Traumatic brain injury (TBI) affects over 10 million people annually and is induced by a mechanical force to the head. The subsequent injury is focal, diffuse, or a combination of both. Following a focal TBI, astrocytes become reactive and form a border that is thought to prevent blood leakage from broken vessels reaching the healthy surrounding brain. However, it remains unknown whether the blood brain barrier (BBB) is repaired on vessels damaged in the injury. In contrast, blood vessel breakage is rare in diffuse mild TBI (mTBI), but BBB impairment is abundant. Our lab previously demonstrated that, in the case of diffuse mTBI, astrocytes fail to assemble a protective border or to repair the BBB, leading to continual leakage of blood-borne factors into surrounding tissue even months after the injury. BBB disruption is linked to numerous neurodegenerative disorders; thus, it is of interest to have tools to assess BBB damage in the context of TBI to determine potential therapeutic targets. In the present study, we test the applicability of tools from other fields in a novel context: BBB and TBI. We show that mice expressing a green fluorescent protein (GFP) tag on the tight junction protein zona occludens 1 (ZO-1) can be employed to assess BBB changes after injury. We further demonstrate that, while protein cross-linking with paraformaldehyde (PFA) fixation frequently renders BBB protein antigens unrecognizable by antibodies, a 3% glyoxal fixation protocol allows for effective visualization and quantification of BBB and vasculature proteins after TBI using immunohistochemistry. Finally, we show that peripheral injection of the small, fluorescently-tagged molecule cadaverine can be used to reveal BBB damage several weeks after focal stabwound injury, which has not been previously reported.