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.

Sodium bicarbonate and salbutamol facilitate recovery from hyperkalemia-induced electrocardiogram abnormalities in bullfrog hearts.

Hyperkalemia is a common electrolyte abnormality frequently complicated with chronic kidney disease. By injecting potassium chloride (KCl) solutions intravenously into bullfrogs, we reproduced typical electrocardiogram (ECG) abnormalities of hyperkalemia in the frog hearts, such as the peaked T waves and the widening of QRS complexes. Simultaneous recordings of cardiac action potentials showed morphological changes that synchronized with those of ECG. After 100 mM KCl injection, the widened QRS complexes continued for a while and gradually restored to their baseline widths. However, pre-treatment with sodium bicarbonate or salbutamol, which directly or indirectly stimulates Na+/K+-ATPase activity, significantly facilitated the recovery from the widened QRS duration, indicating the transcellular movement of potassium ions from the extracellular fluid into the intracellular stores.

Hematological differentiation of bladder rupture and complete/partial urethral obstruction in castrated Hanwoo (Korean indigenous cattle) with urolithiasis.

This case report describes the hematological and radiological examination of urinary bladder rupture and complete urethral obstruction. associated with urolithiasis in Hanwoo. Hyponatremia, hypochloremia, azotemia, and hyperglycemia were observed in both urethral obstruction and urinary bladder rupture. However, cattle with urethral obstruction showed hyperkalemia and mild hyperglycemia, whereas cattle with bladder rupture showed marked hyperglycemia and normal potassium levels. In ultrasonography, the urethral obstruction showed a dilated bladder with a thick bladder wall. In contrast to previous literature, in this study, severe electrolyte changes such as severe hyponatremia, hypochloremia, and hyperkalemia occurred in a case of complete urethral obstruction.

HYPERKALEMIA IN FOUR ANESTHETIZED RED WOLVES (CANIS RUFUS).

Four clinically healthy red wolves (Canis rufus) developed hyperkalemia during routine anesthetic procedures. All cases were anesthetized using a combination of dexmedetomidine (10-24 mcg/kg), ketamine (2-3 mg/kg), and either midazolam (0.25-0.5 mg/kg) or butorphanol (0.2-0.48 mg/kg). Additional anesthetics were given to effect. Total anesthetic time ranged from 60 to 420 min. Three out of four cases were treated using terbutaline (0.01 mg/kg SC), which successfully resolved the hyperkalemia. No bradyarrhythmias were seen in any cases where electrocardiography (ECG) was monitored (3/4). All cases recovered from anesthesia, with one prolonged recovery. All animals are clinically healthy at the time of writing. Factors including anesthetic duration, the use of α-2 agonists, hyperthermia, and genetics are discussed as possible triggers for hyperkalemia. Serial blood gases, with electrolyte measurements, are recommended during anesthesia of red wolves, particularly when anesthetic time may be prolonged or the patient suffers from hyperthermia. Terbutaline appears to be a successful treatment should hyperkalemia arise.

Methodology-related pseudohyperkalemia associated with marked muscle enzyme leakage in a dog.

BACKGROUND: As hyperkalemia may be life-threatening, it is critical to recognize artifactually increased potassium concentrations. Pseudohyperkalemia may occur in myopathies when using the VetScan2 analyzer (VS2), but the degree of pseudohyperkalemia and relationships relative to creatine kinase activity (CK) are unknown. OBJECTIVES: We aimed to determine what degree of muscle enzyme leakage, as reflected by increased serum CK activity, results in cases with falsely elevated potassium concentrations when measured by the VS2. We also sought to establish if a linear relationship exists between potassium concentrations measured by the VS2 and CK activity. METHODS: Serum samples from dogs with increased CK activity and with CK activity within the reference interval and without clinically relevant biochemical alterations were used to create diluted samples having various CK activities. Potassium concentrations and CK activities were determined on VS2 and Cobas c501 (Cobas) analyzers. Wilcoxon signed rank, Bland-Altman, and Passing-Bablok analyses were used to compare potassium concentrations generated by the VS2 and Cobas analyzers. Least squares regression analysis was performed to evaluate if a linear relationship exists between VS2 potassium concentrations and Cobas CK activities. RESULTS: Potassium concentrations from the VS2 were higher (median and standard deviation (SD) = 5.2 +/- 0.46 mmol/L) than those from the Cobas analyzer (4.4 +/- 0.35 mmol/L; P < 0.000), and a positive mean bias was found (mean difference = 0.774 mmol/L; 95% Confidence Interval (CI) = 0.706-0.842; limits of agreement = 0.21-1.34). Passing-Bablok regression showed a positive proportional bias for potassium concentrations on the VS2 compared with paired Cobas results (Slope = 1.328; 95% CI = 1.100-1.500) but did not reveal systematic bias (Intercept = -0.714; 95% CI = -1.46-0.265). Least squares regression analysis showed a poor non-significant relationship (R2 = 0.19) between potassium measured by the VS2 and CK measured by the Cobas analyzer. CONCLUSIONS: A defined threshold value of CK activity at which potassium concentration begins to falsely increase when measured on the VS2 was not established as data widely varied. A poor non-significant relationship between potassium concentrations and CK activities did not allow prediction of the threshold at which falsely increased potassium concentrations would be expected on the VS2.

