Perianesthetic metabolic acidosis is associated with 2% dorzolamide eye drops in dogs that underwent ophthalmic surgery: a retrospective study (2019-2022).

OBJECTIVE: To evaluate whether the administration of 2% dorzolamide ophthalmic solution in dogs undergoing ophthalmic surgery is associated with perianesthetic metabolic acidosis. ANIMALS: 60 dogs, with or without dorzolamide administration, underwent arterial blood gas analysis immediately after anesthesia for ophthalmic surgery between 2019 and 2022; a total of 60 surgeries were evaluated. METHODS: This was a retrospective cross-sectional study. Logistic regression analysis was performed to investigate the association between the administration of 2% dorzolamide ophthalmic solution in dogs and the development of metabolic acidosis. Additionally, the influence of various potential risk factors, including age, body weight, sex, use of topical or systemic NSAIDs, and preoperative medications on the occurrence of metabolic acidosis, was evaluated. RESULTS: A significant association was found between the use of 2% dorzolamide ophthalmic solution and perianesthetic metabolic acidosis (OR, 6.79; 95% CI, 2.00 to 23.02; P = .002). Furthermore, topical dorzolamide administration was significantly associated with both perianesthetic hypokalemia (OR, 3.52; 95% CI, 1.11 to 11.20; P = .033) and perianesthetic hyperchloremia (OR, 9.25; 95% CI, 1.71 to 50.01; P = .010). CLINICAL RELEVANCE: The use of 2% dorzolamide ophthalmic solution is associated with perianesthetic metabolic acidosis, hypokalemia, and hyperchloremia in dogs. It is prudent to be aware of these risks, especially before anesthesia.

Effect of Aerosolised Salbutamol Administration on Arterial Potassium Concentration in Anaesthetised Horses.

Aerosolized salbutamol has been associated with hypokalemia in horses undergoing colic surgery. The objective of this study was to evaluate the effect of aerosolized salbutamol on arterial potassium concentration ([K +]) in healthy anaesthetized horses undergoing elective surgery. Anesthetic records were reviewed from healthy adult horses undergoing elective surgery over a 3-year period with two complete sets of arterial electrolyte (sodium [Na +], potassium [K +], chloride [Cl -], calcium [Ca 2+]) concentration measurements. Records were excluded if intra-operative electrolyte supplementation, antimicrobial administration or noncrystalloid fluid administration were documented or if salbutamol was administered prior to electrolyte measurement. Sixty records which fulfilled inclusion criteria were divided into two groups depending on whether or not aerosolized salbutamol (2µg kg -1) (to treat hypoxemia) was administered after baseline electrolyte measurement and before the second electrolyte measurement. Aerosolized salbutamol was administered (Group S) in 22 horses and not administered (group NS) in 38 horses. There was a significant reduction in [K +] and [Ca 2+] between baseline and the second electrolyte measurement in both groups (P< .001). The reduction in [K +] between baseline and the second electrolyte measurement was significantly greater in group S (12.3%) compared to group NS (6.9%) (P= .017) and was significantly associated with salbutamol administration (P= .04). The results of this study indicate that monitoring [K +] is important in anaesthetized horses, particularly after aerosolized salbutamol administration.

Polimiopatia hipocalêmica e hipertensão secundária a hiperaldosteronismo primário felino / Hypokalemic polymyopathy and secondary hypertension to feline primary hyperaldosteronism

O hiperaldosteronismo se define pela hipersecreção de aldosterona pelas suprarrenais, resultando em excesso de sódio e redução de potássio sanguíneo. Esta hipersecreção deve-se à síntese autônoma de aldosterona por células adrenais hiperplásicas ou neoplásicas, que agem independentemente da estimulação pelo sistema renina-angiotensina. A doença acomete felinos de adultos maduros a idosos. O excesso de aldosterona culmina em hipertensão sistêmica e/ou hipocalemia, que levam à fraqueza muscular e alterações oculares. O diagnóstico é baseado em exames laboratoriais e de imagem, e o tratamento pode ser clínico ou cirúrgico. O prognóstico é considerado favorável quando as medicações são capazes de melhorar as manifestações clínicas ou quando é possível realizar o procedimento cirúrgico. O presente trabalho visa relatar o caso de um felino macho de 13 anos, castrado, sem raça definida, com hipocalemia persistente secundária a um presuntivo tumor adrenal.

