Hyperaldosteronism in a cat with metastasised adrenocortical tumour

In a 12-year-old male shorthaired cat with attacks of hypokalaemic muscular weakness in spite of oral potassium supplementation, highly elevated plasma aldosterone concentrations in combination with low plasma renin activity pointed to primary hyperaldosteronism. Ultrasonography and computed tomography revealed a large left-sided adrenal tumour growing into the phrenicoabdominal vein and the caudal vena cava. The tumour and its intravascular extension were surgically removed, but the subsequent stenosis of the caudal vena cava caused congestion and renal failure. At autopsy pulmonary micrometastases of the aldosteronoma were found.     

Successful use of short‐term mechanical ventilation to manage respiratory failure secondary to profound hypokalemia in a cat with hyperaldosteronism

Objective – To report successful management of respiratory failure due to severe hypokalemia in a cat with hyperaldosteronism, including short‐term mechanical ventilation strategies and aspects of medical and surgical treatment. Case Summary – A cat presented with bilateral pelvic limb weakness that rapidly progressed to tetraparesis and respiratory muscle failure. Point‐of‐care testing revealed severe hypokalemia (1.9 mmol/L) and mild azotemia. Initial management included endotracheal intubation, mechanical ventilation, and aggressive potassium supplementation. Spironolactone was started due to a high index of suspicion for hyperaldosteronism. A right adrenal mass visualized during abdominal ultrasonographic examination and a serum aldosterone level greater than 3329 pmol/L confirmed the diagnosis. The cat made a full recovery following surgical removal of a right adrenal adenoma. New or Unique Information Provided – We report successful management of respiratory failure in a cat with hyperaldosteronism using short‐term mechanical ventilation. Respiratory failure due to severe hypokalemia should be considered a complication of hyperaldosteronism in cats and may require mechanical ventilation. However, full recovery is possible.     

Primary hyperaldosteronism in two cats.

A condition of primary hyperaldosteronism resulting from an adrenal tumor in two cats is presented and was characterized by hypertension, hypokalemia, inappropriate kaliuresis, low normal plasma renin activity, and markedly increased serum aldosterone concentration. One of the two cats underwent a laparotomy, and in this case hypertension and hypokalemia resolved following the removal of an adrenal tumor.     

Primary hyperaldosteronism: expanding the diagnostic net

PRACTICAL RELEVANCE: Primary hyperaldosteronism is probably the most common adrenocortical disorder in cats. As in humans, it is often unrecognised, which excludes a potentially large number of cats from appropriate treatment. PATIENT GROUP: Affected cats present at a median age of 13 years (range 5-20 years). A breed or sex predilection has not been documented. The excessive secretion of mineralocorticoids usually leads to hypokalaemia and/or systemic arterial hypertension. Most affected cats present with muscular weakness and/or ocular signs of arterial hypertension. DIAGNOSTICS: In any cat presenting with hypokalaemia and/or arterial hypertension, other potential causes should be excluded. The ratio of plasma aldosterone concentration to plasma renin activity (aldosterone:renin ratio) is currently the best screening test for feline primary hyperaldosteronism. Diagnostic imaging is required to differentiate between adrenocortical neoplasia and bilateral hyperplasia, and to detect any distant metastases. CLINICAL CHALLENGES: The differentiation between adrenocortical neoplasia and bilateral hyperplasia is imperative for planning optimal therapy, but the limited sensitivity of diagnostic imaging may occasionally pose a problem. For confirmed unilateral primary hyperaldosteronism, unilateral adrenalectomy is the treatment of choice, and offers an excellent prognosis, but potentially fatal intra- and postoperative haemorrhage is a reported complication and risk factors have yet to be identified. EVIDENCE BASE: Only a few case reports are available on which to base the optimal diagnostic and therapeutic approach to feline primary hyperaldosteronism. This article reviews the physiology of aldosterone production and the pathophysiology of primary hyperaldosteronism, and summarises the currently available literature on the feline disease. Practical suggestions are given for the diagnostic investigation of cats with suspected primary hyperaldosteronism.     

