Department of Small Animal Medicine and Surgery, University of Georgia, Athens, Georgia, USA.
J Vet Emerg Crit Care (San Antonio). 2023 Nov-Dec;33(6):715-721. doi: 10.1111/vec.13352. Epub 2023 Nov 9.
To describe the presentation of rebound hyperkalemia as a delayed side effect of albuterol toxicity in a dog.
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.
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.
描述沙丁胺醇中毒后反弹性高钾血症作为一种迟发性副作用的表现。
一只 3 岁雌性已绝育的杂种犬因沙丁胺醇中毒而出现严重低钾血症、高乳酸血症和高血糖症。该犬还出现窦性心动过速和全身无力。治疗采用静脉输液和补钾,并用连续心电图进行监测。初始表现 12 小时后,低钾血症得到纠正,此时停止了液体和钾的补充。此后窦性心动过速未再发生,但犬出现了室性早搏伴快速二联律(即时速率 300 次/分)。超声心动图显示心脏大小和功能正常。在就诊后 24 小时,尽管已停止液体和钾补充 12 小时,该犬仍出现严重高钾血症。连续进行静脉和尿液电解质检查以确定电解质的分数排泄率。这些数据证实了反弹性高钾血症(7.0mmol/L),与钾的分数排泄明显增加一致,这是由于细胞内钾的释放。给予葡萄糖补液治疗,直至就诊后 36 小时。高钾血症得到纠正,犬在住院 44 小时后出院。
本病例记录了犬沙丁胺醇中毒治疗后反弹性高钾血症。该病例强调了在治疗血清低钾血症时了解体内总钾分布的重要性。如沙丁胺醇中毒时的跨细胞钾转移可导致即使在停止补钾后也会出现反弹性高钾血症。本病例进一步探讨了电解质分数排泄在阐明电解质紊乱病因和管理中的作用。