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:-
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
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.
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.
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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