Myotrauma in mechanically ventilated patients

Excerpt

In 1988, Knisely et al. “noted marked thinning of the muscular portions of the diaphragm” in neonates following prolonged mechanical ventilation [1]. This provided the first evidence that adverse patient–ventilator interactions can cause deleterious structural changes in the diaphragm, a phenomenon recently termed myotrauma [2]. Extensive experimental and clinical investigation has confirmed the existence of myotrauma and characterized its prevalence and clinical impact [2, 3]. Diaphragm myotrauma is a serious concern because it leads to acute diaphragm weakness (referred to as ventilator-induced diaphragm dysfunction; see Table 1 for terminology) and can therefore impair patients’ ability to be liberated from mechanical ventilation. Prolonged mechanical ventilation predisposes patients to nosocomial complications and strongly predicts long-term morbidity and mortality [4]. Preventing myotrauma might therefore accelerate liberation from mechanical ventilation and significantly improve outcomes for critically ill patients. This paper focuses on the adverse patient–ventilator interactions involved in myotrauma and their implications for management; the cellular pathways have recently been reviewed [3, 5]. …