Brain Shock—Toward Pathophysiologic Phenotyping in Traumatic Brain Injury

Severe traumatic brain injury (TBI) is a heterogeneous pathophysiologic entity where multiple interacting mechanisms are operating. This viewpoint offers an emerging, clinically actionable understanding of the pathophysiologic heterogeneity and phenotypic diversity that comprise secondary brain injury based on multimodality neuromonitoring data. This pathophysiologic specification has direct implications for diagnostic, monitoring, and therapeutic planning. Cerebral shock can be helpfully subanalyzed into categories via an examination of the different types of brain tissue hypoxia and substrate failure: a) ischemic or flow dependent; b) flow-independent, which includes oxygen diffusion limitation, mitochondrial failure, and arteriovenous shunt; c) low extraction; and d) hypermetabolic. This approach could lead to an alternative treatment paradigm toward optimizing cerebral oxidative metabolism and energy crisis avoidance. Our bedside approach to TBI should respect the pathophysiologic diversity involved; operationalizing it in types of “brain shock” can be one such approach.