ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults

Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults
Author:
Mark D Siegel, MD
Section Editor:
Polly E Parsons, MD
Deputy Editor:
Geraldine Finlay, MD
Literature review current through: Jan 2024.
This topic last updated: Jan 31, 2024.

INTRODUCTION — Acute respiratory distress syndrome (ARDS) is an acute, diffuse, inflammatory form of lung injury that is associated with a variety of etiologies. Recognizing and promptly treating ARDS is critical to reduce the associated high mortality.

The clinical presentation, diagnostic evaluation, and complications of ARDS are reviewed here. The epidemiology, pathogenesis, etiology, management, and prognosis of ARDS are discussed separately. (See "Acute respiratory distress syndrome: Epidemiology, pathophysiology, pathology, and etiology in adults" and "Acute respiratory distress syndrome: Prognosis and outcomes in adults" and "Acute respiratory distress syndrome: Ventilator management strategies for adults" and "Acute respiratory distress syndrome: Fluid management, pharmacotherapy, and supportive care in adults" and "Acute respiratory distress syndrome: Investigational or ineffective therapies in adults".)

CLINICAL FEATURES — Patients with ARDS present with the features of ARDS itself as well as features due to the inciting event [1]. However, the manifestations are so nonspecific that the diagnosis is often missed until the disease progresses.

Findings of ARDS — ARDS should be suspected in patients with progressive symptoms of dyspnea, an increasing requirement for oxygen, and alveolar infiltrates on chest imaging within 6 to 72 hours of an inciting event (table 1).

History and physical — Patients typically present with dyspnea and a reduction in arterial oxygen saturation after 6 to 72 hours (or up to a week) following an inciting event (table 1). On examination patients may have tachypnea, tachycardia, and diffuse crackles. When severe, acute confusion, respiratory distress, cyanosis, and diaphoresis may be evident. Cough, chest pain, wheeze, hemoptysis, and fever are inconsistent and mostly driven by the underlying etiology.

Laboratory tests — Laboratory tests are nonspecific. A complete blood count may reveal a range of white blood cell counts (normal, elevated, or decreased) with or without a left shift (stress response). Routine chemistries may have evidence of organ injury reflective of severe hypoxemia or associated shock and systemic inflammation (eg, acute kidney injury [AKI] or transaminitis). The prothrombin time and activated partial thromboplastin time may be prolonged, and D-dimer elevated, but laboratory evidence for disseminated intravascular coagulopathy (DIC) is generally limited to patients with associated sepsis or malignancy. (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults".)

By definition, arterial blood gas analysis shows hypoxemia, which is often initially accompanied by acute respiratory alkalosis, and an elevated alveolar-arterial oxygen gradient (calculator 1). The development of acute hypercapnic respiratory acidosis is an ominous sign and may represent severe ARDS with impending respiratory arrest. Metabolic acidosis from hypoxemia is unusual and, if present, is more likely to be due to the precipitating etiology (eg, sepsis) or associated organ injury (eg, AKI).

Imaging — Imaging findings are variable and depend upon the severity of ARDS. The initial chest radiograph typically has bilateral diffuse alveolar opacities with dependent atelectasis (image 1), although findings can be subtle [2]. Computed tomography (CT) of the chest may show widespread patchy and/or coalescent airspace opacities that are usually more apparent in the dependent lung zones (image 2) [3-5]. The opacities can be subtle (eg, patchy ground glass), particularly in early ARDS, but can become consolidative in appearance as severity worsens [2].

The radiographic appearance of ARDS changes over time, the details of which are discussed below. (See 'Clinical course' below.)

Bedside lung ultrasound remains investigational but preliminary studies report an 83 to 92 percent sensitivity for the diagnosis of ARDS compared with CT chest [6].

Findings of the inciting event — Clinical findings related to the underlying etiology may also exist at presentation (table 1). As an example, in patients with ARDS due to pneumonia-induced sepsis there may be fever, hypotension, leukocytosis with left shift, lobar consolidation, and lactic acidosis; or patients with shock may also have evidence of organ failure, including transaminitis and AKI.

Presenting features of the inciting event frequently mask the manifestations of ARDS. As an example, the opacities from pancreatitis-related atelectasis may mimic ARDS, ultimately leading to a delay in diagnosis.

Clinical features of the common causes of ARDS are discussed separately:

Sepsis (see "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis", section on 'Clinical presentation')

Infectious or aspiration pneumonia (see "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults", section on 'Clinical evaluation' and "Aspiration pneumonia in adults", section on 'Clinical features')

Trauma and burns (see "Initial management of trauma in adults" and "Overview of inpatient management of the adult trauma patient", section on 'Introduction')

Pancreatitis (see "Clinical manifestations and diagnosis of acute pancreatitis")

Smoke inhalation (see "Inhalation injury from heat, smoke, or chemical irritants" and "Carbon monoxide poisoning")

Shock (see "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock", section on 'Clinical manifestations')

Transfusion-related acute lung injury (see "Transfusion-related acute lung injury (TRALI)")

Cardiothoracic surgery (see "Overview of pulmonary resection", section on 'Complications' and "Postoperative complications among patients undergoing cardiac surgery", section on 'Pulmonary dysfunction')

Hematopoietic stem cell transplant (see "Pulmonary complications after autologous hematopoietic cell transplantation")

Drug toxicity (see "Amiodarone pulmonary toxicity" and "Overview of pulmonary disease in people who inject drugs", section on 'Noncardiogenic pulmonary edema')

INITIAL DIAGNOSTIC EVALUATION — The diagnostic evaluation is focused on identifying ARDS and its cause (table 1) and assessing for potential mimicking etiologies (algorithm 1). (See 'Differential diagnosis' below.)

General evaluation and testing — For most patients with suspected ARDS, initial testing typically involves the following:

A thorough history and clinical examination – Clinicians should inquire about fever, productive cough, pleuritic chest pain, and witnessed aspiration (may suggest infectious or aspiration pneumonia), orthopnea (may suggest cardiogenic pulmonary edema), and hemoptysis (may suggest cancer, vasculitis, or alveolar hemorrhage). They should also inquire about history of asthma (may suggest vasculitis), cardiac dysfunction, cancer, stem cell transplant, or pulmonary fibrosis (may suggest cardiogenic pulmonary edema, lymphangitic tumor spread, immune reaction, or interstitial pneumonitis, respectively), and about abdominal symptoms (pain, vomiting, or diarrhea may suggest pancreatitis, colitis, or viscus rupture). Clinicians should seek evidence of recent trauma, surgery, smoke or other toxin inhalation, sick contacts, environmental or occupational exposures (eg, animal exposure and fire eating), travel, pregnancy, transplant, transfusions, fetal delivery, illicit drug use (inhaled, intravenous, and oral), and recent changes in prescribed medications (eg, antibiotics, amiodarone, chemotherapy).

