION — The Berlin Definition of ARDS (published in 2012) has replaced the American-European Consensus Conference’s definition of ARDS (published in 1994) [2-4]. However, it should be recognized that most evidence is based upon prior definitions. The current diagnostic criteria for ARDS are provided separately. (See "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults", section on 'Diagnosis'.)
EPIDEMIOLOGY — The incidence of acute respiratory distress syndrome (ARDS) was determined in a multicenter, population-based, prospective cohort study in the United States [5]. The study followed 1113 patients with ARDS for 15 months beginning in 1999 or 2000:
●The age-adjusted incidence was 86 per 100,000 person-years for individuals with an arterial oxygen tension to fraction of inspired oxygen (PaO2/FiO2) ratio ≤300 mmHg and 64 per 100,000 person-years for individuals with a PaO2/FiO2 ≤200 mmHg.
●The incidence increased with patient age from 16 per 100,000 person-years among individuals 15 to 19 years of age to 306 per 100,000 person-years among individuals 75 to 84 years of age.
●Extrapolation of the data suggested that there are approximately 190,000 cases of ARDS in the United States each year [5].
Within intensive care units, approximately 10 to 15 percent of admitted patients and up to 23 percent of mechanically ventilated patients meet criteria for ARDS [6-10]. As an example, in a multicenter, international study of nearly 30,000 intensive care unit (ICU) patients, 10 percent of admissions to the ICU were due to ARDS [10]. The majority of patients with ARDS (80 percent) required mechanical ventilation. Among those with ARDS, the majority (47 percent) had moderate ARDS while the remainder had mild (30 percent) or severe disease (23 percent). ARDS was responsible for 23 percent of patients mechanically ventilated in the ICU.
The incidence of ARDS varies geographically and may be higher in the United States and Europe than in other countries [10,11].
The incidence of ARDS may be decreasing. A prospective cohort study from a single institution reported that the incidence of ARDS decreased from 82.4 cases per 100,000 person-years in 2001 to 38.9 cases per 100,000 person-years in 2008 [12]. This was attributable to a decline in hospital-acquired ARDS, since the incidence of ARDS at hospital presentation did not change. Those who developed ARDS had more severe disease, more comorbidities, and more predisposing conditions. These findings may reflect changes in the delivery of care at this institution only; studies from other institutions are necessary before it can be concluded that the incidence of ARDS is declining in general.
PATHOPHYSIOLOGY — Healthy lungs regulate the movement of fluid to maintain a small amount of interstitial fluid and dry alveoli. This is interrupted by lung injury, causing excess fluid in both the interstitium and alveoli. Consequences include impaired gas exchange, decreased compliance, and increased pulmonary arterial pressure.
Baseline — Normal lung function requires that dry, patent alveoli be closely situated to appropriately perfused capillaries (picture 1) [13]. The normal pulmonary capillary endothelium is selectively permeable: fluid crosses the membranes under the control of hydrostatic and oncotic forces, while serum proteins remain intravascular.
The Starling equation describes the forces that direct fluid movement between the vessels and the interstitium [14]. A simplified version of the equation is:
Q = K x [(Pmv - Ppmv) - rc (πmv - πpmv)]
where Q represents the net transvascular flow of fluid, K the permeability of the endothelial membrane, Pmv the hydrostatic pressure within the lumen of the microvessels, Ppmv the hydrostatic pressure in the perimicrovascular space, rc the reflection coefficient of the capillary barrier, πmv the oncotic pressure in the circulation, and πpmv the oncotic pressure in the perimicrovascular compartment. (See "Pathophysiology and etiology of edema in adults".)
The balance of hydrostatic and oncotic forces normally allows small quantities of fluid into the interstitium, but three mechanisms prevent alveolar edema (figure 1A-D) [14]:
●Retained intravascular protein maintains an oncotic gradient favoring reabsorption
●The interstitial lymphatics can return large quantities of fluid to the circulation
●Tight junctions between alveolar epithelial cells prevent leakage into the air spaces
Injury — Acute respiratory distress syndrome (ARDS) is a consequence of an alveolar injury producing diffuse alveolar damage (picture 2 and picture 3) [15]. The injury causes release of pro-inflammatory cytokines such as tumor necrosis factor, interleukin (IL)-1, IL-6, and IL-8 [16-21]. These cytokines recruit neutrophils to the lungs, where they become activated and release toxic mediators (eg, reactive oxygen species and proteases) that damage the capillary endothelium and alveolar epithelium [15,22-26].
