Learning objective: Develop an algorithm for diagnosis and staging of thyroid tumours in dogs and adrenal tumours in dogs and cats. Understand rational application of different treatment modalities in different situations.
Cats with thyroid tumours typically present for clinical signs of hyperthyroidism, dogs for a palpable mass. Although dogs with thyroid tumours are rarely hyperthyroid, elevated T4 in a dog is almost certainly due to a thyroid tumour (rather than hyperplasia). Thyroid carcinoma represents the least common cause of feline hyperthyroidism. Once a thyroid tumour in a dog is palpable, it is almost certainly malignant. Because size and mobility is an important prognostic factor in canine thyroid tumours, early detection via routine neck palpation as part of regular physical examination should be emphasised in dogs. Carcinoma should be considered in hyperthyroid cats with extremely elevated T4, very large or fixed goitre. Screening for metastasis is warranted in cats with suspected thyroid carcinoma, and treatment with surgery or I 131 may be more effective than medical management, however the true best approach is not defined.
In evaluation of a dog with a suspected thyroid tumour, our general approach is as follows:
- Confirm cervical mass is of thyroid origin and assess resectability - thyroid origin can be confirmed with imaging (ultrasound or CT scan) and cytology, though cytology is not specific for malignancy (often thyroid carcinomas have few cytologic criteria of malignancy). Mobility is best assessed under heavy sedation or general anesthesia. If a thyroid tumour appears to be relatively fixed/immobile, contrast CT scan should be avoided if I 131 treatment is a possibility. Total T4 should be evaluated in every case (± TSH, free T4 if TT4 is low)
- Staging for metastasis - evaluation of local lymph nodes (LN) - generally submandibular and prescapular - is recommended. Cytology should be performed in all local LN, with excision for histopathology in any concerning for metastasis. Imaging (ultrasound or CT) may increase suspicion of LN metastasis but should not be considered a substitute for cytology. Thoracic imaging (CT is more sensitive but radiographs reasonable) ± abdominal imaging (ultrasound or CT) should also be performed.
- If tumour is mobile and there is no gross metastasis, surgery is recommended.
- If tumour is fixed/non-resectable and no gross metastasis, definitive radiation therapy (RT) is preferred, with I 131 considered next best option if external beam RT is not available. Chemotherapy (see below) may also be an option of I 131 is not available.
- If tumour is metastatic - I 131 can still be effective (risk of radiation pneumonitis or liver injury with diffuse pulmonary or hepatic metastasis), palliative external beam RT can be considered if significant clinical signs from primary tumour, or chemotherapy.
- Surgical excision of the affected thyroid gland is approached via a ventral midline cervical approach. The sternohyoid and sternothyroid muscles are bluntly separated on the midline and retracted laterally to expose the thyroid gland on either side of the trachea.
- The extracapsular technique is used for removal of thyroid tumours. The blood supply to the thyroid gland is via the cranial and caudal thyroid arteries. The cranial and caudal thyroid artery and vein, and any other large vessels associated with the tumor are ligated. Canine thyroid carcinomas can invade into or be adhered to adjacent tissues. The recurrent laryngeal nerve and vagosympathetic trunk (within the carotid sheath) are identified and spared if possible. The jugular vein, carotid artery, vagosympathetic trunk and laryngeal recurrent nerve can be sacrificed unilaterally with acceptable morbidity if required.
- The contralateral thyroid gland should be visualised at the time of surgery.
- Potential complications after thyroidectomyectomy include hemorrhage and anemia, hypothyroidism, laryngeal paralysis and megaesophagus.
Radiation therapy (RT):
- For non-resectable primary tumours, definitive RT results in median survival times of several years, though maximal tumour shrinkage can take months to >1 year. Adjuvant RT following surgery is commonly recommended to prevent local regrowth for incompletely excised tumours but there is limited information on effectiveness.
- Palliative RT for the primary is a reasonable option for dogs with metastatic disease or owners for whom definitive RT is not feasible. Many tumours will shrink, at least partially.
