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.

Rebound hyperkalemia in a dog with albuterol toxicosis after cessation of potassium supplementation.

OBJECTIVE: To describe the presentation of rebound hyperkalemia as a delayed side effect of albuterol toxicity in a dog. CASE SUMMARY: A 3-year-old female neutered mixed-breed dog was presented for albuterol toxicosis that led to a severe hypokalemia, hyperlactatemia, and hyperglycemia. The dog also experienced sinus tachycardia and generalized weakness. Treatment was instituted with intravenous fluid therapy and potassium supplementation, and the dog was monitored with a continuous electrocardiogram. Resolution of hypokalemia was documented 12 hours after initial presentation, at which time fluid therapy and potassium supplementation were discontinued. There were no further periods of sinus tachycardia, but instead the dog developed ventricular ectopy with rapid couplets (instantaneous rates of 300/min). An echocardiogram revealed normal cardiac size and function. Twenty-four hours after presentation, the patient developed severe hyperkalemia, despite discontinuation of fluids and potassium supplementation for 12 hours. Serial venous and urinary electrolytes were performed for determination of the fractional excretion of electrolytes. These data confirmed rebound hyperkalemia (7.0 mmol/L), consistent with a markedly increased fractional excretion of potassium, and secondary to the release of potassium from inside the cells. Fluid therapy with dextrose supplementation was provided until 36 hours postpresentation. The hyperkalemia resolved, and the dog was discharged after 44 hours of hospitalization. NEW OR UNIQUE INFORMATION PROVIDED: This case documents rebound hyperkalemia following treatment of albuterol toxicosis in a dog. This case highlights the importance of understanding the distribution of total body potassium when treating serum hypokalemia. Transcellular shifts of potassium, as in the case of albuterol toxicosis, can lead to rebound hyperkalemia even after discontinuation of potassium supplementation. This case further explores the utility of fractional excretion of electrolytes in elucidating the etiology and management of electrolyte disturbances.

Model-based exploration of hypokalemia in dairy cows.

Hypokalemia in dairy cows, which is characterized by too low serum potassium levels, is a severe mineral disorder that can be life threatening. In this paper, we explore different originating conditions of hypokalemia-reduced potassium intake, increased excretion, acid-base disturbances, and increased insulin-by using a dynamic mathematical model for potassium balance in non-lactating and lactating cows. The simulations confirm observations described in literature. They illustrate, for example, that changes in dietary intake or excretion highly effect intracellular potassium levels, whereas extracellular levels vary only slightly. Simulations also show that the higher the potassium content in the diet, the more potassium is excreted with urine. Application of the mathematical model assists in experimental planning and therefore contributes to the 3R strategy: reduction, refinement and replacement of animal experiments.

Determinants of hypokalemia following hypertonic sodium bicarbonate infusion.

The hypokalemic response to alkali infusion has been attributed to the resulting extracellular fluid (ECF) expansion, urinary potassium excretion, and internal potassium shifts, but the dominant mechanism remains uncertain. Hypertonic NaHCO3 infusion (1 N, 5 mmol/kg) to unanesthetized dogs with normal acid-base status or one of the four chronic acid-base disorders decreased plasma potassium concentration ([K+]p) at 30 min in all study groups (Δ[K+]p, - 0.16 to - 0.73 mmol/L), which remained essentially unaltered up to 90-min postinfusion. ECF expansion accounted for only a small fraction of the decrease in ECF potassium content, (K+)e. Urinary potassium losses were large in normals and chronic respiratory acid-base disorders, limited in chronic metabolic alkalosis, and minimal in chronic metabolic acidosis, yet, ongoing kaliuresis did not impact the stability of [K+]p. All five groups experienced a reduction in (K+)e at 30-min postinfusion, Δ(K+)e remaining unchanged thereafter. Intracellular fluid (ICF) potassium content, (K+)i, decreased progressively postinfusion in all groups excluding chronic metabolic acidosis, in which a reduction in (K+)e was accompanied by an increase in (K+)i. We demonstrate that hypokalemia following hypertonic NaHCO3 infusion in intact animals with acidemia, alkalemia, or normal acid-base status and intact or depleted potassium stores is critically dependent on mechanisms of internal potassium balance and not ECF volume expansion or kaliuresis. We envision that the acute NaHCO3 infusion elicits immediate ionic shifts between ECF and ICF leading to hypokalemia. Thereafter, maintenance of a relatively stable, although depressed, [K+]e requires that cells release potassium to counterbalance ongoing urinary potassium losses.

