Suspected albuterol toxicosis in a dog

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

Suspected Albuterol Intoxication In A Dog

A suspected case of intoxication of a dog by the beta₂-adrenergic agonist albuterol is discussed. Clinical abnormalities observed included hypokalemia, weakness, tachycardia, tachypnea, hyperthermia, and delirium. Treatment with high-dose potassium supplementation helped to resolve these abnormalities.
Adrenergic control of potassium homeostasis is beta₂-mediated and causes the intracellular uptake of potassium, primarily in liver and muscle. The mechanism of action of albuterol in decreasing serum potassium, its clinical applications in humans, and possible application in dogs are discussed.     

Effects of hypercalcemia on serum concentrations of magnesium, potassium, and phosphate and urinary excretion of electrolytes in horses

OBJECTIVE: To determine effects of experimentally induced hypercalcemia on serum concentrations and urinary excretion of electrolytes, especially ionized magnesium (iMg), in healthy horses. ANIMALS: 21 clinically normal mares. PROCEDURES: Horses were assigned to 5 experimental protocols (1, hypercalcemia induced with calcium gluconate; 2, hypercalcemia induced with calcium chloride; 3, infusion with dextrose solution; 4, infusion with sodium gluconate; and 5, infusion with saline [0.9% NaCl] solution). Hypercalcemia was induced for 2 hours. Dextrose, sodium gluconate, and saline solution were infused for 2 hours. Blood samples were collected to measure serum concentrations of electrolytes, creatinine, parathyroid hormone, and insulin. Urine samples were collected to determine the fractional excretion of ionized calcium (iCa), iMg, sodium, phosphate, potassium, and chloride. RESULTS: Hypercalcemia induced by administration of calcium gluconate or calcium chloride decreased serum iMg, potassium, and parathyroid hormone concentrations; increased phosphate concentration; and had no effect on sodium, chloride, and insulin concentrations. Hypercalcemia increased urinary excretion of iCa, iMg, sodium, phosphate, potassium, and chloride; increased urine output; and decreased urine osmolality and specific gravity. Dextrose administration increased serum insulin; decreased iMg, potassium, and phosphate concentrations; and decreased urinary excretion of iMg. Sodium gluconate increased the excretion of iCa, sodium, and potassium. CONCLUSIONS AND CLINICAL RELEVANCE: Hypercalcemia resulted in hypomagnesemia, hypokalemia, and hyperphosphatemia; increased urinary excretion of calcium, magnesium, potassium, sodium, phosphate, and chloride; and induced diuresis. This study has clinical implications because hypercalcemia and excessive administration of calcium have the potential to increase urinary excretion of electrolytes, especially iMg, and induce volume depletion.     

Use of a point-of-care urine drug test in a dog to assist in diagnosing barbiturate toxicosis secondary to ingestion of a euthanized carcass

Objective – To describe a case of barbiturate toxicosis in a dog secondary to ingestion of a previously buried euthanized goat carcass and to discuss the utility of urine drug testing in diagnosing barbiturate toxicosis.
Case Summary – A 6-year-old neutered male Border Collie was presented to a university veterinary teaching hospital for evaluation of ataxia and acute collapse. Past pertinent history included Addison's disease that had been managed for 1 year. A companion dog was seen 12 hours earlier chewing on the partially decomposed head of a goat that had been euthanized 47 days previously and buried on the owner's property. The dog was laterally recumbent, unresponsive to stimuli, and hypothermic on physical examination. Initial blood work revealed hyponatremia and hyperkalemia, with a Na/K ratio of 18.5. The dog was volume resuscitated and received an injection of dexamethasone sodium phosphate due to a suspected Addisonian crisis. Despite this treatment, the dog remained laterally recumbent and unresponsive to stimuli. A urine drug screen was performed and was positive for barbiturates. A diagnosis of barbiturate toxicosis secondary to ingestion of a euthanized goat carcass was made. The dog was treated supportively over 12 hours with IV fluids and activated charcoal. The dog was able to walk 11 hours after presentation and was subsequently discharged from the hospital.
New or Unique Information Provided – Urine drug testing is a fast, easy, and point-of-care test that may be useful in dogs to assist in the diagnosis of barbiturate intoxication. Proper disposal of euthanized animals is necessary to prevent toxicosis and possible death of companion animals and wildlife.     

