geboy veterinary madicine: papervet: Carotid body tumor in dog: A case report

Aortic body tumors are reported to occur 4 to 5 times more frequently than carotid body tumors in dogs (2,4). These tumors usually express neuroendocrine markers that can be detected by using immunohistochemical staining, such as neuron specific enolase (NSE), synaptophysin, and chromogranin A (4–6). Ultrastructurally, the cytoplasm of the tumor cells contains neurosecretory dense core granules (7).

Many carotid body tumors are malignant, in contrast to aortic body tumors (8), and occasionally metastasize to regional lymph nodes, lung, liver, pancreas, bone, and kidney (9–11).

We diagnosed a carotid body tumor in an 8-year-old, female, white puli dog. The owners observed that the dog became moody and inactive, and developed hoarseness. The dog was given long-acting antibiotics and a combined vitamin (A + D3 + E) injection. After this treatment, the dog’s physical status slightly improved. The dog was returned to the clinic after 37 d with the following signs: distress, hyperpnea, dyspnea, increased intra-ocular pressure (glaucoma) of the left eye, and bilateral dilation of the pupils. At the beginning of the clinical examination, the dog collapsed and was given oxygen after intubation. On physical examination, an extensive, firm mass surrounding the larynx was found, but the parotid, mandibular, and the retropharyngeal lymph nodes were normal. The owners opted for euthanasia.

Necropsy disclosed a 105- × 30-mm, firm, and multilobulated tumor in the left lateral laryngeal region (Figure 1). The swelling extended to the Y-shaped fusion of the linguofacial and maxillary veins forming the external jugular vein, but it was not associated with these veins. Medial to this branching, the tumor masked the bifurcation of the common carotid artery, the origin of the occipital, lingual, and facial arteries, and the vagosympathetic trunk. The tumor was not associated with the neighboring salivary glands. Caudal to the tumor, the common carotid artery was distended. The tumor was dark tan to purple, well circumscribed, and encapsulated. The cut surface revealed a greyish-red septate mass around the internal carotid artery, with multiple areas of hemorrhage and cystic degeneration (Figure 2).

Figure 1

Carotid body tumor (dotted line) in the dog as seen during autopsy. A: sternothyroid muscle, B: B: laryngeal prominence.

Figure 2

The cross-section of the common carotid artery (dotted line) and its relation with the tumor mass.

Histologically, the tumor tissue was divided into lobules by prominent branching trabeculae of connective tissue contiguous with the fibrous capsule, and many blood vessels were present. The cells were polygonal or oval, and they contained variable amounts of granular, slightly basophilic cytoplasm. Areas of spindle cells and giant cells with bizarre-shaped, double, and enlarged nuclei with prominent nucleoli were encountered (Figure 3). Nuclear anaplasia and hyperchromatism were seen, but mitotic figures were rare. Immunohistochemical evaluation utilized 4-μm paraffinembedded tissue sections and standard streptavidin-biotin indirect immunoperoxidase methods with a panel of commercially available mouse and rabbit anti-human primary monoclonal antibodies recognizing alpha-smooth muscle actin (DAKO Corp.), vimentin (HRP, DAKO Corp.), cytokeratin (MNF116, DAKO Corp.), desmin (DAKO Corp.), neuron-specific enolase (NSE, DAKO Corp.), synaptophysin (SYN, Biogenics Corp.), S-100 (DAKO Corp.), and Ki-67 (DAKO Corp.). The positive controls were feline pancreas (NSE, SYN) and canine skin (S-100). Negative controls included staining reactions in which the primary antibody was omitted.

Figure 3

Areas of spindle-shaped cells, with binucleate cells and enlarged nuclei with prominent nucleoli. Hematoxylin and eosin stain; magnification: Bar = 100 μm.

All tumor cells were negative for cytokeratin (MNF 116), desmin, S-100, and smooth muscle actin, and strongly positive for vimentin and synaptophysin. Some tumor cells also stained positively for neuron-specific enolase, and the number of Ki-67 positive cells was low. By electron microscopy, the neoplastic cells contained neurosecretory dense core granules (Figure 4). The location of the tumor and its morphological and immunohistochemical features pointed to the diagnosis of paraganglioma (carotid body tumor).

Figure 4

In the electron micrograph, characteristic chief cells possessed abundant dense core granules in the cytoplasm adjacent to the nucleus. Bar = 0.15 μm.