On examination, the clinician should assess for signs of acute cardiogenic pulmonary edema (eg, raised jugular venous pressure, crackles, murmurs, S3/S4 gallops, and lower extremity edema) and pneumonia (eg, dullness on percussion, rales, egophony, or bronchial breath sounds). The abdomen should be examined for tenderness and distension and/or absent bowel sounds to suggest subdiaphragmatic etiologies for ARDS. The skin should be examined for burns, rashes, wounds, track marks, and systemic manifestations of septic emboli; lymph nodes should be examined for size and tenderness (eg, possible infections or cancer); and dentition examined for possible source of sepsis. Volume status (eg, mucus membrane assessment and skin turgor) should also be assessed and fluid balance calculated, if feasible.

Occasionally, volume status can be difficult to assess clinically, especially in older patients, and bedside hemodynamic tools may provide supplementary data to help inform the clinician in this regard. (See 'Excluding acute cardiogenic pulmonary edema' below.)

Laboratory studies – Laboratory studies should include complete blood count, chemistries, liver function tests, coagulation studies, and arterial blood gas analysis. Some clinicians also measure D-dimer, troponin, and lactate levels to investigate common etiologies that can cause or mimic ARDS. Brain natriuretic peptide (BNP) levels are often ordered when assessing cardiogenic pulmonary edema (see 'Excluding acute cardiogenic pulmonary edema' below). Lipase should be checked in patients with abdominal symptoms, particularly if the patient has no other obvious risk factors for ARDS.

Imaging – All patients with suspected ARDS should have a chest radiograph since abnormal imaging is essential for the diagnosis of ARDS. Chest radiography is also critical to evaluate for etiologies of ARDS (eg, lobar consolidation and air bronchograms consistent with pneumonia) as well as for conditions that mimic ARDS, particularly acute cardiogenic pulmonary edema (eg, pulmonary venous congestion, pleural effusions, Kerley B lines, and cardiomegaly).

While CT of the chest is not necessary for the diagnosis, it may be helpful when there is a need for a more detailed pulmonary evaluation (eg, seeking evidence for cavitation or pleural effusions or chronic interstitial lung disease that may be missed on chest radiograph).

Additional imaging may be performed when specific etiologies for ARDS are suspected. For example, CT or magnetic resonance imaging of the brain (eg, for trauma patients), or CT of the abdomen (eg, for patients with suspected pancreatitis, abscess, colitis, peritonitis, appendicitis), or pelvis (for patients with suspected retained fetal products) may be useful to search for evidence of associated pathologies.

Electrocardiography – Electrocardiography should also be obtained to look for evidence of cardiac dysfunction, including arrhythmias, obvious changes consistent with right or left ventricular strain, or ST segment changes to suggest ischemia.

Microbiologic studies – When feasible, respiratory tract sampling (eg, sputum or endotracheal aspirates) for gram stain and culture of the sputum and/or endotracheal aspirates should be obtained. Urinary legionella and streptococcal antigen should also be sent when pneumonia is suspected, along with cultures of other body fluids such as blood and urine as the patient's presentation dictates. Interpretation of sputum culture should be performed in the context of gram stain.

Excluding acute cardiogenic pulmonary edema — The most important condition to exclude is acute cardiogenic pulmonary edema, which can be difficult to distinguish from ARDS. In practice, most clinicians use clinical evaluation and BNP or N-terminal proBNP (NT-proBNP), with or without transthoracic echocardiography to confirm or exclude pulmonary edema:

Clinical assessment – Cardiogenic pulmonary edema is usually due to left ventricular systolic or diastolic dysfunction, but may also be due to fluid overload, severe hypertension, or severe kidney disease. It may be distinguished from ARDS by evidence of cardiac dysfunction (eg, an S3 or S4 gallop, new or changed murmur), elevated right-sided filling pressures (eg, elevated jugular venous pressure, leg edema), or related radiographic abnormalities (eg, pulmonary venous congestion, Kerley B lines, cardiomegaly, and pleural effusions). A response to diuresis can also confirm the diagnosis retrospectively. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults", section on 'Clinical manifestations' and "Approach to diagnosis and evaluation of acute decompensated heart failure in adults", section on 'Chest radiograph'.)

BNP or NT-proBNP – In patients with suspected ARDS, BNP alone in general is not a reliable indicator for distinguishing ARDS from edema. Rather, it should be used in conjunction with clinical assessment to make this distinction. One observational study found that a plasma BNP level less than 100 pg/mL identified ARDS with a sensitivity and specificity of 27 and 95 percent, respectively [7]. Thus, a plasma BNP level below 100 pg/mL may favor ARDS, but higher levels neither confirm heart failure nor exclude ARDS [7,8]. (See "Heart failure: Clinical manifestations and diagnosis in adults", section on 'Natriuretic peptide'.)

Transthoracic echocardiography (TTE) – In patients with suspected ARDS, TTE may be performed to seek evidence of cardiac dysfunction when cardiogenic pulmonary edema cannot be excluded by clinical evaluation, laboratory findings, or imaging. TTE is not routinely needed if clinical suspicion for cardiogenic pulmonary edema is low and the workup clearly points to noncardiogenic causes of pulmonary infiltrates. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults", section on 'Echocardiography' and "Heart failure: Clinical manifestations and diagnosis in adults", section on 'Echocardiography'.)

A normal ejection fraction may favor ARDS while severe aortic or mitral valve dysfunction, severe diastolic dysfunction, or a severely reduced left ventricular ejection fraction may favor cardiogenic pulmonary edema. However, these findings are not specific. For example, some precipitants of ARDS (eg, septic shock) can cause an acute cardiomyopathy that develops concomitantly with ARDS [9,10]. Conversely, if left heart function appears normal, pulmonary edema may occur due to volume overload (eg, pulmonary edema from blood product transfusions, fluid overload from aggressive fluid resuscitation). In addition, ARDS can coexist with cardiogenic pulmonary edema; while the diagnosis of ARDS requires that hydrostatic edema be excluded, it is clear that patients with volume overload can develop acute lung injury, supported by the observation of elevated pulmonary artery wedge pressures when pulmonary artery catheters are placed in patients with ARDS [11].

For those in whom the diagnosis of acute cardiogenic pulmonary edema remains uncertain (which is rare), additional testing may be indicated. (See 'Ensuring normal fluid status' below.)

ADDITIONAL TESTING

Diagnosis and etiology is apparent — In most patients a preliminary diagnosis of ARDS and its etiology can be confirmed with initial evaluation while patients receive supportive therapy (eg, oxygen, low tidal volume mechanical ventilation, and conservative fluid management (algorithm 1)). In such individuals, no further investigations are necessary, particularly if they show signs of stabilization and/or improvement. (See "Acute respiratory distress syndrome: Fluid management, pharmacotherapy, and supportive care in adults" and "Acute respiratory distress syndrome: Ventilator management strategies for adults".)

Diagnosis and etiology is unclear — In a small proportion of patients, additional testing may be required in the following circumstances:

When initial evaluation does not sufficiently exclude acute cardiogenic pulmonary edema or suggest a specific cause for ARDS (eg, no obvious risk factors)

When an unusual etiology (eg, fungal pneumonia) or an alternate condition that mimics ARDS (eg, diffuse alveolar hemorrhage, pneumocystis pneumonia) are suspected

Suspicion for any of these potential situations may be raised during the initial evaluation or when patients develop progressive hypoxemia despite adequate supportive care.