- I 131, where available, may be a more attractive option in dogs with metastatic disease because it has the potential to be effective against both the primary tumour and metastases. In dogs without metastasis, median survival time after I 131 is approximately 2 years, and with metastasis approximately 1 year. Use of I 131 as an adjuvant treatment following surgery is commonly done in humans but its true utility is not fully established in dogs. Scintigraphy is required prior to I 131 treatment to assess for uptake. If iodinated contrast has been performed, scintigraphy and I 131 treatment must be delayed for a minimum of 4 weeks (preferably 6–8 weeks).
- Hypothyroidism and myelosuppression can occur following I 131 treatment, and hypothyroidism can occur after external beam RT also.
- In dogs with unresectable or metastatic disease, responses to carboplatin, doxorubicin, and toceranib (Palladia) are reported. In my practice, toceranib is generally my first choice because it can be given long term if effective and well-tolerated. Use of adjuvant chemotherapy following surgery for high-risk tumours is often recommended but has not been thoroughly evaluated for effects on survival. Tumours considered high-risk are large tumours (>4–5 cm diameter likely to have higher metastatic risk), or those with lymph node metastasis.
Adrenal tumours are more common in dogs than in cats, and may be of cortical (adenoma/carcinoma) or medullary (phaeochromocytoma) origin. Animals may present for effects of products of functional adrenal tumours (hyperadrenocorticism, intermittent weakness or other signs due to catecholamine release, rarely weakness due to hypokalaemia from a mineralocorticoid secreting tumour), but non-functional adrenal tumours may have no clinical signs and be found incidentally on abdominal imaging for other concerns, or may present with abdominal pain or haemorrhage directly related to the tumour. Pre-operative diagnosis of adrenal tumours can be challenging, except in the case of obvious adrenal dependent hyperadrenocorticism. In small (<2 cm), incidentally diagnosed adrenal tumours, ‘watchful waiting’ is likely reasonable. Consideration should be given to screening for a primary tumour elsewhere, as metastasis to the adrenal glands can also occur. In larger adrenal tumours or those with vascular invasion, malignancy is more likely and further investigation is warranted. If possible, identification of functional tumours prior to surgery is desirable for appropriate planning for perioperative management. Staging with thoracic and abdominal imaging (CT preferred, otherwise thoracic radiographs and abdominal imaging) is indicated in any concerning adrenal mass to evaluate for vascular invasion and screen for metastasis. Testing for functional status should include assessment for hyperadrenocorticism and evaluation of urine catecholamine/metanephrines. Fine needle aspiration and cytology of adrenal masses in many cases can distinguish between the two main tumour types. There are potential risks with this procedure, however in the little published data available it overall seems safe.
The primary treatment for adrenal tumours is surgical excision. This can be achieved by open ventral midline laparotomy approach or via a retroperitoneal approach. For smaller adrenal masses without caval invasion, laparoscopic adrenalectomy is possible. Tumour invasion into the phrenicoabdominal vein and caudal vena cava require venotomy to remove the tumour emboli. In the case of phaeochromocytoma, pre-operative use of phenoxybenzamine decreases the perioperative mortality rate. After the perioperative period, outcomes for both adrenal carcinomas and phaeochromocytomas can be very good in dogs. Vascular invasion, emergency surgery for haemorrhage, and large tumour size increases the perioperative risk but do not necessarily impact on long-term outcome.
In non-resectable adrenal tumours, stereotactic radiation therapy has been recently reported with good outcomes (several year survival time). Adjuvant therapy following surgery has not been established in companion animals. For adrenal dependent hyperadrenocorticism, if surgery is not a good option medical therapy can be attempted. Mitotane can be used as a cytotoxic agent (higher doses than required for pituitary dependent hyperadrenocorticism are typically required, and approaches to ablate the adrenal tissue are described), or trilostane to control clinical signs can also be considered. Other chemotherapy agents have not been evaluated in companion animals with adrenal gland tumours.