Presumptive renal tubular acidosis secondary to topiramate administration in a cat.

OBJECTIVE: To describe renal tubular acidosis (RTA) and secondary acquired hyperaldosteronism in a cat as an adverse effect of topiramate therapy. CASE SUMMARY: An 8-year-old neutered female cat on chronic oral topiramate therapy at a recommended dose (11.9 mg/kg q 8 h) for seizure control was presented with severe metabolic acidosis and hypokalemia. Plasma electrolyte and acid-base analysis identified a severe metabolic acidosis (pH 7.153, reference interval: 7.31-7.46), hypokalemia (2.08 mmol/L [2.08 mEq/L], reference interval: 3.5-4.8 mmol/L [3.5-4.8 mEq/L]), and ionized hypercalcemia (1.85 mmol/L [1.85 mEq/L], reference range: 1.1-1.4 mmol/L [1.1-1.4 mEq/L]). Urinalysis revealed a urine specific gravity of 1.021 and a pH of 7.0. Diagnostic workup suggested distal RTA as a cause of the cat's acid-base and electrolyte disturbances. Aldosterone concentration was moderately increased, suggestive of secondary hyperaldosteronism. The metabolic abnormalities resolved with supportive care and discontinuation of topiramate. NEW OR UNIQUE INFORMATION PROVIDED: Topiramate is suggested to have led to the development severe RTA in a cat.

Retrospective evaluation of acute salbutamol (albuterol) exposure in dogs: 501 cases.

OBJECTIVE: To determine the common clinical signs, with onset and duration, treatments given, and outcome in dogs with acute, accidental exposure to salbutamol. DESIGN: Retrospective study. ANIMALS: Five hundred and one canine cases reported to the UK's Veterinary Poisons Information Service (VPIS). MEASUREMENTS AND MAIN RESULTS: A review of all records in the VPIS database for dogs exposed to salbutamol was carried out. After applying inclusion and exclusion criteria, the records of 501 dogs were further analyzed. The most common clinical signs were tachycardia (80.6%), tachypnea (32.9%), depression (21.0%), and vomiting (19.2%). The dose was unknown in most cases as the dogs typically pierced a salbutamol inhaler. The blood potassium concentration was measured in at least 142 dogs and hypokalemia was reported in 21.2% (106/501), 18 (17%) of which had associated weakness, twitching, or collapse. Three dogs had paralysis probably as a result of hypokalemia, although no potassium concentration was reported in these cases. Arrhythmias occurred in 17 dogs (3.4%), and 7 required pharmacological intervention. There were no reports of persistent cardiac injury or thermal injury from the compressed gas present in some salbutamol products. Signs were rapid in onset, generally within 1-3 h, and, where time to outcome was recorded (n = 172), 78% of dogs recovered within 24 h. Of the 501 dogs, no treatment was required in 27.9%. Beta-blockers were used in 39.5%, intravenous fluids in 28.7%, and potassium supplementation in 15.8%. Overall, 30 dogs remained asymptomatic (6.0%), 469 recovered (93.6%), and 2 dogs (0.4%) died. CONCLUSIONS: Most dogs exposed to salbutamol rapidly develop clinical signs; these were commonly increased heart and respiration rates. Hypokalemia and arrhythmias (particularly ventricular arrhythmias) are potential complications. Any dog that chews a salbutamol inhaler should be assessed promptly for signs of toxicosis. Prognosis in dogs with acute salbutamol exposure is good, but more guarded in those with severe tachycardia and at risk of cardiac injury.