Further testing may involve reevaluation of fluid status, additional laboratory tests, right heart catheterization, bronchoscopy with bronchoalveolar lavage (BAL), and rarely, lung biopsy. Choosing among these tests is individualized and depends upon the suspected condition that needs to be confirmed or excluded as well as the safety of testing and the therapeutic and prognostic value of the test.

Ensuring normal fluid status — Patients should be clinically reevaluated for fluid status. For patients whose fluid status is assessed as normal and cardiogenic pulmonary edema has been sufficiently excluded, no additional testing for fluid status is required. For those in whom fluid status remains uncertain, we suggest the following.

Formal echocardiography – A transthoracic echocardiogram (TTE; if not already performed) with or without shunt testing can assess left ventricular function and valvular pathology. Rarely, transesophageal echocardiography (TEE) is valuable if endocarditis or complex valvular etiology is suspected. (See "Transthoracic echocardiography: Normal cardiac anatomy and tomographic views" and "Transesophageal echocardiography: Indications, complications, and normal views".)

Right heart catheterization (RHC) – While there is no value to routine RHC for either the diagnosis or management of ARDS [12,13], it may occasionally be useful if fluid status remains uncertain despite other means of testing. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults", section on 'Swan-Ganz catheter'.)

Bedside ultrasound – Bedside lung ultrasonography may be helpful in distinguishing B lines with a smooth pleural morphology (which may indicate cardiogenic pulmonary edema) from B lines with irregular pleural morphology (which may suggest ARDS) [14,15]. (See "Indications for bedside ultrasonography in the critically ill adult patient", section on 'Evaluation of the etiology of cardiopulmonary failure' and "Indications for bedside ultrasonography in the critically ill adult patient", section on 'Basic critical care echocardiography'.)

Choosing among these tests is clinician dependent and should take into account clinician expertise, procedural safety, and diagnostic sensitivity of the selected test.

Bronchoscopy (bronchoalveolar lavage, brush) — Bronchoscopy is most useful when the cause of ARDS is uncertain and concern is raised that the etiology may require specific treatment. For example, bronchoscopy may help clinicians identify infectious etiologies for ARDS, typically pneumonia, by providing specimens for culture when sputum is unavailable or unrevealing (eg, invasive mycotic infections, tuberculosis [TB], or pneumocystis). Bronchoscopy may also help clinicians diagnose specific noninfectious causes of ARDS (eg, acute eosinophilic pneumonia [AEP]) or conditions that mimic ARDS (eg, diffuse alveolar hemorrhage, lymphangitic carcinomatosis) by providing specimens for cytologic or biochemical analysis.

Bronchoscopy is generally considered valuable when the following is suspected:

Occult infection/pneumonia – Bilateral pneumonia is both a cause and mimicker of ARDS. Thus, many patients with ARDS end up being treated empirically with antibiotics. This was illustrated by an autopsy study that found pneumonia in 58 percent of patients with ARDS, although pneumonia was suspected antemortem in only 20 percent [16]. In addition, 20 percent of patients thought to have pneumonia did not have histologic evidence of pneumonia. Bronchoscopy may be useful when specific organisms need to be ruled out or are suspected. Examples include patients with a history of TB exposure, immunosuppression, risk factors for fungus (travel history, neutropenia), select viruses (eg, cytomegalovirus [CMV] in transplant patients, varicella in pregnant women) or parasites (eg, travel), suspected nocardia species (eg, coexistent brain lesion), actinomyces species (eg, trauma), or resistant organisms in patients with bronchiectasis. Specific testing includes:

Serology and site-specific cultures – This includes fungal, blood, and site-specific cultures (including cerebrospinal fluid), influenza antigen, viral titers (eg, CMV, Epstein Barr virus), cryptococcal antigen, and beta-D glucan and galactomannan levels.

BAL – BAL is important in identifying culprit organisms if sputum or endotracheal aspirates are unrevealing (eg, fungal, pneumocystis jirovecii, actinomyces, and nocardia species).

Select inflammatory conditions or occult cancer – Conditions including diffuse alveolar hemorrhage (DAH) or AEP can be readily identified on BAL. Elevated eosinophils on BAL may also be useful for the diagnosis of eosinophilic granulomatosis with polyangiitis (EGPA, also known as Churg-Strauss syndrome) or chronic eosinophilic pneumonia (CEP). Less commonly, invasive malignancy may be identified on BAL cytology. (See 'Acute eosinophilic pneumonia' below and 'Pulmonary vasculitis' below and 'Disseminated malignancy' below.)

Others – Recovery of recognizable food particles or lipid-laden macrophages on BAL may suggest aspiration pneumonitis or lipoid pneumonia, although definitive diagnosis of lipoid pneumonia usually requires biopsy. Recovery of cancer cells may support lymphangitis or tumor embolism. (See "Aspiration pneumonia in adults" and "Pulmonary tumor embolism and lymphangitic carcinomatosis in adults: Diagnostic evaluation and management" and "Pulmonary tumor embolism and lymphangitic carcinomatosis in adults: Diagnostic evaluation and management", section on 'Bronchoscopy'.)

Once the decision is made to proceed with bronchoscopy, the airways should be visually inspected for edema, infections, secretions, foreign bodies, lipid or food particles, and endobronchial masses. Lavage fluid, with or without bronchial brushings, should be taken from the most affected regions of the lung. Samples should be analyzed for cell count (including eosinophils), microbiologic analysis (routine, fungal, viral), galactomannan level, and cytologic analysis for organisms (eg, fungus, CMV, mycobacterium, actinomyces, and nocardia species) and for malignancy. (See "Basic principles and technique of bronchoalveolar lavage" and "Role of bronchoalveolar lavage in diagnosis of interstitial lung disease" and "Flexible bronchoscopy in adults: Overview" and "Flexible bronchoscopy in adults: Preparation, procedural technique, and complications" and "Flexible bronchoscopy in adults: Associated diagnostic and therapeutic procedures".)

Bronchoscopy in mechanically ventilated patients with hypoxemia has a similar spectrum of complications to that in spontaneously breathing patients (eg, barotrauma, bleeding, hypotension, hypoxemia) but the risk of complications is assumed to be higher (particularly barotrauma and hypoxemia). The performance of bronchoscopy in mechanically ventilated patients as well as contraindications and complications of bronchoscopy in this population are discussed separately. (See "Flexible bronchoscopy in adults: Indications and contraindications", section on 'Special populations' and "Flexible bronchoscopy in adults: Preparation, procedural technique, and complications".)

The decision to proceed with bronchoscopy should weigh the procedural risk against its diagnostic sensitivity for the suspected condition(s). Conditions with a high sensitivity include infections (particularly before antibiotics are started), DAH, and AEP. In contrast, its diagnostic sensitivity for many of the interstitial lung diseases (eg, acute interstitial pneumonitis [AIP], acute exacerbations of idiopathic pulmonary fibrosis [AEIPF], cryptogenic organizing pneumonia [COP], acute fibrinous organizing pneumonia [AFOP]) or pulmonary vasculitis is poor. If bronchoscopy is not considered safe, mini-BAL may be an alternative, although the sensitivity is likely lower than bronchoscopy. The role of bronchoscopy in the diagnosis of ventilator-associated pneumonia is discussed separately. (See "Clinical presentation and diagnostic evaluation of ventilator-associated pneumonia", section on 'Invasive respiratory sampling'.)

