Each canine adrenal gland consists of the outer cortex and the central medulla. The cortex is responsible for producing aldosterone, glucocorticoids and sex hormones. Tumours of the medulla secrete catecholamines and the most common tumour is the pheochromocytoma. There is little sex or breed consistency with adrenal tumours, although not surprisingly dogs tend to be older. Glucocorticoid-secreting tumours (cushingoid) tend to be seen in larger bred dogs. Adrenal tumours are often functional and clinical signs relate to the hormones they produce. 41% of tumors arise in the cortex and of these 10–20% invade the vena cava. 32% of adrenal tumours are pheos but 30–50% invade the vena cava. This might be because the central location and proximity to the phrenicoabdominal vein allows for tumor to grow down this into the cava. 27% of adrenal tumours are metastatic, with metastasis in decreasing order of frequency: carcinoma highest incidence (pulmonary CA, mammary CA, prostatic CA, gastric CA, pancreatic CA), melanoma, histiocytic sarcoma, hemangiosarcoma, TCC, MCT, lymphoma, OSA, SCC, leiomyosarcoma, mesothelioma, islet cell tumor, CSA, cholangiosarcoma, renal CA, FSA, nasal CA, C-cell tumor, anal sac adenoCA, liposarcoma, sweat gland CA, granulosa cell tumour.
Presentation is variable. Most present for paraneoplastic signs if functional. These include:
Functional Cortical Tumours
Glucocorticoid-secreting tumours; Cushingoid signs - polyuria/polydipsia, polyphagia, pot belly, thin skin.
Aldosterone-secreting tumours (Conn's syndrome); muscle weakness through hypokalaemia, sudden onset blindness through hypertension from hypernatraemia.
Functional Medullary Tumours
Catecholamine secretion leads to weakness, collapse, weight loss, anxiety, panting, depression, hypertension, sudden-onset blindness.
Diagnosis of adrenal tumours is otherwise difficult, especially if non-functional. The majority will not be visible on abdominal radiographs unless large. The adrenal gland is located in the retroperitoneal space just cranial to each kidney. The right adrenal sits between the kidney and liver and is very difficult to identify, making left-sided tumours marginally easier to detect radiographically when present. Approximately 10% are calcified. Many are found on abdominal ultrasound, which raises a dilemma as to whether this mass is responsible for the clinical signs being investigated, or if it incidental. Evidence of invasion into local structures including the kidney and vena cava confirm the mass is malignant and so increase the index of suspicion that the mass is a significant finding. Clinical signs with adrenal tumours (especially pheos) can be vague and intermittent, and physical examination findings can be variable. Abnormalities in laboratory tests are often nonspecific and not hugely helpful. These are typically older dogs and so many have concurrent diseases that complicate the overall picture.
Hormone testing is useful to diagnose an adrenocortical tumour, starting with an ACTH stimulation test as a screening tool, with a high dose dexamethasone suppression test used to differentiate between pituitary and adrenal masses. It is harder to definitively diagnose a pheo in dogs with hormone testing. Catecholamine assays or urinary catecholamine and their metabolites are prone to false positives and have not been found to be useful in dogs.
Whether or not an adrenal tumor needs to be removed depends on a number of factors, not counting cost, surgeon familiarity with the anatomy, and availability of intra-operative and post-operative high-end care. The mere presence of an adrenal mass is not in itself an indication, as many are found incidentally, and can be followed by ultrasound for several months or longer without a significant change in growth. Evidence of invasion, rapid growth, obvious paraneoplastic signs, or clinical signs due to the physical presence (pain, ascites) are all indications that surgery is warranted.
If there are no clinical signs attributable to the mass, and there is no local invasion, then it is quite acceptable to re-ultrasound in a month and determine rate (or lack) of growth before committing the dog and owner to surgery.
CT imaging is recommended wherever possible when surgery is being considered or if vena cava invasion is suspected or known. A CT more accurately delineates extent of tumour thrombus within the vena cava, phrenicoabdominal veins and involvement or displacement of the renal vessels, important for surgical planning. The CT will also identify any obviously enlarged lymph nodes that can be inspected or excised after adrenalectomy. A high quality CT allows for accurate pre-operative planning of where tourniquets need to be placed, how many need to be used, likely involvement of the kidneys (esp. left renal vein), muscular invasion, and importantly early detection of nodal metastasis and lung metastasis. The exact likelihood of metastasis varies depending on the source read, from 0–50%, but an attempt should be made to rule it out prior to surgery.
Pre-op stabilization for functional cortical tumours is not normally necessary although some surgeons will prescribe trilostane or mitotane before excision of a functional cortical tumour. Before excising a suspected pheochromocytoma however, phenoxybenzamine (0.6 mg/kg po BID for a median of 20 days) has been associated with a lower morbidity, as is decreased age, lack of intra-operative arrhythmias and decreased surgery time (likely linked to increased surgical familiarity and availability of experienced surgical assistance).
The exact techniques for adrenalectomy will be covered with case examples in the lecture. This will include simple excisions, dealing with invasion of the phrenicoabdominal vein, renal vein and/or vena cava, and a paracostal approach for difficult right-sided tumours invading the liver. Standard operating instruments are used with the addition of vascular clamps (e.g., Satinskys), long dissecting instruments and DeBakey forceps, and equipment available to prepare Rumel tourniquets intra-operatively.
Bilateral adrenalectomy is to be considered in cases with bilateral, often asymmetrical enlargement. Both adrenals should be removed in a single procedure with dexamethasone being given pre-operatively and DOCP started intra-operatively to counter the inevitable Addisonian complications. These patients can do very well, often living months-years on supplemental therapy.
Post-operative management post functional adrenalectomy is not as many consider a roller-coaster of de-stabilisation, but only as long as patients have been appropriately stabilised before surgery, surgery was well planned and executed, an experienced critical care team is available and due consideration and pre-emptive treatment given for potential complications. Many cases have uneventful recoveries and leave after 48 hours under observation, but the worst can be affected by thromboembolic disease, persistent endocrine disease from functional metastasis, acute renal failure from temporary renal pedicle occlusion during surgery often compounded by concurrent nephrectomy, haemorrhage, pancreatitis, ileus and cardio-vascular and electrolyte abnormalities.
Long-term outcome can be excellent following adrenalectomy, with a median survival long over a year to be expected, regardless of tumour histogenesis. Metastasis is not commonly documented and local recurrence is unusual. Often the cause of death is not adrenal tumour-related, rather another old age disease.