Acute nontraumatic rhabdomyolysis in a Greyhound after albuterol toxicosis.

OBJECTIVE: To describe the clinical features of rhabdomyolysis due to albuterol toxicosis in a Greyhound. CASE SUMMARY: A 4-year-old neutered male Greyhound was presented for albuterol toxicosis leading to severe hypokalemia and respiratory paralysis. After 3 hours of mechanical ventilation, pigmenturia and marked enlargement, firmness, and pain of the left thigh muscles were noted. Severe hyperkalemia and cardiac arrhythmias were identified after turning the patient. After discontinuation of mechanical ventilation, other muscles became involved, and the patient developed acute kidney injury and concern for multiple organ dysfunction syndrome over the next 5 days. On day 6, the patient was euthanized, and necropsy revealed myocardial and skeletal muscle necrosis, myoglobinuria, and acute tubular degeneration. NEW OR UNIQUE INFORMATION PROVIDED: To the authors' knowledge, this is the first case of albuterol toxicosis leading to rhabdomyolysis.

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.

Retrospective evaluation of albuterol inhalant exposure in dogs: 36 cases (2007-2017).

OBJECTIVE: To describe the clinical features, clinicopathological features, treatment, and outcome of dogs presented for albuterol exposure. DESIGN: Retrospective case series from January 2007 to December 2017. SETTING: Tertiary veterinary facility. ANIMALS: Thirty-six client-owned dogs presenting for known or suspected albuterol exposure secondary to chewing on albuterol metered-dose inhalers (MDIs). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: All dogs presented with clinical signs attributable to albuterol exposure. The most common physical examination abnormality was sinus tachycardia, noted in 34 of 36 (94%) dogs. Twenty-seven patients (75%) were admitted to the hospital for therapy, with a median length of hospitalization of 20.5 hours (16.75-24.5). Thirty-two of 36 dogs had serum electrolytes evaluated at admission, with 22 of 32 (69%) presenting with hypokalemia ([K+] < 3.62 mmol/L]). Hyperlactatemia ([lactate] > 2.80 mmol/L) was noted in 23 of 28 (82%) dogs. A negative correlation was found between serum lactate and potassium (r = -0.64, r2  = 0.40, P = 0.0003). Hyperglycemia ([glucose] > 6.44 mmol/L) was noted in 20 of 30 (67%) dogs. Beta antagonist therapy was utilized in 20 of 36 (56%) of dogs. CONCLUSIONS: Although uncommon, albuterol intoxication can lead to significant clinical and electrolyte abnormalities. Albuterol-induced hypokalemia and associated tachyarrhythmias can be successfully managed, and albuterol intoxication has an excellent prognosis for survival to discharge. A minimum database should be evaluated in all dogs presenting for suspected albuterol exposure, with lactate and glucose monitored carefully in dogs with moderate or severe hypokalemia given the correlation found.

Hypokalemia associated with topical administration of dorzolamide 2% ophthalmic solution in cats.

OBJECTIVE: To evaluate the effect of dorzolamide 2% ophthalmic solution on serum potassium and other hematologic parameters in cats. MATERIALS AND METHODS: Part I: Medical records from a single institution were retrospectively reviewed. Inclusion criteria consisted of cats diagnosed with glaucoma for which appropriate clinicopathological data were available both prior to and after the initiation of therapy with dorzolamide 2% ophthalmic solution. Part II: Healthy adult cats were enrolled in a prospective double-masked, randomized, cross-over study. Either dorzolamide 2% ophthalmic solution or placebo was administered OU t.i.d. for 6 weeks. Serum potassium, sodium, chloride, glucose, ALP, and ALT levels were assessed every 2 weeks. After a 2-week washout period, each cat was given the opposite topical preparation, and the study process was repeated. RESULTS: Part I: Of the twenty-seven eligible cases, hypokalemia developed in 29.6% (n = 8). While female spayed cats were significantly more likely to become hypokalemic, serum potassium was not significantly affected by age, weight, dosing frequency, or number of eyes treated. Part II: Ten cats participated in the study. Potassium values were significantly lower in cats receiving dorzolamide 2% ophthalmic solution compared to placebo at each time point throughout the 6-week study period. Additionally, chloride values were significantly greater in the treatment group at week two and four compared to the placebo group. CONCLUSIONS: Administration of dorzolamide 2% ophthalmic solution has a measurable effect on serum potassium level in cats and may result in clinical hypokalemia. Therefore, routine electrolyte monitoring is advised for feline patients receiving this medication.