Endobronchial biopsy is generally not indicated in patients with ARDS unless an occult endobronchial mass is identified during bronchoscopy.

Guidance regarding performing bronchoscopy in patients with high-risk infections, such as coronavirus disease-2019 (COVID-19), Ebola virus, and other highly infectious microorganisms is described separately. (See "Flexible bronchoscopy in adults: Overview", section on 'Infection control'.)

Lung biopsy — Lung biopsy is rarely performed during the diagnostic evaluation of patients with suspected ARDS. In most circumstances, sufficient evidence is available from less invasive studies to provide a diagnosis of ARDS and identify the etiology or a mimicking disorder. Indications for lung biopsy vary but include patients in whom a diagnosis has not been achieved with less invasive means, patients in whom a specific pathology and/or reversible etiology is suspected (eg, lupus vasculitis, COP), or those in whom diagnostic information may inform therapeutic and prognostic decisions including withdrawal of ventilator support [17-19]. Examples where a lung biopsy may be useful include suspicion for an invasive fungal or other lung infection, COP, AEIPF, suspected AIP, pulmonary vasculitis, or invasive cancer (eg, leukemic infiltrates, lymphangitic spread, tumor emboli). The decision to biopsy is an individualized one that needs to be discussed with surrogates; in all cases, the risk of biopsy should be weighed against the benefits of obtaining diagnostic information that can inform therapeutic and prognostic decisions. Importantly, the sensitivity or lack thereof of biopsy and the uncertain likelihood of identifying irreversible etiologies should be clearly explained before proceeding with biopsy. (See "Communication in the ICU: Holding a meeting with families and caregivers".)

Data to support the value of lung biopsy in critically ill patients are derived from retrospective case series [17,20-24]. In most studies, lung biopsy, which was mostly obtained in patients already receiving broad spectrum antibiotics and steroids, provided a diagnosis in roughly two-thirds of cases. As examples:

In a meta-analysis of 14 case series (total of 512 patients), the most common diagnoses were "fibrosis/pneumonitis" (25 percent), infection (eg, CMV, fungus; 20 percent), and diffuse alveolar damage ([DAD]; ie, ARDS or AIP; 16 percent) [20].

In contrast, in a smaller review of 30 patients, a larger proportion (almost three quarters) had DAD (the most common pathology that underlies ARDS) on biopsy [24].

This variability likely reflects the wide variation in practice among clinicians when choosing lung biopsy in this population. Therapeutic decisions were altered in the majority (up to two-thirds) of patients who underwent biopsy, ranging from the implementation of a new or escalation of a prior therapy (most often steroids) to the withdrawal of unnecessary therapy or life-sustaining treatment [17,20-24]. Approximately one-third of patients experienced complications that were generally well tolerated (eg, pneumothorax). While studies report no procedure-related deaths, the mortality after diagnostic biopsy is generally greater than 50 percent, likely reflecting identification of etiologies not responsive to therapy. Survival tends to be best in those in whom a steroid-responsive disease is identified.

In most cases, although the risk of complications is likely greater, video-assisted lung biopsy is preferred over transbronchial biopsy since, in general, it has a higher diagnostic yield for the potential etiologies of interest in this population and the majority of reported studies only include patients that have undergone surgical biopsy. However, two small retrospective studies have reported a diagnostic yield for transbronchial biopsy in ventilated critically ill patients [21,22] that is similar to that reported for surgical lung biopsy.

DIFFERENTIAL DIAGNOSIS — A variety of conditions may present as acute hypoxemic respiratory failure with bilateral alveolar opacities and, therefore, should be considered whenever ARDS is suspected [25]. It is important to note that an almost limitless number of pulmonary conditions can present with bilateral infiltrates and hypoxemia. It is therefore imperative that previous diagnostic studies done prior to admission, particularly chest radiographs and CT scans, be reviewed to document that the abnormalities identified are new.

Acute cardiogenic pulmonary edema — Distinguishing acute cardiogenic pulmonary edema from ARDS is essential for the diagnosis of ARDS and is discussed above. (See 'Excluding acute cardiogenic pulmonary edema' above and 'Ensuring normal fluid status' above.)

Bilateral pneumonia — Bilateral pneumonia may mimic ARDS but may also be an etiology of ARDS. (See 'Bronchoscopy (bronchoalveolar lavage, brush)' above.)

Diffuse alveolar hemorrhage — Several conditions are associated with diffuse alveolar hemorrhage (DAH), a condition that mimics ARDS (table 2). Up to two-thirds will present with hemoptysis, and some patients present with sudden-onset respiratory distress, symptoms that are unusual for patients with ARDS. Bronchoscopy and bronchoalveolar lavage (BAL) are also helpful in distinguishing DAH from ARDS. In DAH, the clinician may appreciate frothy bloody secretions throughout the airways, increasing red blood cells in serial BAL specimens, and hemosiderin-laden macrophages in the BAL fluid. However, these findings are not specific and more subtle forms of hemorrhage may not be evident on BAL. (See "The diffuse alveolar hemorrhage syndromes" and 'Bronchoscopy (bronchoalveolar lavage, brush)' above.)

Inflammatory or autoimmune conditions — Several specific acute inflammatory conditions may mimic ARDS but can be distinguished by a more indolent time of onset (eg, longer than one week) and by specific pathological findings on biopsy. Some conditions may present in a manner that is indistinguishable from ARDS with the acute onset of bilateral lung infiltrates and hypoxemia. Whether the term ARDS should be used to describe these conditions is a matter of uncertainty; nonetheless, it is important to consider these diagnoses, some of which are reversible with specific treatments. With the exception of acute eosinophilic pneumonia (AEP), which can be diagnosed bronchoscopically, most can only be definitively distinguished from ARDS on lung biopsy.

Acute eosinophilic pneumonia — AEP occurs in previously healthy individuals and is characterized by cough, fever, dyspnea, and sometimes chest pain. It can be distinguished from ARDS on BAL specimens by the identification of a large number of eosinophils, typically 35 to 55 percent of all recovered cells [26,27]. Peripheral eosinophilia may or may not be present [28].