Fanconi's Syndrome in a Dog With Primary Hypoparathyroidism

An 11 -year-old castrated male mixed breed dog was referred for evaluation of muscle twitching, polyuria, polydipsia, anorexia, and periocular alopecia. Primary hypoparathyroidism was diagnosed by documenting decreased serum concentrations of parathyroid hormone and ionized calcium. Neurological, gastrointestinal, and dermatological signs resolved after calcium repletion. Initially, 1,25-dihydroxycholecalcif erol PO was required to correct the hypocalcemia. Dihydrotachysterol, in combination with oral calcium supplementation, was used for long-term maintenance of normal serum calcium concentration. Aminoaciduria, glucosuria, and hyperchloremic metabolic acidosis were consistent with a diagnosis of Fanconi's syndrome. This diagnosis was further supported by the presence of hypokalemia and increased urinary fractional excretion of sodium, potassium, calcium, phosphorus, and magnesium. Renal tubular dysfunction resolved after oral supplementation with calcium and vitamin D₃. Fanconi's syndrome in this dog may have been caused by decreased serum concentration of 1,25-dihydroxycholecalciferol, which was secondary to decreased parathyroid hormone production.     

Use of recombinant human factor VIIa in 2 patients with postoperative noncompressible,abdominal hemorrhage

Objective

To describe the clinical presentation, clinical course, and successful management of noncompressible, abdominal hemorrhage with recombinant human factor VIIa (rFVIIa) in 2 postoperative patients.

Case Summary

A 14-year-old neutered female Border Terrier and a 9-year-old neutered male domestic shorthair were treated with rFVIIa to treat noncompressible abdominal hemorrhage in the postoperative period. The dog presented for a septic abdomen following endoscopic intestinal biopsies 10 days prior and was found to have a jejunal perforation along with a fractured liver lobe and hepatic lymphoma at the time of exploratory laparotomy. The cat presented for a spontaneous hemoabdomen associated with hepatic amyloidosis. Clinically significant hemorrhage occurred in the perioperative and postoperative period and both patients received massive transfusions and antifibrinolytic therapy. Despite these interventions, the patients continued to have ongoing abdominal hemorrhage and surgical attempts at hemostasis were not attempted due to the friable nature of the liver at the time of surgery. Both patients received rFVIIa intravenously every 3 hours at a dose between 70 and 90 μg/kg as indicated by the clinical picture, which subsequently decreased transfusion requirements.

New or Unique Information Provided

This case report describes the use of rFVIIa in a cat and a dog with severe, noncompressible abdominal hemorrhage in combination with standard hemostatic interventions.     

Disorders of potassium homeostasis

Hypokalemia and hyperkalemia are common problems that may be artifactual, iatrogenic, or due to altered body homeostatic mechanisms. ECG may help one to recognize hyperkalemia but not hypokalemia. Excessive K supplementation is a common iatrogenic cause of hyperkalemia whereas fluid therapy is a common cause of iatrogenic hypokalemia. The most common causes of spontaneous hyperkalemia are renal failure and hypoadrenocorticism whereas the most common causes of spontaneous hypokalemia are vomiting, diarrhea, and renal wasting. Symptomatic therapy is usually done until the underlying cause(s) is resolved.     

Potassium depletion in cats: renal and dietary influences

Excessive urinary potassium loss was diagnosed in 7 cats with persistent hypokalemia and high serum creatinine concentrations. Renal tubular acidosis (proximal or distal) was not evident in the affected cats. Plasma aldosterone concentrations and plasma renin activities in affected cats were not significantly different from control values. Potassium depletion and hypokalemia were attributed to the combined effects of decreased dietary potassium intake and excessive urinary potassium losses. It was concluded that increased urinary potassium excretion may represent a basic response to renal dysfunction in cats. Data suggested that dietary potassium supplementation improved renal function in most cats in this study.     

Effect of N‐Acetylcysteine Supplementation on Intracellular Glutathione,Urine Isoprostanes,Clinical Score,and Survival in Hospitalized Ill Dogs

Background

Antioxidant depletion and lipid peroxidation have been correlated with disease severity and associated with poor outcomes.