Refeeding syndrome in small ruminants receiving parenteral nutrition.

BACKGROUND: Small ruminants presented to tertiary care facilities commonly suffer from severe protein-calorie malnutrition. Some of these patients require parenteral nutrition (PN; amino acids and dextrose with or without lipids) during hospitalization. Refeeding syndrome, a potentially fatal shift of electrolytes seen in malnourished patients during refeeding, may occur. OBJECTIVE: (a) To report the prevalence of refeeding syndrome in small ruminants receiving PN and (b) to determine risk factors for the development of refeeding syndrome. ANIMALS: Hospitalized small ruminants (n = 20) that received PN from 2010 to 2018 and that had serial (≥2) monitoring of serum electrolyte concentrations after initiation of PN. METHODS: Retrospective case series. Refeeding syndrome was defined as the presence of at least 2 of the following electrolyte abnormalities after initiation of PN: hypophosphatemia, hypokalemia, hypomagnesemia, or some combination of these. Data was analyzed using Fisher's exact test, followed by univariate logistic regression. RESULTS: Eleven of 20 (55%) animals met the definition of refeeding syndrome. Mean minimum serum phosphorus concentration in animals with refeeding syndrome was 1.96 ± 0.69 mg/dL (reference range, 4.2-7.6 mg/dL). Eleven of 20 animals survived to discharge. Survival rate did not differ significantly between refeeding cases (4/11, 36.3%) and nonrefeeding cases (7/9, 77.8%; P = .09). Mean serum phosphorus concentration was significantly lower in nonsurvivors than in survivors (1.88 ± 0.10 mg/dL vs 4.32 ± 0.70 mg/dL, P = .006). CONCLUSIONS AND CLINICAL IMPORTANCE: We report the prevalence of refeeding syndrome in small ruminants receiving PN. Clinicians should anticipate refeeding syndrome after initiation of PN and consider pre-emptive supplementation with phosphorus, potassium, magnesium, or some combination of these.

Complex Disease Management: Managing a Cat with Comorbidities.

Many older cats often suffer concurrently from multiple conditions. By focusing on the common concerns, rather than conflicting requirements, a management program can be devised. Optimize hydration, nutrition, and ensure comfort though providing analgesia and a low-stress environment in which the patient's feline-specific nature is respected both in the clinic and at home. Additional requirements, such as hyperphosphatemia or hypokalemia, can be met using treatments outside of diet, if necessary.

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.

Retrospective evaluation of the severity of and prognosis associated with potassium abnormalities in dogs and cats presenting to an emergency room (January 2014-August 2015): 2441 cases.

OBJECTIVE: To determine the severity, concurrent clinical signs, and disease processes associated with potassium abnormalities in dogs and cats presenting to a veterinary emergency department and associated mortality. DESIGN: Retrospective and descriptive study over 20 months. SETTING: University teaching hospital. ANIMALS: 1916 dog and 525 cat visits. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Medical records from patients with a potassium concentration measured within 24 hours of admission were identified. Hypokalemia and hyperkalemia were defined as a potassium concentration <3.5 mmol/L [3.5 mEq/L] and >5 mmol/L [5 mEq/L], respectively. Associated disease processes and pathophysiologic risk factors for potassium abnormalities were reviewed for moderate to severe potassium abnormalities (<3 mmol/L or ≥6 mmol/L) [<3 mEq/L or ≥6 mEq/L]. Mortality associated with normokalemia, mild, and moderate to severe dyskalemia were evaluated. Overall prevalence of abnormal potassium concentration was 27% in dogs and 40% in cats. Moderate to severe hypokalemia and hyperkalemia were present in 3% of dogs and 8% of cats, and 2% of dogs and 7% of cats, respectively. Moderate to severe hypokalemia was most commonly associated with gastrointestinal disease (48% of dogs and 44% of cats) while moderate to severe hyperkalemia was most commonly associated with urinary tract disease (60% of dogs and 97% of cats). Dogs with hypokalemia and dogs and cats with hyperkalemia (P < 0.001) had significantly greater mortality than those with normokalemia. Dogs with mild hypokalemia and mild hyperkalemia (P < 0.0001) had higher mortality than dogs with normokalemia, but this was not found in cats. CONCLUSIONS: Dyskalemia was common in this population and was associated with greater mortality. Moderate to severe potassium abnormalities were uncommon in this population and occurred most frequently in animals with gastrointestinal and urinary tract disease.