Diagnostic predictivity of transtubular potassium gradient for primary hypoadrenocorticism in hyperkalemic dogs: a cross-sectional study.

OBJECTIVES: Transtubular potassium gradient has never been evaluated in the diagnosis of primary hypoadrenocorticism in dogs. The objective of this study is to evaluate the diagnostic utility of transtubular potassium gradient for the diagnosis of primary hypoadrenocorticism in dogs with serum K+ > 5.5 mol/L. MATERIALS AND METHODS: Cross-sectional study including dogs with primary hypoadrenocorticism and dogs with other disease. Differences in signalment and laboratory parameters between groups were assessed by binary logistic regression modelling. Variables significantly associated with primary hypoadrenocorticism were evaluated for their diagnostic accuracy of this condition by receiver operator characteristic curve analysis and by multivariable logistic regression analysis, respectively. RESULTS: Dogs with primary hypoadrenocorticism (n=39) were significantly younger than hyperkalemic dogs without primary hypoadrenocorticism (n=41). Moreover they had higher serum and urinary concentrations of Na+ and Na+ :K+ , but lower transtubular potassium gradient than hyperkalemic dogs without hypoadrenocorticism. Serum Na+ (sNa+ ) had the highest diagnostic accuracy (area under the curve [AUC]: 0.87, 95% confidence interval, 0.78 to 0.96), followed by the transtubular potassium gradient (AUC: 0.81, 0.72 to 0.91), however the accuracy of the two AUCs was not statistically different. The transtubular potassium gradient-sNa+ additive index (i.e. transtubular potassium gradient+sNa+ /10) had a greater accuracy (AUC: 0.88, 0.79 to 0.94) than transtubular potassium gradient or sNa+ , although it was not statistically superior to the latter. The multivariable logistic regression model showed that transtubular potassium gradient (adjusted odds ratio [aOR]: 0.51, 0.3 to 0.84), sNa+ (aOR: 0.86, 0.78 to 0.95) and spayed female (aOR: 24.96, 2.32 to 267.66) were associated with primary hypoadrenocorticism. CLINICAL SIGNIFICANCE: Transtubular potassium gradient-sNa+ additive index can contribute to decision-making on diagnosis of primary hypoadrenocorticism in dogs presenting with hyperkalaemia.

Transient P' waves in a hyperkalemic cat: artifact or dissociation?

A 15-year-old Sphynx cat was referred for cervical ventroflexion, ataxia, and lethargy associated with hypokalemia. After administration of supplemental potassium, the cat became severely hyperkalemic. Transient P' (vs. pseudo P' waves) were detected on the electrocardiogram. Over the course of hospitalization, the cat's potassium normalized, and the abnormal P' waves did not recur. These images are presented to highlight the differential diagnoses for this type of electrocardiogram. Diagnostic considerations included complete or transient atrial dissociation (as a rare consequence of hyperkalemia), atrial parasystole, and various electrocardiographic artifacts. Definitive diagnosis of atrial dissociation requires an electrophysiologic study or echocardiographic documentation of two independent atrial rhythms with associated mechanical activity, but these were unavailable in this case.

Retrospective evaluation of acute hyperkalemia of unknown origin during general anesthesia in dogs.