Squamous cell carcinoma of the anal sac in two cats

This report describes two cases of feline anal sac squamous cell carcinoma. Cat 1 was managed with a multimodal approach combining surgical resection, radiation therapy and systemic therapy (toceranib phosphate; Palladia™) until local recurrence was identified at 236 days postsurgery. At that time, the cat received carboplatin. With the tumour being progressive, the cat was euthanased 552 days post initial surgery. Cat 2 was managed palliatively with a non-steroidal anti-inflammatory (meloxicam) and supportive medications. Unfortunately, with further decline in quality of life following initial diagnosis, the cat was euthanased 28 days later. Squamous cell carcinoma should be considered as a possible differential diagnosis when a cat is presented for investigation of an anal sac mass.     

Hyperadrenocorticism in six cats

The case records of six cats with hyperadrenocorticism presented to the Department of Clinical Veterinary Medicine, University of Cambridge, over an 11-year period were reviewed. Signalment and clinical signs were similar to previous reports but, in contrast to other reports, only three cats had diabetes mellitus on presentation. Abdominal radiographs revealed an adrenal mass in one case, obesity in all cases but no hepatomegaly. The adrenal glands were identified ultrasonographically in three out of six cases. Clinicopathological findings were non-specific. The diabetic cats had a significantly lower serum potassium concentration than the non-diabetic cats (P<0·05). Results of adrenocorticotrophic hormone (ACTH) stimulation tests were supportive of a diagnosis of hyperadrenocorticism in the five cats in which they were performed. Five cats had pituitary-dependent hyperadrenocorticism (PDH) and one had an adrenal tumour. Differentiation between the two forms of hyperadrenocorticism was possible preoperatively in five out of six cats. Adrenal histopathology confirmed hyperplasia in four cats and adenocarcinoma in one cat. Three cats with PDH underwent bilateral adrenalectomy and two of these cats had low, flat ACTH stimulation tests postoperatively and survived for significant periods. The cat with an adrenal tumour underwent partial unilateral adrenalectomy, maintained a positive ACTH stimulation test postoperatively and was euthanased one week after surgery.     

Use of abdominal ultrasonography in the diagnosis of primary hyperaldosteronism in a cat

A 13-year-old castrated male cat was examined because of a 2-week history of weakness, cervical ventroflexion, and dysphagia. Clinicopathologic abnormalities included hypokalemia and high serum creatine kinase activity. Abdominal ultrasonography revealed a 15-mm spherical mass in the area of the left adrenal gland. Plasma aldosterone concentration was high, and plasma renin activity was low. Findings were diagnostic of primary hyperaldosteronism. The cat responded well to intravenous and oral potassium supplementation while in the hospital. The owner declined surgery; therefore, repeated follow-up abdominal ultrasonography was recommended. The cat did well clinically with medical management alone until day 334, when it was lost to follow-up.     

Hypokalaemic episodic polymyopathy in cats fed a vegetarian diet

A previously undocumented hypokalaemic condition with a cyclical nature, comprising acute bouts of polymyopathy followed by spontaneous recoveries, is described in the cat. Cats being fed a high protein vegetarian diet developed recurrent episodes of polymyopathy, characterised by ventroflexion of the head and neck, stiff forelimb gait, lateral head-resting and generalised muscle weakness. Plasma potassium concentrations (mean +/- standard deviation) were reduced from 3.28 +/- 0.33 mmol/l at the beginning of the experiment to 2.45 +/- 0.24 mmol/l during bouts of myopathy. This hypokalaemia was associated with increased creatine kinase activities indicative of muscle damage, and decreased urinary potassium concentrations, and was caused by insufficient dietary potassium. Cats that received the same diet supplemented with potassium did not develop hypokalaemic polymyopathy. Spontaneous recoveries of affected cats were not associated consistently with increases in plasma potassium concentrations. Plasma taurine concentrations decreased and glutamic acid increased markedly in all cats fed the experimental diet. There was no evidence of thiamin deficiency associated with the high glutamic acid intake. Veterinarians should be aware that hypokalaemic cats, and in particular those on potassium-deficient diets, may show cyclical disease with episodes of polymyopathy recurring after periods of spontaneous clinical recovery. This condition in cats may be a useful animal model for familial hypokalaemic periodic paralysis in humans.     

Treatment of Aldosterone‐Secreting Adrenocortical Tumors in Cats by Unilateral Adrenalectomy: 10 Cases (2002–2012)

Background

Primary hyperaldosteronism (PHA) in cats occurs as a consequence of excessive hormone production by an adrenocortical tumor. Median survival time, association between tumor type and prognosis, and the likelihood that cats require continued medical therapy after surgery have not been systematically evaluated.