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)

Comparative study on 3 oral potassium formulations for treatment of hypokalemia in dairy cows.

BACKGROUND: Hypokalemia is of clinical relevance in cattle. Different mostly empirical treatment options are suggested. HYPOTHESIS/OBJECTIVES: To evaluate if oral administration of potassium influences the plasma concentration, the intracellular concentration in erythrocytes and in muscle, renal excretion of potassium, and to assess if there are differences in the efficacy of the potassium formulations. ANIMALS: Thirty cows with hypokalemia (plasma concentration <3.5 mmol/L) were systematically allocated to 3 treatment groups (10 cows/group). METHODS: The cows received 52 g of potassium in different formulations: group B-potassium chloride bolus (release over 12 hours); group G-potassium propionate gel (release over 2 hours); and group S-potassium chloride solution (immediately available). Potassium concentrations were repeatedly measured in plasma, erythrocytes, muscle, and urine using ICP-OES. RESULTS: Plasma potassium concentrations for all preparations increased within 30 minutes and the increase lasted for 12 hours. The concentrations of potassium in the erythrocytes and in the muscle, renal potassium excretion, and total urine volume were not affected by administration of any product. There were no differences between the treatments groups. The feed intake increased in 50% of cows within 2 hours after potassium application, which may contribute to the increase of plasma potassium concentration. CONCLUSIONS AND CLINICAL IMPORTANCE: All the studied potassium formulations are equally effective to treat hypokalemia in dairy cows for over 12 hours but do not influence intracellular concentration or renal excretion of potassium. The plasma potassium concentration should be reevaluated after 12 hours.

Acute barium poisoning in a dog after ingestion of handheld fireworks (party sparklers).

OBJECTIVE: To report a case of acute barium poisoning in a dog subsequent to ingestion of a common handheld pyrotechnic (sparkler). CASE SUMMARY: A 5-year-old female neutered German Shorthaired Pointer presented with acute onset of generalized flaccid muscle paralysis and fasciculations, ptyalism, and an irregular heart rhythm. Marked hypokalemia (1.9 mmol/L [mEq/L]; reference range [3.5-5.8 mmol/L [mEq/L]), acidemia (pH 7.20; reference range 7.38-7.44), and hypoventilation (PvCO2 55 mm Hg; reference range 40-50 mm Hg) were present on admission. Treatment consisted of fluid therapy, aggressive IV potassium chloride supplementation, gastric lavage, and oral magnesium sulfate administration. Based on history and clinical presentation, barium intoxication after ingestion of handheld firework (sparklers) was suspected and a serum sample was submitted for barium analysis. The serum barium concentration determined by inductively coupled plasma/mass spectrometry was 2,000 µg/L, a 3 orders of magnitude elevation above previously reported normal values in dogs. Within 18 hours of admission, the clinical signs resolved and the blood potassium concentration normalized. The animal was discharged home 36 hours after admission. On follow-up performed after 1 and 5 years, no health issues were apparent. NEW INFORMATION PROVIDED: To the authors' knowledge, this is the first report of acute, life-threatening barium toxicosis characterized by flaccid paralysis, acidemia, and severe hypokalemia occurring in a dog after ingestion of a popular pyrotechnic (sparkler) containing barium nitrate. Clinical signs may resolve within 24 hours with appropriate supportive care including aggressive potassium supplementation and chelation therapy.

