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Adult Respiratory Distress Syndrome

Adult respiratory distress syndrome (ARDS) is a form of pulmonary edema that can quickly lead to acute respiratory failure. It's also known as shock, stiff, white, wet, or Da Nang lung. It 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, 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.

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). It remains unclear whether ARDS stems from DIC or develops independently. Patients with three concurrent ARDS risk factors have an 85% probability of developing ARDS.


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 of microemboli developing.

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 nitrous oxide, ammonia, and chlorine), 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.

Signs and Symptoms

  • Shortness of breath
  • Labored, rapid breathing
  • Low blood pressure or shock
  • Often, persons affected by ARDS are so sick they are unable to complain of symptoms.

    Diagnostic tests

    Arterial blood gas (ABG) analysis (with the patient breathing room air) initially shows a reduced partial pressure of arterial oxygen (Pao2) of less than 60 mm Hg and a decreased partial pressure of arterial carbon dioxide (Paco2) of 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 to identify the cause of pulmonary edema by measuring pulmonary artery wedge pressure (PAWP). This procedure also allows collection of samples of pulmonary artery, mixed venous blood that shows decreased oxygen saturation, reflecting tissue hypoxia. Normal PAWP values in ARDS are 12 mm Hg or less.

    Serial chest X-rays in early stages show bilateral infiltrates. In later stages, findings demonstrate lung fields with a ground-glass appearance and, eventually (with irreversible hypoxemia), "whiteouts" of both lung fields.

    Differential diagnosis must rule out cardiogenic pulmonary edema, pulmonary vasculitis, and diffuse pulmonary hemorrhage. Etiologic tests may involve sputum analyses (including Gram stain and culture and sensitivity); blood cultures (to identify infectious organisms); toxicology tests (to screen for drug ingestion); and various serum amylase tests (to rule out pancreatitis).


    Therapy focuses on correcting the cause of the syndrome, if possible, and preventing progression of life-threatening hypoxemia and respiratory acidosis. Supportive care consists of administering humidified oxygen by a tightly fitting mask, which facilitates the use of continuous positive airway pressure (CPAP). However, this therapy alone seldom fulfills the ARDS patient's ventilatory requirements. If the patient's hypoxemia doesn't subside with this treatment, he may require intubation, mechanical ventilation, and positive end-expiratory pressure (PEEP). Other supportive measures include fluid restriction, diuretic therapy, and correction of electrolyte and acid-base imbalances.

    When a patient with ARDS needs mechanical ventilation, sedatives, narcotics, or neuromuscular blocking agents (such as vecuronium) may be ordered to minimize restlessness (and thereby oxygen consumption and carbon dioxide production) and to facilitate ventilation.

    When ARDS results from fatty emboli or a chemical injury, a short course of high-dose corticosteroids may help if given early. Treatment with sodium bicarbonate may be necessary to reverse severe metabolic acidosis, and fluids and vasopressors may be needed to maintain blood pressure. Nonviral infections require treatment with antimicrobial drugs.


    To help reduce your chances of getting ARDS, seek timely treatment for any direct or indirect injury to the lungs.

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