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Acute Respiratory Distress Syndrome

Kenneth T Horlander, MD, Consulting Staff, Department of Pulmonary and Critical Care Medicine, West Georgia Health System and Emory Clark-Holder Clinic
James Gruden, MD, Consulting Staff, Department of Radiology, Mayo Clinic of Scottsdale

Updated: Aug 13, 2008

Introduction

Background

Acute respiratory distress syndrome (ARDS) was first described by Ashbaugh and colleagues in 1967.1 The authors reported the condition as an acute onset of severe respiratory distress, cyanosis (hypoxemia) that is refractory to oxygen therapy, diffuse abnormalities on chest radiographs (CXRs), and decreased lung compliance. In 1994, the American-European Consensus Conference (AECC) on ARDS formulated their definition of ARDS as follows2 :

  • Acute onset of symptoms
  • The ratio of the alveolar partial pressure of oxygen (PaO2) to the fraction of inspired oxygen (FIO2) of 200 mm Hg or less
  • Bilateral infiltrates on CXRs
  • Pulmonary arterial wedge pressure of 18 mm Hg or less or no clinical signs of left atrial hypertension

The radiographic abnormalities of ARDS reflect the leakage of fluid with a high protein content into the alveolar spaces because of alveolar epithelial injury, or diffuse alveolar damage. ARDS is a syndrome that is defined by its clinical features. The condition may result from intrathoracic or extrathoracic events of various etiologies, such as inflammatory, infectious, vascular, or traumatic etiologies. Determining the causative event may be clinically important for proper treatment.3,4,5,6,7

ARDS is a syndrome that commonly begins after exposure to a known risk factor. Why some people develop ARDS and others do not is still unknown. The risk factors for ARDS include primary pulmonary etiologies (eg, aspiration, pneumonia, toxic inhalation, pulmonary contusion) and extrapulmonary etiologies (eg, sepsis, pancreatitis, multiple blood transfusions, trauma, use of drugs such as heroin). Sometimes, ARDS is not only a reaction to another event but also the result of a known cause, such as an acute interstitial pneumonia (AIP) or a severe, extensive, infectious pneumonia.

For excellent patient education resources, visit eMedicine's Lung and Airway Center. Also, see eMedicine's patient education article Acute Respiratory Distress Syndrome.

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Pathophysiology

The diagnostic criterion standard for acute respiratory distress syndrome (ARDS) is pathologic evidence of diffuse alveolar damage that has been obtained from lung tissue via biopsy. However, biopsy may not be possible because of the patient's clinical condition. If a biopsy is performed, ARDS can be categorized by its pathologic phases, which are similar regardless of the cause of ARDS. The pathologic findings often follow a similar time course, but this can vary between patients. The ARDS phases are as follows:

  • The exudative phase occurs within hours after the initial pulmonary insult and usually lasts 2-7 days. At this early stage of ARDS, the clinical findings are correlated with the microscopic findings of hyaline membranes, loss of the alveolar epithelium, edema, and hemorrhage (see Image 5).
  • The proliferative phase, which usually occurs 7-28 days after the initial pulmonary insult, follows the exudative phase. In this early proliferative phase, type 2 pneumocytic proliferation is present, along with widening of the septa and interstitial fibroblast proliferation (see Image 6).
  • The late proliferative, or fibrotic, phase of ARDS is the result of cellular proliferation that leads to the deposition of collagen and proteoglycans. Extensive fibroblast proliferation with incorporation of the hyaline membranes is a characteristic finding in this stage of ARDS (see Image 7).
  • Interstitial fibrosis develops in some patients. Pulmonary vascular abnormalities are common, such as microvascular thrombi and vascular remodeling.

Frequency

United States

The annual incidence of acute respiratory distress syndrome (ARDS) has been reported to be 150,000 cases; however, this number is suspect because of differing definitions for ARDS. Previously, the National Institutes of Health (NIH) Acute Respiratory Distress Syndrome Network enrolled many ARDS patients into clinical trials. The ARDS incidence rate estimates from those trials agreed with an earlier NIH estimate of 75 cases per 100,000 persons per year.

