A dog with squamous cell carcinoma in the middle ear

Abstract

An 8-year-old, castrated male golden retriever was referred for lethargy and inappetance. Severe pain was elicited on palpation of the left temporomandibular joint region. Computed tomography revealed aggressive bone destruction of the left bulla. Squamous cell carcinoma was diagnosed. Malignant tumor in the canine middle ear is rare.

An 8-year-old, 43-kg, castrated male golden retriever was presented to the Western College of Veterinary Medicine with a week-long history of lethargy and inappetance. The dog had been treated intermittently for idiopathic pericardial/pleural/abdominal effusion for 2 y. Previous treatment included pericardiocentesis followed by pericardial fenestration. Once pericardial fenestration had been performed, pericardial effusion had not recurred for 10 mo. The dog had also been administered anti-inflammatory and anti-bacterial/fungal ear drops for otitis externa for unknown periods.

Case description

On the physical examination, severe pain was elicited on attempts to open the mouth. Pain was also evident during palpation of the region of the left tympanic bulla and left temporomandibular area. Regional lymph nodes were normal in size on palpation. There was no evidence of fluid accumulation or other abnormalities on thoracic and abdominal radiographic or ultrasonographic examination. Complete blood counts revealed mild nonregenerative anemia and a serum chemistry panel was within normal reference intervals.

The dog was anesthetized with hydromorphone (Hydromorphone injection USP; Sandoz, Quebec), 0.1 mg/kg body weight (BW), IV, as a premedication followed by propofol, (Rapinovet; Schering-Plough Animal Health, Quebec), 0.7 mg/kg BW, IV, and diazepam (Diazepam injection USP; Sandoz, Quebec), 0.4 mg/kg BW, IV, as induction, and maintained with isoflurane (IsoFlo; Abbott Laboratories, Saint-Laurent, Quebec). Under anesthesia, otoscopic examination was performed. The left vertical ear canal was unremarkable in appearance. No masses were evident within the left horizontal ear canal; however, the canal was collapsed due to extraluminal compression. No tympanic membrane was evident, but a structure resembling an ossicle could be visualized against a gray mass medial to the ear canal. A computed tomography (CT) examination was performed to evaluate the extent of the lesion. Extensive destruction of the left bulla (Figure 1), as well as of a portion of the adjacent mandibular condyle and the base of the zygoma, was evident. After the CT examination, left ventral bulla osteotomy was performed, revealing a 4-cm diameter soft tissue mass on the ventral aspect of the tympanic bulla. The bulk of this mass was removed and submitted for histopathological examination. Aerobic and anaerobic cultures were also taken. The mass was invading the skull and dorsal aspect of the bulla. In order to avoid causing neurological complications, curettage of these areas was not performed.

Figure 1.

Computed tomographic images show severe bone destructive lesion with a central focus on the left tympanic bulla (arrows).

On histopathological examination, the tumor was found to be composed of multiple, irregularly anastomosing sheets of highly pleomorphic, neoplastic squamous cells with variable incomplete maturation and multiple large foci of keratinized cells (Figure 2A). These cells had a variable N:C ratio with variable amounts of cytoplasm that ranged from basophilic and finely granular to eosinophilic and glassy. Large round and indented nuclei were present with 1–2 markedly enlarged, variably shaped nucleoli. Marked anisocytosis and anisokaryosis were seen and approximately 7 mitotic figures were found per 10 high power fields. Considering these findings, a definitive diagnosis of squamous cell carcinoma (SCC) was made (Figure 2B). No organisms were detected by histopathological or cultural examination.

Figure 2.

Histopathology of the mass resected from the left tympanic bulla. Hematoxylin and eosin stain. A — Multiple foci of keratinized cells (*) are seen. A — densely proliferating area is also seen in the right half. Magnification 100×. Bar = 160 μm. B — Magnified view of Figure 2A. Several mitotic figures are seen (arrow). Magnification 1000×. Bar = 16 μm.

