Possible reasons for predisposition to VALI include:

An injured lung may be at risk for further injury
Cyclic atelectasis is particularly common in an injured lung

Pathogenesis
Overdistension of alveoli and cyclic atelectasis (atelectotrauma) are the primary causes for alveolar injury during positive pressure mechanical ventilation. Severe injury to alveoli causes swelling of the tissues (edema) in the lungs, bleeding of the alveoli, loss of surfactant (decrease in lung compliance) and complete alveoli collapse (biotrauma). High flow rates are associated with rheotrauma, high volumes with volutrauma and pressures with barotrauma. Collectively these may be converted into a single unit of mechanical power. Diagnosis
VALI does not need to be distinguished from progressive ALI/ARDS because management is the same in both. Additionally, definitive diagnosis of VALI may not be possible because of lack of sign or symptoms. Prevention
Preventing alveolar overdistension
Alveolar overdistension is mitigated by using small tidal volumes, maintaining a low plateau pressure, and most effectively by using volume-limited ventilation. A 2018 systematic review by The Cochrane Collaboration provided evidence that low tidal volume ventilation reduced post operative pneumonia and reduced the requirement for both invasive and non invasive ventilation after surgery

Preventing cyclic atelectasis (atelectotrauma)
Applied positive end-expiratory pressure (PEEP) is the principal method used to keep the alveoli open and lessen cyclic atelectasis. Open lung ventilation
Open lung ventilation is a ventilatory strategy that combines small tidal volumes (to lessen alveolar overdistension) and an applied PEEP above the low inflection point on the pressure-volume curve (to lessen cyclic atelectasis).
Brain disease
Wernickes encephalopathy (WE), Korsakoff syndrome (also called alcohol amnestic disorder), and Wernicke–Korsakoff syndrome are forms of dry beriberi.Wernickes encephalopathy is the most frequently encountered manifestation of thiamine deficiency in Western society, though it may also occur in patients with impaired nutrition from other causes, such as gastrointestinal disease, those with HIV/AIDS, and with the injudicious administration of parenteral glucose or hyperalimentation without adequate B-vitamin supplementation. This is a striking neuro-psychiatric disorder characterized by paralysis of eye movements, abnormal stance and gait, and markedly deranged mental function.Korsakoff syndrome, in general, is considered to occur with deterioration of brain function in patients initially diagnosed with WE. This is an amnestic-confabulatory syndrome characterized by retrograde and anterograde amnesia, impairment of conceptual functions, and decreased spontaneity and initiative.Alcoholics may have thiamine deficiency because of:

Inadequate nutritional intake:  Alcoholics tend to intake less than the recommended amount of thiamine. Decreased uptake of thiamine from the GI tract:  Active transport of thiamine into enterocytes is disturbed during acute alcohol exposure. Liver thiamine stores are reduced due to hepatic steatosis or fibrosis. Impaired thiamine utilization:  Magnesium, which is required for the binding of thiamine to thiamine-using enzymes within the cell, is also deficient due to chronic alcohol consumption. The inefficient use of any thiamine that does reach the cells will further exacerbate the thiamine deficiency.