International

The incidence for acute respiratory distress syndrome (ARDS) is about 18 cases per 100,000 persons per year for acute lung injury (ALI) and 13.5 cases per 100,000 persons per year for ARDS, as reported by the Acute Respiratory Failure (ARF) Study Group in Sweden, Denmark, and Iceland.8

Mortality/Morbidity

Mortality in acute respiratory distress syndrome (ARDS) is commonly secondary to multiorgan dysfunction. Less alveolar epithelial damage indicates a better likelihood of the patient recovering pulmonary function.9,10

Differential Diagnoses

Aspiration Pneumonia
Congestive Heart Failure
Pneumonia, Atypical Bacterial
Pneumonia, Pneumocystis Carinii
Pneumonia, Typical Bacterial
Pneumonia, Viral

Other Problems to Be Considered

Diffuse pneumonia of any origin (although pneumonia can be a cause of ARDS)
Cardiogenic edema
Massive aspiration (although aspiration, too, can be a cause of ARDS)
Pulmonary hemorrhage
Severe acute respiratory syndrome (SARS)

Congestive heart failure (CHF) can mimic ARDS. A Swan-Ganz catheter is used to measure the left ventricular end-diastolic pressure to rule out CHF. According to the AECC definition, the pulmonary artery wedge pressure (pulmonary artery occlusion pressure) for ARDS, as measured with a Swan-Ganz catheter, should be 18 mm Hg or less.

Some investigators believe that distinguishing CHF from ARDS may be difficult and arbitrary at times, and they propose a classification for permeability edema. The 4 categories are as follows: (1) hydrostatic edema, (2) permeability edema due to diffuse alveolar damage or ARDS, (3) permeability edema without diffuse alveolar damage, or (4) mixed (hydrostatic and permeability edema).11

The cause of ARDS is commonly an immune reaction to an otherwise nonrelated event; other times, the condition results from a direct insult to the lung that causes pathologically identical changes as ARDS. This is the case for diffuse pneumonias of any origin and is commonly seen with viral pneumonia. SARS is a good example of a probable infectious pneumonia that is ARDS, pathologically and clinically. Experts have speculated that the cause is from a coronavirus that may be transmitted via respiratory secretions and develops after 2-11 days of a febrile illness.

Radiography

Findings

Chest radiograph findings of acute respiratory distress syndrome (ARDS) vary widely depending on the stage of the disease. The most common chest radiograph findings are bilateral, predominantly peripheral, somewhat asymmetrical consolidation with air bronchograms. Septal lines and pleural effusions, however, are uncommon (see Images 1-4). Differential diagnosis considerations include pneumonias such as those due to aspiration, diffuse alveolar hemorrhage, and pulmonary edema of any cause.

Early findings on the chest radiograph include normal or diffuse alveolar opacities (consolidation), which are often bilateral and which obscure the pulmonary vascular markings. Later, these opacities progress to more extensive consolidation that is diffuse, and they are often asymmetric. Again, effusions and septal lines are not usually seen on chest radiographs of patients affected by ARDS, although these findings are commonly seen in patients with CHF. Radiographic findings tend to stabilize (part of the clinical definition of ARDS); if further radiographic worsening occurs after 5-7 days, another disease process should be considered.

Chest radiograph correlation with the pulmonary pathologic findings is useful because steroids may be helpful at the beginning of the fibrotic process in ARDS.7 In the early exudative phase, chest radiographs show 3 general findings: (1) a bilateral, whiteout appearance; (2) asymmetric consolidations; and (3) a central bat-wing consolidative appearance.12 In the fibrotic phase, chest radiographs may have an interstitial appearance, which is not necessarily due to fibrosis, because this finding may completely resolve in many patients who survive. Pathologic specimens have been analyzed, and the findings of severe lung fibrosis do not correlate with any specific portable chest radiograph findings, including reticular patterns. Computed tomography (CT) scans provide more detailed and more reliable information in areas of consolidation and fibrosis.