Electrocardiographic findings in 130 hospitalized neonatal calves with diarrhea and associated potassium balance disorders.

BACKGROUND: Hyperkalemia in neonatal diarrheic calves can potentially result in serious cardiac conduction abnormalities and arrhythmias. OBJECTIVES: To document electrocardiographic (ECG) findings and the sequence of ECG changes that are associated with increasing plasma potassium concentrations (cK+ ) in a large population of neonatal diarrheic calves. ANIMALS: One hundred and thirty neonatal diarrheic calves (age ≤21 days). METHODS: Prospective observational study involving calves admitted to a veterinary teaching hospital. RESULTS: Hyperkalemic calves (cK+ : 5.8-10.2, blood pH: 6.55-7.47) had significantly (P < .05) longer QRS durations as well as deeper S wave, higher T wave, and higher ST segment amplitudes in lead II than calves, which had both venous blood pH and cK+ within the reference range. The first ECG changes in response to an increase in cK+ were an increase in voltages of P, Ta, S, and T wave amplitudes. Segmented linear regression indicated that P wave amplitude decreased when cK+ >6.5 mmol/L, S wave amplitude voltage decreased when cK+ >7.4 mmol/L, QRS duration increased when cK+ >7.8 mmol/L, J point amplitude increased when cK+ >7.9 mmol/L, and ST segment angle increased when cK+ >9.1 mmol/L. P wave amplitude was characterized by a second common break point at cK+ = 8.2 mmol/L, above which value the amplitude was 0. CONCLUSIONS AND CLINICAL IMPORTANCE: Hyperkalemia in neonatal diarrheic calves is associated with serious cardiac conduction abnormalities. In addition to increased S and T wave amplitude voltages, alterations of P and Ta wave amplitudes are early signs of hyperkalemia, which is consistent with the known sensitivity of atrial myocytes to increased cK+ .

Pharmacokinetic and pharmacodynamic properties of orally administered torsemide in healthy horses.

BACKGROUND: Diuretic treatment is the mainstay for management of congestive heart failure in horses, and its use has been restricted to injectable medications because no currently data supports the use of PO administered loop diuretics. OBJECTIVES: To determine the pharmacokinetic and pharmacodynamic properties of PO administered torsemide and, determine if PO administered torsemide, could be used as an alternative to injectable diuretics in the horse. ANIMALS: Six healthy adult mares. METHODS: A 2-phase, prospective study, that consisted of pharmacokinetic profiling of a single dose (6 mg/kg PO) and pharmacodynamic effects of long-term torsemide administration (2 mg/kg PO q12h) for 6 days in healthy horses. RESULTS: Pharmacokinetic analysis identified a peak concentration (Cmax ) of 10.14 µg/mL (range, 6.79-14.69 µg/mL) and elimination half-life (T1/2 ) 9.2 hours (range, 8.4-10.4 hours). The area under the plasma drug concentration over time curve (AUC) was 80.7 µg × h/mL (range, 56.5-117.2 µg × h/mL). A statistically significant increase in urine volume and decrease in urine specific gravity were found from day 0 (baseline) to day 6 (P < .0001). Significant alterations in biochemical variables included hyponatremia, hypokalemia, hypochloremia, and increased serum creatinine concentration. Mean arterial blood pressure significantly decreased on day 6 (57.7 ± 8.8 mm Hg, P = .001) as compared with baseline (78 ± 6.1 mm Hg). Serum aldosterone concentrations significantly increased after 6 days of torsemide administration (P = .0006). CONCLUSIONS AND CLINICAL IMPORTANCE: PO administered torsemide (4 mg/kg/day) successfully reached therapeutic concentrations in blood, induced clinically relevant diuresis, and resulted in moderate pre-renal azotemia and electrolyte disturbances.