Damage to the capillary endothelium allows protein to escape from the vascular space. The oncotic gradient that favors resorption of fluid is lost and fluid pours into the interstitium, overwhelming the lymphatics [27]. The ability to upregulate alveolar fluid clearance may also be lost [28]. Increase in interstitial fluid, combined with damage to the alveolar epithelium, causes the air spaces to fill with bloody, proteinaceous edema fluid and debris from degenerating cells. In addition, functional surfactant is lost, resulting in alveolar collapse.
Consequences — Lung injury has numerous consequences including impairment of gas exchange, decreased lung compliance, and increased pulmonary arterial pressure.
●Impaired gas exchange – Impaired gas exchange in ARDS is primarily due to ventilation-perfusion mismatching: physiologic shunting causes hypoxemia, while increased physiologic dead space impairs carbon dioxide elimination [29,30]. A high minute volume is generally needed to maintain a normal arterial carbon dioxide tension (PaCO2), although hypercapnia is uncommon. (See "Measures of oxygenation and mechanisms of hypoxemia".)
●Decreased lung compliance – Decreased pulmonary compliance is one of the hallmarks of ARDS [31]. It is a consequence of the stiffness of poorly or nonaerated lung, rather than the pressure-volume characteristics of residual functioning lung units [32]. Even small tidal volumes can exceed the lung's inspiratory capacity and cause a dramatic rise in airway pressures [31].
●Pulmonary hypertension – Pulmonary hypertension (PH) occurs in up to 25 percent of patients with ARDS who undergo mechanical ventilation [33-35]. Causes include hypoxic vasoconstriction, vascular compression by positive airway pressure, parenchymal destruction, airway collapse, hypercarbia, and pulmonary vasoconstrictors [36]. The clinical importance of PH in most patients with ARDS is uncertain. PH severe enough to induce cor pulmonale is rare, but it is associated with an increased risk of death [37,38].
PATHOLOGIC STAGES — ARDS tend to progress through three relatively discrete pathologic stages (the exudative stage, proliferative stage, and fibrotic stage), the details of which are discussed separately. (See "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults", section on 'Pathologic diagnosis and stages'.)
ETIOLOGIES AND PREDISPOSING FACTORS — Acute respiratory distress syndrome (ARDS) has traditionally been conceptualized as a pattern of lung injury and clinical manifestations that can be caused by a variety of insults. However, the validity of the assumption that different inciting events cause a similar pattern of lung injury and similar clinical features has been questioned because numerous studies have found more severe reductions in lung compliance and less responsiveness to positive end-expiratory pressure (PEEP) when the ARDS was due to a pulmonary process than when it was due to an extrapulmonary precipitant, such as sepsis [39-42].
More than 60 possible causes of ARDS have been identified and other potential causes continue to emerge as adverse pulmonary reactions to new therapies are observed (table 1). However, only a few common causes account for most cases of ARDS [9,43-46]. In one study of 107 patients in a medical intensive care unit, the most common etiologies were pneumonia (40 percent), sepsis (32 percent), and aspiration (9 percent) [47]. Factors that may predispose a patient to develop ARDS, but probably can't cause ARDS, have also been identified.
Sepsis — Sepsis is the most common cause of ARDS [43,44,48,49]. It should be the first etiology considered whenever ARDS develops in a patient who is predisposed to serious infection or in association with a new fever or hypotension. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis".)
The risk of developing ARDS may be particularly high among septic patients with a history of alcoholism [50-52]. This was illustrated by a prospective cohort study that determined the incidence of ARDS in 220 patients with septic shock [51]. The incidence of ARDS among patients who chronically abuse alcohol was 70 percent, compared to 31 percent among patients who did not chronically abuse alcohol. A possible explanation for these findings is that alcoholism may decrease the concentration of glutathione in the epithelial lining fluid, predisposing the lung to oxidative injury [50,53,54]. Alternatively, chronic alcohol abuse may increase the risk of ARDS by enhancing inappropriate leukocyte adhesion to endothelial cells [55].
