What are the clinical manifestations of a patient with Ventilator-Induced Lung Injury (VILI)?

From the Guidelines

A patient who has suffered ventilator-induced lung injury (VILI) typically presents with worsening respiratory status and increasing oxygen requirements, and may develop acute respiratory distress syndrome (ARDS) characterized by decreased lung compliance, making breathing more difficult, as noted in the study by 1. The clinical presentation of a patient with VILI may include:

• Tachypnea (rapid breathing)
• Dyspnea (shortness of breath)
• Increased work of breathing with accessory muscle use
• Hypoxemia despite increasing ventilator support
• Signs of systemic inflammation, including fever, tachycardia, and hemodynamic instability
• Chest imaging revealing new or worsening bilateral infiltrates

Management of VILI involves:

• Protective ventilation strategies with lower tidal volumes (4-6 mL/kg predicted body weight) and limiting plateau pressures to <30 cmH2O, as recommended by 1
• Appropriate PEEP titration
• Considering prone positioning for severe cases, which has been shown to improve oxygenation and reduce mortality in patients with severe ARDS, as noted in the study by 1
• Pharmacologic interventions, such as sedation with propofol, dexmedetomidine, or midazolam, to improve ventilator synchrony
• Neuromuscular blockade with cisatracurium (typically 37.5 mg/hr infusion) for severe cases
• Judicious fluid management to prevent fluid overload and minimize the risk of pulmonary edema, as discussed in the study by 1

The pathophysiology of VILI involves excessive mechanical forces, including volutrauma from overdistension, atelectrauma from repetitive opening/closing of alveoli, and biotrauma from inflammatory mediator release, which damage the delicate alveolar structures and trigger inflammation that can progress to systemic inflammatory response, as described in the study by 1. The use of prone positioning has been shown to reduce the incidence of ventilator-associated pneumonia and improve oxygenation, as noted in the study by 1. However, the optimal duration and timing of prone positioning are still unclear, and further research is needed to determine the best approach, as discussed in the study by 1. Overall, the management of VILI requires a multifaceted approach that includes protective ventilation strategies, pharmacologic interventions, and careful consideration of the patient's hemodynamic and respiratory status, as recommended by 1.

From the Research

Ventilator-Induced Lung Injury (VILI) Overview

• VILI is a significant risk to patients receiving positive-pressure ventilation (PPV) 2.
• It is caused by the application of excessive end-inspiratory volumes and transpulmonary pressures, leading to lung injury 3.
• The prevention of VILI has become a main goal of current ventilator strategies for patients with acute respiratory distress syndrome (ARDS) and those with normal lungs requiring mechanical ventilation 3.

Clinical Presentation of VILI

• Patients with VILI may exhibit elevated levels of cytokines, indicating an inflammatory process activated by PPV 2.
• The clinical presentation of VILI cannot be distinguished from exacerbation of the primary condition in patients with ARDS or acute lung injury (ALI) 2.
• VILI can lead to significant changes in lung structure and function, resulting from an imbalance between lung stress and strain 4.

Ventilatory Strategies to Prevent VILI

• Lung-protective ventilator strategies are considered standard practice in the care of patients with ARDS 5.
• The use of low tidal volume ventilation (approximately 6 mL/kg) and adequately adjusted positive end-expiratory pressure (PEEP) are recommended to prevent VILI 5, 2, 4.
• The optimal setting of PEEP remains unsettled, but it should be set to maximize alveolar recruitment while avoiding overdistention 5.
• Noninvasive ventilation has gained preference in the past decade, but it also has the potential to cause harm, especially in patients with de novo respiratory failure 6.

Management and Prevention of VILI

• Alveolar pressure exposure (plateau pressure) should be limited to less than 32 cm H2O 2.
• Tidal volume should be set at approximately 6 mL/kg or further guided by plateau pressure limitation 2.
• The results of preliminary studies investigating the preventative potential of respiratory acidosis, prone positioning, or careful vascular pressure management seem promising 2.
• Combined modulation of the mechanisms of VILI genesis could have a potential to impact outcomes 6.