Objectives

To determine the median survival time of cats with PHA treated by unilateral adrenalectomy. To examine if tumor type, anesthesia time, or tumor location (left or right side) affect survival and if affected cats require continued postoperative treatment for persistent hypertension or hypokalemia.

Animals

Ten client‐owned cats.

Methods

Retrospective study. Cats were diagnosed with PHA based on clinical signs, increased plasma aldosterone concentration, and advanced imaging. Cats underwent unilateral adrenalectomy. Survival time (days alive after surgery) was determined for each cat. Factors affecting median survival time were investigated, including histopathology, anesthesia time, and location (side) of the tumor.

Results

Eight of 10 cats survived to discharge from the hospital post adrenalectomy. Overall median survival was 1,297 days (range 2–1,582 days). The only significant factor affecting median survival time was anesthesia time >4 hours. Tumor type and location (side) did not significantly affect median survival time. No cats required continued medical treatment for PHA.

Conclusions and Clinical Importance

Although PHA in cats is still considered an uncommon condition, it should be considered in middle to older aged cats with hypokalemic polymyopathy and systemic hypertension. Surgical correction by unilateral adrenalectomy is a viable approach to definitive treatment of PHA with no need for continued medical management.     

Feline hypertension: clinical findings and response to antihypertensive treatment in 30 cases

Systolic hypertension was diagnosed in 30 cats. At diagnosis, 16 of those were found to be in chronic renal failure only, while five were azotaemic and either receiving treatment for hyperthyroidism (four cases) or were untreated hyperthyroid cases (one case). Two cases were untreated hyperthyroid cases with no evidence of azotaemia and the remaining seven cases had no definitive diagnosis of the underlying cause of their hypertension. The successful treatment used for the majority of cases was amlodipine, which lowered systolic blood pressure from 202.5+/-16.8 to 153.2+/-21.6 mmHg (mean+/-SD; n=29) within the first 50 days. Each case was followed for at least three months, or to the end of its natural life, and each cat was re-examined every six to eight weeks. Systolic blood pressure was kept below a target value of 165 mmHg in 58 per cent of cases treated for three months or longer. At the time of writing, 19 of the cases had died or been euthanased with a median treatment time of 203 days, one case was lost to follow-up and 10 cases were still alive, nine of which had been treated for six months or more. Amlodipine can be used for long-term control of feline systemic hypertension.     

Idiopathic hyperaldosteronism in a dog

Idiopathic hyperaldosteronism was diagnosed in an 8-year-old castrated male Yorkshire Terrier, based on increased concentration of plasma aldosterone, hypertension, hypernatremia, decreased natriuresis, hypokalemia, and hyperkaluria. Unilateral adrenalectomy was performed after visualization of a nodule on the right adrenal gland. Hyperplasia of the zona glomerulosa and increased postoperative aldosterone concentrations supported the diagnosis of idiopathic hyperaldosteronism.     

Functioning unilateral adrenocortical carcinoma in a dog

An 11-year-old, 24-kg, intact female Siberian husky dog in anestrus had a 2-month history of polyuria and polydipsia. The dog had signs of mineralocorticoid excess such as hypertension and hypokalemia refractory to potassium supplementation. Abdominal ultrasound revealed an irregular mass in the left adrenal gland. The ACTH stimulation test for aldosterone concentration did not reveal hyperaldosteronism. Unilateral adrenalectomy was performed and histopathology identified adrenal cortical carcinoma. All clinical signs of mineralocorticoid excess ceased after surgery.     

Severe systemic hypertension in a cat with pituitary-dependent hyperadrenocorticism

A seven-year-old Burmese cat was presented with sudden onset blindness. On physical examination, the cat had bilateral retinal detachment and severe systemic hypertension. Further clinical investigations revealed pituitary-dependent hyperadrenocorticism. Antihypertensive therapy was discontinued when the hypertension resolved after bilateral adrenalectomy. Systolic blood pressure remained normal until 19 months post-operatively when systemic hypertension recurred and was attributed to chronic kidney disease. The cat was euthanased 47 months after initial presentation. A pituitary adenoma was identified at post-mortem examination. This case illustrates that systemic hypertension can occur secondary to hyperadrenocorticism in the cat.     

