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.     

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.     

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.     

Adrenalectomy and caval thrombectomy in a cat with primary hyperaldosteronism

A 13-year-old, castrated male, domestic longhaired cat was diagnosed with primary hyperaldosteronism from an adrenal gland tumor and a thrombus in the caudal vena cava. Clinical signs included cervical ventriflexion, lethargy, weakness, inappetence, and diarrhea. Laboratory tests revealed hypokalemia, normonatremia, hyperglycemia, hypophosphatemia, and elevated creatine kinase activity. Hypokalemia worsened despite oral potassium supplementation. An adrenalectomy and caval thrombectomy were successfully performed utilizing deliberate hypothermia followed by progressive rewarming.     

Primary hyperaldosteronism in the cat: a series of 13 cases

Thirteen cases of feline primary hyperaldosteronism were diagnosed based on clinical signs, serum biochemistry, plasma aldosterone concentration, adrenal imaging and histopathology of adrenal tissue. Two cases presented with blindness caused by systemic hypertension, whilst the remaining 11 cases showed weakness resulting from hypokalaemic polymyopathy. Elevated concentrations of plasma aldosterone and adrenocortical neoplasia were documented in all cases. Seven cases had adrenal adenomas (unilateral in five and bilateral in two) and six had unilateral adrenal carcinomas. Three cases underwent medical treatment only with amlodipine, spironolactone and potassium gluconate; two cases survived for 304 and 984 days until they were euthanased because of chronic renal failure, whilst the third case was euthanased at 50 days following failure of the owner to medicate the cat. Ten cases underwent surgical adrenalectomy following a successful stabilisation period on medical management. Five cases remain alive at the time of writing with follow-up periods of between 240 and 1803 days. Three cases were euthanased during or immediately following surgery because of surgical-induced haemorrhage. One cat was euthanased 14 days after surgery because of generalised sepsis, whilst the remaining cat was euthanased 1045 days after surgery because of anorexia and the development of a cranial abdominal mass. It is recommended that primary hyperaldosteronism should be considered as a differential diagnosis in middle-aged and older cats with hypokalaemic polymyopathy and/or systemic hypertension and should no longer be considered a rare condition.     

Bone marrow hypoplasia in a cat treated with griseofulvin

Three weeks after initiation of griseofulvin treatment for dermatophytosis (40 mg/kg of body weight, q 12 h), an 8-yr-old domestic shorthair cat developed depression, vomiting, and pyrexia. Abnormalities found during physical examination included bilateral mydriasis, visual impairment, grade-II/V systolic murmur and multiple areas of alopecia. The cat was pancytopenic; serum biochemical abnormalities included hyperbilirubinemia, hyperglycemia, hyponatremia, and hypokalemia, and urinalysis revealed proteinuria, glycosuria, and bilirubinuria. Examination of a bone marrow aspirate revealed profound hypoplasia of all precursors. Griseofulvin toxicosis was diagnosed on the basis of the temporal relationship of drug administration with onset of clinical, hematologic, and biochemical abnormalities and failure to identify an infective or neoplastic cause for the bone marrow hypoplasia. The condition was refractory to treatment and the cat was euthanatized. Pathologic changes in the bone marrow were consistent with severe hypoplasia of all bone marrow precursors.     

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.     

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.     

Clinical,virological, imaging and pathological findings in a SARS CoV-2 antibody positive cat

This paper reports a presumptive severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in a cat. A cat with respiratory disease living with three individuals with coronavirus disease 2019 showed bilateral ground-glass opacities in the lung on X-ray and computed tomography. The clinical swabs were negative for SARS-CoV-2 RNA, but the serum was positive for SARS-CoV-2 antibodies. Interstitial pneumonia and prominent type 2 pneumocyte hyperplasia were noted on histopathology. Respiratory tissues were negative for SARS-CoV-2 RNA or antigen, but the cat was positive for feline parvovirus DNA. In conclusion, the respiratory disease and associated pathology in this cat could have been due to exposure to SARS-CoV-2.     

