Acute Respiratory Distress Syndrome

Description

Acute respiratory distress syndrome (ARDS) is a form of noncardiogenic pulmonary edema. It results from lung inflammation and presents as acute hypoxemia and bilateral pulmonary infiltrates.
- Acute lung injury (ALI) is a milder form of ARDS.
- Hyaline membrane disease is a pediatric form of ARDS (caused by a decrease in surfactant).
Causes stem from either pulmonary or extrapulmonary sources.
Histologically, affected alveolar units are filled with protein-rich edematous fluid and cellular debris; this occurs in a heterogenous manner.
Diagnosis is based on the history, ABG, and chest radiography.
Treatment consists of supportive measures (supplemental oxygen, mechanical ventilation) while the lungs heal.

Epidemiology

Incidence

In the US, approximately 200,000 cases per year

Morbidity

Can lead to multiorgan failure syndrome, GI ulcers, cardiac dysfunction, acute renal failure, malnutrition, and chronic issues such as myopathy and psychiatric problems
Lung function recovers significantly 6–12 months after initial injury.

Mortality

Estimated 25–40%, but is influenced by a variety of coexisting conditions such multisystem organ failure

Etiology/Risk Factors

Lung dysfunction due to direct lung injury:
- Pneumonia (frequent cause, high mortality)
- Aspiration
- Mechanical ventilation
- Lung contusion
- Inhalational injury
- Near drowning
Extrapulmonary sources:
- Sepsis (frequent cause, high mortality; elderly patients are more susceptible)
- Trauma
- Pancreatitis
- Polysubstance abuse: Cocaine, opioid
- Massive blood transfusions
- Ischemia-reperfusion injury
- CNS injury
- Air/fat embolism
- Cardiopulmonary bypass

Physiology/Pathophysiology

Early: "Exudative phase" translates into ventilation/perfusion mismatch (shunting) and hypoxia, decreased lung compliance, and increased work of breathing. It is associated with the following:
- Diffuse alveolar and capillary endothelial injury
- Influx of protein-rich fluid into alveoli
- Release of tumor necrosis factor, interleukin-1, and interleukin-8
- Procoagulant activity as protein C and S levels fall and levels of tissue factor and plasminogen activator inhibitor-1 increase
- Pneumocyte type 1 apoptosis with resultant accumulation of necrotic cellular debris in the alveolar lumen. Pneumocyte type 2 dysfunction reduces surfactant production.
Late: Fibroproliferative changes occur later and are characterized by:
- Chronic inflammation resulting from the proliferation of pneumocyte type 2 and macrophages, and neutrophils filling the alveolar space.
- Fibrosis (associated with increase mortality).
- Neovascularization

Prevantative Measures

Pneumonia should be diagnosed and treated aggressively.
Identify patients at risk for pulmonary aspiration (e.g., full stomach, reflux disease, active vomiting, recent oral contrast for radiological study, altered mental status) and implement appropriate maneuvers to reduce risk (gastric tube suctioning, prokinetic agents, reverse Trendelenburg, rapid sequence induction).
Mechanical ventilation should be weaned as tolerated.
Prevention of multiorgan dysfunction:
- Diagnose and treat sources of infection aggressively (e.g., urinary tract infection in the elderly) to avoid sepsis.
- Limit blood transfusions, as appropriate. Consider blood salvaging techniques, blood filters, and collection from donors without multiple HLA exposures.

Diagnosis ⬆ ⬇

The diagnosis of ARDS can coexist with other (extrapulmonary) diagnoses.
- History: Acute dyspnea or hypoxemia related to trauma, sepsis, drug overdose, massive transfusion, aspiration, or acute pancreatitis
- Physical examination: Tachypnea and tachycardia are nonspecific. Auscultation may reveal bilateral rales. Cyanosis, fever, hypothermia.
- ABG: PaO₂/FiO₂ ratio <200; a ratio <300 suggests ALI. Initially a respiratory alkalosis is seen. If ARDS is secondary to sepsis, the ABG may reveal a respiratory acidosis with or without respiratory compensation.
- CXR is initially patchy and located peripherally; it progresses rapidly to diffuse bilateral involvement with a ground-glass appearance.
- PCWP 18 mm Hg with no clinical evidence of cardiac failure.
- TEE may be helpful to determine pulmonary artery pressures and intravascular volume status.
- CT scan: Heterogeneous alveolar involvement