Generalised amyloidosis in two Siamese cats: spontaneous liver haemorrhage and chronic renal failure

Two cases are reported, illustrating the antemortem diagnosis of systemic amyloidosis in Siamese cats. A cat presenting with inappetence and depression was diagnosed as having systemic amyloidosis with spontaneous haemorrhage from the liver. In another cat from the same breeding cattery, chronic renal failure due to systemic amyloidosis was an incidental finding. Little treatment was possible in either case and both were later euthanased. The two cats had similar renal and hepatic pathology but different signs of disease.     

Oesophageal squamous cell carcinoma in two cats

Two cases of feline oesophageal squamous cell carcinoma are described. In both cases, diagnosis was achieved by radiography, endoscopy and cytology, and later confirmed by histology. One cat underwent oesophagectomy followed by end-to-end anastomosis, but died three days postsurgery; the second cat was euthanased after diagnosis.     

Feline adrenal disorders

Although only recently discovered, feline adrenal disorders are becoming increasingly more recognized. Feline adrenal disorders include diseases such as hyperadrenocorticism (Cushing's syndrome) and hyperaldosteronism (Conn's syndrome). The clinical signs of feline hyperadrenocorticism, which include unregulated diabetes mellitus and severe skin atrophy, are unique to the cat. Other signs of feline hyperadrenocorticism, such as potbellied appearance, polydipsia, polyuria, and susceptibility to infections are also seen in dogs with hyperadrenocorticism. Conn's syndrome has only recently been described in the cat and is in fact more common in cats than in dogs. Characterized by severe hypokalemia, hypertension, and muscle weakness, Conn's syndrome may be misdiagnosed as renal failure. The clinician should become familiar with the clinical signs of adrenal disorders in cats and the common diagnostic tests used to diagnose these syndromes in cats as they differ from those in the dog. Treatment of feline adrenal disorders may be challenging; the clinician should become familiar with common drugs used to treat adrenal disorders in cats.     

Pseudomembranous cystitis, an unusual condition associated with feline urine outflow obstruction: Four cases

The clinical follow-up of four cats presumptively diagnosed with pseudomembranous cystitis is described. All presented with acute urine outflow obstruction and acute renal failure. Urethral catheterisation was performed without difficulty but ultrasonography and contrast radiography consistently revealed abnormal bladder wall and content. One cat was euthanased, the remaining three underwent an exploratory cystotomy. Abundant inflammatory and necrotic tissue covering an ulcerated bladder mucosa was removed. All cats recovered uneventfully. No definitive cause was identified but the clinical course of the disease was not typical of idiopathic cystitis.     

Hypertensive retinopathy in a cat

A 12-year-old cat presented for sudden blindness was diagnosed with hypertensive retinopathy on the basis of ophthalmologic and ultrasonic examination. Renal failure due to a large intranephric cyst obstructing the right ureter and renal artery was the suggested cause of the systemic hypertension. The cat died 8 hours after unilateral nephrectomy.     

Effects of benazepril hydrochloride in cats with experimentally induced or spontaneously occurring chronic renal failure

We examined effects of an angiotensin converting-enzyme inhibitor, benazepril hydrochloride (BH), on renal hypertension and chronic renal failure (CRF) in cats. For experimental CRF, healthy cats (n=5) underwent 7/8 renal ablation. After renal insufficiency and hypertension were confirmed by blood urea nitrogen (BUN), serum creatinine, creatinine clearance and telemetric recording of systemic blood pressure, BH was administered orally once daily at 0.9 to 2.0 mg/kg/day for 2 to 3 weeks. Within 2 months after renal ablation, renal failure and hypertension developed as evidenced by significant increases in BUN, serum creatinine and systemic blood pressure (p<0.01 or 0.05) and significantly decreased creatinine clearance accompanied by elevated plasma renin activity, angiotensin I and II, and aldosterone (p<0.01 or 0.05). BH administration corrected systemic hypertension (p<0.05) and significantly reduced angiotensin II and aldosterone (p<0.05). Upon discontinuation of BH, these values returned to the pre-administration levels. Studies on spontaneous CRF enrolled 11 cats with spontaneously occurring CRF. BH was administered orally to 6 cats once daily for 24 weeks at a final dose of 1.0 mg/kg/day, while 5 cats served as control. BH administration reduced serum creatinine and urinary protein concentration in every cat. Results demonstrate that in cats, loss of renal mass leads to activation of the renin-angiotensin-aldosterone system and associated renal hypertension, and indicate that BH is effective in correcting renal hypertension and may provide renal benefits to cats with CRF.