Respiratory muscle fatigue.

The contribution of respiratory muscle fatigue to the development of ventilatory failure has been the subject of considerable interest and has stimulated much research. Experimental studies in dogs have shown respiratory muscle fatigue to be a cause of ventilatory failure in both cardiogenic and septic shock models. In clinical conditions resulting in acute or chronic hypercapnia, respiratory muscle fatigue is believed to occur; however, the specific role of fatigue has been difficult to prove.     

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.     

Primary hyperaldosteronism in a dog with concurrent lymphoma

An 11-year-old, male castrated English springer spaniel was presented for muscle weakness, lethargy and anorexia while undergoing treatment of Stage IV lymphoma. Persistent hypokalemia prompted multiple diagnostic tests. Serum aldosterone levels, surgical exploration and histopathology confirmed primary hyperaldosteronism. Hyperaldosteronism is a rarely reported endocrinopathy in the dog. This report describes a case in which immunohistochemistry was utilized to confirm the diagnosis of an aldosterone-secreting tumour.     

Primary mycoplasma pneumonia associated with reversible respiratory failure in a cat

A young adult cat was evaluated for respiratory failure. Diagnostic testing, including computed tomography and culture, documented a primary Mycoplasma species pneumonia. The cat was treated aggressively with supportive care, including mechanical ventilation and appropriate antibiotics including doxycycline, and made a complete recovery. This is a unique case in respect of the severity of the Mycoplasma species pneumonia as well as the cat's recovery from severe lung injury.     

What is your diagnosis? Abdominal mass aspirate in a cat with an increased Na:K ratio

Abstract: A 13‐year‐old domestic shorthair cat was presented for evaluation of pollakiuria. Laboratory abnormalities included mild hypercholesterolemia, moderate hypertriglyceridemia, and a mild increase in the Na:K ratio (43, reference interval 32–41). Abdominal ultrasonography revealed urinary calculi and a soft tissue mass between the right caudate liver lobe and the right kidney. Surgery was done to remove the cystic calculi, and aspirates of the mass were obtained. Cytologic specimens contained a population of large, round to angular cells with round nuclei, coarse irregularly stippled chromatin, 1–2 prominent round to angular nucleoli, and abundant pale basophilic cytoplasm distended by numerous well‐delineated vacuoles. Rare binucleated cells and micronuclei, and moderate anisocytosis, anisokaryosis, and anisonucleoleosis were noted. The cytologic interpretation was adrenal neoplasia, consistent with adrenal carcinoma. Approximately 4 months later, the cat developed vomiting, dehydration, weakness, and cervical ventroflexion. Serum biochemical alterations at that time included marked hypokalemia (2.4 mmol/L, reference interval 3.4–5.6 mmol/L) and a markedly increased Na:K ratio (65, reference interval 32–41). Mean systolic blood pressure was 205 mmHg. Surgical removal of the mass was accomplished via right adrenalectomy and a diagnosis of adrenal carcinoma was confirmed histologically. Plasma aldosterone concentration (measured preoperatively) was 1358 pmol/L (reference interval 194–388 pmol/L). Primary hyperaldosteronism caused by a functional adrenal carcinoma is an uncommon condition in cats.     

Primary aldosteronism (Conn's syndrome) in a cat; a case report and review of comparative aspects

An aged cat was presented with a history of chronic relapsing weakness and depression. Profound hypokalaemia was detected in association with increased serum aldosterone levels and marginally subnormal plasma renin activity. A diagnosis of primary aldosteronism (Conn's syndrome) was made and the cat was successfully treated for 2 ½ months with spironolactone. When renal failure developed, the cat was destroyed and at autopsy a large adrenal cortical adenocarcinoma was found.     

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.     

