Ventilator-Induced Lung Injury (VILI)

Ventilator-induced lung injury (VILI) is lung damage caused or aggravated by mechanical ventilation itself. The same positive-pressure breaths that support gas exchange can overstretch alveoli, repeatedly open and close unstable lung units, and trigger inflammation, so that the supportive therapy becomes a source of harm. Recognising VILI reframed mechanical ventilation around protecting the lung rather than only normalising blood gases.

Definition

Ventilator-induced lung injury is acute lung injury attributable to mechanical ventilation, encompassing overdistension injury (volutrauma), pressure-related air leak (barotrauma), injury from repeated alveolar opening and collapse (atelectrauma), and the inflammatory cascade these forces provoke (biotrauma).

Scope

This entry explains the mechanisms of VILI, the concepts of volutrauma, barotrauma, atelectrauma, and biotrauma, and how the evidence on protective ventilation flows from these mechanisms. It is a conceptual and educational topic and does not provide ventilator settings or treatment instructions for individual patients.

Core questions

• How can a life-supporting therapy injure the lung?
• What distinguishes volutrauma, barotrauma, atelectrauma, and biotrauma?
• Why does limiting tidal volume and pressure reduce harm?
• What is the role of positive end-expiratory pressure in preventing atelectrauma?

Key concepts

• Volutrauma (overdistension)
• Barotrauma (high-pressure air leak)
• Atelectrauma (repetitive alveolar opening and collapse)
• Biotrauma (mechanotransduced inflammation)
• Transpulmonary pressure
• Driving pressure
• Mechanical power

Mechanisms

VILI arises when mechanical forces exceed what lung tissue can tolerate. Excessive end-inspiratory volume and transpulmonary pressure overstretch alveolar walls (volutrauma), high airway pressures can rupture alveoli and cause air leak (barotrauma), and cyclic opening and collapse of unstable units shears tissue (atelectrauma). These physical insults activate inflammatory signalling (biotrauma), and the released mediators can injure the lung further and reach the systemic circulation. The injurious dose integrates volume, pressure, flow, and rate, a concept summarised as mechanical power. Protective strategies limit tidal volume, plateau and driving pressure, and use positive end-expiratory pressure to keep alveoli open and reduce atelectrauma (Slutsky-Ranieri-2013).

Clinical relevance

VILI is central to why modern ventilation is protective rather than simply corrective, and it underlies the appraisal of nearly every ventilation trial. This entry describes the mechanisms and supporting evidence; it explains how harm is generated and is not a source of individual ventilator or treatment instructions.

Epidemiology

VILI is difficult to count as a discrete diagnosis because it overlaps with the underlying lung injury, but its importance is inferred from randomised trials in which less injurious ventilation reduced mortality, implying that a meaningful share of harm in earlier practice was iatrogenic (Amato-1998; ARDSnet-2000).

Evidence & guidelines

The clearest evidence for VILI comes from trials showing that protective ventilation strategies reduce mortality compared with higher tidal volumes and pressures (Amato-1998; ARDSnet-2000), a principle carried into professional-society guidelines on ventilation in ARDS (Fan-2017-guideline). This entry conveys the direction of that evidence without specifying numeric limits.

History

Animal studies from the 1970s onward showed that high-volume, high-pressure ventilation could itself injure the lung, shifting attention from pressure alone (barotrauma) to volume (volutrauma) and to the cyclic-collapse and inflammatory mechanisms of atelectrauma and biotrauma. The clinical proof came from protective-ventilation trials in the late 1990s and 2000, which demonstrated survival benefit from less injurious ventilation and made VILI prevention a guiding aim (Amato-1998; ARDSnet-2000; Slutsky-Ranieri-2013).

Debates

Which single parameter best captures injurious ventilation?

Tidal volume, plateau pressure, driving pressure, and integrated mechanical power have each been proposed as the most relevant target for limiting VILI, and which is most useful at the bedside remains an active question.

Key figures

• Arthur Slutsky
• V. Marco Ranieri
• Marcelo Amato
• Luciano Gattinoni

Seminal works

• slutsky-ranieri-2013
• amato-1998
• ardsnet-2000

Frequently asked questions

What is the difference between barotrauma and volutrauma?

Barotrauma refers to injury and air leak associated with high airway pressures, whereas volutrauma refers to injury from overdistension of the lung by excessive volume; experimental work suggests that overdistension (volume) rather than pressure per se is the dominant driver of injury.

What is atelectrauma?

Atelectrauma is lung injury caused by the repeated opening and collapse of unstable alveolar units during the respiratory cycle; positive end-expiratory pressure is used to keep these units open and reduce this cyclic shear.