Acute Respiratory Distress Syndrome
A form of pulmonary edema, acute respiratory distress syndrome (ARDS) can quickly lead to acute respiratory failure. Also known as shock, stiff, white, wet, or Da Nang lung, ARDS may follow direct or indirect lung injury.
Increased permeability of the alveolocapillary membranes allows fluid to accumulate in the lung interstitium, alveolar spaces, and small airways. This results in impaired surfactant production, causing the lung to stiffen. This impairs ventilation, reducing oxygenation of pulmonary capillary blood. Difficult to recognize, the disorder can prove fatal within 48 hours of onset if not promptly diagnosed and treated.
Although this four-stage syndrome can progress to intractable and fatal hypoxemia, patients who recover may have little or no permanent lung damage.
In some patients, the syndrome may coexist with disseminated intravascular coagulation (DIC). Whether ARDS stems from DIC or develops independently remains unclear. Patients with three concurrent ARDS risk factors have an 85% probability of developing ARDS.
Causes
Trauma is the most common cause of ARDS, possibly because trauma-related factors, such as fat emboli, sepsis, shock, pulmonary contusions, and multiple transfusions, increase the likelihood that microemboli will develop.
Other common causes of ARDS include anaphylaxis, aspiration of gastric contents, diffuse pneumonia (especially viral), drug overdose (for example, heroin,
aspirin, and ethchlorvynol), idiosyncratic drug reaction (to ampicillin and hydrochlorothiazide), inhalation of noxious gases (such as ammonia, chlorine, and nitrous oxide), near-drowning, and oxygen toxicity.
aspirin, and ethchlorvynol), idiosyncratic drug reaction (to ampicillin and hydrochlorothiazide), inhalation of noxious gases (such as ammonia, chlorine, and nitrous oxide), near-drowning, and oxygen toxicity.
Less common causes of ARDS include coronary artery bypass grafting, hemodialysis, leukemia, acute miliary tuberculosis, pancreatitis, thrombotic thrombocytopenic purpura, uremia, and venous air embolism.
Complications
Severe ARDS can lead to metabolic and respiratory acidosis and ensuing cardiac arrest.
Assessment
As you conduct your assessment, be alert for rapid, shallow breathing; dyspnea; tachycardia; hypoxemia; intercostal and suprasternal retractions; crackles and rhonchi; restlessness; apprehension; agitation; mental sluggishness; and motor dysfunction. ARDS is staged from I to IV, and each stage has typical signs. (See Recognizing ARDS stages.)
Diagnostic tests
Arterial blood gas (ABG) analysis (with the patient breathing room air) initially shows a reduced partial pressure of arterial oxygen (PaO2) (less than 60 mm Hg) and a decreased partial pressure of arterial carbon dioxide (PaCO2) (less than 35 mm Hg). Hypoxemia despite increased supplemental oxygen is the hallmark of ARDS. The resulting blood pH usually reflects respiratory alkalosis. As ARDS worsens, ABG values show respiratory acidosis (increasing PaCO2 [more than 45 mm Hg]) and metabolic acidosis (decreasing bicarbonate levels [less than 22 mEq/L]) and declining PaO2 despite oxygen therapy.
Pulmonary artery catheterization helps identify the cause of pulmonary edema by measuring pulmonary artery wedge pressure (PAWP). This procedure also allows sample collection of pulmonary artery and mixed venous blood that show decreased oxygen saturation, reflecting tissue
hypoxia. Normal PAWP values in ARDS are 12 mm Hg or less.
Serial chest X-rays in early stages initially may be normal because bilateral infiltrates may not appear for up to 24 hours. In later stages, findings demonstrate lung fields with a ground-glass appearance and, eventually (with irreversible hypoxemia), “whiteouts” of both lung fields.
Recognizing ARDS stages
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
