The Carotid Body Tumor

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THE CAROTID BODY TUMOR

Introduction:

Among the nonchromaffin paragangliomas, the carotid body tumor is second in frequency to the glomus jugulare tumor. Despite the large number of published cases, these tumors are relatively uncommon. Several authors have suggested that the carotid body tumor represents a proliferative response of the normal organ to some unknown disturbance within the nervous system, rather than a true neoplasm. Bungeler (1952) suggested that this was some form of adaptive hyperplasia, which was produced by traumatic destruction of the cortical projection fields of the X nerve. In contrast to this hypothesis, is the realization that a significant number of these lesions undergo malignant transformation with metastasis, which establishes the carotid body tumor as a true neoplasm.

Study of the familial occurrence of chemodectomas has established a definite genetic influence in the development of these neoplasms. This hereditary factor is especially prominent in multicentric cases.

Saldana et al. (1973) found that chemodectomas were 10 times more frequent in high-altitude dwellers than in sea-level residents. They proposed that hypoxia, acting from birth, served as a stimulus for chemoreceptor tissue hyperplasia, which eventually led to tumor formation.

Epidemiology:

These tumors have been reported in all stages of life. There appears to be a slight predilection for women in the incidence of these tumors. There is no preferential laterality.

Clinical Manifestations:

Slow growth
Lateral cervical mass that is pulsatile
Superior & medial extension may produce a pharyngeal bulge with displacement of the tonsil, soft palate & uvula to the opposite side.
Rare extension into the nasopharynx.
Pain may occur; however, the vast majority of lesions are painless.
Dysphagia
Syncope with or without associated diaphoresis, nausea, trembling & blurred vision
Hoarseness
Dyspnea & Cough
Horner’s Syndrome

Differential Diagnosis: