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Background
Frontobasal skull injuries, while accounting for a relatively small portion of head trauma patients, can lead to a spectrum of complications, including CSF leak, encephaloceles, orbital apex syndromes, cranial nerve palsies, and vascular injuries. Although rare, frontobasal skull injuries can involve critical neurovascular structures, resulting in acute and subacute vascular complications with various clinical outcomes, ranging from spontaneously resolved mild intimal injury to fatal ruptured pseudoaneurysm and vessel transection. Detecting these vascular injuries can be difficult, due to subtle radiological findings, complex skull base anatomy, and different timelines for symptom presentation. Failure to recognize and address these vascular complications promptly can lead to significant morbidity and mortality. This educational exhibit will focus on the anatomy and pathophysiology of frontobasal skull fractures and related vascular complications, as well as imaging techniques for evaluating these injuries.

Educational Goals / Teaching Points
In this educational exhibit, we will emphasize the anatomy and fracture patterns of the frontobasal skull. We will provide a case-based review of arterial and venous vascular complications from frontobasal injuries.

Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
Skull base fractures have been reported in 3.5–24% of overall head fractures and 4% of overall head injuries. Motor vehicle collisions (MVCs) are the most common cause of skull base injury, with most injuries from direct impact with rigid objects. Vascular injuries have been reported in 8.5% of cases of blunt skull base fractures, with a high association of fractures involving the sella turcica-sphenoid sinus complex and petrous carotid canal. Vascular complications from frontobasal trauma involving ECA branches and the ICA may result in extravasation/laceration, dissection, pseudoaneurysm, or arteriovenous fistula. The various onset and insidious presentation of these vascular complications often make them challenging to identify clinically and radiologically. Findings on the initial CTA assessment can be subtle and may result in delayed diagnosis if not recognized. With the advent of high-resolution CT imaging, the diagnostic sensitivity for detecting skull fractures has been greatly enhanced. CT or MR angiograms are noninvasive techniques for evaluating vascular injuries, offering viable alternatives to digital subtraction angiography (DSA). In cases where ambiguity arises, vessel wall imaging can provide supplementary diagnostic value for assessing vascular dissections and pseudoaneurysms in patients suspected of having vascular injuries.

Conclusion
Frontobasal trauma can result in vascular complications with immediate and delayed clinical and radiological manifestations. Understanding the anatomy, mechanism of injury, pathophysiology of vascular abnormalities, and advantages and limitations of available imaging modalities can help radiologists to make an accurate and timely diagnosis to guide clinical management.