Introduction
Weakening and eventual rupture of the carotid artery is one of the most devastating complications of advanced head and neck cancer treatment. The clinical signs and symptoms related to compromise of the carotid are referred to as carotid blowout syndrome (CBS). Although CBS represents a relatively uncommon complication of head and neck therapy, awareness of this entity is paramount, since it can be rapidly fatal without prompt diagnosis and intervention. Notably, CBS may involve the common, internal, and/or external carotid arteries.
Risk factors for CBS include radical neck resection, lack of supporting healthy tissues, prior radiation therapy, radiation necrosis, carotid exposure, wound infection, pharyngocutaneous fistula, and recurrent or persistent carcinoma. Depending on the acuity of the clinical presentation, computed tomographic angiography (CTA) is a suitable modality for evaluating asymptomatic or mildly symptomatic CBS. The most common associated CTA findings include soft tissue necrosis, exposed artery, viable tumor, pseudoaneurysm, and contrast extravasation. On catheter angiography, the lumen of an exposed artery may appear normal, but overlying involvement can be readily detected by CTA. On the other hand, the gold standard for identification of luminal abnormalities of the exposed artery is catheter angiography. As surgical management in the carotid blowout scenario is often difficult or impossible, endovascular treatment such as coil embolization (deconstructive management) or use of a covered stent grafts (reconstructive management) has supplanted surgical treatment in the establishment of immediate hemostasis ( Fig. 49.1 ).
The carotid artery and its branches receive most of their blood supply from the vasa vasorum in the adventitia. Compromise of the carotid artery can therefore occur not only secondary to direct involvement of the vessel wall but also as a result of vessel wall ischemia secondary to direct damage to the vasa vasorum. As such, a variety of imaging findings demonstrating exposure of the vessel to a variety of insults indicates eventual carotid blowout if action is not taken. These insults include overlying soft tissue deficiency, encasement by tumor, and/or exposure to infection. CBS has been classified into three stages: (I) threatened, (II) impending, and (III) acute carotid blowout ( Fig. 49.2 ), representing a progression of presentations ranging from exposure of the vessel at one end of the spectrum to frank hemorrhage at the other.
Temporal Evolution: Overview
Threatened (type I) carotid blowout is defined as physical examination or imaging findings indicating carotid exposure without evidence of active bleeding. Perhaps the most important point to understand about this first step in the classification is that despite the absence of bleeding, impending hemorrhage is inevitable unless action is taken to protect the vessel ( Figs. 49.3 and 49.4 ). Impending (type II) carotid blowout (sentinel hemorrhage) is defined as transient hemorrhage that resolves spontaneously or with simple packing or pressure ( Fig. 49.5 ). Acute (type III) carotid blowout represents profuse hemorrhage that cannot be controlled by packing or pressure and is rapidly fatal if not treated immediately. Of note, hemorrhage may occur through either the skin or the mucosa and only rarely as an expanding hematoma ( Fig. 49.6 ).