OBJECTIVE: To report and characterize cases of acute hyperkalemia of unknown origin in dogs under anesthesia. STUDY DESIGN: Multicentric retrospective clinical study. ANIMALS: Medical records of 19 client-owned dogs that developed acute hyperkalemia during anesthesia. METHODS: Anesthetic records of dogs developing acute hyperkalemia from January 2015 to December 2022 were evaluated. Data collected included demographics, duration of anesthesia until the episode, electrolytes and blood gas measurements, electrocardiogram (ECG) abnormalities, drugs used as part of the anesthetic protocol, hyperkalemia treatment and outcome. RESULTS: A total of 13 cases met the inclusion criteria with documented acute hyperkalemia with no apparent underlying cause during anesthesia. Dogs were [mean ± standard deviation (range)] 6.5 ± 5.0 (3-10) years old and weighed 18.0 ± 14.3 (5.1-40.0) kg. All dogs were administered dexmedetomidine and an opioid as part of the premedication. All dogs had inhalation anesthesia of >60 minutes' duration. The first clinical sign was bradycardia that was minimally responsive to anticholinergic administration and was often accompanied by moderate/severe hypotension. These signs were rapidly followed by ECG changes compatible with hyperkalemia and/or cardiac arrest. Rapid identification and treatment for hyperkalemia, with or without dexmedetomidine reversal, resulted in survival of 12 dogs and one fatality. CONCLUSIONS AND CLINICAL RELEVANCE: Unknown origin hyperkalemia is a life-threatening complication that can occur during general anesthesia. In healthy dogs, preanesthetic administration of dexmedetomidine in association with an opioid and followed by inhalation anesthesia of more than 1 hour duration may predispose to this complication. A sudden decrease in heart rate >90 minutes after dexmedetomidine administration, or ECG changes, may warrant measurement of blood potassium concentrations.

High temperature and hyperkalemia cause exit block of action potentials at the atrioventricular junction of rainbow trout (Oncorhynchus mykiss) heart.

At critically high temperatures, atrioventricular (AV) block causes ventricular bradycardia and collapse of cardiac output in fish. Here, the possible role of the AV canal in high temperature-induced heart failure was examined. To this end, optical mapping was used to measure action potential (AP) conduction in isolated AV junction preparations of the rainbow trout (Oncorhynchus mykiss) heart during acute warming/cooling in the presence of 4 or 8 mM external K+ concentration. The preparation included the AV canal and some atrial and ventricular tissue at its edges, and it was paced either from atrial or ventricular side at a frequency of 0.67 Hz (40 beats min-1) to trigger forward (anterograde) and backward (retrograde) conduction, respectively. The propagation of AP was fast in atrial and ventricular tissues, but much slower in the AV canal, causing an AV delay. Acute warming from 15 °C to 27 °C or cooling from 15 °C to 5 °C did not impair AP conduction in the AV canal, as both anterograde and retrograde excitations propagated regularly through the AV canal. In contrast, anterograde conduction through the AV canal did not trigger ventricular excitation at the boundary zone between the AV canal and the ventricle when extracellular K+ concentration was raised from 4 mM to 8 mM at 27 °C. Also, the retrograde conduction was blocked at the border between the AV canal and the atrium in high K+ at 27 °C. These findings suggest that the AV canal is resistant against high temperatures (and high K+), but the ventricular muscle cannot be excited by APs coming from the AV canal when temperature and external K+ concentration are simultaneously elevated. Therefore, bradycardia at high temperatures in fish may occur due to inability of AP of the AV canal to trigger ventricular AP at the junctional zone between the AV canal and the proximal part of the ventricle.

Effect of inhaled albuterol on whole blood potassium concentrations in dogs.

BACKGROUND: Albuterol by inhalation (IH) is a common treatment for hyperkalemia in humans but its effect on blood potassium concentrations in dogs is unknown. OBJECTIVE: Determine whether albuterol (IH) decreases blood potassium concentrations in healthy normokalemic dogs and if effects are dose-dependent. ANIMALS: Ten healthy dogs. METHODS: Prospective, crossover experimental study. Albuterol sulfate was administered at a low-dose (90 µg) in phase I and, 7 days later, high-dose (450 µg) in phase II. Blood potassium and glucose concentrations (measured via blood gas analyzer) and heart rates were obtained at baseline and then 3, 5, 10, 15, 30, 60, 90, 120, 180, and 360 minutes after inhaler actuation. RESULTS: Blood potassium concentrations decreased rapidly after albuterol delivery with a significant reduction compared to baseline within 30 minutes in both phases (P = .05). The potassium nadir concentration of phase I occurred at 60 minutes (mean, SD; 4.07 mmol/L, 0.4) and was significantly decreased from baseline, (4.30 mmol/L, 0.3; t(9) = 2.40, P = .04). The potassium nadir concentration of phase II occurred at 30 minutes (mean, SD; 3.96 mmol/L, 0.39) and was also significantly decreased from baseline, (4.33 mmol/L, 0.4; t(9) = 2.22, P = .05). The potassium nadir concentration decreased by 0.1 mmol/L for each 10 µg/kg increase in dose of albuterol (P = .01). Five dogs had ≥1 hyperglycemic measurement (ie, >112 mg/dL). No median heart rate was tachycardic nor was any mean blood glucose concentration hyperglycemic at any time point. CONCLUSION AND CLINICAL IMPORTANCE: Albuterol IH decreases blood potassium concentrations in a dose-dependent manner without clinically meaningful alterations to heart rate or blood glucose concentrations in healthy dogs. The mean decrease in potassium concentration at the high-dose of albuterol was modest (0.38 mmol/L).