Pulmonary vasculitis — Pulmonary vasculitis (eg, systemic lupus erythematosus, granulomatosis with polyangiitis [granulomatosis with polyangiitis formerly Wegner's granulomatosis], Goodpasture's syndrome, eosinophilic granulomatosis with polyangiitis [EGPA or Churg-Strauss syndrome]) is a rare phenomenon that may be suspected in patients with a known rheumatologic diagnosis or underlying asthma (EGPA), or in those that present with hemoptysis. These conditions may be distinguished from ARDS by serology including a rheumatologic panel (eg, antinuclear antibody [ANA], antidouble stranded DNA) or vasculitis panel (eg, c- and p-antineutrophil cytoplasmic autoantibody [ANCA], anti-glomerular basement membrane antibody [anti-GBMA]). Although EGPA may be suspected on the basis of elevated eosinophils on BAL, BAL is not typically diagnostic and lung biopsy is often needed. (See "Anti-GBM (Goodpasture) disease: Pathogenesis, clinical manifestations, and diagnosis" and "Granulomatosis with polyangiitis and microscopic polyangiitis: Respiratory tract involvement" and "Clinical features and diagnosis of eosinophilic granulomatosis with polyangiitis (Churg-Strauss)" and 'Lung biopsy' above and "Clinical manifestations and diagnosis of systemic lupus erythematosus in adults", section on 'Clinical manifestations'.)

Cryptogenic organizing pneumonia (COP) — COP may be suspected in patients who present with the symptoms of nonresolving pneumonia heralded by a flu-like illness. BAL usually contains a smaller proportion of macrophages and higher proportions of lymphocytes, neutrophils, and eosinophils than healthy patients. The diagnosis is made by ruling out infectious causes of pneumonia and documenting typical pathologic changes on lung biopsy. (See "Cryptogenic organizing pneumonia" and 'Lung biopsy' above.)

Acute interstitial pneumonitis (AIP; Hamman-Rich syndrome) — AIP is a rare and fulminant form of diffuse lung injury that has a presentation similar to ARDS. Many people consider AIP a subset of idiopathic ARDS since its clinical manifestations are similar and both demonstrate diffuse alveolar damage (DAD) on histopathology. The distinguishing characteristic is that ARDS is typically associated with an identifiable risk factor, whereas AIP is not. When AIP is suspected, lung biopsy is usually required since bronchoscopic BAL is not diagnostic. (See "Acute interstitial pneumonia (Hamman-Rich syndrome)" and 'Lung biopsy' above.)

Acute exacerbation of idiopathic pulmonary fibrosis (AEIPF) — Like ARDS, the pathological findings of AEIPF are dominated by DAD/AIP, but the prognosis is substantially worse. This diagnostic possibility is easily overlooked in patients with previously undiagnosed interstitial lung disease. The diagnosis is suggested by careful review of previous and current chest radiographic and CT images that may reveal changes consistent with underlying IPF. When AEIPF is suspected, lung biopsy is usually required since bronchoscopic BAL is not diagnostic. (See "Acute exacerbations of idiopathic pulmonary fibrosis" and 'Lung biopsy' above.)

Acute fibrinous organizing pneumonia (AFOP) — AFOP is a rare alveolar filling disease that can be idiopathic, follow organ transplantation, or be associated with infection, collagen vascular disease, drug reactions, and environmental exposures [29]. It can only be distinguished pathologically on lung biopsy from the diffuse alveolar damage pattern classically associated with ARDS. (See "Interpretation of lung biopsy results in interstitial lung disease", section on 'Rare histopathologic interstitial pneumonia patterns'.)

Disseminated malignancy — Cancer can disseminate through the lungs (invasive cancer), lymphatics (lymphangitic spread), or blood vessels so rapidly that the ensuing respiratory failure may be mistaken for ARDS. It should be suspected in patients with malignancy (lymphoma, acute leukemia, or solid tumors) (table 3) who have progressive unexplained dyspnea and hypoxemia not responding to supportive therapy such as antibiotics. Cytological preparation of bronchoscopic specimens (eg, brushings, lavage) sometimes reveals malignant cells. Rarely, bronchoscopy may reveal an endobronchial lesion not detected on imaging and pulmonary artery catheter sampling may detect malignant cells. Lung biopsy is typically diagnostic. (See "Pulmonary tumor embolism and lymphangitic carcinomatosis in adults: Diagnostic evaluation and management" and 'Lung biopsy' above.)

Others — Embolic syndromes may present with hypoxemia and bilateral opacities. They usually have an abrupt onset in an appropriate clinical setting such as in patients with orthopedic fractures (fat embolism syndrome [FES]) or peripartum patients (amniotic fluid embolism syndrome [AFES]). Occasionally, fat or amniotic fluid debris may be identified on BAL to support a clinical diagnosis of fat embolism or amniotic fluid embolism, although this is not diagnostic. Pulmonary embolism (PE) is also typically abrupt in onset but bilateral opacities are unusual unless complicated by infarction and pneumonitis. PE can be easily distinguished on CT pulmonary angiography. Air embolism should always be suspected when patients experience sudden-onset respiratory distress in the setting of a known risk factor, intravenous catheter insertion, or trauma. A transthoracic echocardiogram may identify air in the intravascular space. (See "Fat embolism syndrome" and "Amniotic fluid embolism" and "Air embolism" and "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism".)

DIAGNOSIS — For most patients, ARDS is a clinical diagnosis. Although ARDS can be diagnosed histopathologically (eg, classically diffuse alveolar damage [DAD] in the early stages), clinicians typically only perform lung biopsy to confirm or exclude other important etiologies that can cause or mimic ARDS. Because it is under-recognized, it is essential to have a high clinical suspicion for ARDS in those at risk.

Clinical diagnosis — ARDS can be diagnosed once cardiogenic pulmonary edema and alternative causes of acute hypoxemic respiratory failure and bilateral infiltrates have been excluded. The "global definition" proposed in 2024 expands on the previous Berlin definition [30-32]:

Respiratory symptoms must have begun within one week of a known clinical insult, or the patient must have new or worsening symptoms during the past week. In the proposed "global definition," it is proposed that the clinical onset of ARDS may be more indolent and be present before intubation in some instances.

Bilateral opacities must be present on a chest radiograph or CT scan. The proposed "global definition" also includes bilateral opacities diagnosed by ultrasonography performed by a trained operator. The opacities must not be fully explained by pleural effusions, lobar collapse, lung collapse, or pulmonary nodules.

The patient's respiratory failure must not be fully explained by cardiogenic edema or fluid overload.

A moderate to severe impairment of oxygenation must be present, as defined by the ratio of arterial oxygen tension (PaO2) to fraction of inspired oxygen (FiO2). The "global definition" includes ratio of peripheral oxygen saturation (SpO2) to FiO2 as an assessment of oxygenation.

Nonintubated patients – The "global definition" includes diagnosis in nonintubated patients. ARDS is considered present when the PaO2/FiO2 is ≤300 mmHg or the SpO2/FiO2 is ≤315 mmHg (if the SpO2 ≤97 percent) while on humidified high-flow oxygen delivered via nasal cannulae (HFNC) ≥30 L/minute or noninvasive ventilation (eg, continuous positive airway pressure [CPAP]) ≥5 cm H2O end-expiratory pressure.

Intubated patients – The severity of the hypoxemia defines the severity of the ARDS:

-Mild ARDS – The PaO2/FiO2 is >200 mmHg but ≤300 mmHg on ventilator settings that include positive end-expiratory pressure (PEEP) or CPAP ≥5 cm H2O. Alternatively, the SpO2/FiO2 is >235 mmHg but ≤315 mmHg (if the SpO2 ≤97 percent).

