What is Patient Self-Inflicted Lung Injury (P-SILI) in Acute Respiratory Distress Syndrome (ARDS)?

Patient Self-Inflicted Lung Injury (P-SILI) in ARDS

Patient self-inflicted lung injury (P-SILI) is a form of lung damage caused by vigorous spontaneous inspiratory efforts in ARDS patients, where high respiratory drive generates excessive transpulmonary pressures and harmful mechanical forces that worsen existing lung injury. 1

Pathophysiological Mechanisms

P-SILI develops through several distinct but interconnected mechanisms that occur when patients with ARDS generate strong inspiratory efforts:

Excessive Transpulmonary Pressure

• High inspiratory effort creates excessive transpulmonary pressure leading to over-distension of already injured lung tissue, similar to ventilator-induced lung injury but driven by the patient's own respiratory muscles rather than the ventilator. 2
• The negative intrathoracic pressures generated during vigorous spontaneous breathing can be as damaging as excessive positive pressure from mechanical ventilation. 1

Regional Lung Injury Patterns

• Inhomogeneous distribution of transpulmonary pressure variations across the lung leads to cyclic opening and closing of non-dependent lung regions, causing repetitive alveolar collapse and re-expansion injury. 2
• The "pendelluft" phenomenon occurs where gas shifts from non-dependent to dependent lung regions during inspiration, creating local overdistension in already vulnerable areas. 2, 3

Pulmonary Edema Aggravation

• Increased transvascular pressure from vigorous inspiratory efforts favors worsening of pulmonary edema by increasing the pressure gradient across damaged capillary membranes. 2
• This creates a vicious cycle where worsening edema increases respiratory drive, which further aggravates lung injury. 3, 4

Clinical Context and Risk Factors

P-SILI occurs most commonly in two clinical scenarios:

During Noninvasive Ventilation

• High tidal volumes and strongly negative intrathoracic pressures during NIV or high-flow nasal oxygen contribute to P-SILI, particularly in patients with moderate or severe hypoxemia (PaO₂/FiO₂ <200 mmHg). 1
• Approximately 16% of ARDS patients may be managed without invasive mechanical ventilation, but these patients are at risk for P-SILI if respiratory effort is not controlled. 1

During Mechanical Ventilation with Preserved Spontaneous Breathing

• P-SILI can develop even during mechanical ventilation when patients maintain spontaneous respiratory activity with excessive effort. 3
• Patient-ventilator dyssynchrony compounds the problem by creating additional harmful pressure swings. 2

Clinical Recognition

Signs of Increased Work of Breathing

• Look for visible use of accessory respiratory muscles, paradoxical abdominal motion, tachypnea >30 breaths/minute, and nasal flaring as indicators of potentially injurious respiratory effort. 3, 4
• Agitation, inability to speak in full sentences, and diaphoresis suggest excessive respiratory drive. 4

Physiological Measurements

• Driving pressure ≥18 cmH₂O before procedures like bronchoscopy indicates increased risk of derecruitment and P-SILI. 5
• Elevated PaCO₂ ≥48 mmHg combined with high respiratory rate suggests inadequate ventilatory capacity relative to drive. 5
• Esophageal pressure monitoring can quantify inspiratory effort, though this is not routinely available in all centers. 2, 3

Prevention and Management Strategies

Early Intubation Considerations

• Patients with moderate to severe ARDS (PaO₂/FiO₂ <200 mmHg) showing signs of excessive respiratory effort should be considered for early intubation rather than prolonged trials of noninvasive support. 1
• Delayed intubation in patients with worsening P-SILI is associated with worse outcomes. 1

Ventilatory Management

• Apply higher PEEP strategies (targeting moderate to severe ARDS levels) to reduce the intensity of spontaneous effort while maintaining some respiratory muscle activity. 6
• Higher PEEP can facilitate "safe" spontaneous breathing by reducing the work required to trigger breaths and preventing cyclic alveolar collapse. 6
• Maintain low tidal volumes (4-8 ml/kg predicted body weight) and plateau pressures ≤30 cmH₂O even when spontaneous breathing is present. 1

Sedation and Neuromuscular Blockade

• Use adequate sedation to control excessive respiratory drive without completely eliminating spontaneous breathing in most cases. 5
• Consider neuromuscular blocking agents in severe ARDS (PaO₂/FiO₂ <150 mmHg) when signs of injurious respiratory effort persist despite optimized ventilator settings and sedation. 5, 6
• The goal is to prevent expiratory efforts that cause derecruitment while avoiding prolonged paralysis. 5

Adjunctive Therapies

• Implement prone positioning for >12 hours daily in severe ARDS (PaO₂/FiO₂ <100 mmHg), which reduces ventilatory demands and may decrease P-SILI risk. 1, 5
• Consider combining prone positioning with helmet NIV or high-flow nasal oxygen in selected patients, though close monitoring for P-SILI signs is essential. 1

Critical Pitfalls to Avoid

• Do not delay intubation in patients with worsening respiratory distress on noninvasive support, as this is associated with significantly worse outcomes. 1
• Avoid assuming that spontaneous breathing is always beneficial—in severe ARDS with high respiratory drive, uncontrolled spontaneous effort can be more harmful than controlled mechanical ventilation. 2, 3
• Do not use high-frequency oscillatory ventilation as a rescue strategy for P-SILI, as it may worsen hemodynamics and increase right ventricular failure risk. 5
• Monitor for right ventricular dysfunction, which can be exacerbated by lung derecruitment and increased afterload from P-SILI. 5

Evidence Limitations

While the concept of P-SILI is supported by strong physiological reasoning, experimental data, and clinical observations, no randomized controlled trial has yet demonstrated that strategies specifically targeting P-SILI prevention improve mortality or other patient-centered outcomes. 2, 4 However, the mechanistic understanding is sufficiently compelling that clinicians should remain vigilant for signs of injurious respiratory effort and intervene accordingly based on the principles outlined above. 3, 7