Having the pathological diagnosis, the clinical signs can be explained in a coherent way. The hoarse voice can be explained by the compression of the laryngeal nerves. Hyperpnea and dyspnea can be explained on the basis of the dysregulation of the chemoreceptors of the carotid body. In human patients with hypertonia or arteriosclerosis, collapse may result from volume changes of the carotid sinus, with activation of the stretch receptors and consequential downregulation of the blood pressure (12). Compression of the internal carotid artery also affects the tissues perfused by this artery on the same side, including the eye. The majority of the retinal blood supply arrives from the internal ophthalmic artery via the central retinal artery; therefore, the unilateral ocular signs were probably the result of retinal ischemia rather than glaucoma. The phenomenon is referred to as amaurosis fugax in human medicine (13).

Carotid body tumors are rare neoplasms that tend to splay the carotid bifurcation as they enlarge, and can extend along the internal carotid to the base of the skull. The paraganglioma is histologically similar to the normal carotid body, except that cell clusters tend to be larger and contain vascular areas and giant cells with bizarre-shaped nuclei, binucleation, and karyomegaly with prominent nucleoli. Nuclear pleomorphism and cellular hyperchromatism are common and should not be considered as the only indicator of malignancy (14). In fact, there are no clear histologic characteristics of malignancy, except for the presence of metastases, which were absent in the present case.

Footnotes

Dr. Deim’s current address is Central Veterinary Institute, Department of Mammalian Pathology, Budapest Tabornok u.2 1149 Hungary.

References

1.Johnson KH. Aortic body tumors in the dog. J Am Vet Med Assoc. 1968;152:154–160.

2.Hayes HM, Sass B. Chemoreceptor neoplasia: A study of the epidemiological features of 357 canine cases. Zentralbl Veterinarmed [A]. 1988;35:401–408.

3.Tillson DM, Fingland RB, Andrews GA. Chemodectoma in a cat. J Am Anim Hosp Assoc. 1994;30:586–590.

4.Kimura N, Sasano N, Yamada R, Satoh J. Immunohistochemical study of chromogranin in 100 cases of pheochromocytoma, carotid body tumour, medullary thyroid carcinoma and carcinoid tumour. Virchows Archiv A Pathol Anat Histopathol. 1988;413:33–38.

5.Brown PJ, Rema A, Gartner F. Immunohistochemical characteristics of canine aortic and carotid body tumours. J Vet Med A Physiol Pathol Clin Med. 2003;50:140–144. [PubMed]

6.Johnson TL, Zarbo RJ, Lloyd RV, Crissman JD. Paragangliomas of the head and neck: Immunohistochemical neuroendocrine and intermediate filament typing. Mod Pathol. 1988;1:216–223. [PubMed]

7.Kliewer KE, Cochran AJ. A review of the histology, ultrastructure, immunohistology, and molecular biology of extra-adrenal paragangliomas. Arch Pathol Lab Med. 1989;113:1209–1218. [PubMed]

8.Obradovich JE, Withrow SJ, Powers BE, Walshaw R. Carotid body tumors in the dog. Eleven cases (1978–1988). J Vet Intern Med. 1992;6:96–101. [PubMed]

9.Szczech GM, Blevins WE, Carlton WW, et al. Chemodectoma with metastasis to bone in a dog. J Am Vet Med Assoc. 1973;162:376–378. [PubMed]

10.Capen CC. Endocrine system. In: Jubb KVF, Kennedy PC, Palmer N, editors. Pathology of Domestic Animals. 4. San Diego, Calif: Acad Pr; 1993. pp. 345–347.

11.Callanan JJ, McNeil PE, Andersen TJ, Laird H. Metastatic aortic body tumour causing neck pain in a dog. J Small Anim Pract. 1991;32:525–528.

12.Kapoor WN, Karpf M, Wieand S, Peterson JR, Levey GS. A prospective evaluation and follow-up of patients with syncope. N Engl J Med. 1983;309:197–204. [PubMed]

13.De Schryver EL, Algra A, Donders RC, van Gijn J, Kappelle LJ. Type of stroke after transient monocular blindness or retinal infarction of presumed arterial origin. J Neurol Neurosurg Psychiatry. 2006;77:734–738. [PubMed]

14.Sander CH, Whitenack DL. Canine malignant carotid body tumor. J Am Vet Med Assoc. 1970;156:606–610. [PubMed]