Hypothesis/Objectives

Supplementing dogs with N‐acetylcysteine (NAC) during the first 48 hours of hospitalization will increase cysteine, normalize glutathione concentrations, and decrease the degree of lipid peroxidation associated with illness.

Animals

Sixty systemically ill hospitalized client‐owned dogs and 14 healthy control dogs.

Methods

Randomized investigator‐blinded, placebo‐controlled prospective study. Dogs were randomized to treatment with NAC (n = 30) versus placebo (n = 30). Antioxidants, urine 8‐isoprostane/creatinine (IP/Cr), and clinical score were determined before and after treatment with NAC. Glutathione, cysteine, and vitamin E concentrations were quantified using high‐performance liquid chromatography. Atomic absorption spectroscopy and enzyme‐linked immunosorbent assays were used to quantify selenium and isoprostane concentrations, respectively.

Results

Ill dogs had significantly lower vitamin E concentrations (27 versus 55 μg/mL; P = .0005) as well as elevated IP/Cr ratios (872 versus 399 pg/mg; P = .0007) versus healthy dogs. NAC supplementation significantly increased plasma cysteine (8.67 versus 15.1 μM; P < .0001) while maintaining glutathione concentrations. Dogs in the placebo group experienced a statistically significant decrease in glutathione concentrations (1.49 versus 1.44 mM; P = .0463). Illness severity and survival were unchanged after short duration NAC supplementation.

Conclusions

Ill dogs experience systemic oxidative stress. Supplementation with NAC during the first 48 hours of hospitalization stabilized erythrocyte glutathione concentrations. The clinical impact of this supplementation and glutathione concentration stabilization was undetermined.     

Renal excretion of urea and electrolytes in sheep after extracellular fluid expansion with an isotonic solution of sodium chloride

Sheep of the Merino breed, given 10.11 g nitrogen daily (after Czechoslovak Standard CSN 46 7007) were studied for the effect of the expansion of the extracellular fluid (ECF) by an infusion of an isotonic solution of NaCl (at a rate of 5% of live weight), as exerted on the renal excretion of urea and on the sodium and potassium electrolytes. The high natriuresis, induced by the expansion of ECF, resulted in a statistically significant increase in the clearance of urea, free water, and solutions, and in higher diuresis. An increase was observed in the excretion of urea with urine (UureaV; P < 0.005) and in the excretion of the studied electrolytes of sodium (UNaV; P < 0.001) and potassium (UKV; P < 0.005) by the same route. No variation was recorded in the clearance of inulin as a measure of the glomerular filtration rate (GFR). The fractional excretion of urea, sodium, and potassium also showed a significant increase. The results imply that the fractional excretion of urea increases under the conditions of artificially induced natriuresis.     

Reference limits for urinary fractional excretion of electrolytes in adult non-racing Greyhound dogs

OBJECTIVE: To determine reference limits for urinary fractional excretion of electrolytes in Greyhound dogs. METHODS: Urinary fractional excretion was calculated using a spot clearance method preceded by a 16 to 20 hour fast in 48 Greyhound dogs. Raw data analysed using the bootstrap estimate was used to calculate the reference limits. RESULTS: The observed range for urinary fractional excretion in Greyhound dogs was 0.0 to 0.77% for sodium, 0.9 to 14.7% for potassium, 0 to 0.66% for chloride, 0.03 to 0.22% for calcium and 0.4 to 20.1% for phosphate. Expressed as percentages, the suggested reference limits for fractional excretion in Greyhound dogs are as follows: sodium < or = 0.72, potassium < or = 12.2, chloride < or = 0.55, calcium < or = 0.13 and phosphate < or = 16.5. CLINICAL SIGNIFICANCE: Veterinary practitioners may use these reference limits for urinary electrolyte fractional excretion when investigating renal tubular disease in Greyhound dogs.     