Suspected vagal reflex and hyperkalaemia inducing asystole in an anaesthetised horse.

A 10-year-old 466 kg mustang gelding presented to an equine referral hospital for surgical repair of nasal, frontal and lacrimal bone fractures from an unknown trauma. Surgical repair was performed under general anaesthesia, including a right-sided maxillary regional anaesthetic block with mepivacaine hydrochloride. Progressive hyperkalaemia was documented perianaesthetically (T-3 mins; 134 mins after induction; potassium 6.4 mmol/L (ref 3.5-5.1 mmol/L). Perianaesthetic bradycardia was attributed to alpha -2 agonist infusion administration, and other characteristic ECG changes (flattened P waves, narrow T waves of increased amplitude, prolonged QRS complex) were not documented. Asystole occurred 137 min after induction of anaesthesia; however, a review of the available literature suggests the degree of hyperkalaemia documented was unlikely to be the primary cause of asystole but may have been a contributing factor. It is hypothesised that a trigeminocardiac reflex was the primary contributory factor to asystole in the described case, and may represent a maxillomandibulocardiac reflex that has not been previously described in the horse.

Third-degree atrioventricular block with narrow QRS complexes in a case of hypoadrenocorticism in a dog.

A 4-year-old dog presented with lethargy and bradycardia (heart rate 40 bpm). Electrocardiogram diagnosed third-degree atrioventricular block with narrow QRS complexes. An atropine response test did not result in a change of the heart rate. Venous blood gas documented moderate hyperkalaemia and an adrenocorticotrophic hormone stimulation test was consistent with hypoadrenocorticism. The patient repeatedly converted to sinus rhythm with normalisation of serum potassium levels following medical treatment. This is the first report of third-degree atrioventricular block in a patient with hypoadrenocorticism that was not vagally mediated and did not require pacemaker implantation, with conversion to sinus rhythm following treatment of the hyperkalaemia.

Insulin accelerates recovery from QRS complex widening in a frog heart model of hyperkalemia.

Hyperkalemia is one of the most common electrolyte disorders. By injecting various concentrations of potassium chloride (KCl) solutions intravenously into bullfrogs, we demonstrated characteristic electrocardiogram (ECG) abnormalities of hyperkalemia in frog hearts. The widened QRS complexes induced by 100 mM KCl injection were accompanied by an increase in the resting membrane potential in cardiomyocytes and a decreased slope of phase 0 in the action potential. Recording both ECG waveforms and the cardiac action potential enabled us to reveal the mechanisms of hyperkalemia-induced ECG abnormalities. Additionally, pre-treatment with insulin, a powerful stimulator of Na+/K+-ATPase activity, significantly accelerated the recovery from the widened QRS complexes in the ECG, demonstrating a pronounced shift of extracellular potassium ions into the intracellular space.

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.

Acute hyperkalemia as anesthetic complication in a diabetic dog undergoing tumor excision.

A mixed-breed dog with a history of diabetes mellitus underwent surgical removal of multiple colonic adenocarcinomas. The dog acutely developed electrocardiographic changes compatible with hyperkalemia during manipulation of the tumors, which was confirmed and treated. Although it was not possible to confirm clinical tumor lysis syndrome in this dog, the hyperkalemia and resultant arrhythmia that occurred during tumor manipulation were suggestive of acute tumor lysis syndrome. Key clinical message: Hyperkalemia is a serious anesthetic and intraoperative complication that should be considered in dogs undergoing solid tumor resection due to the potential risk of developing acute tumor lysis syndrome. Diabetic patients may also be at increased risk of developing hyperkalemia. Both the potassium concentration and ECG should be routinely monitored during these procedures.

