Computed tomography is the most reliable imaging modality for detecting and determining the extent of nasopharyngeal carcinoma. Indeed, CT, with its view of the deep tissue planes, may detect a lesion that is predominantly submucosal and without mucosal abnormality and that might be missed on a fiberoptic examination.
The hallmark of nasopharyngeal carcinoma is deep infiltration of surrounding tissues. This is manifest on CT by obliteration (asymmetry) of the parapharyngeal space, carotid sheaths, and retropharyngeal space. Obliteration of the parapharyngeal space is a sign that the pathologic process is virulent enough to breach the pharyngobasilar fascia and thus have free access to spread anywhere from the base of the skull to the oropharynx within the parapharyngeal space. On CT scans, such extension is evident by obliteration of the normal fatty density that surrounds the airway, deep musculature, and vessels. Nasopharyngeal malignancies may bulge into the airway or distort its normal superficial contours.
Intracranial extension of a nasopharyngeal tumor is almost always related to destruction of the middle cranial fossa floor. The tumor may grow directly through the skull base or follow the carotid sheath and produce a bonv defect in the region of the foramen lacerum. This mode of spread often results in cranial nerve deficits.
Carcinoma of the nasopharynx frequently metastasizes to the regional lymph nodes on one or both sides of the neck. On CT scans, lymph node extension to the highest jugular and lateral retropharyngeal nodes is manifest by obliteration of the tissue planes around the carotid sheath and just under the lateral pharyngeal recess.
Although invasive inflammatory lesions (mucormycosis, malignant otitis externa) may produce a CT appearance simulating that of a nasopharyngeal carcinoma, the clinical circumstances usually indicate the appropriate diagnosis.
The adenoids represent a portion of the large circle of lymphatic tissue surrounding the oral respiratory passageway at the level of the posterior tongue and the tonsils. The amount of adenoid tissue within the nasopharynx varies greatly among individual patients. Younger persons tend to have larger amounts that often fill the entire pharyngeal recesses and, not infrequently, almost the entire airway. Hypertrophied or inflamed adenoids can produce ominous nasopharyngeal masses on both physical examination and CT scans. However, unlike malignancies and aggressive inflammatory lesions that cross the pharyngobasilar fascia, hypertrophied adenoid masses do not alter the symmetry of the deep tissue planes.
Juvenile Nasopharyngeal Hemangiofibromas
Juvenile nasopharyngeal hemangiofibromas are highly vascular, locally invasive, nonencapsulated tumors that occur almost exclusively in adolescent males. Clinical symptoms include severe recurrent epistaxis, nasal obstruction, facial deformity, and nasal speech. The tumor begins in the nasopharynx and progressively increases in size, eventually eroding the anterior structures, obstructing the nasal passages, and entering the maxillary sinuses on one or both sides.
Plain lateral radiographs demonstrate a variable-sized nasopharyngeal mass that typically causes anterior bowing of the posterior wall of the ipsilateral maxillary antrum (anterior-bowing sign). Although often considered pathognomonic of a juvenile nasopharyngeal heman-giofibroma, an identical appearance can occur with other slow-growing noninvasive lesions involving the retro-maxillary region (lymphoepithelioma, schwannoma, fibrous histiocytoma). On CT, the enhancing nasopharyngeal mass extends into the pterygopalatine fossa and sphenoid sinus.
Angiography remains the most accurate means of establishing a definitive radiographic diagnosis of juvenile nasopharyngeal hemangiofibroma. Depending on the size of the neoplasm and in what direction extension has occurred, blood supply to the tumor may also be derived from the internal carotid system and from muscular branches of the vertebral arteries. The angiographic appearance is characteristic, with dilated nodular tumor vessels from a hypertrophied internal maxillary artery feeding the densely hypervascular lesion.
Surgical resection of juvenile nasopharyngeal hemangiofibroma is considered the therapy of choice in those lesions without intracranial involvement. Because the tumor is such a vascular lesion, preoperative angiographic embolization is often used to significantly reduce intraoperative blood loss.