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Home :: Acute Respiratory Distress Syndrome

Acute Respiratory Distress Syndrome (ARDS)

Alternative names :- Non-cardiogenic pulmonary edema; Increased-permeability pulmonary edema; Stiff lung; Shock lung; Adult respiratory distress syndrome; Acute respiratory distress syndrome

A form of pulmonary edema that causes acute respiratory failure, adult respiratory distress syndrome (ARDS, shock lung, stiff lung) results from increased permeability of the alveolocapillary membrane. Fluid accumulates in the lung interstitium, alveolar spaces, and small airways, causing the lung to stiffen. Effective ventilation is thus impaired, prohibiting adequate oxygenation of pulmonary capillary blood. Severe ARDS can cause intractable and fatal hypoxemia; however, patients who recover may have little or no permanent lung damage.


ARDS results from a variety of respiratory and nonrespiratory insults, such as:-

  • aspiration of gastric contents
  • sepsis (primarily gram-negative), trauma (lung contusion, head injury, long bone fracture with fat emboli), or oxygen toxicity.
  • viral, bacterial, or fungal pneumonia or microemboli (fat or air emboli or dis­seminated intravascular coagulation)
  • drug overdose (barbiturates, glutethimide, narcotics) or blood transfusion
  • smoke or chemical inhalation (nitrous oxide, chlorine, ammonia).
  • hydrocarbon and paraquat ingestion
  • pancreatitis, uremia, or miliary tuberculosis (rare)
  • neardrowning.

Altered permeability of the alveolocapillary membranes causes fluid to accumulate in the interstitial space. If the pulmonary lymphatics can't remove this fluid, interstitial edema develops. The fluid collects in the peribronchial and peribronchiolar spaces, producing bronchiolar narrowing.

Hypoxemia occurs as a result of fluid accumulation in alveoli and subsequent alveolar collapse, causing the shunting of blood through nonventilated lung regions. In addition, regional differences in compliance and airway narrowing cause regions of low ventilation and inadequate perfusion, which also contribute to hypoxemia.

Signs and symptoms

  • Shortness of breath
  • Labored, rapid breathing
  • Low blood pressure or shock (low blood pressure accompanied by organ failure)

Often, persons affected by ARDS are so sick they are unable to complain of symptoms.


On room air, arterial blood gas (ABG) analysis initially shows a decreased (Pao2) - < 60 mm Hg - and a decreased partial pressure of arterial car­bon dioxide (Paco2)- < 35 mm Hg. The resulting pH usually reflects respiratory alkalosis. As ARDS becomes more severe, ABG values indicate respiratory acidosis (a Paco2 > 45 mm Hg) and metabolic acidosis (a bicarbonate level < 22 mEq/L) as well as a decreasing Pao2 despite oxygen therapy.

  • Pulmonary artery (PA) catheterization helps identify the cause of pulmonary edema by evaluating PA wedge pressure (PAWP); allows collection of PA blood, which shows decreased oxygen saturation, reflecting tissue hypoxia; measures PA pressure; and measures cardiac output by thermodilution techniques.
  • Serial chest X-rays initially show bilateral infiltrates; in later stages, groundglass appearance and, eventually (as hypoxemia becomes irreversible), "white­outs" of both lung fields.

A differential diagnosis must rule out cardiogenic pulmonary edema, pulmonary vasculitis, and diffuse pulmonary hemorrhage. To establish the cause, laboratory work should include a sputum Gram stain, culture and sensitivity tests, and blood cultures to detect infections; a toxicology screen for drug ingestion; and, when pancreatitis is a consideration, a serum amylase determination.


When possible, treatment is designed to correct the underlying cause of ARDS and to prevent progression and potentially fatal complications of hypoxemia and respiratory acidosis. Supportive medical care consists of administering humidified oxygen by a tight-fitting mask, which allows for the use of continuous positive airway pressure. Hypoxemia that doesn't respond adequately to these measures requires ventilatory support with intubation, volume ventilation, and positive end-expiratory pressure (PEEP). Other supportive measures include fluid restriction, diuretics, and the correction of electrolyte and acid­base abnormalities.

Special considerations
  • Frequently assess the patient's respiratory status. Be alert for retractions on inspiration. Note rate, rhythm, and depth of respirations, and watch for dyspnea and the use of accessory muscles of respiration. On auscultation, listen for adventitious or diminished breath sounds. Check for clear, frothy sputum that may indicate pulmonary edema.
  • Observe and document the hypoxemic patient's neurologic status (level of consciousness, mental sluggishness).
  • Maintain a patent airway by suctioning, using sterile, nontraumatic technique. Ensure adequate humidification to help liquefy tenacious secretions.
  • Closely monitor heart rate and blood pressure. Watch for arrhythmias that may result from hypoxemia, acid-base disturbances, or electrolyte imbalance.
  • Reposition the patient often and note any increase in secretions, temperature, or hypotension that may indicate a deteriorating condition.
  • Perform passive range-of-motion exercises, or help the patient perform active exercises, if possible. Provide meticulous skin care. Allow periods of uninterrupted sleep.

Expectations (prognosis)

The death rate in ARDS is approximately 20-30%. Although survivors may recover normal lung function, many individuals suffer permanent lung damage, which can range from mild to severe.

Many people who survive ARDS suffer memory loss or other problems with thinking after they recover. This is related to brain damage caused by reduced access to oxygen while the lungs were malfunctioning.

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