-Moderate ARDS – The PaO2/FiO2 is >100 mmHg but ≤200 mmHg on ventilator settings that include PEEP ≥5 cm H2O. Alternatively, the SpO2/FiO2 is >148 mmHg but <235 mmHg (if the SpO2 ≤97 percent).

-Severe ARDS – The PaO2/FiO2 is ≤100 mmHg on ventilator settings that include PEEP ≥5 cm H2O. Alternatively, the SpO2/FiO2 is ≤148 mmHg (if the SpO2 ≤97 percent).

Resource-limited settings – The "global definition" incudes an allowance for resource-limited settings, in which PEEP ≥5 cm H2O or minimum flow rate for HFNC is not required for diagnosis.

Determining the PaO2/FiO2 requires arterial blood gas (ABG) analysis. To calculate the PaO2/FiO2 ratio, the PaO2 is measured in mmHg and the FiO2 is expressed as a decimal between 0.21 and 1 (calculator 2). As an example, if a patient has a PaO2 of 60 mmHg while receiving 80 percent oxygen, then the PaO2/FiO2 ratio is 75 mmHg (ie, 60 mmHg/0.8). For patients in whom an ABG cannot be obtained, the ratio of SpO2 measured by pulse oximetry to FiO2 may be an appropriate substitute, according to one retrospective study that found that an SpO2/FiO2 ratio of 315 predicted a PaO2/FiO2 of 300 (the threshold for ARDS) with a sensitivity of 91 percent and a specificity of 56 percent [33]. A study published by the National Institutes of Health Prevention and Early Treatment of Acute Lung Injury (PETAL) Network investigated the use of a nonlinear imputation method to estimate the PaO2/FiO2 ratio from available measurements of the SpO2/FiO2 (table 4) [34]. Among 1034 ABGs, of which 650 were associated with an SpO2 less than or equal to 96 percent, the nonlinear technique was superior to other measures used to impute the PaO2/FiO2 ratio, particularly when the SpO2 was ≤96 percent. Thus, while useful, this approach may be less reliable for patients with mild ARDS.

Because the international consensus definition of ARDS specifies no criteria relating to the underlying etiology, some uncertainty remains with respect to which conditions should or should not be included under the ARDS diagnostic umbrella. Generally included are disorders that are known to cause diffuse alveolar damage and have the potential to resolve over time. Thus, viral or diffuse bacterial pneumonia and acute inhalational injuries are included, whereas eosinophilic pneumonia and diffuse alveolar hemorrhage associated with collagen vascular diseases are not.

Pathologic diagnosis and stages — Patients with ARDS tend to progress through three pathologic stages (figure 1) [29,35]. Thus, the histopathology associated with ARDS depends upon the stage during which pre or postmortem tissue is obtained and if obtained late in the course of disease, it may show features of all three stages. The early phase typically reveals histopathology consistent with DAD, while the later phases (if the patient survives) are characterized by fibroproliferation and fibrosis.

Early exudative stage (DAD) – The early exudative stage during the first 7 to 10 days is characterized by DAD. DAD is a nonspecific reaction to lung injury from a variety of causes (table 5). It is characterized by interstitial edema, acute and chronic inflammation, type II cell hyperplasia, and hyaline membrane formation (picture 1) [36-38]. Further details are provided separately. (See "Interpretation of lung biopsy results in interstitial lung disease", section on 'Organizing pneumonia'.)

The relationship between the clinical definition of ARDS and DAD has been described in several studies [19,39]. In one autopsy study of 356 patients who met clinical criteria for ARDS at the time of death, the sensitivity and specificity of the Berlin definition were 89 and 63 percent, respectively [39]. Among patients meeting clinical criteria for ARDS, 45 percent had DAD on autopsy. The presence of DAD correlated with severity, with DAD being found in 12, 40, and 58 percent of those with mild, moderate, and severe ARDS, respectively. Pneumonia was the most common pathologic finding among patients who met clinical criteria for ARDS but did not have DAD. Further investigation is needed to determine whether DAD can predict prognosis or response to therapy.

Fibroproliferative stage – After approximately 7 to 10 days, a proliferative stage develops, characterized by resolution of pulmonary edema, proliferation of type II alveolar cells, squamous metaplasia, interstitial infiltration by myofibroblasts, and early deposition of collagen (picture 2). It is unknown how long this phase lasts but is probably in the realm of two to three weeks.

Fibrotic stage – Some patients progress to a fibrotic stage, characterized by obliteration of normal lung architecture, fibrosis, and cyst formation. The degree of fibrosis ranges from minimal to severe.

The proportion of patients that progress through the early phase to reach the later phases is unknown.

CLINICAL COURSE — The first several days of ARDS are characterized by hypoxemia requiring a moderate to high concentration of inspired oxygen and positive end-expiratory pressure. The bilateral alveolar infiltrates and diffuse crackles are persistent during this period and patients may be tenuous due to severe hypoxemia. Most patients who survive this initial course begin to exhibit better oxygenation and decreasing alveolar infiltrates over the next several days. This may permit the amount of ventilatory support to be decreased and weaning to begin. (See "Weaning from mechanical ventilation: Readiness testing" and "Initial weaning strategy in mechanically ventilated adults".)

Some patients, the proportion of which is unknown, have persistent, severe hypoxemia and remain ventilator-dependent, which may represent the fibroproliferative phase of ARDS. The fibroproliferative phase of ARDS is characterized radiographically by progression from airspace opacification to a coarser reticular pattern of lung infiltration. These changes within the lung parenchyma are often accompanied by persistent hypoxemia, low lung compliance, high dead space, and sometimes by progressive pulmonary hypertension. The course may become dominated by persistent ventilator dependence. This phase needs to be distinguished from ventilator-associated pneumonia (VAP) or ventilator-induced lung injury. (See "Ventilator-induced lung injury" and "Clinical presentation and diagnostic evaluation of ventilator-associated pneumonia".)

The lungs of patients who survive the fibroproliferative phase enter into an extended phase of resolution and repair. Hypoxemia and pulmonary infiltrates gradually improve over weeks to months. Cardiopulmonary function often returns to near baseline levels by six months or longer after the initial lung injury. However, many survivors of severe ARDS are left with lung function, cognitive, emotional, and physical deficits. (See "Acute respiratory distress syndrome: Prognosis and outcomes in adults" and "Post-intensive care syndrome (PICS) in adults: Clinical features and diagnostic evaluation".)

COMPLICATIONS — Patients with ARDS are at high risk for complications related to mechanical ventilation or critical illness.

Complications related to mechanical ventilation include:

Barotrauma – Among patients who are mechanically ventilated, ARDS is a risk factor for pulmonary barotrauma due to the physical stress of positive pressure mechanical ventilation on acutely damaged alveolar membranes. Barotrauma can be an early or late complication of ARDS. The diagnosis, prevention, and management of pulmonary barotrauma are discussed in detail separately. (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults".)

