Acute Respiratory Distress Syndrome (ARDS)

Definition and Etiology

Syndrome of rapid-onset hypoxemic respiratory failure with:

1. Diffuse pulmonary infiltrates on chest radiograph

2. Arterial PaO (mmHg)/FIO (inspired oxygen fraction) _ 200 2 2

3. No contribution of pulmonary congestion (pulmonary capillary wedge pressure

_ 18 mmHg).

Acute lung injury (ALI) is a similar syndrome, withPa O /FIO _ 300. Caused 2 2

by many medical and surgical disorders (Table 12-1), but_80% of cases caused

by sepsis, bacterial pneumonia, trauma, multiple transfusions, gastric acid aspiration,

and drug overdose. Risk factors include older age, chronic alcohol

abuse, metabolic acidosis, and severity of critical illness.

Clinical Course and Pathophysiology

Natural history marked by three phases:

1. Exudative phase—Marked by disruption of normally tight alveolarcapillary

membrane withconsequent collection of protein-rich alveolar wall and

airspace edema withcollection of cytokines in edema fluid. Exudative phase

duration is typically _7 days, marked by dyspnea, tachypnea, and severe hypoxemia;

differential includes cardiogenic pulmonary edema, diffuse pneumonia,

alveolar hemorrhage.

2. Proliferative phase—If recovery does not occur, some pts will develop

progressive lung injury and evidence of pulmonary interstitial inflammation and

fibrosis. Duration approximately days 7–21.

3. Fibrotic phase—Although the majority of patients recover within 3–4

weeks of the initial insult, some experience progressive fibrosis, necessitating

prolonged ventilatory support predisposing to complications of long-term intensive

care. Many investigators believe the incidence of this final phase of ARDS was in part a reaction to now-abandoned ventilator strategies that employed

large tidal volumes and high lung inflation pressures.

TREATMENT

Progress in recent therapy has emphasized the importance of general critical

care of patients withARDS in addition to new ventilator strategies. General

care requires:

• Treatment of underlying cause of lung injury

• Minimizing procedural complications

• Avoidance of preventable complications suchas venous thromboembolism

and GI hemorrhage with appropriate prophylactic regimes

• Recognition and treatment of nosocomial infections

• Adequate nutritional support.

Mechanical Ventilatory Support A substantial improvement in outcome

of ARDS has occurred with recognition that overdistention of normal

lung units withpositive pressure can produce or exacerbate lung injury, causing

or worsening ARDS. This finding has prompted the introduction of ventilator

strategies aimed at limiting alveolar distention while still ensuring adequate

tissue oxygenation.

Current practice is to use low tidal volumes (_ 6 mL/kg predicted body

weight); see http://www.ardsnet.org/. Low tidal volumes are combined with

the use of positive end-expiratory pressure (PEEP) at levels that strive to

achieve adequate oxygenation with the lowest FIO . Other techniques that may 2

improve oxygenation while limiting alveolar distention include extending the

time of inspiration on the ventilator and placing the patient in the prone position.

Ancillary Therapies In general, patients withARDS should receive intravenous

fluids only sufficient to achieve an adequate cardiac output and

tissue oxygen delivery. There is no survival advantage to increasing oxygen

delivery by overresuscitation, and fluids should be given only in sufficient

volumes to maintain adequate organ function as assessed by urine output,

acid-base statues, arterial pressure. There is no current evidence to support

the use of glucocorticoids or other pharmacologic therapies in ARDS, except

as needed to treat the underlying cause of the condition.

Outcomes

Mortality from ARDS has declined steadily over the past 15 years with improvements in general care and then the introduction of low tidal volume ventilation.

Current mortality is 41–65%, withmost deaths due to nonpulmonary

causes.