AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Adult respiratory distress syndrome (ARDS) is a diffuse pulmonary parenchymal injury associated with noncardiogenic pulmonary edema and resulting in severe respiratory distress and hypoxemic respiratory failure. The pathologic hallmark is diffuse alveolar damage (DAD), but lung tissue rarely is available for a pathologic diagnosis. Therefore, diagnosis is made on clinical grounds, according to the following criteria set forth by the American-European Consensus Conference:

• Acute onset
• Bilateral infiltrates
• Pulmonary artery wedge pressure less than 19 mm Hg (or no clinical signs of congestive heart failure)
• PaO₂/FIO₂ ratio less than 200 (ARDS) or less than 300 (acute lung injury [ALI]): ALI is a milder clinical expression of the injury of ARDS that may or may not progress to ARDS.

Pathophysiology

DAD results in loss of the integrity of the alveolar-capillary barrier, transudation of protein-rich fluid across the barrier, pulmonary edema, and hypoxemia from intrapulmonary shunting. ARDS has a diversity of predisposing conditions, including direct pulmonary injury (eg, pulmonary infection or aspiration) and indirect injury (eg, sepsis, pancreatitis, multiple trauma). Frequently, ARDS develops in association with other organ dysfunction, in which case it is part of the multiple organ dysfunction syndrome (MODS).

The exact mechanism by which the predisposing condition results in DAD is not known fully, but most likely it is mediated, at least in part, by reactive oxygen radicals and proteolytic enzymes from neutrophils. Other mechanisms mediated by cytokines, complement, or endotoxin also may be involved.

The following 3 phases in the pathogenesis of ARDS have been described:

• Exudative phase is the initial phase, with injury to the endothelium and epithelium, inflammation, and fluid exudation.
• Fibroproliferative phase follows the exudative phase and is characterized by the influx and proliferation of fibroblasts and other cellular elements. In this phase, injury may begin to resolve or become persistent.
• In those who recover, the fibrosis phase of healing is marked by resolution of inflammation and development of varying degrees of pulmonary fibrosis.

Frequency

United States

Incidence of ARDS is hard to quantify because of its varying definitions in epidemiological studies. Estimated incidence in the US is 150,000-200,000 cases per year. Most cases occur following admission to the hospital. Patients presenting to the ED with ARDS are rare. However, patients with direct pulmonary injury such as pulmonary aspiration, toxic inhalation, or blunt thoracic trauma may develop ARDS during their stay in the ED.

Mortality/Morbidity

• Overall risk of mortality is reported to be 40-70%, with prospective studies demonstrating an average of about 60%. Most survivors have few long-term sequelae. Survivors of severe cases may have persistent pulmonary fibrosis with symptoms of restrictive lung disease.
• Factors that influence mortality rate include age (higher rate in those older than 65 y) and coexisting organ failure (higher rate with increasing number of concomitantly failing organs).

Age

No age predilection exists. ARDS can occur in children as well as in adults. Incidence may be higher in adults because of a higher incidence of predisposing conditions (eg, major trauma, sepsis, pancreatitis).

CLINICAL

Section 3 of 11  

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• Medication
• Follow-up
• Miscellaneous
• Multimedia
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History

• ARDS can follow a variety of pulmonary or nonpulmonary insults, and the presence of such factors should alert physicians to the potential for development of ARDS.
• Onset of symptoms in ARDS can follow the predisposing condition from 4 hours to several days; thus, the timing of symptom onset may vary greatly.
• Dyspnea is present in all cases except those in which alteration in sensorium is present.
• Other symptoms, if present, typically are related to the predisposing condition.

Physical

Findings on physical examination are not specific for ARDS and can be found in pulmonary edema of any cause.

• Labored breathing and tachypnea (almost universally present)
• Cyanosis and moist skin
• Tachycardia
• Hyperventilation
• Scattered crackles
• Increased work of breathing
• Agitation
• Lethargy followed by obtundation

Causes

• Many conditions have been found to precipitate ARDS. In some cases a predisposing condition cannot be identified. The following is a partial list of the most common predisposing conditions:
• • Infection - Pneumonia of any etiology (especially viral) and systemic sepsis (especially gram negative)
  • Shock - Any type, particularly septic and traumatic shock
  • Aspiration - Gastric contents, near drowning, and toxic inhalation
  • Trauma - Pulmonary contusion, fat embolization, and multiple trauma
  • Other - Systemic inflammatory response syndrome, pancreatitis, postcardiopulmonary bypass, massive blood transfusion, drug ingestion (eg, heroin, methadone, barbiturates, salicylates)

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

Cardiogenic pulmonary edema

WORKUP

Section 5 of 11  

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• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Arterial blood gases analysis (ABGs) is the most important laboratory test and allows detection and documentation of hypoxemia.
• • Hypocapnia is a typical finding early in ARDS, but hypercapnia can be seen later as ventilatory failure progresses.
  • PaO₂ less than 50 mm Hg with an FIO₂ more than 0.6
• Other laboratory studies are nonspecific and are obtained as indicated by the underlying or predisposing conditions.

Imaging Studies

• The chest radiograph reveals characteristic diffuse alveolar-interstitial infiltrates in all lung fields.
• • In early cases, the radiographic findings may not be fully developed.
  • Additional localized pulmonary findings may be present if the predisposing condition involves a pulmonary process.
• Chest CT may be helpful in advanced cases but is not necessary for diagnosis.
• Echocardiography may be helpful to exclude a cardiogenic etiology for pulmonary edema.