Suspected albuterol toxicosis in a dog

CASE DESCRIPTION: A 6-year-old male castrated Shetland Sheepdog was evaluated because of severe hypokalemia and progressive paresis. CLINICAL FINDINGS: Physical examination revealed fever, tachypnea, mydriasis, hyperemic mucous membranes, severe forelimb paresis, and hind limb paraplegia. The dog had superficial and deep pain sensation in all 4 limbs. Forelimb spinal reflexes were considered normal, but hind limb reflexes were normal to slightly hyperreflexive. The panniculus reflex was considered to be normal, and cranial nerve reflexes were intact. A CBC revealed mild leukocytosis and erythrocytosis, and serum biochemical analysis revealed severe hypokalemia. Thoracic and abdominal imaging did not reveal relevant findings. Blood pressure and ECG findings were within reference limits. Questioning of the owner revealed possible exposure to albuterol via ingestion of medication intended for the owner's horse. Results of serum testing via immunoassay were suggestive of albuterol toxicosis. TREATMENT AND OUTCOME: Treatment included IV administration of an electrolyte solution and supplemental potassium chloride. The rate of potassium chloride supplementation was slowly decreased as serum potassium concentration increased. No other medical intervention was required, and the dog made a rapid and complete recovery. CLINICAL RELEVANCE: Ingestion of albuterol can lead to profound physical and serum biochemical abnormalities. Appropriate historical information should be obtained to identify possible sources and routes of exposure to intoxicants. Albuterol-induced hypokalemia can be successfully managed medically.     

Treatment of a dog with severe baclofen intoxication using hemodialysis and mechanical ventilation

Objective: This case report describes the successful management of a dog with coma and respiratory depression due to severe baclofen intoxication. Case summary: A Doberman Pinscher mixed breed dog ingested 500 mg (20 mg/kg) of baclofen. Signs of severe intoxication included coma and profound respiratory muscle weakness. The dog was supported with positive pressure ventilation and treated with one session of hemodialysis. Weaning from the ventilator was achieved within 4 hours of hemodialysis, and recovery from coma occurred over the following 12–36 hours. The dog regained full neurologic function and was normal at discharge following 3 days of hospitalization. New or unique information provide: Severe central nervous system depression and respiratory depression due to baclofen intoxication can be life threatening. In addition to other supportive care, hemodialysis may hasten recovery and ventilatory support may be essential to achieve a positive outcome. With successful treatment, toxicity can be decreased and the associated life‐threatening central nervous system and ventilatory depression can resolve. Prognosis for return of normal function is excellent.     

Urinary aldosterone to creatinine ratio in cats before and after suppression with salt or fludrocortisone acetate

Background: The endocrine diagnosis of primary hyperaldosteronism in cats currently is based on an increased plasma aldosterone to renin ratio, which has several disadvantages for use in veterinary practice. Objectives: To establish a reference range for the urinary aldosterone to creatinine ratio (UACR) and to determine whether oral administration of either sodium chloride or fludrocortisone acetate is effective for use in a suppression test. Animals: Forty‐two healthy cats from an animal shelter and 1 cat with primary hyperaldosteronism from a veterinary teaching hospital. Methods: Morning urine samples for determination of the basal UACR were collected from 42 healthy cats. For the suppression tests, urine samples for the UACR were collected after twice daily oral administration for 4 consecutive days of either sodium chloride, 0.25 g/kg body weight (n = 22) or fludrocortisone acetate, 0.05 mg/kg body weight (n = 15). Results: The median basal UACR was 7.2 × 10^?9 (range, 1.8–52.3 × 10^?9), with a calculated reference range of <46.5 × 10^?9. Administration of sodium chloride resulted in adequate salt loading in 10 of 22 cats, but without significant reduction in the UACR. Administration of fludrocortisone resulted in a significant decrease in the UACR (median, 78%; range, 44–97%; P < .001) in healthy cats. In the cat with an aldosterone‐producing adrenocortical carcinoma, the basal UACR and the UACR after fludrocortisone administration were 32 × 10^?9 and 36 × 10^?9, respectively. Conclusions and Clinical Importance: Using the UACR for an oral fludrocortisone suppression test may be useful for the diagnosis of primary hyperaldosteronism in cats.