Hyperaldosteronism is defined by the hypersecretion of aldosterone by the adrenal glands resulting in excess sodium and reduced blood potassium. This hypersecretion is due to the autonomous synthesis of aldosterone by hyperplastic or neoplastic adrenal cells, which act independently of stimulation by the renin-angiotensin system. The disease affects felines in the age group from mature adults to the elderly. The excess of aldosterone culminates in systemic hypertension and/or hypokalemia, which leads to muscle weakness and ocular changes. The diagnosis is based on laboratory and imaging tests and treatment can be clinical or surgical. The prognosis is considered favorable when the medications are able to improve the clinical manifestations or when it is possible to perform the surgical procedure. The present paper aims to report the case of a 13-year-old male cat, castrated, crossbred, with persistent hypokalemia secondary to a presumptive adrenal tumor.

Retrospective study of the efficacy of oral potassium supplementation in cats with kidney disease.

OBJECTIVES: The aim of this study was to assess the effect of three oral potassium supplements (potassium gluconate tablets [PGT], potassium gluconate granules [PGG] and potassium citrate granules [PCG]) on hypokalemia and serum bicarbonate in cats with chronic kidney disease (CKD). METHODS: Medical records (2006-2016) were retrospectively searched for cats that had been prescribed an oral potassium supplement for management of their CKD-associated hypokalemia. For inclusion, laboratory work had to be available at the time of hypokalemia diagnosis, and at recheck within 1-6 weeks. Treatment response was defined in three ways: any increase in potassium, an increase in potassium to within the normal reference interval, and an increase to >4 mEq/l. RESULTS: Thirty-seven cats met inclusion criteria (16 PGT, 11 PGG, 10 PCG). Dosing ranged from 0.21 to 1.6 mEq/kg/day for PGT, from 0.25 to 1.48 mEq/kg/day for PGG and from 0.04 to 1.34 mEq/kg/day for PCG. After supplementation, 36/37 cats had an increase in potassium, 34/37 increased to within the reference interval and 24/37 had an increase in potassium to >4 mEq/l. There was a statistically significant difference in serum potassium post-supplementation for all three treatments: PGT (P = 0.0001), PGG (P = 0.001) and PCG (P = 0.002). There was a positive correlation between PGT dose and change in potassium concentration (P = 0.04), but there was no significant correlation for PGG or PCG. In cats that had data available, serum bicarbonate increased >2 mEq/l in 1/6 PGT, 1/6 PGG and 3/4 PCG cats. CONCLUSIONS AND RELEVANCE: All three potassium supplements were effective in treating hypokalemia secondary to CKD in the majority of cats despite variable dosing. Data were limited to assess the alkalinizing effect and prospective studies are needed.

Hipoparatireoidismo secundário ao uso prolongado de omeprazol em um cão: relato de caso / Secondary hypoparathyroidism to omeprazole prolonged use in a dog: case report

O hipoparatireoidismo, quer seja primário ou secundário, é uma doença rara em cães, causada pela diminuição da secreção de paratormônio pelas paratireoides, que leva a sinais clínicos resultantes da hipocalcemia. O omeprazol vem sendo cada vez mais utilizado na medicina veterinária visando à diminuição na produção de líquor, mas existem poucos estudos sobre os efeitos colaterais relacionados ao uso crônico dessa medicação. Relata-se o caso de um cão macho da raça Yorkshire Terrier, com quatro anos de idade, com sinais clínicos de dor, sendo verificada calcificação em pelve e divertículo renal. Segundo o proprietário, o cão fazia uso de omeprazol há mais de dois anos devido ao histórico de hidrocefalia. Os exames laboratoriais evidenciaram anemia microcítica hipocrômica, hipocalemia, hiperfosfatemia, hipocalcemia, hipomagnesemia e hipercalciúria. A dosagem do paratormônio sérico confirmou o hipoparatireoidismo. Após a suspensão do omeprazol, as alterações encontradas nos exames se normalizaram, confirmando que a causa do hipoparatireoidismo era o uso crônico da medicação.(AU)

Primary or secondary hypoparathyroidism is a rare disease in dogs caused by the decreased secretion of parathormone from the parathyroid glands, leading to clinical signs of hypocalcemia. Omeprazole has been increasingly used in veterinary medicine in order to reduce the production of cerebrospinal fluid, but there are few reports of side effects related to its chronic use. We report a case of a four-year-old male Yorkshire terrier with clinical signs of pain, calcification in the pelvis and renal diverticulum. According to the owner, the dog had been receiving omeprazole for over 2 years because of the history of hydrocephalus. Hematological exams revealed hypochromic microcytic anemia, hypokalemia, hyperphosphatemia, hypocalcemia, hypomagnesemia besides hypercalciuria. The determination of serum parathyroid hormone concentrations confirmed hypoparathyroidism. After interrupting omeprazole, the altered features on the exams returned to normal values, confirming that the cause of hypoparathyroidism was the chronic use of the drug.(AU)

Concentration of Potassium in Plasma, Erythrocytes, and Muscle Tissue in Cows with Decreased Feed Intake and Gastrointestinal Ileus.