Procedures

• Sputum should be collected for Gram stain and cultures (eg, bacterial, fungal, viral) if a pulmonary infection is present. These are best obtained from the lower respiratory tract shortly after endotracheal (ET) intubation.
• Bronchoscopy with bronchoalveolar lavage may be helpful to identify occult pulmonary infection but is usually performed in the ICU.
• A pulmonary artery catheter may be helpful to exclude cardiogenic causes but usually is placed in the ICU.

TREATMENT

Section 6 of 11  

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• Medication
• Follow-up
• Miscellaneous
• Multimedia
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Prehospital Care

• Prehospital care should focus on the ABCs of life support, particularly with rapidly developing cases.
• Institute pulse oximetry and manage hypoxemia with supplemental oxygen.
• ET intubation is indicated for refractory hypoxemia or marked respiratory distress.

Emergency Department Care

• Airway and support of ventilation and oxygenation are the initial priorities of management. Perform ET intubation for hypoxemia refractory to supplemental oxygen or for clinical signs of respiratory failure.
• Mechanical ventilation with positive end-expiratory pressure (PEEP) of 5-10 cm H₂O is effective in reducing intrapulmonary shunting and improving oxygenation.
• • Initiate with an FIO₂ of 1 and decrease only while monitoring pulse oximetry, maintaining the oxygen saturation at 92-94%.
  • Select an initial tidal volume of 8-10 mL/kg and respiratory rate of 10/minute.
  • Pressure-controlled ventilation offers several advantages over volume-controlled modes.
  • Hypercapnia alone on these settings should not prompt an increase in ventilator settings unless pH is less than 7.1 (permissive hypercapnia).
• Monitor vital signs frequently, especially with mechanical ventilation, since marked decreases in venous return can result with subsequent impairment of cardiovascular function.
• An intravenous (IV) line should be available at all times for fluid and/or medication administration.
• Avoid excessive fluid administration. Use only what is necessary to treat signs of intravascular volume depletion or hypotension.
• Treat the underlying etiology.

Consultations

Obtain critical care consultation for hypoxemia or hypercapnia that persists despite mechanical ventilation or hemodynamic instability refractory to therapy.

MEDICATION

Section 7 of 11  

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As of yet, no medication has been shown to affect the pulmonary inflammatory process of ARDS directly. Late cases with a persistent fibroproliferative phase may respond to steroids, but these cases are not seen in the ED. Administer antibiotics following appropriate cultures in cases of pulmonary or extrapulmonary infection leading to ARDS. The mainstays of therapy are cardiopulmonary support and treatment/eradication of the underlying or predisposing conditions. Cardiovascular instability despite fluid administration is managed with catecholamines, such as dopamine and/or dobutamine.

FOLLOW-UP

Section 8 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Admit all patients to the ICU. Patients with early ARDS with mild pulmonary findings may deteriorate rapidly.

Complications

• Multiple organ failure
• Death
• Permanent lung disease
• Oxygen toxicity
• Barotrauma
• Superinfection

Prognosis

• Mortality rate averages 60%.
• Nonsurvivors usually die from sepsis or multiple organ failure.
• Survivors usually have a good outcome with minimal, if any, persistent pulmonary symptoms.
• Survivors of severe cases may have some degree of permanent pulmonary fibrosis and symptoms of restrictive lung disease.

Patient Education

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

MISCELLANEOUS

Section 9 of 11  

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Medical/Legal Pitfalls

• Failure to recognize patient's risk for rapid progression of respiratory failure

MULTIMEDIA

Section 10 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Chest radiograph of a patient with adult respiratory distress syndrome (ARDS).
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Media type:  X-RAY

Media file 2:  Histologic section of the lung showing diffuse alveolar damage in adult respiratory distress syndrome (ARDS).
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Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
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• Follow-up
• Miscellaneous
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• References

• Bidani A, Tzouanakis AE, Cardenas VJ Jr, Zwischenberger JB. Permissive hypercapnia in acute respiratory failure. JAMA. Sep 28 1994;272(12):957-62. [Medline].
• Dantzker DR, Brook CJ, Dehart P, et al. Ventilation-perfusion distributions in the adult respiratory distress syndrome. Am Rev Respir Dis. Nov 1979;120(5):1039-52. [Medline].
• Fowler AA, Hamman RF, Good JT, et al. Adult respiratory distress syndrome: risk with common predispositions. Ann Intern Med. May 1983;98(5 Pt 1):593-7. [Medline].
• Kollef MH, Schuster DP. The acute respiratory distress syndrome. N Engl J Med. Jan 5 1995;332(1):27-37. [Medline].
• Repine JE. Scientific perspectives on adult respiratory distress syndrome. Lancet. Feb 22 1992;339(8791):466-9. [Medline].
• Rinaldo JE, Rogers RM. Adult respiratory-distress syndrome: changing concepts of lung injury and repair. N Engl J Med. Apr 15 1982;306(15):900-9. [Medline].
• Schuster DP. What is acute lung injury? What is ARDS?. Chest. Jun 1995;107(6):1721-6. [Medline].

Article Last Updated: Jan 31, 2005