History
A 17-year-old 6-kg (13.2-lb) castrated male domestic shorthair cat was admitted to the emergency department because of a 3-day history of anorexia and dysphagia. One month previously, the patient had received a diagnosis of a fungal ear infection and was being treated with florfenicol, terbinafine, and mometasone furoate otic solution. Ingestion of the solution had been witnessed by the owner and was suspected to be the cause of the dysphagia.
On physical examination, heart rate, respiratory rate, and rectal temperature were within reference limits. A grade 4/6 holosystolic murmur was auscultated over the left parasternal region, but no gallop rhythm or arrhythmia was appreciated. The remainder of the physical examination was unremarkable. Serum biochemical analysis revealed alkalosis (blood pH, 7.632; reference range, 7.337 to 7.467), hypokalemia (2.8 mmol/L; reference range, 3.6 to 4.8 mmol/L), and high aspartate aminotransferase (188 U/L; reference range, 5 to 42 U/L) and creatine kinase (8,319 U/L; reference range, 14 to 528 U/L) activities. Systolic blood pressure, measured with an ultrasonic Doppler device, was mildly high (180 mm Hg; reference range, 120 to 160 mm Hg). Abdominal radiography was performed (Figure 1).
Determine whether additional imaging studies are required, or make your diagnosis from Figure 1—then turn the page →
Radiographic Findings and Interpretation
On the lateral projection, there is a rounded soft tissue opacity mass in the craniodorsal aspect of the abdomen. The mass is located craniodorsal to the kidneys; it appears to be in the retroperitoneal space because of its summation with the cranial pole of a kidney and its position dorsal to the colon. Both kidneys are also ventrally displaced, which is thought to be a result of an excess amount of retroperitoneal fat that reflects the body condition of the cat. On the ventrodorsal projection, the retroperitoneal mass is not delineated, which is likely the result of superimposition with the vertebral column and intestines. On both the lateral and the ventrodorsal projections, there are small mineral opacities superimposed with both kidneys and the bladder (Figure 2).
Because of the radiographic findings and clinical history, a retroperitoneal neoplasm of adrenal gland origin was considered most likely, but other differential diagnoses included an eccentric renal mass, a retroperitoneal cyst or abscess, and a mass originating from the head of the spleen.
Abdominal ultrasonography was performed to confirm the origin of the mass, assess for vascular involvement, evaluate surgical resectability, and rule out metastasis or comorbidities of other organs. A well-encapsulated, heterogeneously hypoechoic mass (approx 2.9 × 2.0 × 2.2 cm) was identified (Figure 3). The mass was in the left cranial aspect of the abdomen, craniomedial to the left kidney, and surrounded by hyperechoic fat. Adjacent to the mass, color flow Doppler ultrasonography revealed turbulent blood flow in the caudal vena cava without vascular invasion. The mass was considered consistent with a left adrenal gland mass. The right adrenal gland was 0.3 cm in height and considered normal in size. The left kidney measured 4.1 cm in length, and the right kidney measured 3.7 cm in length; both were within reference limits. The caudal pole of the left kidney was flattened with a hyperechoic cortex, consistent with a renal infarct. There was a single small (< 0.3 cm in diameter) hyperechoic shadowing structure in the caudal pole of the left kidney, consistent with a nephrolith, and a small amount of gravity dependent, hyperechoic, shadowing debris in the urinary bladder. These shadowing structures were consistent with the previously noted mineral opacities seen radiographically.
Treatment and Outcome
Hyperaldosteronism caused by an adrenocortical mass was suspected on the basis of findings of hypokalemia, hypertension, and the presence of an adrenal gland mass. A plasma sample was sent to the Michigan State University Diagnostic Center for Population and Animal Health to determine the plasma aldosterone concentration. Because the cat was eating well and was clinically stable, it was discharged from the hospital, with maropitant citrate (2.5 mg/kg [1.14 mg/lb], PO, q 24 h) and clopidogrel (3 mg/kg [1.4 mg/lb], PO, q 12 h) prescribed pending the results of aldosterone testing. The plasma aldosterone concentration was high (1,183 pmol/L; reference range, 194 to 388 pmol/L), consistent with a functional adrenocortical tumor. Because of persistent hypokalemia and dysphagia at the cat's 1-week recheck examination, orally administered spironolactone (2 mg/kg [0.9 mg/lb], q 24 h) and potassium gluconate were added to the treatment regimen. Thereafter, the patient was lost to follow-up.
