Acute Respiratory Distress Syndrome

The condition described in this chapter, which has the nondescript name acute respiratory distress syndrome (ARDS), is a diffuse inflammatory injury of the lungs that is responsible for 10% of ICU admissions and 25% of cases of prolonged mechanical ventilation worldwide (1).

I. Features

A. Pathogenesis

The inciting event in ARDS is activation of circulating neutrophils (as part of the systemic inflammatory response). The activated neutrophils attach to the endothelium in pulmonary capillaries, and subsequently migrate into the lung parenchyma (2). Neutrophil degranulation damages the capillary endothelium, leading to exudation of protein-rich fluid that fills the distal airspaces and impairs pulmonary gas exchange.

B. Predisposing Conditions

ARDS is not a primary disorder, but is a consequence of a variety of infectious and noninfectious conditions.
The conditions that predispose to ARDS are listed in Table 17.1. The most frequent offenders are pneumonia, extrapulmonary sepsis, and aspiration of gastric secretions (1).
Fewer than 10% of cases have no predisposing condition.
The one feature shared by most (but not all) of these conditions is the tendency to trigger a systemic inflammatory response.

Table 17.1 Predisposing Conditions for ARDS

Condition	Prevalence¹
Pneumonia	59.4%
Extrapulmonary Sepsis	16.0%
Aspiration	14.2%
Noncardiogenic Shock	7.5%
Trauma	4.2%
Blood Transfusion	3.9%
Pulmonary Contusion	3.2%
Others²	8.6%
No Predisposing Condition	8.3%
¹From Reference 1, which included 3,022 cases of ARDS from 459 ICUs in 50 countries. The total exceeds 100% because some patients had more than one condition. ²Other predisposing conditions include inhalation injury, burns, drug overdose, cardiopulmonary bypass, necrotizing pancreatitis, and intracranial hemorrhage.

C. Clinical Features

The clinical features of ARDS are shown in Table 17.2 (3). The principal features are acute hypoxemic respiratory failure and bilateral, diffuse pulmonary infiltrates that are not explained by left heart failure or volume overload. Most (>90%) cases of ARDS appear within one week of a known predisposing condition, and 80% of cases require mechanical ventilation (1).

Table 17.2 Clinical Features of ARDS1

Feature	Requirements
Timing	Occurs within one week of a predisposing condition, or one week from symptom onset.
Imaging	Bilateral opacitis (on chest x-ray or CT scan) consistent with alveolar consolidation.
Origin of Edema	No evidence of left heart failure or fluid overload.
Oxygenation²
Mild	PaO₂/FIO₂ = 201–300 mm Hg*
Moderate	PaO₂/FIO₂ = 101–200 mm Hg
Severe	PaO₂/FIO₂ ≤ 100 mm Hg
*(PaO₂/FIO₂ measured with PEEP or CPAP ≥5 cm H₂O)
¹Corresponds to the “Berlin” definition of ARDS, from Reference 3. ²For altitudes >1,000 meters, use PaO₂/FIO₂ × (barometric pressure/760). PaO₂ = arterial PO₂; FIO₂ = fractional concentration of inhaled O₂; PEEP = positive end-expiratory pressure; CPAP = continuous positive airway pressure.

1. Radiographic Appearance

The characteristic appearance of ARDS on a portable chest x-ray is shown in Figure 17.1. The infiltrate has a finely granular or ground-glass appearance, and is evenly distributed throughout both lungs. Also note the lack of a prominent pleural effusion, which helps to distinguish ARDS from cardiogenic pulmonary edema.

Oxygenation

The impairment in oxygenation in ARDS is assessed using the PaO₂/FIO₂ ratio, measured at a positive end-expiratory pressure (PEEP) of ≥5 cm H₂O. (For patients who are not on a ventilator, continuous positive airway pressure, or CPAP, is used instead of PEEP.)

The diagnosis of ARDS requires a PaO₂/FIO₂ ratio <300 mm Hg (with PEEP or CPAP at ≥5 cm H₂O) (3).
Table 17.2 shows a severity of illness classification (mild, moderate, or severe) based on the PaO₂/FIO₂ ratio, which is intended for predicting the likelihood of a fatal outcome. The reported mortality rates for mild, moderate, and severe ARDS are 27%, 32%, and 45% (mean values), respectively (3).

FIGURE 17.1 Portable chest x-ray showing the characteristic appearance of ARDS.

D. Diagnostic Problems

Many clinical features of ARDS are nonspecific, and are shared by other conditions that cause hypoxemic respiratory failure. This creates a tendency for misdiagnosis, as demonstrated by the following observations:

In a study of interobserver variability in the radiographic diagnosis of ARDS, a group of 21 experts in ARDS agreed on the diagnosis (ARDS or no ARDS) in only 43% of cases (4).
In a large retrospective study designed to identify patients with ARDS based on the clinical criteria in Table 17.2, 40% of the cases of ARDS were not clinically recognized (1).
An autopsy study of patients who died with a clinical diagnosis of ARDS showed that only 50% of the patients had postmortem evidence of ARDS (5). This implies that the likelihood of identifying ARDS based on clinical criteria is no greater than the likelihood of predicting heads or tails in a coin toss.

4. The Wedge Pressure

The pulmonary artery occlusion pressure (wedge pressure) has been used to distinguish between ARDS and cardiogenic pulmonary edema; i.e., a wedge pressure ≤18 mm Hg is considered evidence of ARDS (6). This is problematic because the wedge pressure is not a measure of capillary hydrostatic pressure, as explained in Chapter 5, Section II-B. Although the wedge pressure is no longer a required measurement in the diagnosis of ARDS, the limitations of this measurement deserve mention.

II. Mechanical Ventilation

As mentioned earlier, about 80% of patients with ARDS require mechanical ventilation (1). There are two general goals of mechanical ventilation in ARDS: (a) limit the stretch imposed on the distal airspaces during lung inflation, and (b) prevent the distal airspaces from collapsing during lung deflation.

A. Ventilator-Induced Lung Injury

One of the most important discoveries in critical care medicine in the last quarter-century is the role of mechanical ventilation
as a source of lung injury, particularly in patients with ARDS. This injury is related to excessive stretch of distal airspaces, as described next.

1. Inhomogeneity

Although portable chest x-rays show an apparent homogeneous pattern of lung infiltration in ARDS, CT images reveal that the lung infiltration in ARDS is confined to dependent lung regions (7). This is shown in the CT images in Figure 17.2. Note the dense consolidation in the posterior lung regions (which are the dependent lung regions in the supine position). The uninvolved lung in the anterior portion of the thorax is the functional lung volume, and is the region that receives the inflation volumes from the ventilator.

2. Volutrauma

Because the functional lung volume in ARDS is markedly reduced, the usual inflation volumes delivered by mechanical ventilation (10–15 mL/kg) cause overdistension of alveoli and stress-fractures in the alveolar capillary interface (8). This volume-related lung injury is known as volutrauma.

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