A secondary analysis from a multicenter observational cohort study investigated risk factors for the development of ARDS among septic patients presenting to the emergency department or admitted for high risk elective surgery [56]. Of the 2534 patients meeting criteria for sepsis, 156 (6.2 percent) developed ARDS. In a multivariable analysis, risk factors for ARDS included APACHE II score (OR 1.10, 95% CI 1.07–1.13), age (OR 0.97, 95% CI 0.96–0.98), shock (OR 2.57, 95% CI 1.62–4.08), pneumonia (OR 2.31, 95% CI 1.59–3.36), pancreatitis (OR 3.86, 95% CI 1.33–11.24), presence of acute abdomen (OR 3.77, 95% CI1.37–10.41), and quantity of fluid given during the first six hours in liters (OR 1.15, 95% CI 1.03–1.29). When stratified by the presence or absence of shock, total fluid infused was not associated with the development of ARDS in the group with shock (OR 1.05, 95% CI 0.87–1.28), whereas quantity of fluid was associated with ARDS among those without shock (OR 1.21, 95% CI 1.05–1.38). Only 9 percent of the cohort had shock, suggesting that further studies are needed to investigate the relationship between quantity of fluids given and the risk of developing ARDS among septic shock patients.
Aspiration — Observational evidence indicates that ARDS will develop in approximately one-third of hospitalized patients who have a recognized episode of aspiration of gastric contents [43,45,57].
It was initially suggested in a classic study by Mendelson that aspirated contents had to have a pH less than 2.5 to cause severe lung injury [58]; however, subsequent animal studies showed that aspiration of non-acidic gastric contents can also cause widespread damage to the lungs [59]. This suggests that gastric enzymes and small food particles also contribute to the lung injury.
The unexpected development of ARDS may be the only indication that an intubated patient has developed a tracheoesophageal fistula, which is a rare complication of intubation.
Pneumonia — Community acquired pneumonia is probably the most common cause of ARDS that develops outside of the hospital [60]. Common pathogens include Streptococcus pneumoniae [61], Legionella pneumophila, Pneumocystis jirovecii (formerly called Pneumocystis carinii), Staphylococcus aureus, enteric gram negative organisms, and a variety of respiratory viruses [62,63]. (See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults" and "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults".)
Nosocomial pneumonias can also progress to ARDS. Staphylococcus aureus, Pseudomonas aeruginosa, and other enteric gram negative bacteria are the most commonly implicated pathogens. (See "Epidemiology, pathogenesis, microbiology, and diagnosis of hospital-acquired and ventilator-associated pneumonia in adults".)
Severe trauma — ARDS is a complication of severe trauma with approximately 10 percent developing ARDS following trauma [64]. There are several situations during which ARDS seems to be particularly common following trauma [65]:
●Bilateral lung contusion following blunt trauma [66].
●Fat embolism after long bone fractures. In this situation, ARDS typically appears 12 to 48 hours after the trauma. This complication has decreased since immobilization for transport to the hospital became routine [67]. (See "Fat embolism syndrome".)
●Sepsis may be the most common cause of ARDS that develops several days or more after severe trauma or burns.
●Massive traumatic tissue injury may directly precipitate or predispose a patient to ARDS [65,68].
A predictive model taking into account age, APACHE II score, Injury Severity Score (ISS), the presence of blunt traumatic injury, pulmonary contusion, massive transfusion, and flail chest injury has been shown to predict the development of ARDS among at risk patients with severe trauma [69]. Although ARDS can contribute to the length of critical illness following severe trauma, it does not appear to independently increase the risk of death [70]. Trauma-related ARDS has a significantly better prognosis than ARDS that is not related to trauma [71].
