A 71‐year‐old man with excessive alcohol consumption complained of a 2‐week history of left proptosis. Despite progressive visual deterioration for 2 years, he did not receive treatment. His past medical and family history was unremarkable. Physical examination showed 9‐mm proptosis and a firm, solid mass at the lateral aspect of the left orbit. Brain magnetic resonance imaging (MRI) revealed a 31 × 28 × 31‐mm vividly enhanced, left orbital mass with high vascularity and involvement of the left temporalis muscle (Fig. a), causing proptosis of the left eye. Blood chemistry revealed the following: white blood cell count, 8480/μL; hemoglobin level, 15 g/dL; platelet count, 126 × 103/μL; serum albumin level, 4.45 g/dL; serum bilirubin level, 0.82 mg/dL; serum aspartate aminotransferase level, 133 IU/L; serum alanine aminotransferase level, 53 IU/L; and prothrombin time‐international normalized ratio, 1.03. Test results for serum hepatitis B surface antigen and hepatitis C antigen were negative. Orbital mass biopsy revealed metastatic hepatocellular carcinoma (HCC), confirmed on histology (Fig. a,b) and immunohistochemistry (Fig. c,d). Abdominal computed tomography showed multiple huge HCC masses with central necrosis in the right lobe and direct tumor invasion of the inferior vena cava (Fig. b). The serum alpha‐fetoprotein level was 8894 ng/mL (normal range: 0–15). A total of 45 Gy radiation was administered over 15 days to relieve the symptoms of orbital metastasis. However, the patient did not show improvement and died within 2 months.1(a) Contrast MRI revealed a left orbital mass with high vascularity and bone destruction on T1‐weighted imaging (white arrow), causing left eye proptosis. (b) Abdominal computed tomography revealed multiple hepatocellular carcinoma with inferior vena cava invasion (black arrow).2(a and b) Diffuse cluster of polygonal cells with pale, eosinophilic cytoplasm and vesicular nuclei (HE staining, at 100× and 200× magnification). The cells were positively stained for hepatocyte‐specific antigen (c, ×200) and arginase‐1 (d, ×200).Orbital metastasis from HCC is rare. Only 10 patients with orbital metastasis as the first ocular symptom before detection of the primary lesion have been reported. The mechanism of orbital metastasis from HCC is unclear. Metastasis of HCC is known to occur via the hematogenous route, mainly through the inferior vena cava. Because the orbit does not have lymphatic vessels, metastasis is thought to occur primarily through the bloodstream, which is known to occur through the Batson vertebral venous plexus. The Batson venous plexus in the epidural space does not have valves and is connected to the pelvic veins, thoracic veins, and azygos vein. When the pressure in the thoracic and abdominal cavity is increased, reversal of blood flow can cause cancer to spread to the skull, sinus, and orbit through the Batson venous plexus. Histologically, the diagnosis of HCC is based on the trabecular pattern of polygonal cells with large nuclei and granular acidophilic cytoplasm but shows similar architecture in renal cell carcinoma. Primary tumors can be distinguished by immunohistochemical staining for hepatocyte‐specific antigen, anti‐cytokeratin, alpha‐fetoprotein, and arginase‐1. Palliative radiation is the only available treatment for symptom relief in the treatment of orbital metastasis from HCC, but the prognosis is poor and the mean survival time is 8.1months after the diagnosis of extrahepatic metastasis from HCC. Histological and immunohistochemical studies to determine the primary site of cancer may be useful for evaluating treatment and prognosis in patients with an orbital mass.
Journal of Gastroenterology and Hepatology – Wiley
Published: Jan 1, 2018
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