Lung-protective ventilation for SAH patients: are these measures truly protective?

Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) are common in patients with critical neurological illnesses and herald a worse outcome. It has been reported in 15–40 % of patients suffering from an aneurysmal subarachnoid hemorrhage (SAH) [1, 2]. Any type of acute brain injury can trigger ALI/ARDS, but even more so, the systemic inflammatory response syndrome (SIRS) seen in the acute and delayed phases of SAH exposes these patients to this type of catastrophic respiratory deterioration [3]. Furthermore, hemodynamic augmentation has been the mainstay of treatment for vasospasm/delayed cerebral ischemia in patients with SAH and the timing of the initial therapy as well as the utilization of each component (hypertension, hypervolemia, and inotropic enhancement) varies widely [4]. Hypervolemia, stressed cardiac function, and early recourse to blood transfusion can easily lead to pulmonary edema with worse outcomes. But it is easy to understand that in order for the injured and actively ischemic brain to receive adequate oxygen, gas exchange in the lungs must occur optimally [3]. Finally, because nearly a third of mortality after SAH is due to medical and not neurological complications [5, 6], early implementation of strategies to prevent, even partially, the development of ALI/ARDS is primordial. The pathophysiology of ALI/ARDS is complex, and a ‘‘double hit’’ model has been proposed [7]. Severe brain injury results in the ‘‘first hit’’ with an adrenergic surge and systemic inflammation, making the lung more susceptible to injury [3, 7]. The ‘‘second hit’’ results from non-neurological variables such as infections, transfusions, and mechanical ventilation (MV) [3, 7]. One of the major goals of care in such patients should include optimization of oxygen delivery to prevent hypoxemia and, hence, secondary neurological insults. Lung-protective ventilator settings (LPS) have been proposed as a cornerstone in not only the management of but also in the prevention of ALI/ARDS, while injurious ventilator settings (IVS) definitely facilitate the appearance of this lung failure [8, 9]. In this issue of the journal, Marhong and colleagues [10] report a single-center retrospective experience of ventilator practices in a mixed intensive care unit (ICU) in adult SAH patients. The authors describe the incidence of ALI/ARDS as well as the adherence to LPS. They included only patients who required MV within 72 h of their admission. Authors [10] define LPS as tidal volume (TV) B 8 mL/kg of predicted body weight, positive end-expiratory pressure (PEEP) C 5 cm H2O, and peak or plateau pressure B30 cm H2O. The development of ARDS was defined by PaO2/FiO2 B300 along with new bilateral lung opacities on chest X-ray within a day of hypoxemia. Currently accepted thresholds for lung-protective ventilation (LPS) [8, 9] were not met in approximately onethird of patient days, suggesting that this is a target for quality improvement. But initial MV settings were not associated with the subsequent development of ARDS. Furthermore, Marhong et al. [10] found no correlation between one, two, or all three components of LPS, or even IVS and the subsequent occurrence of ARDS. Readers G. Kapinos (&) Departments of Neurosurgery & Neurology, Hofstra North Shore-LIJ School of Medicine, North Shore-LIJ Health System, 300 Community Drive, Tower, 9th floor, Manhasset, NY 11030, USA e-mail: kapigreg@gmail.com