Massive transfusion — Transfusion of more than 15 units of red blood cells is a risk factor for the development of ARDS [44]. Because the need for massive transfusion identifies patients at high risk for ARDS from other causes, it may be difficult to determine the degree to which transfusions are independently responsible for lung injury [72]. Transfusion of smaller volumes of packed red blood cells may also increase the risk of developing ARDS, as well as increase the risk of mortality among patients with established ARDS [73]. (See "Massive blood transfusion".)
Transfusion-related acute lung injury — Transfusion of even one unit of a plasma-containing blood product sometimes causes ARDS [74,75]. Fresh frozen plasma, platelet, and packed red blood cell transfusions have all been implicated. By definition, respiratory distress becomes apparent within six hours of completion of the transfusion. The mechanism is incompletely understood and may be multifactorial. (See "Transfusion-related acute lung injury (TRALI)".)
Lung and hematopoietic stem cell transplantation — During the first two or three days after surgery, lung transplant recipients are prone to primary graft failure. This devastating form of ARDS is attributed to imperfect preservation of the transplanted lung. (See "Primary lung graft dysfunction".)
Hematopoietic stem cell transplant patients are at risk for ARDS due to a variety of infectious and noninfectious causes. Noninfectious insults include idiopathic pneumonia syndrome, engraftment syndrome, and diffuse alveolar hemorrhage [76]. The lung injury appears to be partly related to the inflammation associated with chemoradiation conditioning regimens, as well as T cell alloreactivity. (See "Pulmonary complications after allogeneic hematopoietic cell transplantation: Causes" and "Pulmonary complications after autologous hematopoietic cell transplantation".)
Drugs and alcohol — ARDS can occur following an overdose. Drugs that have been implicated include aspirin, cocaine, opioids, phenothiazines, and tricyclic antidepressants [77,78]. Idiosyncratic reactions to other drugs (eg, protamine, nitrofurantoin), including certain chemotherapeutic agents, occasionally precipitate ARDS after therapeutic doses. Radiologic contrast media can also provoke ARDS in susceptible individuals [79]. Alcohol abuse increases the risk of ARDS due to other causes (eg, sepsis, trauma), but does not cause ARDS [80,81].
Genetic determinants — It seems likely that there are genetic determinants that increase an individual's risk of developing ARDS, since only a small proportion of the patients who are exposed to typical insults actually develop ARDS [82]. Studies that link mutations in the surfactant protein B (SP-B) gene to an increased risk of ARDS support this notion [83,84]. Insertion-deletion polymorphisms associated with the angiotensin converting enzyme (ACE) gene have also been suggested as a possible risk factor for ARDS [85], although not all studies support this observation [86]. Mutations in the selectin P ligand gene (SELPLG) have also be proposed as susceptibility genes involved in the development of ARDS among individuals of European and African descent [87]. A genome-wide association study (GWAS) of patients of European decent with sepsis-induced ARDS reported a reduced association between the development of ARDS and the geners9508032 located within the Fms-related tyrosine kinase-1 (FLT1) gene which encodes vascular endothelial growth factor-1 (VEGF-1) [88].
Other risk factors — Other possible risk factors for ARDS include cigarette smoking [89,90], cardiopulmonary bypass [91,92], thoracic surgery [93], pneumonectomy [94], acute pancreatitis [95], obesity [96,97], blood type A [98], near drowning [57,99,100], and exposure to particulate matter with an aerodynamic <2.5 micrometers (PM2.5) and ozone [101]. (See "Drowning (submersion injuries)".)
Venous air embolism can occasionally cause ARDS. Outside of the operating room, the most common portal of entry for the air is a central venous catheter left open to the air [102]. (See "Air embolism".)
LUNG INJURY PREDICTION SCORE — The lung injury prediction score (LIPS) identifies patients who are unlikely to develop ARDS. This was demonstrated by a prospective cohort study of 5584 patients, in which seven percent of the cohort developed ARDS, resulting in a negative predictive value (ie, the percent of patients with a LIPS <4 who will not develop ARDS) of 97 percent [103]. A LIPS >4 predicted ARDS with a sensitivity and specificity of 69 and 78 percent, respectively. A smaller study, using a retrospective derivation and prospective validation cohorts reported similar results [104].