Nosocomial infection – Nosocomial infections (eg, ventilator-associated pneumonia [VAP], or catheter-related infections, Clostridioides difficile) are an important cause of morbidity and mortality in patients with ARDS [40-43]. In addition, being mechanically ventilated for ARDS compared with non-ARDS related conditions is a risk factor for VAP. Further details regarding nosocomial infections are discussed separately. (See "Risk factors and prevention of hospital-acquired and ventilator-associated pneumonia in adults" and "Clinical presentation and diagnostic evaluation of ventilator-associated pneumonia" and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults" and "Intravascular non-hemodialysis catheter-related infection: Clinical manifestations and diagnosis" and "Intravascular non-hemodialysis catheter-related infection: Treatment" and "Clostridioides difficile infection in adults: Clinical manifestations and diagnosis".)

Other consequences of mechanical ventilation or underlying disorders (eg, sepsis) – These include multiorgan failure, critical care neuromyopathies, and sleep disturbance. (See "Clinical and physiologic complications of mechanical ventilation: Overview".)

Other complications that frequently occur during the hospital course of patients with ARDS include the following:

Delirium – ARDS is commonly complicated by delirium, the etiology of which is likely multifactorial [44]. (See "Diagnosis of delirium and confusional states" and "Sedative-analgesia in ventilated adults: Management strategies, agent selection, monitoring, and withdrawal".)

Critically ill patients are also at high risk for:

Deep venous thrombosis (see "Clinical presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity")

Gastrointestinal bleeding due to stress ulceration (see "Stress ulcers in the intensive care unit: Diagnosis, management, and prevention")

Poor nutrition (see "Nutrition support in intubated critically ill adult patients: Initial evaluation and prescription")

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute respiratory failure and acute respiratory distress syndrome in adults" and "Society guideline links: Assessment of oxygenation and gas exchange".)

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

Clinical features – Acute respiratory distress syndrome (ARDS) should be suspected in patients with progressive symptoms of dyspnea, an increasing requirement for oxygen, and alveolar infiltrates on chest imaging within 6 to 72 hours (and up to one week) of an inciting event (table 1). The features of ARDS may be masked by those of the underlying etiology and are so nonspecific that the diagnosis may be missed until ARDS progresses. (See 'Clinical features' above.)

Initial diagnostic evaluation – Initial evaluation includes the following (algorithm 1) (see 'Initial diagnostic evaluation' above):

A thorough history and examination

Routine laboratory studies (complete blood count, chemistries, liver function tests, coagulation studies, arterial blood gas analysis, sputum Gram stain and culture, urinary legionella, and streptococcal antigen)

Chest radiograph (image 1 and image 2)

In most patients, acute cardiogenic pulmonary edema is excluded by clinical evaluation and brain natriuretic peptide (BNP) or N-terminal proBNP, with or without transthoracic echocardiography. In most patients, a preliminary diagnosis of ARDS and its etiology can be confirmed, and no further investigations are necessary.

Additional testing – In a small proportion of patients, additional testing may be required when initial evaluation does not sufficiently exclude acute cardiogenic pulmonary edema, another condition that mimics ARDS (eg, diffuse alveolar hemorrhage [DAH (table 2)]), when no etiology is identified, or when an unusual etiology (eg, fungal pneumonia) is suspected.

Further testing may involve the following:

Reevaluation of fluid status

Additional laboratory tests (eg, vasculitis serology)

Right heart catheterization

Bronchoscopy

Bronchoalveolar lavage

Lung biopsy (rarely needed)

Choosing among these tests is individualized and dependent upon the suspected condition that needs to be confirmed or excluded, the safety of testing, and the therapeutic and prognostic value of the test. (See 'Diagnosis and etiology is unclear' above.)

Differential diagnosis – A variety of conditions may present similarly to ARDS or as causes of ARDS, with specific etiologies requiring individualized treatment. Examples include DAH, inflammatory conditions (acute eosinophilic pneumonia, acute interstitial pneumonitis, acute exacerbations of idiopathic pulmonary fibrosis, cryptogenic organizing pneumonia, acute fibrinous organizing pneumonia, pulmonary vasculitis), and disseminated malignancy. (See 'Diagnosis and etiology is unclear' above and 'Differential diagnosis' above.)

Diagnosis – In most patients, ARDS is a clinical diagnosis of exclusion.

Clinical criteria – Patients must have all of the following:

-New or worsening respiratory symptoms during the previous week, following a known clinical insult

-Bilateral opacities on chest imaging

-Findings must not be fully explained by cardiogenic edema/fluid overload or other etiologies

-Hypoxemia must be present on minimal ventilator settings (defined by the ratio of arterial oxygen tension or peripheral oxygen saturation on pulse oximetry to fraction of inspired oxygen)

Pathologic – Few patients are diagnosed on lung biopsy; the early phase of ARDS classically reveals histopathology consistent with diffuse alveolar damage (picture 1), while the later phases (if the patient survives) are characterized by fibroproliferation and fibrosis (picture 2 and table 5). (See 'Diagnosis' above.)

Clinical course – Patients who survive the initial course usually begin to exhibit better oxygenation and decreasing alveolar infiltrates over the next several days such that ventilator weaning may begin (figure 1). Some patients, however, remain ventilator-dependent and demonstrate persistent interstitial infiltrates (fibroproliferative phase) followed by pulmonary fibrosis (fibrotic phase). (See 'Clinical course' above.)

Complications – Patients with ARDS may endure complications due to mechanical ventilation (eg, pulmonary barotrauma, nosocomial pneumonia) and critical illness (eg, delirium). (See 'Complications' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledge John Hansen-Flaschen, MD, who contributed to earlier versions of this topic review.