BACKGROUND: Healthy cows consume large amounts of potassium and a sudden loss in appetite can lead to hypokalemia. The routine method to evaluate potassium homeostasis is the measurement of the extracellular potassium in plasma or serum, but this does not provide information about the intracellular potassium pool. HYPOTHESIS/OBJECTIVES: To evaluate potassium homeostasis by comparing the extracellular and intracellular potassium concentration in cows with reduced feed intake and gastrointestinal ileus. ANIMALS: Twenty cows 1-3 days postpartum (group 1) and 20 cows with gastrointestinal ileus (group 2). METHODS: Observational cross-sectional study. Plasma potassium was measured by using an ion-sensitive electrode. Intracellular potassium was measured in erythrocytes and muscle tissue (muscle biopsy) by using inductively coupled plasma optical emission spectroscopy. RESULTS: Cows of group 1 did not have hypokalemia. Overall cows with gastrointestinal ileus were hypokalemic (mean ± SD, 2.9 mmol/L ± 0.78), but potassium concentration in erythrocytes and muscle tissue was not lower than in postpartum cows. Intracellular potassium in erythrocytes varied very widely; group 1: 3497-10735 mg/kg (5559 ± 2002 mg/kg), group 2: 4139-21678 mg/kg (7473 ± 4034 mg/kg). Potassium in muscle tissue did not differ between group 1 (3356 ± 735 mg/kg wet weight) and group 2 (3407 ± 1069 mg/kg wet weight). No association between extracellular and intracellular potassium concentrations was detected. CONCLUSIONS AND CLINICAL IMPORTANCE: That measurement of plasma potassium concentration is not sufficient to evaluate potassium metabolism of cows.

Clinical findings, diagnostics and outcome in 33 cats with adrenal neoplasia (2002-2013).

OBJECTIVES: The objective of this retrospective study was to describe the clinical signs and diagnostic findings in cats with histopathologically confirmed adrenal neoplasms, and to assess correlations with survival data. METHODS: Study data were acquired by reviewing medical records for all cats diagnosed with adrenal neoplasms at seven referral institutions between 2002 and 2013. Inclusion criteria required a histopathologic diagnosis of an adrenal neoplasm (ante-mortem or on necropsy). RESULTS: Thirty-three cats met the inclusion criteria for the study. The most common presenting complaints included weakness (n = 12), respiratory signs (n = 4), blindness (n = 4) or gastrointestinal signs (n = 3). Laboratory abnormalities included hypokalemia (n = 18), alkalemia (n = 12), elevated creatine kinase (>3000, n = 5) and azotemia (n = 4). In addition, hypertension was noted in 13 cats. Thirty cats were diagnosed with cortical tumors (17 carcinomas, 13 adenomas) and three cats were diagnosed with pheochromocytomas. Twenty-five cats underwent tests to evaluate the function of the adrenal tumors; 19/25 cats had functional tumors (hyperaldosteronism [n = 16], hypercortisolemia [n = 1], high estradiol [n = 1], and hypersecretion of aldosterone, estradiol and progesterone [n = 1]). Twenty-six cats underwent adrenalectomy, one cat was medically managed and six were euthanized without treatment. Long-term survival postoperatively ranged from 4-540 weeks, with 20 (77%) cats surviving the perioperative period of 2 weeks. The only variable that was found to be negatively associated with survival was female sex. The most common complications noted during the perioperative period were hemorrhage and progressive lethargy and anorexia. CONCLUSIONS AND RELEVANCE: Surgical treatment for feline adrenal tumors (regardless of tumor type) resulted in good long-term survival. Given that pre- and postoperative hypocortisolemia was identified in this study, and, in addition, hypersecretion of more than one adrenal hormone occurred in one cat, adrenal panels prior to surgery may be beneficial as part of the preoperative work-up.

Periodic hypokalaemic polymyopathy in Burmese and closely related cats: a review including the latest genetic data.

