Capillary stalling after traumatic brain injury: an emerging microcirculatory contributor to secondary brain injury.
- 1Department of Clinical Medicine, North Sichuan Medical College, Nanchong, Sichuan, China.
- 2Department of Emergency Medicine, The General Hospital of Western Theater Command, Chengdu, Sichuan, China.
Abstract
Secondary brain injury after traumatic brain injury (TBI) has traditionally been understood and managed through the lens of intracranial pressure, cerebral perfusion pressure, and global cerebral blood flow. Yet a substantial proportion of patients continue to exhibit persistent tissue hypoxia and metabolic crisis even when these macrocirculatory parameters appear adequately controlled. Capillary stalling-the transient or sustained interruption of red blood cell transit within individual or focal capillary networks-may represent an under-recognized microcirculatory disorder that conventional macrovascular monitoring cannot capture. This review synthesizes evidence supporting capillary stalling as a potentially distinct and reversible component of post-traumatic microvascular failure. We examine candidate mechanisms of capillary flow interruption after TBI, including endothelial injury and glycocalyx disruption, leukocyte plugging, pericyte contraction, platelet activation and microthrombosis, red blood cell dysfunction, and edema-associated extravascular compression. These mechanisms can generate marked capillary flow heterogeneity, impair oxygen extraction, and contribute to metabolic crisis, neuroinflammation, and secondary neuronal injury. We further discuss why conventional bedside monitoring-including intracranial pressure, cerebral perfusion pressure, global cerebral blood flow, brain tissue oxygenation, and microdialysis-may fail to detect capillary-level flow abnormalities, and we review established and emerging detection strategies from experimental two-photon microscopy to clinical surrogates. Finally, we evaluate potential microcirculation-targeted therapeutic avenues. Direct evidence of capillary stalling in human TBI remains limited; accordingly, it should currently be viewed as a biologically plausible and testable contributor to secondary brain injury rather than an established dominant driver.
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BibTeX
@article{lei2026capillary,
title = {{Capillary stalling after traumatic brain injury: an emerging microcirculatory contributor to secondary brain injury.}},
author = {Xiaolong Lei and Yan Yang and Xiaokun Yang and Kai Tao},
journal = {Frontiers in neurology},
year = {2026},
month = oct,
doi = {10.3389/fneur.2026.1971528},
url = {https://europepmc.org/article/MED/42903673},
note = {CC BY},
}
RIS
TY - JOUR
TI - Capillary stalling after traumatic brain injury: an emerging microcirculatory contributor to secondary brain injury.
AU - Xiaolong Lei
AU - Yan Yang
AU - Xiaokun Yang
AU - Kai Tao
PY - 2026
DA - 2026/10/06
JO - Frontiers in neurology
DO - 10.3389/fneur.2026.1971528
UR - https://europepmc.org/article/MED/42903673
AB - Secondary brain injury after traumatic brain injury (TBI) has traditionally been understood and managed through the lens of intracranial pressure, cerebral perfusion pressure, and global cerebral blood flow. Yet a substantial proportion of patients continue to exhibit persistent tissue hypoxia and metabolic crisis even when these macrocirculatory parameters appear adequately controlled. Capillary stalling-the transient or sustained interruption of red blood cell transit within individual or focal capillary networks-may represent an under-recognized microcirculatory disorder that conventional macrovascular monitoring cannot capture. This review synthesizes evidence supporting capillary stalling as a potentially distinct and reversible component of post-traumatic microvascular failure. We examine candidate mechanisms of capillary flow interruption after TBI, including endothelial injury and glycocalyx disruption, leukocyte plugging, pericyte contraction, platelet activation and microthrombosis, red blood cell dysfunction, and edema-associated extravascular compression. These mechanisms can generate marked capillary flow heterogeneity, impair oxygen extraction, and contribute to metabolic crisis, neuroinflammation, and secondary neuronal injury. We further discuss why conventional bedside monitoring-including intracranial pressure, cerebral perfusion pressure, global cerebral blood flow, brain tissue oxygenation, and microdialysis-may fail to detect capillary-level flow abnormalities, and we review established and emerging detection strategies from experimental two-photon microscopy to clinical surrogates. Finally, we evaluate potential microcirculation-targeted therapeutic avenues. Direct evidence of capillary stalling in human TBI remains limited; accordingly, it should currently be viewed as a biologically plausible and testable contributor to secondary brain injury rather than an established dominant driver.
SN - 1664-2295
ER -