Acute Lung Injury in Patients with Severe Brain Injury: A Double Hit Model

Abstract

The presence of pulmonary dysfunction after brain injury is well recognized. Acute lung injury (ALI) occurs in 20% of patients with isolated brain injury and is associated with a poor outcome. The "blast injury" theory, which proposes combined "hydrostatic" and "high permeability" mechanisms for the formation of neurogenic pulmonary edema, has been challenged recently by the observation that a systemic inflammatory response may play an integral role in the development of pulmonary dysfunction associated with brain injury. As a result of the primary cerebral injury, a systemic inflammatory reaction occurs, which induces an alteration in blood-brain barrier permeability and infiltration of activated neutrophils into the lung. This preclinical injury makes the lungs more susceptible to the mechanical stress of an injurious ventilatory strategy. Tight CO2 control is a therapeutic priority in patients with acute brain injury, but the use of high tidal volume ventilation may contribute to the development of ALI. Establishment of a therapeutic regimen that allows the combination of protective ventilation with the prevention of hypercapnia is, therefore, required. Moreover, in patients with brain injury, hypoxemia represents a secondary insult associated with a poor outcome. Optimal oxygenation may be achieved by using an adequate FiO2 and by application of positive end-expiratory pressure (PEEP). PEEP may, however, affect the cerebral circulation by hemodynamic and CO2-mediated mechanisms and the effects of PEEP on cerebral hemodynamics should be monitored in these patients and used to titrate its application.

Pulmonary Complications in Patients with Brain Injury

“…Although the level of adrenaline subsequently falls, it keeps 3 times higher than normal for about ten days. [2][3]7,[9][10] This catecholamine release elevates intravascular pressure thus damaging the endothelium and producing pulmonary edema due to disruption of the alveolar-capillary barrier. The initial hydrostatic edema becomes a protein-rich edema that goes into interstitial and alveolar spaces.…”

“…The initial hydrostatic edema becomes a protein-rich edema that goes into interstitial and alveolar spaces. 3,7,[9][10] The amount of fluid that leaks through the endothelium depends on the severity of capillary hypertension. Furthermore, in case of structural damage to the capillary wall, plasma will pass to the interstitial and alveolar spaces.…”

“…Its severity is related to the magnitude of the brain injury and it is associated with high morbidity rates and up to 7% mortality. 8,10,25 NPE may be triggered by different brain conditions, including seizures, stroke and traumatic brain injury ( Figure 3). NPE is most common in seizures during the post-critical period, affecting to up to one third of patients in status epilepticus.…”

“…), [14][15][16][17][18] used. 3,10 All of this increases lung capillary permeability and results in bilateral pulmonary infiltrates that lead to severe hypoxemia with a low PaO 2 /FiO 2 ratio (<300 mm Hg in ALI, <200 mm Hg in ARDS) and decreased lung compliance.…”

“…It has been shown that use of high tidal volumes (9-11 ml/kg) stimulates inflammatory response and lung injury induced by the ventilator. 10,25,[31][32] Even neurocritical patient's ventilation in prone possition results in improved brain tissue oxygenation in severe hypoxemia with minimal effect on Intracranial pressure (ICP) and Cerebral Perfusion Pressure (CPP).…”