Review of the pathophysiology of alterations in potassium homeostasis

The 2 interrelated systems of external and internal balance that regulate potassium homeostasis must function properly if normal plasma potassium concentration and total body potassium content is to be maintained. Should external balance fail, with renal or gastrointestinal wasting of potassium, hypokalemia with depletion of total body potassium may result. In the absence of this type of potassium wasting, hypokalemia most often is caused by redistribution, with potassium moving from the extracellular-fluid into cells and total body potassium content remaining unaltered. Likewise, factors regulating internal balance may redistribute potassium from cells into the extracellular fluid and cause hyperkalemia, but with normal total body potassium content. Should the kidneys or urinary system fail to excrete potassium, hyperkalemia with an increase in total body potassium content would result.     

Comparison of fractional excretion and 24-hour urinary excretion of sodium and potassium in clinically normal cats and cats with induced chronic renal failure.

The influence of induced chronic renal failure on 24-hour urinary excretion and fractional excretion of sodium and potassium was studied in cats. Induction of chronic renal failure significantly increased fractional excretion of potassium (P less than 0.0001) and sodium (P less than 0.05); however, 24-hour urinary excretion of sodium and potassium decreased slightly following induction of chronic renal failure. Fractional excretion and 24-hour urinary excretion of sodium and potassium were compared by linear regression in clinically normal cats, cats with chronic renal failure, and clinically normal and affected cats combined. In clinically normal cats, linear regression revealed only moderate correlation between fractional excretion and 24-hour urinary excretion for sodium and potassium. Linear regression of these same relationships in cats with chronic renal failure, and in clinically normal cats and cats with chronic renal failure combined, indicated low correlation. Fractional excretions of sodium and potassium were not reliable indicators of 24-hour urinary excretion of these electrolytes in cats with chronic renal failure or unknown glomerular filtration rate. Fractional excretion of potassium and sodium correlated only moderately with 24-hour urinary excretion in clinically normal cats.     

Effect of sampling time on urinary electrolytes following oral furosemide administration in dogs with myxomatous mitral valve disease

Introduction/ObjectivesUrine chemistry has received growing attention to estimate the diuretic response in dogs with cardiac disease.The aim of the study was to evaluate the impact of time elapsed between the oral furosemide administration and sample collection on urine chemistry in dogs with myxomatous mitral valve disease (MMVD) receiving diuretic therapy in American College of Veterinary Internal Medicine (ACVIM) stage C.Materials and methodsSeventy-three dogs with MMVD ACVIM stage C and 106 healthy dogs were prospectively included. Dogs with MMVD were divided, based on the time of sampling, in morning group (MMVD-MG) of one to 6 h and an evening group (MMVD-EG) over 6 h from oral furosemide administration. Analogously, healthy dogs sampled between 9 a.m. and 1 p.m. and between 2 and 7 p.m. were divided in a morning group (H-MG) and an evening group (H-EG), respectively. Urine chemistry, including fractional excretion of electrolytes, was evaluated and compared among groups.ResultsHigher excretion of sodium and chloride and higher urine sodium to urine potassium ratio (uNa⁺:uK⁺) were detected in MMVD-MG than MMVD-EG (P = 0.021, P = 0.038, and P = 0.016, respectively). Natriuresis, chloriuresis, and uNa⁺:uK+ were higher in MMVD-MG than H-MG, while no differences were found in the comparison between H-MG and H-EG and between MMVD-EG and H-EG.ConclusionsUrinary electrolyte excretion is significantly increased within 6 h from furosemide administration in MMVD ACVIM stage C dogs. Time of sampling from furosemide administration significantly affects urine chemistry in MMVD dogs and should be considered in clinical practice and the research field.     

Correction of Hyperkalemia in Dogs with Chronic Kidney Disease Consuming Commercial Renal Therapeutic Diets by a Potassium‐Reduced Home‐Prepared Diet

