Acute respiratory distress syndrome (ARDS)
Acute respiratory distress syndrome (ARDS) is a life-threatening lung injury that allows fluid to leak into the lungs. Breathing becomes difficult and oxygen cannot get into the body. The severity of ARDS is based on the level of oxygenation impairment:
- mild, Pao2 /Fio2 ratio between 200 and 300 mm Hg;
- moderate, Pao2 /Fio2 ratio between 100 and 200 mm Hg; and
- severe, Pao2 /Fio2 ratio less than 100 mm Hg.
Common risk factors for ARDS include sepsis, aspiration of gastric contents, shock, infection, lung contusion, nonthoracic trauma, toxic inhalation, neardrowning, and multiple blood transfusions. About onethird of ARDS patients initially have sepsis syndrome.
Damage to capillary endothelial cells and alveolar epithelial cells is common to ARDS regardless of cause or mechanism of lung injury, resulting in increased vascular permeability and decreased production and activity of surfactant; these abnormalities lead to interstitial and alveolar pulmonary edema, alveolar collapse, and hypoxemia.
The signs and symptoms of ARDS can vary in intensity, depending on its cause and severity, as well as the presence of underlying heart or lung disease. They include:
- Severe shortness of breath
- Labored and unusually rapid breathing
- Low blood pressure
- Confusion and extreme tiredness
ARDS is marked by the rapid onset of profound dyspnea that usually occurs 12–48 hours after the initiating event. Labored breathing, tachypnea, intercostal retractions, and crackles are noted on physical examination.
Chest radiography shows diffuse or patchy bilateral infiltrates that rapidly become confluent; these characteristically spare the costophrenic angles. Air bronchograms occur in about 80% of cases.
Heart size is usually normal, and pleural effusions are small or nonexistent. Marked hypoxemia occurs that is refractory to treatment with supplemental oxygen.
Many patients with ARDS demonstrate multiple organ failure, particularly involving the kidneys, liver, gut, central nervous system, and cardiovascular system.
Since ARDS is a physiologic and radiographic syndrome rather than a specific disease, the concept of differential diagnosis does not strictly apply. Normal-permeability (“cardiogenic” or hydrostatic) pulmonary edema must be excluded, however, because specific therapy is available for that disorder.
Emergent echocardiogram or measurement of pulmonary capillary wedge pressure by means of a flowdirected pulmonary artery catheter may be required in selected patients with suspected cardiac dysfunction; routine use in ARDS is discouraged.
The first principle in management is to identify and treat the primary condition that has led to ARDS. Meticulous supportive care must then be provided to compensate for the severe dysfunction of the respiratory system associated with ARDS and to prevent complications.
Treatment of the hypoxemia seen in ARDS usually requires tracheal intubation and positive-pressure mechanical ventilation. The lowest levels of PEEP (used to recruit atelectatic alveoli) and supplemental oxygen required to maintain the Pao2 above 55 mm Hg (7.13 kPa) or the Sao2 above 88% should be used. Efforts should be made to decrease Fio2 as soon as possible in order to avoid oxygen toxicity.
PEEP can be increased as needed as long as cardiac output and oxygen delivery do not decrease and airway pressures do not increase excessively. Prone positioning frequently improves oxygenation by helping recruit atelectatic alveoli and may yield a mortality benefit in severe ARDS. In one placebo-controlled randomized trial, neuromuscular blockade (by continuous infusion of cisatracurium at 37.5 mg/h) for 48 hours upon initiation of mechanical ventilation was associated with improved mortality and more ventilator-free days in patients with Pao2 / Fio2 ratio less than 120 mm Hg.
A variety of mechanical ventilation strategies are available. The most significant advance in the treatment of ARDS over the past 20 years has been the recognition of the potential for excessive alveolar stretch to cause lung injury, and the widespread adoption of low tidal volume ventilation. A multicenter study of 800 patients demonstrated that a protocol using volume-control ventilation with low tidal volumes (6 mL/kg of ideal body weight) resulted in an 8.8% absolute mortality reduction over therapy with standard tidal volumes (defined as 12 mL/kg of ideal body weight).
Approaches to hemodynamic monitoring and fluid management in patients with acute lung injury have been carefully studied. A prospective RCT comparing hemodynamic management guided either by a pulmonary artery catheter or a central venous catheter using an explicit management protocol demonstrated that a pulmonary artery catheter should not be routinely used for the management of acute lung injury.
A subsequent randomized, prospective clinical study of restrictive fluid intake and diuresis as needed to maintain central venous pressure less than 4 mm Hg or pulmonary artery occlusion pressure less than 8 mm Hg (conservative strategy group) versus a fluid management protocol to target a central venous pressure of 10–14 mm Hg or a pulmonary artery occlusion pressure 14–18 mm Hg (liberal strategy group), showed that patients in the conservative strategy group experienced faster improvement in lung function and spent significantly fewer days on mechanical ventilation and in the ICU without an improvement in death by 60 days or worsening nonpulmonary organ failure at 28 days.
Oxygen delivery can be increased in anemic patients by ensuring that hemoglobin concentrations are at least 7 g/dL (70 g/L); patients are not likely to benefit from higher levels. Increasing oxygen delivery to supranormal levels through the use of inotropes and high hemoglobin concentrations is not clinically useful and may be harmful. Strategies to decrease oxygen consumption include the appropriate use of sedatives, analgesics, and antipyretics.
A large number of innovative therapeutic interventions to improve outcomes in ARDS patients have been or are being investigated. Unfortunately, to date, none have consistently shown benefit in clinical trials.
Systemic corticosteroids have been studied extensively with variable and inconsistent results. While a few small studies suggest some specific improved outcomes when given within the first 2 weeks after the onset of ARDS, mortality appears increased when corticosteroids are started more than 2 weeks after the onset of ARDS. Therefore, routine use of corticosteroids is not recommended.