Related Experiment Video
Updated: Apr 7, 2026
Effects of Blast-induced Neurotrauma on Pressurized Rodent Middle Cerebral Arteries
Published on: April 1, 2019
Lethal now or lethal later: The natural history of Grade 4 blunt cerebrovascular injury
Margaret H Lauerman1, Timothy Feeney, Clint W Sliker
1From the Divisions of Critical Care (M.H.L., T.F., B.R.B., A.L., R.T., M.B., T.M.S., D.M.S.), and Radiology (C.W.S., N.S.), R Adams Cowley Shock Trauma Center, University of Maryland School of Medicine, Baltimore, Maryland.
Insights
Grade 4 blunt cerebrovascular injury (BCVI4) poses a significant stroke risk, particularly in the internal carotid artery (ICA). Early anticoagulation assessment is crucial for managing BCVI4 stroke risk.
Area of Science:
- Trauma surgery
- Neurology
- Vascular surgery
Background:
- Grade 4 blunt cerebrovascular injury (BCVI4) is associated with a high stroke incidence.
- Limited understanding exists regarding the natural history and stroke pathophysiology of BCVI4.
Purpose of the Study:
- To investigate the natural history and stroke formation mechanisms in patients with Grade 4 BCVI.
- To determine stroke rates, mortality, and influencing factors in BCVI4.
Main Methods:
- Retrospective review of 82 patients with BCVI4 over 4 years.
- Analysis of BCVI4-related stroke rates, mortality, and stroke mechanisms.
- Examination of vessel changes and their correlation with stroke development.
Main Results:
- Stroke rate was 2.9% for vertebral artery BCVI4 and 70% for internal carotid artery (ICA) BCVI4.
- Stroke mechanisms included embolic, thrombotic, and combined types.
- ICA BCVI4 strokes involved recanalization and embolic mechanisms; 67% occurred within 10 hours of admission.
Conclusions:
- BCVI4 presents diverse stroke etiologies.
- Early risk-benefit assessment for anticoagulation/antiplatelet therapy is essential.
- Consider endovascular occlusion for contraindications; explore aggressive medical therapy to reduce stroke risk.
Background:
Grade 4 blunt cerebrovascular injury (BCVI4) has a known, significant rate of stroke. However, little is known about the natural history of BCVI4 and the pathophysiology of subsequent stroke formation.
Methods:
A 4-year review of patients with BCVI4 at the R Adams Cowley Shock Trauma Center was performed. Rates of BCVI4-related stroke, stroke-related mortality, and overall mortality were calculated. The relationship of change in vessel characteristics and BCVI4-related stroke was examined, as was the mechanism of stroke formation.
Results:
There were 82 BCVI4s identified, with 13 carotid artery (ICA) and 69 vertebral artery BCVI4s. BCVI4-related stroke rate was 2.9% in vertebral artery BCVI4 and 70% in ICA BCVI4 patients surviving to reimaging. Stroke mechanisms included embolic strokes, thrombotic strokes, and combined embolic and thrombotic strokes. Peristroke vessel recanalization and an embolic stroke mechanism were seen in 100% of ICA BCVI4-related strokes developing after admission. BCVI4-related stroke occurred within 10 hours of hospital admission in 67% of the patients with strokes. Contraindications to anticoagulation were present in most patients with BCVI4-related stroke developing after admission.
Conclusion:
Multiple etiologies of stroke formation exist in BCVI4. Early risk-benefit analysis for initiation of anticoagulation or antiplatelet agents should be performed in all patients with BCVI4, and the use of endovascular vessel occlusion should be considered in those with true contraindications to anticoagulation. However, more aggressive medical therapy may be needed to lessen BCVI4-related stroke development.
Level Of Evidence:
Prognostic study, level IV; therapeutic study, level V.
