ARDS associated acute brain injury: from the lung to the brain

Abstract

A complex interrelation between lung and brain in patients with acute lung injury (ALI) has been established by experimental and clinical studies during the last decades. Although, acute brain injury represents one of the most common insufficiencies in patients with ALI and acute respiratory distress syndrome (ARDS), the underlying pathophysiology of the observed crosstalk remains poorly understood due to its complexity. Specifically, it involves numerous pathophysiological parameters such as hypoxemia, neurological adverse events of lung protective ventilation, hypotension, disruption of the BBB, and neuroinflammation in such a manner that the brain of ARDS patients-especially hippocampus-becomes very vulnerable to develop secondary lung-mediated acute brain injury. A protective ventilator strategy could reduce or even minimize further systemic release of inflammatory mediators and thus maintain brain homeostasis. On the other hand, mechanical ventilation with low tidal volumes may lead to self-inflicted lung injury, hypercapnia and subsequent cerebral vasodilatation, increased cerebral blood flow, and intracranial hypertension. Therefore, by describing the pathophysiology of ARDS-associated acute brain injury we aim to highlight and discuss the possible influence of mechanical ventilation on ALI-associated acute brain injury.

Keywords: Acute brain injury; Acute lung injury; Acute respiratory distress syndrome; Blood–brain barrier disruption; Brain–lung interactions; Hypoxemia; Inflammation; Mechanical ventilation.

Fig. 1

Extrapulmonal complications in patients with ARDS

Fig. 2

Role of inflammation in the development of ARDS-associated secondary brain injury. Hypoxemia and mechanical ventilation elicit a number of systemic responses including release of inflammatory mediators in the systemic circulation followed by potential BBB dysfunction, endothelial cell activation, altered lymphocyte trafficking, and impairment of cerebral and systemic blood flow. These afferent signals and circulating inflammatory mediators might induce neuroinflammation, microglial activation, neuronal death, and cerebral oedema, contributing potentially to the development of ARDS-associated encephalopathy