GLOBAL IMPORTANCE: Hypokalaemic polymyopathy is a genetic disease of Burmese cats that has been encountered in Australasia, Europe and South Africa. CLINICAL FEATURES: Affected cats usually present with signs of muscle weakness and muscle pain in the first year of life. Although certain clinical features, such as ventroflexion of the head and neck, are especially characteristic, some cats do not display these signs. Usually weakness is periodic or episodic, but occasionally it is incessant. DIAGNOSTIC CHALLENGES: In the past, diagnosis was problematic in that clinical signs and a lowered serum potassium concentration were not always observed synchronously. This necessitated serial serum potassium concentration determinations, testing of serum creatine kinase activity and exclusion of other potential causes of muscle disease in cats (including muscular dystrophies, Toxoplasma myositis, immune-mediated polymyositis, organophosphorus intoxication and envenomations). Signs in affected cats often waxed and waned, possibly in response to changes in dietary factors and stress, and some cats could apparently 'grow out of' the condition. RECENT ADVANCES AND FUTURE PROSPECTS: Recent molecular genetics research has identified a single nonsense mutation in the gene (WNK4) coding for lysine-deficient 4 protein kinase, an enzyme present primarily in the distal nephron. The underlying pathomechanism in affected cats is therefore likely to be a potassium wasting nephropathy, as this enzyme is involved in complex sodium/potassium exchange mechanisms in the kidney. Additional functional characterisation of the condition is warranted to define precisely how, why and when the serum potassium concentration declines. The diagnosis of Burmese hypokalaemia is now straightforward, as an inexpensive PCR test can identify affected homozygous individuals, as well as carriers. The elimination of this condition from the Burmese breed, and also from pedigree cats infused with Burmese lines, such as the Bombay, Tonkinese and Tiffanie breeds, should therefore be possible.

Hypokalaemia in a hyperthyroid domestic shorthair cat with adrenal hyperplasia.

A 13-year-old female domestic shorthair cat presented with polyphagia and weight loss. Marked systolic hypertension was found on examination. Elevated total thyroxine levels confirmed hyperthyroidism, and hypokalaemia was also documented. A euthyroid state and normotension were achieved following 4 weeks of treatment with carbimazole and amlodipine. Despite potassium supplementation, the hypokalaemia worsened. Abdominal ultrasonography revealed left adrenomegaly. Plasma aldosterone concentrations were initially in the lower half of the reference interval and, when repeated 2 months later, were undetectable. Urea and creatinine remained in the lower half of the reference interval throughout treatment, and urine specific gravity suggested good urine concentrating ability. The fractional excretion of potassium confirmed a renal source of potassium loss. Blood gas analysis was unremarkable. It was theorised that an aldosterone precursor was causing signs of mineralocorticoid excess and undetectable plasma aldosterone levels. Treatment with an aldosterone receptor antagonist successfully increased the serum potassium concentration. Owing to difficulties administering medication and associated effects on life quality the cat was euthanased. Adrenal hyperplasia was apparent on post-mortem histopathology.

Manual ventilation therapy and aggressive potassium supplementation in the management of respiratory failure secondary to severe hypokalaemia in a cat with exocrine pancreatic insufficiency.

A domestic shorthair cat was referred for progressive muscle weakness and dyspnoea. The cat had a 2-month history of severe weight loss, small intestinal diarrhoea, polyphagia and polyuria/polydipsia. Biochemical analysis and venous blood gas evaluation revealed severe hypokalaemia [1.7 mmol/l; reference interval (RI): 3.5-5.1 mmol/l] and hypoventilation (partial pressure of carbon dioxide = 68 mmHg; RI: 34-38 mmHg). Aggressive potassium supplementation was initiated. The cat was manually ventilated until serum potassium increased to 3 mmol/l. A diagnosis of exocrine pancreatic insufficiency (EPI) was made based on clinical signs and serum feline trypsin-like immunoreactivity (0.1 µg/l; RI: 12-82 µg/l). Medical management of the EPI resulted in clinical recovery.

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.

Hypokalaemic paresis, hypertension, alkalosis and adrenal-dependent hyperadrenocorticism in a dog.

Generalised paresis, severe hypokalaemia and kaliuresis, metabolic alkalosis and hypertension, characteristic of mineralocorticoid excess, were identified in a dog with hyperadrenocorticism due to a functional adrenocortical carcinoma. Aldosterone concentration was decreased and deoxycorticosterone concentration increased in the presence of hypokalaemia. These metabolic abnormalities resolved with resection of the carcinoma. Mineralocorticoid excess in dogs with hyperadrenocorticism is generally considered to be of little clinical significance but resulted in the acute presentation of this patient. The possible pathogenesis of mineralocorticoid excess in this case of canine hyperadrenocorticism is discussed.

Primary hyperaldosteronism in a domestic ferret with an adrenocortical adenoma.

