Objectives: Spontaneous recanalization of a chronic total occlusion of the extra-cranial internal carotid artery is an under-reported clinical entity. This paper reviews the different etiologies of internal carotid artery occlusion, its natural course, as well as the significance and our recommendations for the management of spontaneous internal carotid artery recanalization. Methods: A review of literature on etiology, diagnosis, and treatment of internal carotid artery occlusion and recanalization was conducted. PubMed database was searched using the terms “internal carotid occlusion” and “recanalization”. Articles were reviewed and studies involving the management of internal carotid artery occlusion and spontaneous recanalization were included. We subsequently developed a management algorithm for chronic total occlusion of the internal carotid artery and spontaneous recanalization of such lesions based on the available evidence. Results: Common etiologies of chronic total occlusion of the internal carotid artery include carotid atherosclerotic disease, cardioembolic, and carotid dissection. Progression of an asymptomatic to symptomatic occlusion is estimated at 2–8% annually. Well-compensated patients can be asymptomatic. In others, clinical symptoms range from ipsilateral or global hypoperfusion to embolic stroke in some cases of spontaneous recanalization. Spontaneous recanalization occurs in 2.3–10.3% of patients but rarely results in a cerebrovascular event. Conclusions: Progression of an asymptomatic chronic total occlusion of the internal carotid artery to symptomatic is infrequent. The management algorithm of chronic total occlusion of the internal carotid artery and spontaneous recanalization of the internal carotid artery must be tailored to the patient based on symptoms, etiology of the lesion, imaging findings, surgical risk, and reliability for follow-up.

Objectives: The indication, timing, and choice of the treatment modality for penetrating aortic ulcers (PAUs) and intramural hematoma (IMH) are frequently challenging. This article reviews these pathologies and their relation to aortic dissection and proposes a diagnostic and treatment algorithm. Methods: A review of literature on diagnosis and treatment of PAU and IMH was conducted. The PubMed database was searched using the terms “penetrating aortic ulcer” and “aortic intramural hematoma”. Articles were reviewed and the studies involving diagnosis and management of PAU and IMH were included. We subsequently proposed a management algorithm for PAU and IMH based on available evidence. Results: PAU and IMH are distinct entities from aortic dissection, although they carry a significant risk of progression into dissection, aneurysm, and rupture. PAU and IMH originating in zone 0 of the aorta generally require surgical treatment. When the origin is beyond zone 0, a trial of medical therapy is recommended. Progression of disease on imaging studies, persistent uncontrolled pain, and certain high-risk features warrant surgery. High-risk features signaling risk of disease progression include PAU with IMH, PAU depth more than 10 mm, PAU diameter more than 20 mm, IMH thickness more than 10 mm, and maximum initial aortic diameter more than 40 mm. Conclusions: High-quality evidence regarding the treatment of PAU and IMH is lacking. These entities can have a malignant course when they are present with associated symptoms and/or when they have associated high-risk features on imaging. An aggressive surgical approach is necessary in that group of patients.