  1. Hudson LD, Milberg JA, Anardi D, Maunder RJ. Clinical risks for development of the acute respiratory distress syndrome. Am J Respir Crit Care Med 1995; 151:293.
  2. Rubenfeld GD, Caldwell E, Granton J, et al. Interobserver variability in applying a radiographic definition for ARDS. Chest 1999; 116:1347.
  3. Goodman LR. Congestive heart failure and adult respiratory distress syndrome. New insights using computed tomography. Radiol Clin North Am 1996; 34:33.
  4. Gattinoni L, Presenti A, Torresin A, et al. Adult respiratory distress syndrome profiles by computed tomography. J Thorac Imaging 1986; 1:25.
  5. Pelosi P, Crotti S, Brazzi L, Gattinoni L. Computed tomography in adult respiratory distress syndrome: what has it taught us? Eur Respir J 1996; 9:1055.
  6. Chiumello D, Umbrello M, Sferrazza Papa GF, et al. Global and Regional Diagnostic Accuracy of Lung Ultrasound Compared to CT in Patients With Acute Respiratory Distress Syndrome. Crit Care Med 2019; 47:1599.
  7. Levitt JE, Vinayak AG, Gehlbach BK, et al. Diagnostic utility of B-type natriuretic peptide in critically ill patients with pulmonary edema: a prospective cohort study. Crit Care 2008; 12:R3.
  8. Rudiger A, Gasser S, Fischler M, et al. Comparable increase of B-type natriuretic peptide and amino-terminal pro-B-type natriuretic peptide levels in patients with severe sepsis, septic shock, and acute heart failure. Crit Care Med 2006; 34:2140.
  9. Bouhemad B, Nicolas-Robin A, Arbelot C, et al. Acute left ventricular dilatation and shock-induced myocardial dysfunction. Crit Care Med 2009; 37:441.
  10. Landesberg G, Gilon D, Meroz Y, et al. Diastolic dysfunction and mortality in severe sepsis and septic shock. Eur Heart J 2012; 33:895.
  11. Ferguson ND, Meade MO, Hallett DC, Stewart TE. High values of the pulmonary artery wedge pressure in patients with acute lung injury and acute respiratory distress syndrome. Intensive Care Med 2002; 28:1073.
  12. National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network, Wheeler AP, Bernard GR, et al. Pulmonary-artery versus central venous catheter to guide treatment of acute lung injury. N Engl J Med 2006; 354:2213.
  13. Richard C, Warszawski J, Anguel N, et al. Early use of the pulmonary artery catheter and outcomes in patients with shock and acute respiratory distress syndrome: a randomized controlled trial. JAMA 2003; 290:2713.
  14. Mojoli F, Bouhemad B, Mongodi S, Lichtenstein D. Lung Ultrasound for Critically Ill Patients. Am J Respir Crit Care Med 2019; 199:701.
  15. Copetti R, Soldati G, Copetti P. Chest sonography: a useful tool to differentiate acute cardiogenic pulmonary edema from acute respiratory distress syndrome. Cardiovasc Ultrasound 2008; 6:16.
  16. Andrews CP, Coalson JJ, Smith JD, Johanson WG Jr. Diagnosis of nosocomial bacterial pneumonia in acute, diffuse lung injury. Chest 1981; 80:254.
  17. Patel SR, Karmpaliotis D, Ayas NT, et al. The role of open-lung biopsy in ARDS. Chest 2004; 125:197.
  18. Papazian L, Thomas P, Bregeon F, et al. Open-lung biopsy in patients with acute respiratory distress syndrome. Anesthesiology 1998; 88:935.
  19. Guerin C, Bayle F, Leray V, et al. Open lung biopsy in nonresolving ARDS frequently identifies diffuse alveolar damage regardless of the severity stage and may have implications for patient management. Intensive Care Med 2015; 41:222.
  20. Wong AK, Walkey AJ. Open Lung Biopsy Among Critically Ill, Mechanically Ventilated Patients. A Metaanalysis. Ann Am Thorac Soc 2015; 12:1226.
  21. Bulpa PA, Dive AM, Mertens L, et al. Combined bronchoalveolar lavage and transbronchial lung biopsy: safety and yield in ventilated patients. Eur Respir J 2003; 21:489.
  22. Baumann HJ, Kluge S, Balke L, et al. Yield and safety of bedside open lung biopsy in mechanically ventilated patients with acute lung injury or acute respiratory distress syndrome. Surgery 2008; 143:426.
  23. Almotairi A, Biswas S, Shahin J. The Role of Open Lung Biopsy in Critically Ill Patients with Hypoxic Respiratory Failure: A Retrospective Cohort Study. Can Respir J 2016; 2016:8715024.
  24. Donaldson LH, Gill AJ, Hibbert M. Utility of surgical lung biopsy in critically ill patients with diffuse pulmonary infiltrates: a retrospective review. Intern Med J 2016; 46:1306.
  25. Schwarz MI, Albert RK. "Imitators" of the ARDS: implications for diagnosis and treatment. Chest 2004; 125:1530.
  26. Pope-Harman AL, Davis WB, Allen ED, et al. Acute eosinophilic pneumonia. A summary of 15 cases and review of the literature. Medicine (Baltimore) 1996; 75:334.
  27. Buchheit J, Eid N, Rodgers G Jr, et al. Acute eosinophilic pneumonia with respiratory failure: a new syndrome? Am Rev Respir Dis 1992; 145:716.
  28. Philit F, Etienne-Mastroïanni B, Parrot A, et al. Idiopathic acute eosinophilic pneumonia: a study of 22 patients. Am J Respir Crit Care Med 2002; 166:1235.
  29. Hughes KT, Beasley MB. Pulmonary Manifestations of Acute Lung Injury: More Than Just Diffuse Alveolar Damage. Arch Pathol Lab Med 2017; 141:916.
  30. The ARDS Definition Task Force. Acute Respiratory Distress Syndrome: The Berlin Definition. JAMA 2012; May 21, 2012:Epub ahead of print.
  31. Ferguson ND, Fan E, Camporota L, et al. The Berlin definition of ARDS: an expanded rationale, justification, and supplementary material. Intensive Care Med 2012; 38:1573.
  32. Matthay MA, Arabi Y, Arroliga AC, et al. A New Global Definition of Acute Respiratory Distress Syndrome. Am J Respir Crit Care Med 2024; 209:37.
  33. Rice TW, Wheeler AP, Bernard GR, et al. Comparison of the SpO2/FIO2 ratio and the PaO2/FIO2 ratio in patients with acute lung injury or ARDS. Chest 2007; 132:410.
  34. Brown SM, Duggal A, Hou PC, et al. Nonlinear Imputation of PaO2/FIO2 From SpO2/FIO2 Among Mechanically Ventilated Patients in the ICU: A Prospective, Observational Study. Crit Care Med 2017; 45:1317.
  35. Tomashefski JF Jr. Pulmonary pathology of the adult respiratory distress syndrome. Clin Chest Med 1990; 11:593.
  36. Katzenstein AL, Myers JL, Mazur MT. Acute interstitial pneumonia. A clinicopathologic, ultrastructural, and cell kinetic study. Am J Surg Pathol 1986; 10:256.
  37. Olson J, Colby TV, Elliott CG. Hamman-Rich syndrome revisited. Mayo Clin Proc 1990; 65:1538.
  38. Fulmer JD, Katzenstein AL. The interstitial lung diseases. In: Pulmonary and Critical Care Medicine, Bone RC (Ed), Mosby Year Book, St. Louis 1993. p.M1.
  39. Thille AW, Esteban A, Fernández-Segoviano P, et al. Comparison of the Berlin definition for acute respiratory distress syndrome with autopsy. Am J Respir Crit Care Med 2013; 187:761.
  40. Seidenfeld JJ, Pohl DF, Bell RC, et al. Incidence, site, and outcome of infections in patients with the adult respiratory distress syndrome. Am Rev Respir Dis 1986; 134:12.
  41. Kollef MH, Silver P, Murphy DM, Trovillion E. The effect of late-onset ventilator-associated pneumonia in determining patient mortality. Chest 1995; 108:1655.
  42. Fagon JY, Chastre J, Vuagnat A, et al. Nosocomial pneumonia and mortality among patients in intensive care units. JAMA 1996; 275:866.
  43. Fagon JY, Chastre J, Hance AJ, et al. Nosocomial pneumonia in ventilated patients: a cohort study evaluating attributable mortality and hospital stay. Am J Med 1993; 94:281.
  44. Ely EW, Margolin R, Francis J, et al. Evaluation of delirium in critically ill patients: validation of the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU). Crit Care Med 2001; 29:1370.
Topic 1637 Version 43.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