If the patient survives, most radiographic abnormalities improve after 10-14 days. The speed and degree of this improvement vary widely from complete resolution before the patient's discharge from the intensive care unit (ICU) to gradual improvement over several months (see Image 1). Factors that affect the speed of recovery are not known, but they may be related to other medical factors (eg, patient's age, underlying disease states) that may have caused the onset of ARDS in the first place.

Therapy for ARDS can affect the chest radiograph appearance. To improve oxygenation, the clinician may place the patient in the prone position. However, large clinical trials have failed to prove any mortality benefit with prone positioning.

Partial liquid ventilation with perflubron has been used to treat ARDS. Perflubron carries gases such as oxygen, and it appears to improve gas exchange and promote lung recruitment. Pulmonary compliance may improve, alveolar hemorrhage may decrease, and pulmonary edema may be reduced, but some investigators question the possible effects, such as increased oxidative damage. This strategy has been under investigation in several clinical trials, and the results appear to be mixed.13,14,15,3,16,4,5

The initial chest radiograph in ARDS patients who have been treated with partial liquid ventilation with perflubron shows opacification in 60-100% of the lung fields; the lateral image reveals a gravity-dependent distribution (see Image 9). Findings of residual perflubron can linger for as long as 138 days, but its levels usually are minimal after 3 weeks.

Mechanical ventilation with positive end-expiratory pressure (PEEP) is another common therapy in ARDS. Chest radiograph findings when PEEP is applied vary from no change to apparent hyperinflation. Higher levels of PEEP may result in barotraumatic changes, which include vesicular rarefactions, pulmonary interstitial emphysema (lucent streaks toward the hilus), radiolucent halos around vessels, pneumatocele formation, subpleural emphysema as manifested by blebs or lucent lines on the chest radiograph, pneumothorax, mediastinal emphysema, and extrathoracic gas collection.17 When PEEP is initially applied or increased, lung opacities may appear to improve; or if PEEP is reduced, the opacities may appear to worsen, despite the fact that the clinical signs are stable or contrary to improvement or worsening of these opacities on radiographs.

Many other methods of mechanical ventilation have been used to treat ARDS. In 2000, the ARDS-NET group completed a trial that showed a mortality benefit of using lower tidal volumes in ARDS.18 At least initially, tidal volumes of 6 mL/kg of ideal body weight should be used rather than the larger tidal volumes that were used in the past. Sometimes this approach requires allowing the arterial carbon dioxide levels to increase because of hypoventilation; this is commonly called permissive hypercapnia.

The AECC definition is usually used in investigations of ARDS. Several entities can mimic ARDS, and attempts to exclude these diseases are important. Lung injury scores are sometimes used in clinical trials, and the chest radiograph interpretation can be weighted 50% or more in these scores. For this reason, some investigators have questioned the reproducibility of chest radiograph readings between clinicians. High interobserver variability in chest radiograph interpretations occurs, even between experts. On the other hand, the chest radiographs are very accurate in the diagnosis of ARDS, with rates as high as 84%. The accuracy of the chest radiograph reading is stage dependent, and observer disagreement is highest in the early disease phases. Accuracy of the clinical diagnosis is also dependent on the pathologic stage.

Computed Tomography

Findings

The diffuse and often nonspecific consolidation that is depicted on chest radiographs in patients with ARDS is, in fact, heterogeneous on CT scans. Also, CT scans show that the parenchymal consolidation in ARDS is in the gravity-dependent areas of the lung.19 Therefore, the disease is not as diffuse as the chest radiograph findings alone suggest.20,21,22,23

A review of chest CT scans in 74 patients with acute respiratory distress syndrome (ARDS) revealed the following findings19 : bilateral abnormalities in almost all the patients, predominantly dependent abnormalities (86%), patchy abnormalities (42%), homogeneous abnormalities (23%), ground-glass attenuation (8%), mixed ground-glass appearance and consolidation (27%), basilar predominant abnormalities (68%), and areas of consolidation with air bronchograms (89%). CT scan findings also provided additional information relative to the chest radiographs in 66% of the patients that directly affected treatment in 22% of the patients.19

On CT scans, ARDS that is due to pulmonary disease tends to be asymmetric, with a mix of consolidation and ground-glass opacification, whereas ARDS that is due to extrapulmonary causes has predominantly symmetric ground-glass opacification. CT scans of ARDS patients with AIP tend to have more symmetric consolidations, more basilar distribution, and more honeycombing (26%) than those patients without AIP (8%).24 In patients with ARDS from either cause, pleural effusions and air bronchograms are common, and Kerley B lines and pneumatoceles are uncommon.