The LIPS is the sum of the points assigned for each of the following predisposing conditions: shock (2 points), aspiration (2 points), sepsis (1 point), pneumonia (1.5 points), orthopedic spine surgery (1.5 points), acute abdominal surgery (2 points), cardiac surgery (2.5 points), aortic vascular surgery (3.5 points), traumatic brain injury (2 points), smoke inhalation (2 points), near drowning (2 points), lung contusion (1.5 points), multiple fractures (1.5 points), alcohol abuse (1 point), obesity (BMI >30, 1 point), hypoalbuminemia (1 point), chemotherapy (1 point), fraction of inspired oxygen >0.35 or >4 L/min (2 points), tachypnea >30 breaths/min (1.5 points), oxyhemoglobin saturation <95 percent (1 point), acidosis (pH <7.35, 1.5 points), and diabetes mellitus (-1 point).
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)
●Basics topics (see "Patient education: Acute respiratory distress syndrome (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by the acute onset of bilateral alveolar infiltrates and hypoxemia. The diagnostic criteria for ARDS are provided separately. (See "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults", section on 'Diagnosis'.)
●Approximately 10 to 15 percent of patients admitted to intensive care units have ARDS. The incidence of ARDS rises with age, ranging from 16 per 100,000 person-years among individuals 15 to 19 years of age to 306 per 100,000 person-years among individuals 75 to 84 years of age. (See 'Epidemiology' above.)
●Healthy lungs regulate the movement of fluid to maintain a small amount of interstitial fluid and dry alveoli. In patients with ARDS, this regulation is interrupted by lung injury, causing excess fluid in both the interstitium and alveoli. Consequences include impaired gas exchange, decreased compliance, and increased pulmonary arterial pressure. (See 'Pathophysiology' above.)
●Patients with ARDS tend to progress through three relatively discrete pathologic stages: the exudative stage, proliferative stage, and fibrotic stage. (See 'Pathologic stages' above and "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults", section on 'Pathologic diagnosis and stages'.)
●More than 60 possible causes of ARDS have been identified and other potential causes continue to emerge as adverse pulmonary reactions to new therapies are observed. However, only a few common causes account for most cases of ARDS; in the medical intensive care unit population, the most common causes include pneumonia, sepsis, and aspiration. Factors that may predispose a patient to develop ARDS have also been identified. (See 'Etiologies and predisposing factors' above.)
1 : Acute respiratory distress in adults.
2 : The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination.
3 : The American-European Consensus Conference on ARDS, part 2: Ventilatory, pharmacologic, supportive therapy, study design strategies, and issues related to recovery and remodeling. Acute respiratory distress syndrome.
4 : Acute respiratory distress syndrome: the Berlin Definition.
5 : Incidence and outcomes of acute lung injury.
6 : Epidemiology of acute lung injury and acute respiratory distress syndrome.
7 : Incidence, clinical course, and outcome in 217 patients with acute respiratory distress syndrome.
8 : Characteristics and outcomes in adult patients receiving mechanical ventilation: a 28-day international study.
9 : Clinical diagnostic criteria of the adult respiratory distress syndrome in the intensive care unit.
10 : Epidemiology, Patterns of Care, and Mortality for Patients With Acute Respiratory Distress Syndrome in Intensive Care Units in 50 Countries.
11 : Epidemiology of acute lung injury.
12 : Eight-year trend of acute respiratory distress syndrome: a population-based study in Olmsted County, Minnesota.
13 : Eight-year trend of acute respiratory distress syndrome: a population-based study in Olmsted County, Minnesota.
14 : Eight-year trend of acute respiratory distress syndrome: a population-based study in Olmsted County, Minnesota.
15 : The acute respiratory distress syndrome.
16 : Lower tidal volume ventilation and plasma cytokine markers of inflammation in patients with acute lung injury.
17 : Lung cytokines and ARDS: Roger S. Mitchell Lecture.
18 : Role of tumor necrosis factor-alpha in the pathophysiologic alterations after hepatic ischemia/reperfusion injury in the rat.
19 : The association between mortality rates and decreased concentrations of interleukin-10 and interleukin-1 receptor antagonist in the lung fluids of patients with the adult respiratory distress syndrome.
