Brain-lung Interaction in Neurotrauma in COVID-19 Patients

Abstract

The recently described coronavirus (SARS-CoV-2) has produced a series of pathological changes after infection of the human body. A significant percentage of infected critically ill patients with COVID-19 will require multiple intensive care strategies to give appropriate support to increase the possibility of favorable evolution. The new coronavirus could invade using the respiratory mucosa and to infect various cell types successively creating a severe inflammatory response. Patients with cerebral neurotrauma have elements associated with the primary and secondary lesions. Lung injury impact brain with hypoxia, hypercapnia, hypocapnia, mediators release, presence of neurotoxic factors, and endothelial activation. On the other hand, brain injury impacts lungs due to increase in intracranial pressure (ICP). There is development of neuroinflammatory phenomena, the activation of sympathetic nervous system, and the presence of intense dopaminergic activity through the hypothalamic-pituitary-adrenal axis. Studies have demonstrated injury at the ultrastructural level in type II pneumocytes after traumatic brain injury.