Hyperkaliémie aiguë comme complication lors de l'anesthésie d'un chien diabétique subissant une excision tumorale. Un chien de race croisée avec une historique de diabète mellitus a subi une chirurgie pour retirer de multiples adénocarcinomes coloniques. Le chien développa de manière aiguë des changements électrocardiographiques compatibles avec une hyperkaliémie durant la manipulation des tumeurs, ce qui fut confirmé et traité. Bien qu'il ne soit pas possible de confirmer un syndrome clinique de lyse des tumeurs chez ce chien, l'hyperkaliémie et l'arythmie qui en résulta durant la manipulation des tumeurs étaient suggestives du syndrome aigu de lyse des tumeurs.Message clinique clé :L'hyperkaliémie est une complication sérieuse lors de l'anesthésie et de la chirurgie qui devrait être considérée chez les chiens subissant la résection d'une tumeur solide dû au risque potentiel de développer le syndrome aigu de lyse des tumeurs. Les patients diabétiques pourraient également présenter un risque plus grand de développer une hyperkaliémie. La concentration de potassium et l'ECG devraient être surveillés de routine durant ces procédures.(Traduit par Dr Serge Messier).

Postmortem urinary tract changes in cats with urethral obstruction.

OBJECTIVE: To report the gross and histopathological postmortem findings of the urinary tract and compare them to clinical severity of disease in cats with urethral obstruction (UO). DESIGN: Retrospective, observational, descriptive study. SETTING: University teaching hospital. ANIMALS: Fourteen cats from 2000 to 2014 with UO that had a complete postmortem examination. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Bladder lesions were moderate-severe in 10 of 14 (71%) and mild in 4 of 14 (29%) cats. Bladder lesions were diffuse in 8 of 14 (57%), multifocal in 3 of 14 (21%), and focal in 3 of 14 (21%) cats. Lymphocytic cystitis was noted in 11 of 14 cats (78%), and neutrophilic cystitis was noted in 10 of 14 (71%) bladders. Urethral lesions were moderate-severe in 4 of 14 (29%), mild in 4 of 14 (29%), and no urethral lesions were identified in 6 of 14 (43%) cats. Ureteral lesions were mild in 1 of 14 (7%), and no ureteral lesions were identified in 13 of 14 (93%) cats. There were moderate-severe histopathological renal lesions in 5 of 14 cats (36%), mild renal lesions in 6 of 14 (43%), and no renal lesions were identified in 3 of 14 cats (21%). Renal lesions were multifocal in 10 of 14 (71%) and regional in 1 of 14 cats (7%). In the kidneys, the most common inflammatory infiltrate was lymphoplasmacytic. The severity of urethral lesions was not associated with the severity of bladder lesions (P = 1.0). Hyperkalemia paralleled the severity of bladder (P = 0.02) and renal lesions (P = 0.04). An association between the severity of bladder lesions and degree of azotemia could not be determined due to small sample size and removal of the most azotemic cats. CONCLUSIONS: Substantial renal and urinary bladder inflammatory lesions were found in cats with UO. The severity of these findings paralleled the severity of blood potassium concentrations.

THE EFFECTS OF PROCEDURE DURATION AND ATIPAMEZOLE ADMINISTRATION ON HYPERKALEMIA IN TIGERS (PANTHERA TIGRIS) AND LIONS (PANTHERA LEO) ANESTHETIZED WITH α-2 AGONISTS.

A retrospective analysis of 40 extended (>2 hr) anesthetic events in eight lions (Panthera leo) and 32 tigers (Panthera tigris) was performed using a hierarchical linear growth curve model to assess the effects of anesthetic time, α-2 adrenoreceptor agonist dosages, administration of atipamezole, and biochemical parameters on rising plasma K+ concentrations. Hyperkalemia was first noted at a mean time of 187 min (range: 131-226 min), with time under anesthesia as a statistically significant predictor of K+ concentration (P < 0.0001). A significant two-way interaction between time and atipamezole administration (P = 0.0082) for rising K+ concentrations was demonstrated, indicating that administration of atipamezole can mitigate the rise in K+ concentrations. Administration of atipamezole beyond 150 min of anesthetic time was less effective in reducing K+ concentrations than if administered earlier. Electrocardiographic abnormalities were noted in eight animals, including three hyperkalemic individuals. Lions developed significantly greater plasma K+ concentrations than tigers (P = 0.0009) during anesthesia. No biochemical parameter was identified as a significant indicator of which individuals will develop hyperkalemia. Clinicians anesthetizing any large nondomestic felid should monitor electrolytes regularly during anesthetic events; consider early, partial- to full-dose reversal of α-2 agonists; and be prepared to correct potentially life-threatening electrocardiographic abnormalities resulting from hyperkalemia.

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.