If a patient is placed in the prone position, as they sometimes are in an attempt to improve oxygenation, the consolidations shift over time to the anterior portions of the lung parenchyma, which are now in the gravity-dependent portions of the lung.25 Because of a lack of positive outcome data, logistics, and possible complications of this procedure, it is not often used. In one study, CT scanning was performed on a cohort of patients about to be placed in the prone position.26 Although good evaluation of the patients' pathologic lung changes were seen, the authors were unable to select out any findings that would predict which patients eventually responded to prone-position ventilation.

CT scanning can be used to detect the pathologic features and complications of ARDS that are occult on chest radiographs largely because the diffuse consolidations of ARDS obscure other findings, which include the following: pleural abnormalities (eg, pneumothorax), parenchymal disease (eg, nodules, focal opacities, interstitial emphysema), and mediastinal disease (eg, enlarged lymph nodes). In one study, pneumothorax was missed on supine chest radiographs and detected with CT scans in one third of the patients. Also, the position of a thoracostomy tube can be better delineated with CT scanning so that the need for repositioning can be determined.

In the later stages of ARDS, CT scanning is more reliable than the chest radiograph in the detection of suspected fibrosis as the changes that accompany fibrosis become more apparent. Findings that are suggestive of fibrosis and better visualized on CT scans include the following: traction bronchiectasis; lobular distortion; intralobular lines; and, in advanced cases, cystic lung destruction (also called honeycombing).

ARDS therapies can also alter the CT scan appearance. The use of perflubron in partial liquid ventilation causes a gravity-dependent patchy or homogeneously white appearance on CT scans. The movement of perflubron out of the lungs has been documented and may occur because of hematogenous spread. Extrapulmonary perflubron may also be present in the lymph nodes, pleural space, mediastinum, and retroperitoneum.

CT scanning has also been used to evaluate patients who survive ARDS. In one study, 6-10 months after ARDS patients were discharged from the hospital, CT images of their chests revealed more ventral than dorsal pulmonary fibrosis in 87% patients.27 The extent of the fibrotic changes correlated with the severity of ARDS as well as the duration of mechanical ventilation during which high peak pressures (>30 mm Hg) or high oxygen levels (>70%) were used.

Nuclear Imaging

Findings

Positron emission tomography (PET) scanning has been used in studies of extravascular lung density (EVD) and pulmonary vascular permeability with the pulmonary transcapillary escape rate (PTCER).28,29 In studies, patients with acute respiratory distress syndrome (ARDS) had a PTCER and EVD that were higher than those of healthy control subjects, and the findings were most dramatic in the early phase of ARDS. The PTCER remained elevated in patients with ARDS, even after the EVD had returned to normal levels.

The PTCER can be used to estimate capillary permeability by watching for the accumulation of injected gallium-68 (68 Ga) citrate, which is attached to native transferrin, in the lung parenchyma. ARDS is a noncardiogenic pulmonary edema condition; therefore, fluid and protein are translocated across the lung vascular endothelium into the interstitium. These measures are used only in experimental studies, not in routine clinical situations.

Multimedia

Anteroposterior (AP) portable chest radiograph in...

Media file 1: Anteroposterior (AP) portable chest radiograph in a patient who had been in respiratory failure for 1 week with the diagnosis of acute respiratory distress syndrome. This image shows an endotracheal tube, a left subclavian central venous catheter in the superior vena cava, and bilateral patchy opacities in mostly the middle and lower lung zones.

Portable chest radiograph in a patient with acute...

Media file 2: Portable chest radiograph in a patient with acute respiratory distress syndrome. The condition evolved over approximately 1 week.