CASE DESCRIPTION: A 6-year-old spayed female domestic ferret was evaluated because of lethargy, alopecia, pruritus, and an abdominal mass. CLINICAL FINDINGS: On initial examination, nonregenerative anemia, mild azotemia, and a large left adrenal gland mass were identified. However, deterioration of the ferret's general condition prevented excision of the mass, and dyspnea, weakness, hypertension, and severe hypokalemia developed. Plasma aldosterone concentration was >3329 pmol/L, confirming a provisional diagnosis of hyperaldosteronism. High concentrations of sex hormones were also observed, but baseline cortisol concentration was within reference limits. TREATMENT AND OUTCOME: Medical treatment included oral administration of spironolactone, potassium gluconate, leuprolide acetate, amlodipine, and benazepril. Inhalation of albuterol proved effective in reducing the dyspnea. In the following weeks, serum potassium concentration returned to within reference limits and hypertension decreased, but dyspnea persisted. Two months after initial examination, the ferret became anorectic and was euthanized. Histologic examination revealed a large left adrenal gland adenoma, progressive chronic nephropathy, severe pulmonary edema, and focal fibrosis in the left ventricle. Immunohistochemical staining of the adrenal gland mass revealed aldosterone within neoplastic adrenocortical cells. CLINICAL RELEVANCE: Findings suggested that primary hyperaldosteronism should be considered as a possible cause in ferrets with hypokalemia, hypertension, and an adrenal gland mass. Early detection of aldosterone-secreting masses might allow for removal of the tumor before irreversible complications occur.

Hypernatremia associated with intracranial B-cell lymphoma in a cat.

An 8-year-old, spayed female, domestic shorthair cat with a history of hyperthyroidism, anorexia, dehydration, cervical ventroflexion, and behavioral changes was referred to the Iowa State University College of Veterinary Medicine. The cat was obtunded, with severe dehydration (15%) and hypothermia (86 degrees F), and severe muscle atrophy and fasciculations. Serum biochemical abnormalities included severe hypernatremia (195 mmol/L, reference interval 155-165 mmol/L), hyperchloridemia (161 mmol/L, reference interval 123-131 mmol/L), and hypokalemia (3.6 mmol/L, reference interval 4.0-5.7 mmol/L). Calculated osmolality was 418 mOsm/kg (reference interval 280-305 mOsm/kg), attributable to the hypernatremia. The cat was kept warm and given fluid and glucocorticoid therapy and supportive measures but remained unresponsive. Hypernatremia and hyperosmolality improved through day 3, when the cat died suddenly. At necropsy, a 1.25-cm mass was found in the area of the thalamus and interthalamic adhesion that extended to the ventral aspect of the cerebrum. The histologic and immunohistochemical diagnosis was B-cell lymphoma. Hypernatremia and hyperosmolality in this cat were attributed to primary adipsia and hypothalamic dysfunction secondary to effacement of central nervous system tissue by neoplastic lymphocytes. To the authors' knowledge, this is the first reported case of central nervous system lymphoma, confirmed by use of immunohistochemical analysis as a B-cell phenotype, associated with hypernatremia. It also is the first reported case of lymphoma in animals limited to the thalamus, hypothalamus, and cerebrum, with no involvement of the spinal cord.

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.

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.

Hepatic carcinoid, hypercortisolism and hypokalaemia in a dog.

A German Shepherd dog was diagnosed with periodic myopathy secondary to persistent hypokalaemia. Hormone analysis revealed excess cortisol secretion. A neuroendocrine carcinoma, thought to be a primary hepatic carcinoid, was detected in the liver. Ectopic adrenocorticotrophin hormone secretion was suspected as the cause of hypercortisolism and hypokalaemia, although this could not be confirmed by immunohistochemical staining.

A potentially misleading presentation and course of acute myelomonocytic leukemia in a dog.

A nine-year-old, castrated male golden retriever had lethargy, fever, massive peripheral lymphadenomegaly, hepatosplenomegaly, and pale mucous membranes. There was a marked leukocytosis (456.3 x 10(3) cells/microliter) with 99% blasts; a moderate, nonregenerative anemia; and marked thrombocytopenia. A tentative diagnosis of acute lymphocytic leukemia was made pending results of cytochemical staining. Despite the severity of the laboratory and clinical findings, the dog exhibited a partial response to an induction chemotherapy protocol commonly used for lymphoma. Subsequent cytochemical staining of the original blood and bone-marrow samples resulted in a revised diagnosis of acute myelomonocytic leukemia (AML-M4). Clinicopathological findings, response to treatment, and clinical outcome in this case of canine AML-M4 are discussed.