From the Guidelines
Diagnosing ventilator-induced lung injury (VILI) requires a high index of suspicion and a combination of clinical assessment, imaging, and laboratory findings in mechanically ventilated patients, as outlined in the American Thoracic Society/European Society of Intensive Care Medicine/Society of Critical Care Medicine clinical practice guideline 1. To diagnose VILI, clinicians should monitor for worsening oxygenation, decreased lung compliance, and increased airway pressures despite stable ventilator settings. Key findings include:
- Worsening oxygenation
- Decreased lung compliance
- Increased airway pressures Chest radiographs or CT scans typically show bilateral infiltrates, ground-glass opacities, or consolidations that weren't present before mechanical ventilation or have worsened during ventilation. Laboratory findings may include elevated inflammatory markers such as C-reactive protein and procalcitonin. Bronchoalveolar lavage often reveals neutrophil predominance and increased protein content, indicating alveolar damage. Clinicians should also review ventilator parameters, looking for risk factors like high tidal volumes (>6 ml/kg predicted body weight), high plateau pressures (>30 cmH2O), or high driving pressures (>15 cmH2O), as these are associated with the development of VILI, according to the guideline 1. The diagnosis is often one of exclusion, ruling out other causes of respiratory deterioration such as pneumonia, pulmonary edema, or pulmonary embolism. Given the potential for VILI to cause significant morbidity and mortality, as highlighted in the guideline 1, a prompt and accurate diagnosis is crucial to guide management and improve patient outcomes.
From the Research
Diagnosing VILI
To diagnose Ventilator-Induced Lung Injury (VILI), it is essential to understand the mechanisms and determinants of the condition. The following points highlight the key aspects of VILI diagnosis:
- VILI results from injury to the blood-gas barrier caused by mechanical ventilation 2.
- The determinants of VILI include the nature, duration, and intensity of the exposure, as well as the pattern of initial insult to the lung 2.
- Clinically significant VILI occurs from volutrauma, barotrauma, atelectrauma, biotrauma, and shear strain 3.
- Differences in regional mechanics are important in VILI pathogenesis 3.
- Ventilator settings, such as tidal volume, respiratory rate, positive end-expiratory pressure, peak, plateau, driving and transpulmonary pressures, energy, mechanical power, and intensity, can act as VILI determinants 4.
- The use of large tidal volume, transfusion of blood products, acidemia, and a history of restrictive lung disease are risk factors associated with the development of acute lung injury 5.
- The physical basis of VILI involves the biophysical characteristics of heterogeneously injured lungs, which increase the parenchymal stress associated with breathing, further aggravated by mechanical ventilation 6.
- Several clinical surrogate measures of lung stress/strain, such as density changes in chest computed tomography, lower and upper inflection points of the pressure-volume curve, plateau pressure, and inflammatory cytokine levels, can be used to titrate mechanical ventilation 6.
Diagnostic Considerations
When diagnosing VILI, consider the following:
- The definition and classification of Acute Respiratory Distress Syndrome (ARDS) 4.
- The role of prone positioning and muscle paralysis in preventing VILI 4.
- The importance of balancing the risk of lung injury with untoward side effects from preventive efforts 3.
- The need to target VILI prevention strategies to subsets of patients at increased risk 3.
- The association between the initial tidal volume and the development of acute lung injury, suggesting that ventilator-associated lung injury may be an important cause of this syndrome 5.