Comments
Radiographic findings for cats with adrenal gland masses are variable depending on the size of the lesion. In the case described in the present report, the left adrenal gland mass was large and observed radiographically as a soft tissue opacity in the retroperitoneal space. The detection of the lesion was aided by the presence of a large amount of retroperitoneal fat that reflected the patient's body condition. Often these masses are not large enough to be readily visible on radiographs; therefore, ultrasonography is a valuable tool to detect adrenal gland abnormalities. Ultrasonographically, normal adrenal glands in cats appear hypoechoic with a surrounding hyperechoic halo of fat and are most frequently bean shaped or ovoid; typical adrenal gland height in healthy cats is approximately 0.36 to 0.38 cm.1 For the cat of the present report, the left adrenal gland was substantially larger (ie, 2.9 × 2.0 × 2.2 cm) on ultrasonographic evaluation.
Adrenal gland tumors are an uncommon neoplasm in cats, making up only 0.2% of neoplasia.2 Of these tumors, adrenocortical carcinomas appear to be the most common; however, adrenocortical adenomas are also found.3 Functional tumors can produce an excess of several hormones, including aldosterone, cortisol, or sex hormones, but overproduction of aldosterone (primary hyperaldosteronism) is most frequently identified.3
The most common clinical signs associated with primary hyperaldosteronism are generalized weakness, dysphagia, and blindness secondary to systemic hypertension and retinal detachment.3,4 Weakness and dysphagia are thought to be the result of hypokalemia, which is seen in most affected cats.3 As neither the clinical signs nor biochemical abnormalities are specific for hyperaldosteronism in cats, diagnostic imaging is particularly useful.
Definitive diagnosis of primary hyperaldosteronism in cats is challenging. A high plasma aldosterone concentration is considered the hallmark, but plasma aldosterone concentration may remain within the reference range in hypokalemic patients.5 This is because the hypokalemia will reduce the stimulus for aldosterone secretion in situations where the adrenal gland tissue remains responsive to regulatory control. Therefore, primary hyperaldosteronism should still be considered in hypokalemic patients with a plasma aldosterone concentration at the upper limit of the reference range.
Unilateral adrenalectomy is currently the treatment of choice for clinically affected cats with primary hyperaldosteronism. If surgery is declined or is not a viable option, medical management of the condition is aimed at treating the hypokalemia and associated hypokalemic polymyopathy and hypertension, if present.4 Although primary hyperaldosteronism in cats is uncommon, recognition of the clinical signs and the diagnostic imaging features of adrenal gland abnormalities can be critical in making a correct diagnosis.
References
1. Combes A, Pey P, Paepe D, et al. Ultrasonographic appearance of adrenal glands in healthy and sick cats. J Feline Med Surg 2013;15:445–457.
2. Lunn KF, Page RL. Tumors of the endocrine system. In: Withrow SJ, Vail DM, eds. Withrow and McEwen's small animal clinical oncology. 5th ed. St Louis: Saunders Elsevier, 2013;504–531.
3. Daniel G, Mahony OM, Markovich JE, et al. Clinical findings, diagnostics and outcome in 33 cats with adrenal neoplasia (2002–2013). J Feline Med Surg 2016;18:77–84.
4. Ash RA, Harvey AM, Tasker S. Primary hyperaldosteronism in the cat: a series of 13 cases. J Feline Med Surg 2005;7:173–182.
5. Schulman RL. Feline primary hyperaldosteronism. Vet Clin North Am Small Anim Pract 2010;40:353–359.