Conceptual model: ARDS is an acute, diffuse, inflammatory lung injury precipitated by a predisposing risk factor, such as pneumonia, nonpulmonary infection, trauma, transfusion, burn, aspiration, or shock. The resulting injury leads to increased pulmonary vascular and epithelial permeability, lung edema, and gravity-dependent atelectasis, all of which contribute to loss of aerated lung tissue. The clinical hallmarks are arterial hypoxemia and diffuse radiographic opacities associated with increased shunting, increased alveolar dead space, and decreased lung compliance. The clinical presentation is influenced by medical management (position, sedation, paralysis, positive end-expiratory airway pressure, and fluid balance). Histological findings vary and may include intraalveolar edema, inflammation, hyaline membrane formation, and alveolar hemorrhage. | |||
Criteria that apply to all ARDS categories | |||
Risk factors and origin of edema | Precipitated by an acute predisposing risk factor, such as pneumonia, nonpulmonary infection, trauma, transfusion, aspiration, or shock. Pulmonary edema is not exclusively or primarily attributable to cardiogenic pulmonary edema/fluid overload, and hypoxemia/gas exchange abnormalities are not primarily attributable to atelectasis. However, ARDS can be diagnosed in the presence of these conditions if a predisposing risk factor for ARDS is also present. | ||
Timing | Acute onset or worsening of hypoxemic respiratory failure within 1 week of the estimated onset of the predisposing risk factor or new or worsening respiratory symptoms. | ||
Chest imaging | Bilateral opacities on chest radiography and computed tomography or bilateral B lines and/or consolidations on ultrasound* not fully explained by effusions, atelectasis, or nodules/masses. | ||
Criteria that apply to specific ARDS categories | |||
Nonintubated ARDS¶ | Intubated ARDS | Modified definition for resource-limited settingsΔ | |
Oxygenation◊ § | PaO2:FIO2 ≤300 mmHg or SpO2:FIO2 ≤315 (if SpO2 ≤97%) on HFNC with flow of ≥30 L/min or NIV/CPAP with at least 5 cm H2O end-expiratory pressure | Mild:¥ 200 < PaO2:FIO2 ≤300 mmHg or 235 < SpO2:FIO2 ≤315 (if SpO2 ≤97%) Moderate: 100 < PaO2:FIO2 ≤200 mmHg or 148 < SpO2:FIO2 ≤235 (if SpO2 ≤97%) Severe: PaO2:FIO2 ≤100 mmHg or SpO2:FIO2 ≤148 (if SpO2 ≤97%) | SpO2:FIO2 ≤315 (if SpO2 ≤97%)¶. Neither positive end-expiratory pressure nor a minimum flow rate of oxygen is required for diagnosis in resource-limited settings. |
ARDS: acute respiratory distress syndrome; CPAP: continuous positive airway pressure; HFNC: high-flow oxygen delivered via nasal cannulae; NIV: noninvasive ventilation; PEEP: positive end-expiratory pressure; SpO2: oxygen saturation as measured by pulse oximetry.
* The ultrasound operator should be well trained in the use of ultrasound for identifying bilateral loss of lung aeration (eg, multiple B lines and/or consolidations) and other ultrasound findings suggestive of noncardiogenic pulmonary edema (eg, pleural line abnormalities).
¶ Estimated FIO2 = ambient FIO2 (eg, 0.21) + 0.03 × O2 flow rate (L/min).
Δ Modified oxygenation criteria can be applied in settings in which arterial blood gas and/or HFNC, NIV, and mechanical ventilation are not routinely available.
◊ Blood gas and oximetry measurements should be made when the patient is comfortably at rest and at least 30 minutes after changes in position, FIO2, or flow rate. For pulse oximetry, ensure an adequate waveform and oximeter placement. SpO2:FIO2 is not valid above saturation values of 97%. Pulse oximetry is not recommended for diagnosis if a hemoglobin abnormality is suspected (eg, methemoglobinemia or carboxyhemoglobinemia).
§ If altitude is >1000 m, apply the following correction factor: (PaO2 or SpO2)/FIO2 × (barometric pressure/760).
¥ For all severity categories of intubated ARDS, a minimum PEEP of 5 cm H2O is required. Patients may move from one category to another throughout their disease course.آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