History
An 8-year-old 22.8-kg (50.2-lb) castrated male German Wirehaired Pointer was examined at the Department of Oncology of the Animal Health Trust for restaging 3 months after incomplete surgical resection of a large hepatocellular carcinoma (HCC) that originated from the dog's left medial hepatic lobe. Prior to that surgery, the dog had not had any evidence of HCC metastasis detected on thoracic or abdominal CT (not shown) but had previously undergone complete excision of a cutaneous mast cell tumor from the preputial area.
Findings on the 3-month follow-up physical examination for restaging were unremarkable, and results of a CBC and serum biochemical analyses were within reference limits. General anesthesia was induced, and CT of the neck, thorax, and abdomen was performed with a 16-row multidetector systema before (not shown) and after (Figure 1) administration of a contrast medium (iopamidol, 300 mg of iodine/mL; total patient dose, 45 mL; IV).
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Diagnostic Image Findings and Interpretation
In transverse plane postcontrast CT images, a well-defined soft tissue-attenuating mass was identified just cranial to the thoracic inlet at the levels of C6 and C7 (Figure 2) The mass appeared round (25 mm in diameter), discrete, and heterogeneous and had poor contrast medium enhancement. The dog's external jugular veins were mostly symmetric and equal in diameter without evidence of congestion, despite the mass occupying most of the intraluminal diameter of the right external jugular vein at 1 site. Adjacent structures appeared unaffected, displaying no mass effect. Results of thoracic and abdominal CT were unremarkable, with no evidence of local recurrence of the previously resected HCC.
The presence of a discrete soft tissue mass led to a high suspicion of neoplasia. Differential diagnoses considered on the basis of findings from diagnostic imaging included hemangioma, hemangiosarcoma (HSA), leiomyoma, leiomyosarcoma, and carotid body tumor. Secondary thrombus formation was considered as a potential component of the intravascular portion of the mass.
Transcutaneous ultrasonographyb revealed a well-defined, heterogeneously echogenic, irregularly spheroidal, expansile mass that extended 1 cm caudally in the lumen of the right external jugular vein. Findings on transcutaneous power Doppler ultrasonography depicted a patent right jugular vein (Figure 3) An ultrasonographically guided fine-needle aspirate sample was obtained from the extraluminal portion of the mass; however, results of cytologic examination were nondiagnostic, with a poorly cellular sample, predominance of free erythrocytes, and a single small aggregate of poorly preserved mesenchymal cells.
Treatment and Outcome
The dog underwent surgical ligation and resection of the caudal two-thirds of the right external jugular vein. Results of histologic evaluation were consistent with incompletely excised HSA, and results of immunohistochemical stainingc,d confirmed that the mass had an endothelial origin.1 Therefore, the dog received adjuvant chemotherapy with doxorubicin (30 mg/m2, IV, q 21 d for 4 treatments).
Four months after surgery, the dog was restaged with CT of the neck, thorax, and abdomen (not shown) and had no evidence of tumor recurrence (local or metastatic). Eight months after surgery, the dog was returned for evaluation of progressive weight loss and hyporexia. The dog's body weight was 21.2 kg (46.7 lb), and abdominal CT revealed multiple well-defined mass lesions throughout the liver. The mass lesions appeared heterogenous and hypoattenuating in precontract CT images and had poor contrast enhancement on postcontrast CT images, consistent with poorly vascularized or partially fluid-filled masses. The masses ranged in diameter from approximately 1 to 15 cm. Results of CT of the neck and thorax were unremarkable. The owner declined sampling of the lesions and elected palliative treatment with prednisolone (1.0 mg/kg [0.45 mg/lb], PO, q 24 h). Although it was not possible to determine the cause of these findings, differential diagnoses included metastatic lesions from HSA, HCC, or, less likely, mast cell tumor.
Comments
Early detection of HSA is difficult because, for a sustained period of time as the tumor grows, its biological behavior is often silent or lacks specific clinical signs that would prompt diagnostic imaging.2 Clinical signs are most commonly associated with advanced disease and include weakness or collapse associated with hemorrhage from ruptures in the primary solid tumor.3 In the dog of the present report, HSA of the right external jugular vein was diagnosed on the basis of results of histologic evaluation, including immunohistochemical staining, of the resected jugular mass incidentally identified with CT used in restaging 3 months after incomplete resection of HCC from the dog's left medial hepatic lobe. Primary intravascular neoplasia of venous origin is rare in dogs; however, leiomyosarcoma in the jugular vein has been described,4 and to our knowledge, the present report is the first to describe HSA arising from an external jugular vein in a dog.
Results of the 3-month follow-up physical and hematologic examinations of the dog in the present report identified no clinical abnormalities; however, use of CT allowed us to identify the venous mass and to verify that the mass had neither local nor metastatic spread detectable. Although the nature of the mass could not be defined from diagnostic imaging, the mass had poor contrast medium enhancement, similar to that described for splenic HSA5 and a uterine remnant HSA6 in dogs. Information obtained from CT was valuable in locating the mass, prompting further diagnostic procedures, and assisting in surgical planning.
Use of transcutaneous power Doppler ultrasonography allowed us to evaluate and confirm patency of the affected vein in the dog of the present report. In addition, ultrasonography was used to further investigate the mass, including obtaining an ultrasonographically guided fine-needle aspirate sample for cytologic examination.
Hemangiosarcoma is an aggressive malignant neoplasm in dogs and is derived from progenitor endothelial cells that originate from incompletely differentiated multipotent bone marrow-derived stem cells near or at the stage of endothelial commitment.7 These early endothelial precursor cells migrate from the bone marrow and into the peripheral vessels.8 Hemangiosar-comas represent about 2% (1,822/81,744) of all canine tumors and are most commonly reported to arise from vasculature of the spleen, liver, skin, subcutis, or right cardiac atrium or auricle.2,9 With the exception of the cutaneous form, HSA that has progressed to the point of detection in dogs typically has an aggressive biological behavior, and a study10 shows that affected dogs have a high tumor-related mortality rate (96% [100/104]) despite surgical or chemotherapeutic intervention because of development of clinical metastatic disease. Surgery is typically used for local control, and adjuvant chemotherapy has become a mainstay in HSA treatment for microscopic disease.2 The use of single-agent doxorubicin-based maximum tolerated dose chemotherapy provides a modest improvement in outcome, with median survival times in the range of 6 to 8 months.11 Dogs with HSA treated with protocols based on doxorubicin combined with vincristine and cyclophosphamide have similar survival times.12 The use of adjuvant metronomic chemotherapy is still debated.2
Acknowledgments
The authors declare that there were no conflicts of interest.
Footnotes
Brivo CT385, GE Healthcare, Chicago, Ill.
iU22 xMatrix-DS, Koninklijke Philips NV, Amsterdam, Netherlands.
Monoclonal mouse anti-human CD31, endothelial cell, clone JC70A, Dako, Glostrup, Denmark.
Polyclonal rabbit anti-human von Willebrand factor, Dako, Glostrup, Denmark.
References
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