Differential Diagnosis

Interstitial/idiopathic pulmonary fibrosis
Lymphangitic carcinoma
Veno-occlusive pulmonary disease
Intravascular fluid overload
Pneumonia and respiratory failure: Ventilator-associated pneumonia, viral, bacterial
Pulmonary hemorrhage
Near drowning
Drug reaction toxicity: Heroin, salicylate
Cardiac disease: Left ventricle failure, mitral stenosis
Toxic shock syndrome
Tumor lysis syndrome

Treatment ⬆ ⬇

Nonpharmacologic interventions are supportive and consist of intubation and mechanical ventilation:
- Tidal volume (6 mL/kg) using predicted body weight and plateau pressures of 30 cm H₂O (Level I evidence per the ARDS Network trial)
- Positive end-expiratory pressure (PEEP); higher PEEP levels do not negatively impact low-VT strategy.
- Prone positioning can improve oxygenation and mortality (Level I evidence).
- Permissive hypercarbia allows for decreased minute ventilation with consequent decreases in shear injury that is imposed on the alveoli with positive pressure ventilation. The pH should be maintained at 7.20.
- Extracorporeal membrane oxygenation and extracorporeal carbon dioxide removal; no outcome improvement has been demonstrated with these techniques.
- Recruitment maneuvers expand atelectatic areas and improve ventilation/perfusion matching. However, they are ineffective in providing sustained oxygen concentration.
- Pressure–volume curve to set VT and PEEP; has uncertain clinical value.
- Open-lung strategy applying high-pressure ventilation (55 cm H₂O) for 5–10 minutes and PEEP of 16 cm H₂O has uncertain value.
- High-frequency oscillatory ventilation and bilevel ventilation improve oxygenation transiently with no benefit in mortality.
Pharmacologic interventions:
- Fluid management: A conservative or restrictive strategy can improve oxygenation. It has been associated with decreased morbidity and mortality.
- Inhaled nitric oxide (INO): Provides short-term reduction of pulmonary artery pressures and oxygen improvement (Level I evidence)
- N-acetylcysteine and procysteine have some benefit in improving lung injury score.
- Corticosteroids and methylprednisolone have been used with benefit in ALI/ARDS patients diagnosed with Pneumocystis carinii pneumonia or at high risk for fat emboli. High doses may benefit patients with unresolved ARDS of more than 7 days duration.
- Nutritional support: Diets with high-fat content and antioxidant nutrition. The use of eicosapentaenoic acid (EPA) and gamma-linoleic acid (GLA) appears to decrease inflammation mediated by arachidonic acid metabolites. Evidence exists to support the use of EPA and GLA in ARDS.
- Surfactant: Evidence demonstrates that there is a lack of improvement in oxygenation, ventilator-free days, or mortality.
- Partial liquid ventilation appears to reduce inflammation and disease progression, but has no obvious benefit in ventilator dependency and mortality.
- Ibuprofen and NSAIDs do not control inflammation mediated by sepsis and are likely of no benefit in ARDS.
- Ketoconazole, pentoxifylline, lisofylline: Studies have not demonstrated a benefit.
Diagnose and provide supportive therapy for extrapulmonary manifestations:
- Renal: Monitor for acute tubular necrosis
- Hepatic: Monitor liver function test for abnormalities such as cholestasis and hepatocellular injury
- Hematologic: Monitor for thrombocytopenia, disseminated intravascular coagulation, and changes in Von Willebrand factor

Follow-Up ⬆ ⬇

After resolution of the acute phase, mechanical ventilation and respiratory therapy should be administered to regain muscle strength.

References ⬆ ⬇

Bernard GR. Acute respiratory distress syndrome. Am J Respir Crit Care Med. 2005;172:798–806.
Briel M , Meade M , Mercat A , et al. Higher versus lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: Systematic review and meta-analysis. JAMA. 2010;303(9):865–873.
Kallet RH. Evidence-based management of acute lung injury and acute respiratory distress syndrome. Resp Care. 2004;49(7):793–809.
The Acute Respiratory Distress Syndrome Network . Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301–1308.

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Basics ⬇

Incidence

Morbidity

Mortality

Diagnosis ⬆ ⬇

Treatment ⬆ ⬇

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