Acute respiratory distress syndrome

Acute respiratory distress syndrome (formerly called adult respiratory distress syndrome) (ARDS) is a form of noncardiogenic pulmonary edema that results from acute damage to the alveoli. It is characterized by acute diffuse infiltrative lung lesions with resulting interstitial and alveolar edema, severe hypoxemia, and respiratory failure. The definition of ARDS includes the following three components:
1. A ratio of Pao2 to Fio2 =200 regardless of the level of PEEP
2. The detection of bilateral pulmonary infiltrates on frontal chest x-ray
3. Pulmonary artery wedge pressure (PAWP) =18 mm Hg or no clinical evidence of elevated left atrial pressure on the basis of chest radiograph or other clinical data
Acute respiratory distress syndrome
Acute respiratory distress syndrome. (a) Lung computed tomography scan showing ground-glass opacification in non-dependent regions with atelectasis and consolidation in dependent regions. There are small pleural effusions. (b) Same patient as shown in (a) using soft-tissue window settings to demonstrate small bilateral effusions layering in the dependent region of both hemithoraces.
Disorders associated with acute respiratory distress syndrome
Disorders associated with acute respiratory distress syndrome
Adult respiratory distress syndrome
In the U.S. there are 75,000 to 100,000 ARDS cases/yr.
• Incidence is 1.5 to 8.3 cases/ 100,000/yr.
• Signs and symptoms
1. Dyspnea
2. Chest discomfort
3. Cough
4. Anxiety
• Physical examination
1. Tachypnea
2. Tachycardia
3. Hypertension
4. Coarse crepitations of both lungs
5. Fever may be present if infection is the underlying etiology.
• Sepsis (>40% of cases)
• Aspiration: near drowning, aspiration of gastric contents (>30% of cases)
• Trauma (>20% of cases)
• Multiple transfusions, blood products
• Drugs (e.g., overdose of morphine, methadone, heroin, reaction to nitrofurantoin)
• Noxious inhalation (e.g., chlorine gas, high O2 concentration)
• Postresuscitation
• Cardiopulmonary bypass
• Pneumonia
• Burns
• Pancreatitis
• A history of chronic alcohol abuse significantly increases the risk of developing ARDS in critically ill patients

• Cardiogenic pulmonary edema
• Viral pneumonitis
• Lymphangitic carcinomatosis
The search for an underlying cause should focus on treatable causes (e.g., infections such as sepsis or pneumonia)
• ABGs
• Hemodynamic monitoring
• Bronchoalveolar lavage (selected patients)
• ABGs:
1. Initially: varying degrees of hyp-oxemia, generally resistant to supplemental oxygen
2. Respiratory alkalosis, decreased Pco2
3. Widened alveolar-arterial gradient
4. Hypercapnia as the disease progresses
• Bronchoalveolar lavage:
1. The most prominent finding is an increased number of polymorphonucleocytes.
2. The presence of eosinophilia has therapeutic implications, since these patients respond to corticosteroids.
• Blood and urine cultures
Chest x-ray examination.
• The initial chest radiogram might be normal in the initial hours after the precipitating event.
• Bilateral interstitial infiltrates are usually seen within 24 hr; they often are more prominent in the bases and periphery.
• “White out” of both lung fields can be seen in advanced stages.
Hemodynamic monitoring
• Hemodynamic monitoring can be used for the initial evaluation of ARDS (in ruling out cardiogenic pulmonary edema) and its subsequent management.
• Although no dynamic profile is diagnostic of ARDS, the presence of pulmonary edema, a high cardiac output, and a low PAWP is characteristic of ARDS.
• It is important to remember that partially treated intravascular volume overload and flash pulmonary edema can have the hemodynamic features of ARDS; filling pressures can also be elevated by increased intrathoracic pressures or with fluid administration; cardiac function can be depressed by acidosis, hypoxemia, or other factors associated with sepsis.

Ventilatory support: mechanical ventilation is generally necessary to maintain adequate gas exchange; assist-control is generally preferred initially with the following ventilator settings:
• Fio2 1.0 (until a lower value can be used to achieve adequate oxygenation). When possible, minimize oxygen toxicity by maintaining Fio2 at <60%.
• Tidal volume: Set initial tidal volume at 5-6 ml/kg of body weight. Aim to maintain plateau pressure (Pplat) at <30 mm Hg.
• PEEP =5 cm H2O to increase lung volume and keep alveoli open. Recent data, however, raise questions about the use of minimal PEEP (5 to 10 cm H2O) in patients with ARDS. The data suggest that the use of more liberal PEEP (10 to 20 cm H2O) might be warranted even without a determination of the lower inflection point.
• Inspiratory flow: 60 L/min.
• Ventilatory rate: high ventilatory rates of 20 to 25 breaths/min are often necessary in patients with ARDS because of their increased physiologic deadspace and
smaller lung volumes. Patients must be monitored for excessive intrathoracic gas trapping (“auto-PEEP” or “intrinsic-PEEP”) that can depress cardiac output.
Identify and treat precipitating conditions:
• Blood and urine cultures and trial of antibiotics in presumed sepsis (routine administration of antibiotics in all cases of ARDS is not recommended)
• Prompt repair of bone fractures in patients with major trauma
• Bowel rest and crystalloid resuscitation in pancreatitis
• Fluid management: optimal fluid and hemodynamic management of patients with ARDS is patient specific; generally, administration of crystalloids is recommended if a downward trend in pulmonary capillary wedge pressures (PCWP) is associated with diminished cardiac index, resulting in prerenal azotemia, oliguria, and relative tachycardia; on the other hand, if PCWP increases with little or no change in cardiac index, one should begin diuretic therapy and use low-dose dopamine (2 to 4
mg/kg/min) to maintain natriuresis and support adequate renal flow.
• Positioning the patient: changes in position can improve oxygenation by improving the distribution of perfusion to ventilated lung regions; repositioning (lateral decubitus positioning) should be attempted in patients with hypoxemia that is not responsive to other medical interventions. Placing patients with acute respiratory failure in a prone position improves their oxygenation but does not improve their survival.
• Corticosteroids: routine use of corticosteroids in ARDS is not recommended; corticosteroids may be beneficial in patients with many eosinophils in the bronchoalveolar lavage fluid; systemic infections should be ruled out or adequately treated before administration of corticosteroids.
• Nutritional support: nutritional support is necessary to maintain adequate colloid oncotic pressure and intravascular volume.
• Tracheostomy: tracheostomy is warranted in patients requiring >2 wk of mechanical ventilation; discussion regarding tracheostomy should begin with patient (if alert and oriented) and family members/legal guardian, after 5 to 7 days of ventilatory support.
• Some form of DVT prophylaxis is indicated in most patients with ARDS.
• Prognosis for ARDS varies with the underlying cause. Prognosis is worse in patients with chronic liver disease, nonpulmonary organ dysfunction, sepsis, and advanced age.
• Elevated values of dead-space fraction [(Paco2 -Peco2 )/Paco2 ] (normal is <0.3) is associated with an increased risk of death.
• Overall mortality varies between 40% and 60%. The majority of deaths is attributable to sepsis or multiorgan dysfunction rather than primary respiratory causes.
Chest radiograph
Chest radiograph appearances in acute respiratory distress syndrome. Bilateral diffuse alveolar shadowing with air bronchograms and no cardiac enlargement.
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