Outline the clinical manifestations, appropriate investigations and treatment of
“volutrauma” in the critically ill patient
Nomenclature used for defining ventilator induced lung damage are complex and continue to evolve. “Volutrauma” should be considered as a potential complication of mechanical ventilation and may be manifest as extra-alveolar air, or acute (ventilator associated) lung injury. A good answer would deal with both aspects.
Exacerbation of acute lung injury is detectable on analysis of BAL fluid, but is hard to differentiate from the inflammatory state associated with the initial lung injury, and its associated conditions. Treatment is the continuation of lung protective strategies (see below).
Extra-alveolar air results from alveolar rupture, and manifestations depend on where the gas passes but include interstitial emphysema, mediastinal emphysema, pneumothorax, pneumoperitoneum, and subcutaneous emphysema. Clinical signs may include haemodynamic and/or respiratory compromise in a ventilated patient (e.g. tension pneumothorax), in particular in a susceptible patient (e.g. obstructive airways disease, heterogeneous lung disease). Manifestations may vary from a subtle deterioration to overwhelming collapse, or may just present with palpable (subcutaneous) emphysema. Investigations should include radiographs to exclude the manifestations mentioned above, and to exclude differential diagnoses. Treatment involves introduction of lung protective strategies to minimise further damage (in particular lower tidal volumes, lower ventilatory rates, lower mean airway pressures, and avoidance of auto-PEEP), drainage of collections of gas (e.g. urgent decompression of tension pneumothorax, and subsequent intercostal catheters, or even subcutaneous tubes). Double lumen tubes and/or differential lung ventilation is occasionally required.
The idea of "volutrauma" is these days more refined; the term has narrowed in its definition to describe only the alveolar overdistension aspect of ventilator-associated lung injury. Question 10 from the first paper of 2012 gives a more thorough answer, which focuses on all aspects of VALI.
Overdistension of alveoli leads to broken cell walls, and leaking pneumocyte contents is highly immunogenic. The ensuing inflammatory response not only creates more lung injury (by inflammation, so called "biotrauma") but contributes to the systemic inflammatory response sydnrome and mlti-organ system failure.
This process is worst when there is heterogenous lung disease: the healthy lung will suffer the side effects of whatever ventilator strategy is being used to improve gas exchange within the diseased lung. Thus, huge tidal volumes are not required to induce this sort of lung injury. The ultimate outcome of volutrauma may actually be pneumothorax and pneumomediastinum, as the alveoli rupture from overdistension.
- Worsening gas exchange
- Increasing organ system failure due to cytokine release
- worsening lactic acidosis
- decreasing lung compliance
- surgical emphysema
- Plateau pressure measurement by inspiratory hold
Treatment of volutrauma
- Lung-protective ventilation
- thoracocentesis for pneumothoraces
- dual-lumen intubation to isolate the affected lung, with the potential to ventilate it independently and a different pressure.
Rocco PR, Dos Santos C, Pelosi P. Pathophysiology of ventilator-associated lung injury. Curr Opin Anaesthesiol. 2012 Apr;25(2):123-30