{"title":"停止补钾后沙丁胺醇中毒犬的反弹性高钾血症。","authors":"Samantha J. Guida DVM, Lisa Bazzle DVM, DACVECC","doi":"10.1111/vec.13352","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Objective</h3>\n \n <p>To describe the presentation of rebound hyperkalemia as a delayed side effect of albuterol toxicity in a dog.</p>\n </section>\n \n <section>\n \n <h3> Case Summary</h3>\n \n <p>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.</p>\n </section>\n \n <section>\n \n <h3> New or Unique Information Provided</h3>\n \n <p>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.</p>\n </section>\n </div>","PeriodicalId":17603,"journal":{"name":"Journal of veterinary emergency and critical care","volume":"33 6","pages":"715-721"},"PeriodicalIF":1.1000,"publicationDate":"2023-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/vec.13352","citationCount":"0","resultStr":"{\"title\":\"Rebound hyperkalemia in a dog with albuterol toxicosis after cessation of potassium supplementation\",\"authors\":\"Samantha J. Guida DVM, Lisa Bazzle DVM, DACVECC\",\"doi\":\"10.1111/vec.13352\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Objective</h3>\\n \\n <p>To describe the presentation of rebound hyperkalemia as a delayed side effect of albuterol toxicity in a dog.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Case Summary</h3>\\n \\n <p>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.</p>\\n </section>\\n \\n <section>\\n \\n <h3> New or Unique Information Provided</h3>\\n \\n <p>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.</p>\\n </section>\\n </div>\",\"PeriodicalId\":17603,\"journal\":{\"name\":\"Journal of veterinary emergency and critical care\",\"volume\":\"33 6\",\"pages\":\"715-721\"},\"PeriodicalIF\":1.1000,\"publicationDate\":\"2023-11-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1111/vec.13352\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of veterinary emergency and critical care\",\"FirstCategoryId\":\"97\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/vec.13352\",\"RegionNum\":3,\"RegionCategory\":\"农林科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"VETERINARY SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of veterinary emergency and critical care","FirstCategoryId":"97","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/vec.13352","RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"VETERINARY SCIENCES","Score":null,"Total":0}
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.
期刊介绍:
The Journal of Veterinary Emergency and Critical Care’s primary aim is to advance the international clinical standard of care for emergency/critical care patients of all species. The journal’s content is relevant to specialist and non-specialist veterinarians practicing emergency/critical care medicine. The journal achieves it aims by publishing descriptions of unique presentation or management; retrospective and prospective evaluations of prognosis, novel diagnosis, or therapy; translational basic science studies with clinical relevance; in depth reviews of pertinent topics; topical news and letters; and regular themed issues.
The journal is the official publication of the Veterinary Emergency and Critical Care Society, the American College of Veterinary Emergency and Critical Care, the European Veterinary Emergency and Critical Care Society, and the European College of Veterinary Emergency and Critical Care. It is a bimonthly publication with international impact and adheres to currently accepted ethical standards.