Portable chest radiograph in a patient with acute...

Media file 3: Portable chest radiograph in a patient with acute respiratory distress syndrome. The condition evolved over approximately 1 week.

Portable chest radiograph in a patient with acute...

Media file 4: Portable chest radiograph in a patient with acute respiratory distress syndrome. The condition evolved over approximately 1 week.

Photomicrograph from a patient with acute respira...

Media file 5: Photomicrograph from a patient with acute respiratory distress syndrome (ARDS). This image shows ARDS in the exudative stage. Note the hyaline membranes and loss of alveolar epithelium in this early stage of ARDS.

Photomicrograph from a patient with acute respira...

Media file 6: Photomicrograph from a patient with acute respiratory distress syndrome (ARDS). This image shows ARDS in the early proliferative stage. Note the type 2 pneumocytic proliferation, with widening of the septa and interstitial fibroblast proliferation.

Photomicrograph from a patient with acute respira...

Media file 7: Photomicrograph from a patient with acute respiratory distress syndrome (ARDS). This image shows ARDS in the late proliferative stage. Note the extensive fibroblast proliferation, with incorporation of the hyaline membranes.

Chest radiograph in a patient with acute respirat...

Media file 8: Chest radiograph in a patient with acute respiratory distress syndrome (ARDS). The patient was treated with perflubron, which is used for partial liquid ventilation.

Portable chest radiograph. This image shows bilat...

Media file 9: Portable chest radiograph. This image shows bilateral opacities that are suggestive of ARDS.

Computed tomography scan in a patient with suspec...

Media file 10: Computed tomography scan in a patient with suspected acute respiratory distress syndrome (ARDS). This image was obtained at the cardiac level with mediastinal window settings and shows bilateral pleural effusions instead of diffuse bilateral lung consolidation. In addition, the presence of some compression atelectasis in the lower lobes is observed.

High-resolution computed tomography scan in a pat...

Media file 11: High-resolution computed tomography scan in a patient with acute respiratory distress syndrome. This image demonstrates a small right pleural effusion, consolidation with air-bronchograms, and some ground-glass-appearing opacities. The findings indicate an alveolar process, in this case, alveolar damage.

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Keywords

ARDS, acute respiratory distress syndrome, adult respiratory distress syndrome, pulmonary insufficiency, lung disease, respiratory tract disease, respiratory failure, respiratory syndrome, respiratory distress syndrome, severe respiratory distress, cyanosis, hypoxemia, diffuse alveolar damage, acute lung injury, ALI

Contributor Information and Disclosures

Author

Kenneth T Horlander, MD, Consulting Staff, Department of Pulmonary and Critical Care Medicine, West Georgia Health System and Emory Clark-Holder Clinic
Kenneth T Horlander, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

James Gruden, MD, Consulting Staff, Department of Radiology, Mayo Clinic of Scottsdale
James Gruden, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Radiology, American Medical Association, American Roentgen Ray Society, American Thoracic Society, Radiological Society of North America, Society for Health Services Research in Radiology, and Society of Thoracic Radiology
Disclosure: Nothing to disclose.

Medical Editor

Judith K Amorosa, MD, FACR, Clinical Professor and Program Director, Department of Radiology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School; Consulting Staff, Department of Radiology, Robert Wood Johnson University Hospital
Judith K Amorosa, MD, FACR is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Association of University Radiologists, Radiological Society of North America, and Society of Thoracic Radiology
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

Eric J Stern, MD, Professor of Radiology, Adjunct Professor of Medicine, Adjunct Professor of Medical Education and Biomedical Informatics, University of Washington School of Medicine; Director of Thoracic Imaging, Harborview Medical Center; Associate Medical Staff, Seattle Cancer Care Alliance
Eric J Stern, MD is a member of the following medical societies: American Roentgen Ray Society, Association of University Radiologists, European Society of Radiology, Radiological Society of North America, and Society of Thoracic Radiology
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Eugene C Lin, MD, Clinical Assistant Professor of Radiology, University of Washington Medical School
Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine
Disclosure: Nothing to disclose.

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