A form of pulmonary edema that causes acute respiratory failure, acute 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.
Causes
ARDS can result from any one of several respiratory and non respiratory causes:
ARDS can result from any one of several respiratory and non respiratory causes:
- 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)
- pancreatitis, hypertransfusion, cardiopulmonary bypass
- near drowning.
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.
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
ARDS initially produces rapid, shallow breathing and dyspnea within hours to days of the initial injury (sometimes after the patient’s condition appears stable). Hypoxemia develops, causing an increased drive for ventilation. Because of the effort required to expand the stiff lung, intercostal and suprasternal retractions result. Fluid accumulation may produce crackles and rhonchi, and worsening hypoxemia causes restlessness, apprehension, mental sluggishness, motor dysfunction, and tachycardia (possibly with transient increased arterial blood pressure).
Severe ARDS causes overwhelming hypoxemia, which, if uncorrected, results in hypotension, decreasing urine output, respiratory and metabolic acidosis and, eventually, ventricular fibrillation or standstill.
ARDS initially produces rapid, shallow breathing and dyspnea within hours to days of the initial injury (sometimes after the patient’s condition appears stable). Hypoxemia develops, causing an increased drive for ventilation. Because of the effort required to expand the stiff lung, intercostal and suprasternal retractions result. Fluid accumulation may produce crackles and rhonchi, and worsening hypoxemia causes restlessness, apprehension, mental sluggishness, motor dysfunction, and tachycardia (possibly with transient increased arterial blood pressure).
Severe ARDS causes overwhelming hypoxemia, which, if uncorrected, results in hypotension, decreasing urine output, respiratory and metabolic acidosis and, eventually, ventricular fibrillation or standstill.
Diagnosis
On room air, arterial blood gas (ABG) analysis initially shows a decreased 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. The resulting pH usually reflects respiratory alkalosis. As ARDS becomes more severe, ABG levels indicate respiratory acidosis (a PaCO2 greater than 45 mm Hg) and metabolic acidosis (a bicarbonate level less than 22 mEq/L) as well as a decreasing PaO2, despite oxygen therapy.
Pulmonary artery (PA) catheterization helps identify the cause of pulmonary edema: It allows evaluation of pulmonary artery wedge pressure (PAWP); collection of PA blood, which shows decreased oxygen saturation, indicating tissue hypoxia; measurement of PA pressure; and measurement of cardiac output via thermodilution.
Serial chest X-rays initially show bilateral infiltrates; in later stages, the X-rays show ground-glass appearance and, eventually (as hypoxemia becomes irreversible), “whiteouts” of both lung fields. This is seen more clearly by the use of computed tomography of the chest.
A differential diagnosis must rule out cardiogenic pulmonary edema, pulmonary vasculitis, and diffuse pulmonary hemorrhage. To establish the cause of ARDS, 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.
On room air, arterial blood gas (ABG) analysis initially shows a decreased 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. The resulting pH usually reflects respiratory alkalosis. As ARDS becomes more severe, ABG levels indicate respiratory acidosis (a PaCO2 greater than 45 mm Hg) and metabolic acidosis (a bicarbonate level less than 22 mEq/L) as well as a decreasing PaO2, despite oxygen therapy.
Pulmonary artery (PA) catheterization helps identify the cause of pulmonary edema: It allows evaluation of pulmonary artery wedge pressure (PAWP); collection of PA blood, which shows decreased oxygen saturation, indicating tissue hypoxia; measurement of PA pressure; and measurement of cardiac output via thermodilution.
Serial chest X-rays initially show bilateral infiltrates; in later stages, the X-rays show ground-glass appearance and, eventually (as hypoxemia becomes irreversible), “whiteouts” of both lung fields. This is seen more clearly by the use of computed tomography of the chest.
A differential diagnosis must rule out cardiogenic pulmonary edema, pulmonary vasculitis, and diffuse pulmonary hemorrhage. To establish the cause of ARDS, 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.
Treatment
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 involves administering humidified oxygen through 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, positive end-expiratory pressure (PEEP), and increased ratio ventilation. Other supportive measures include fluid restriction, diuretics, and the correction of electrolyte and acid-base abnormalities.AuthoPost
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 involves administering humidified oxygen through 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, positive end-expiratory pressure (PEEP), and increased ratio ventilation. Other supportive measures include fluid restriction, diuretics, and the correction of electrolyte and acid-base abnormalities.AuthoPost
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