Background: Hyperkalemia occurs in dogs with chronic kidney disease (CKD). Objectives: (1) To determine the incidence of hyperkalemia in dogs with CKD, (2) to determine the proportion of hyperkalemic dogs that required modification of dietary potassium intake, (3) to evaluate the response to dietary modification. Methods: The hospital database was reviewed retrospectively to identify dogs with CKD and persistent (>5.3 mmol/L on at least 3 occasions) or severe (K ≥ 6.5 mmol/L) hyperkalemia while consuming a therapeutic renal diet. Records of dogs with hyperkalemia that were prescribed a home‐prepared, potassium‐reduced diet were evaluated further. Response was evaluated by changes in body weight, BCS, and serum potassium concentration. Results: One hundred and fifty‐two dogs were diagnosed with CKD, of which 47% had ≥1 documented episode of hyperkalemia, 25% had ≥3 episodes of hyperkalemia, and 16% had ≥1 episodes of severe hyperkalemia (K > 6.5 mmol/L). Twenty‐six dogs (17.2%) with CKD and hyperkalemia were prescribed a potassium‐reduced, home‐prepared diet. The potassium concentration of all hyperkalemic dogs on therapeutic diets (potassium content, 1.6 ± 0.23 g/1,000 kcal of metabolizable energy [ME]) was 6.5 ± 0.5 mmol/L but decreased significantly to 5.1 ± 0.5 mmol/L in 18 dogs available for follow‐up in response to the dietary modification (0.91 ± 0.14 g/1,000 kcal of ME, P < .001). Potassium concentration normalized in all but 1 dog. Conclusions and Clinical Importance: Hyperkalemia is a potential complication of CKD. In a subset of CKD dogs, hyperkalemia can be associated with commercial renal diets and could restrict use of these diets. Appropriately formulated, potassium‐reduced, diets are an effective alternative to correct hyperkalemia.     

Zinc-associated acute pancreatitis in a dog

Zinc-induced haemolytic anaemia is a common phenomenon in dogs in the USA following the ingestion of pennies minted after 1982. A case of acute pancreatitis secondary to zinc toxicosis in a dog is described. Acute pancreatitis has been reported in humans, following the ingestion of liquid zinc chloride, but zinc-associated pancreatitis has not been reported previously in the dog. The mechanism of toxicity is unknown, although the pathophysiology may relate to the role of the pancreas in zinc excretion. Acute pancreatitis as a sequela to zinc toxicosis in the dog represents a complication that may prolong hospitalisation and worsen the prognosis.     

Functioning unilateral adrenocortical carcinoma in a dog

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

Pharmacodynamic assessment of diuretic efficacy and braking in a furosemide continuous infusion model

Introduction

Diuretic failure is a potential life-ending event but is unpredictable and poorly understood. The objectives of this study were to evaluate pharmacodynamic markers of furosemide-induced diuresis and to investigate mechanisms of diuretic braking in dogs receiving constant rate infusion (CRI) of furosemide.

Refractory shock,hypercoagulability, and multiorgan thrombosis associated with hypertrophic osteodystrophy in a dog

Objective

To describe the clinical findings and case progression in a dog presenting with severe systemic inflammatory response, refractory shock, progressive metabolic acidosis, and respiratory failure that was ultimately diagnosed with hypertrophic osteodystrophy (HOD).

Case Summary

A 4-month-old male intact Mastiff presented with a 24-hour history of lethargy and generalized ostealgia. On examination, the dog was recumbent, febrile, and tachycardic with pain on palpation of the abdomen, right femur, and mandible. Appendicular joint radiographs showed changes consistent with osteochondrosis and ulnar-retained cartilaginous cores, with no overt evidence of HOD. Initial treatment included IV fluid therapy, multimodal analgesia, and broad-spectrum antimicrobials. Vasopressor therapy was initiated following hemodynamic decompensation. Synovial fluid cytological analysis and culture revealed nonseptic suppurative inflammation and no bacterial growth, respectively. Blood and urine cultures also yielded no growth. Viscoelastic testing was consistent with hypercoagulability. The dog initially had a metabolic acidosis with appropriate respiratory compensation that progressed to a mixed metabolic and respiratory acidosis despite aggressive therapies that included antimicrobials, vasopressors, positive inotropes, and corticosteroids. Humane euthanasia was elected approximately 32 hours after admission. Necropsy yielded a diagnosis of HOD.

New or Unique Information Provided

This is the first report detailing the occurrence of refractory shock and hypercoagulability associated with HOD in a dog without evidence of another identified comorbidity. HOD should be considered in any young, large-breed dog with generalized ostealgia and signs of systemic illness, even in the absence of classic radiographic abnormalities. Further investigation of coagulation status in dogs with HOD and a secondary systemic inflammatory response is warranted.