20 : Increased interleukin-8 concentrations in the pulmonary edema fluid of patients with acute respiratory distress syndrome from sepsis.
21 : Alveolar neutrophil functions and cytokine levels in patients with the adult respiratory distress syndrome during nitric oxide inhalation.
22 : Role of the neutrophil in adult respiratory distress syndrome.
23 : Felix Fleischner Lecture. The traffic of polymorphonuclear leukocytes through pulmonary microvessels in health and disease.
24 : Serum lipofuscin as a prognostic indicator of adult respiratory distress syndrome and multiple organ failure.
25 : The interdependence of lung antioxidants and antiprotease defense in ARDS.
26 : Plasma elastase levels and the development of the adult respiratory distress syndrome.
27 : Pulmonary vascular permeability during the adult respiratory distress syndrome: a positron emission tomographic study.
28 : Alveolar fluid clearance is impaired in the majority of patients with acute lung injury and the acute respiratory distress syndrome.
29 : Ventilation-perfusion distributions in the adult respiratory distress syndrome.
30 : Effect of tidal volume on gas exchange and oxygen transport in the adult respiratory distress syndrome.
31 : Titration of tidal volume and induced hypercapnia in acute respiratory distress syndrome.
32 : Pressure-volume curve of total respiratory system in acute respiratory failure. Computed tomographic scan study.
33 : Acute cor pulmonale in acute respiratory distress syndrome submitted to protective ventilation: incidence, clinical implications, and prognosis.
34 : Pulmonary hypertension in acute respiratory failure.
35 : Right ventricular function and oxygen transport patterns in patients with acute respiratory distress syndrome.
36 : Effects of levosimendan on right ventricular afterload in patients with acute respiratory distress syndrome: a pilot study.
37 : Pulmonary vascular tone improves pulmonary gas exchange in the adult respiratory distress syndrome.
38 : Early predictive factors of survival in the acute respiratory distress syndrome. A multivariate analysis.
39 : Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease. Different syndromes?
40 : Effect of alveolar recruitment maneuver in early acute respiratory distress syndrome according to antiderecruitment strategy, etiological category of diffuse lung injury, and body position of the patient.
41 : Effects of sustained inflation and postinflation positive end-expiratory pressure in acute respiratory distress syndrome: focusing on pulmonary and extrapulmonary forms.
42 : Pulmonary and extrapulmonary acute respiratory distress syndrome: are they different?
43 : Clinical predictors of the adult respiratory distress syndrome.
44 : Clinical risks for development of the acute respiratory distress syndrome.
45 : Adult respiratory distress syndrome: risk with common predispositions.
46 : The ALIEN study: incidence and outcome of acute respiratory distress syndrome in the era of lung protective ventilation.
47 : Acute lung injury in the medical ICU: comorbid conditions, age, etiology, and hospital outcome.
48 : Identification of patients with acute lung injury. Predictors of mortality.
49 : The risk factors, incidence, and prognosis of ARDS following septicemia.
50 : The role of chronic alcohol abuse in the development of acute respiratory distress syndrome in adults.
51 : Chronic alcohol abuse is associated with an increased incidence of acute respiratory distress syndrome and severity of multiple organ dysfunction in patients with septic shock.
52 : Risk factors for the development of acute lung injury in patients with septic shock: an observational cohort study.
53 : The effects of chronic alcohol abuse on pulmonary glutathione homeostasis.
54 : Effects of chronic hepatic dysfunction on pulmonary glutathione homeostasis.
55 : Elevated plasma and lung endothelial selectin levels in patients with acute respiratory distress syndrome and a history of chronic alcohol abuse.
56 : Early risk factors and the role of fluid administration in developing acute respiratory distress syndrome in septic patients.
57 : Aspiration emergencies.
58 : The aspiration of stomach contents into the lungs during obstetric anesthesia.
59 : Aspiration pneumonitis. Correlation of experimental models with clinical disease.
60 : Incidence and mortality of adult respiratory distress syndrome: a prospective analysis from a large metropolitan hospital.
61 : Adult respiratory distress syndrome (ARDS) due to bacteraemic pneumococcal pneumonia.