Postoperative analgesia included hydromorphone (Hydromorphone inj USP; Sandoz, Quebec), 0.05 mg/kg BW, IV, q4h; ketamine (Vetalar, Bioniche Animal Health Canada, Belleville, Ontario), 1.5 mg/kg BW/h, IV; meloxicam (Metacam injection; Boehringer Ingelheim, Burlington, Ontario), 0.1 mg/kg BW, SC, q24h; and Fentanyl patch (Ran-Fentanyl Transdermal System; Ranbaxy Pharmaceuticals Canada, Mississanga, Ontario), 2.2 mg/kg BW/h, transdermally. A gradual improvement in appetite was observed. Eight days following surgery, radiation therapy with a palliative intent protocol was begun (800 cGy × 3 fractions, on 0, 7, and 21 days, using Theratron 780 cobalt-60 (Atomic Energy of Canada, Mississauga, Ontario). A mild external otitis with erythema (Veterinary Radiation Therapy Oncology Group acute radiation morbidity scoring scheme score 1) was present at day 21 after the start of radiation therapy. No other side effects of radiation were seen. Two weeks after completion of radiation therapy, the dog developed a left bacterial otitis externa and was treated with meloxicam (Metacam; Oral Suspension, Boehringer Ingelheim), 0.1 mg/kg BW, PO, q24h, tramadol (Tramadol; PCCA, London, Ontario), 2.2 mg/kg BW, PO, q12h, and topical otic anti-inflammatory, antifungal, and antibacterial medication (Surolan; Merial Canada, Princeville, Quebec), 6–8 drops, into his left ear, q12h. These medications were continued until the dog was euthanized.

After the radiation therapy was completed, the dog’s appetite and energy level remained good for 70 d, and the dog did not show signs of pain which were observed at the first presentation. However, 70 d after the end of the radiation therapy, the dog was presented to the WCVM due to lethargy and inappetance. Thoracic radiographs revealed multiple nodules in his lung and a slight amount of thoracic fluid accumulation. About 90 mL of thoracic fluid was collected and identified as a nonseptic exudate. The nodules were considered likely to be metastatic lesions, and the dog was sent home. Seventy-six days after the last radiation treatment, the dog was euthanized due to poor prognosis. Postmortem examination was offered but declined by the owner.

Discussion

Tumors of the ear are rarely seen in dogs, but the external ear canal is the most common site of origin (1). Tumors originating from the middle ear are quite rare (2–4), the most common being SCC (5).

Typical clinical signs include aural discharge, odor, pruritus, local pain, and neurological abnormalities, such as Horner’s syndrome or vestibular signs (1,2,6). Neurological signs are seen in only 10% of dogs with malignant ear canal tumors (1). In this dog, the only clinical signs that the owner noted were lethargy and inappetance. On physical examination, severe pain when attempting to open the mouth was the most prominent finding. There are many potential differentials to be considered including retrobulbar abscess, retrobulbar tumor, temporomandibular joint disease, and masticatory muscle myositis. Because the clinical signs of malignant ear tumors are nonspecific, diagnosis can be delayed. Typically, SCC is a locally invasive tumor (1,7); the tumor in this dog was invading tissues adjacent to the bulla during the surgery, and was removed incompletely. As a result, temporomandibular joint involvement was the most likely source of the pain on opening the dog’s mouth.

In this dog, the horizontal ear canal was compressed from the outside and not obviously involved with the tumor. During surgical exploration, the tumor appeared to have arisen from the tympanic bulla or possibly the auditory tube. By contrast, most feline nasopharyngeal polyps extend from the auditory tube into the middle ear (8), and one author also reported nasopharyngeal polyps of the middle ear in 5 dogs (9). However, the auditory tube is lined with columnar respiratory epithelium, thus is unlikely to be the source of an SCC in this case (10,11). On histopathological examination, the tumor dissected from the middle ear contained multifocal areas of necrosis. On the CT examination the bulla was almost completely obliterated, suggesting that the point of origin was the middle ear or distal portion of the external ear canal. These findings all suggest that the tumor in this dog most likely originated within the tympanic bulla.

Many reports have noted that cases of external ear canal tumors are usually accompanied by concurrent superimposed bacterial or fungal infection (1,2,12–14). This dog had a past history of otitis externa and had been treated with ear drops for otitis externa at the first presentation. Thus, the relationship between the SCC and otitis externa in this dog is difficult to determine.

The owner declined curative radiation therapy and elected palliative treatment for relief of pain only. Curative radiation therapy has been shown to be an effective primary or adjunctive therapy to cure or control tumors for dogs with malignant ear tumors and human patients with SCC in the middle ear (15–17). In contrast to the goal of curative radiation therapy, the goal of palliative radiation therapy is relief of pain, not extension of survival. Pain relief was achieved for a period of 70 d in this dog.