62 : Severe community-acquired pneumonia. Etiology, prognosis, and treatment.
63 : Severe community-acquired pneumonia. Epidemiology and prognostic factors.
64 : Incidence of adult respiratory distress syndrome in trauma patients: A systematic review and meta-analysis over a period of three decades.
65 : Current concepts on the adult respiratory distress syndrome.
66 : Pulmonary contusions and critical care management in thoracic trauma.
67 : Fat embolism prophylaxis with corticosteroids. A prospective study in high-risk patients.
68 : Postinjury multiple organ failure: role of extrathoracic injury and sepsis in adult respiratory distress syndrome.
69 : Acute respiratory distress syndrome after trauma: development and validation of a predictive model.
70 : Effect of acute lung injury and acute respiratory distress syndrome on outcome in critically ill trauma patients.
71 : Trauma-associated lung injury differs clinically and biologically from acute lung injury due to other clinical disorders.
72 : C3a and adult respiratory distress syndrome after massive transfusion.
73 : Clinical predictors of and mortality in acute respiratory distress syndrome: potential role of red cell transfusion.
74 : The pathogenesis of transfusion-related acute lung injury (TRALI).
75 : Fresh-frozen plasma and platelet transfusions are associated with development of acute lung injury in critically ill medical patients.
76 : Pulmonary complications of solid organ and hematopoietic stem cell transplantation.
77 : Respiratory failure as a result of drugs, overdoses, and poisonings.
78 : Drug-induced noncardiogenic pulmonary edema.
79 : Radiographic contrast media-induced noncardiogenic pulmonary edema: case report and review of the literature.
80 : Alcohol abuse and acute lung injury: epidemiology and pathophysiology of a recently recognized association.
81 : The Effect of Alcohol Consumption on the Risk of ARDS: A Systematic Review and Meta-Analysis.
82 : Genetic polymorphisms associated with susceptibility and outcome in ARDS.
83 : Polymorphism in the surfactant protein-B gene, gender, and the risk of direct pulmonary injury and ARDS.
84 : Polymorphisms of human SP-A, SP-B, and SP-D genes: association of SP-B Thr131Ile with ARDS.
85 : Angiotensin converting enzyme insertion/deletion polymorphism is associated with susceptibility and outcome in acute respiratory distress syndrome.
86 : Angiotensin-converting enzyme insertion/deletion polymorphism is not associated with susceptibility and outcome in sepsis and acute respiratory distress syndrome.
87 : Genome-Wide Association Study in African Americans with Acute Respiratory Distress Syndrome Identifies the Selectin P Ligand Gene as a Risk Factor.
88 : Sepsis-associated acute respiratory distress syndrome in individuals of European ancestry: a genome-wide association study.
89 : Cigarette smoking, alcohol consumption, and risk of ARDS: a 15-year cohort study in a managed care setting.
90 : Active and passive cigarette smoking and acute lung injury after severe blunt trauma.
91 : Adult respiratory distress syndrome following cardiopulmonary bypass: incidence and prediction.
92 : Lung injury and acute respiratory distress syndrome after cardiopulmonary bypass.
93 : Incidence of mortality and morbidity related to postoperative lung injury in patients who have undergone abdominal or thoracic surgery: a systematic review and meta-analysis.
94 : Prevalence and mortality of acute lung injury and ARDS after lung resection.
95 : From acute pancreatitis to end-organ injury: mechanisms of acute lung injury.
96 : Influence of body mass index on outcome of the mechanically ventilated patients.
97 : Body mass index is associated with the development of acute respiratory distress syndrome.
98 : ABO blood type A is associated with increased risk of ARDS in whites following both major trauma and severe sepsis.
99 : Pulmonary edema associated with salt water near-drowning: new insights.
100 : Drowning.
101 : Impact of Long-Term Exposures to Ambient PM2.5 and Ozone on ARDS Risk for Older Adults in the United States.
102 : Permeability pulmonary edema caused by venous air embolism.
103 : Early identification of patients at risk of acute lung injury: evaluation of lung injury prediction score in a multicenter cohort study.
104 : Acute lung injury prediction score: derivation and validation in a population-based sample.