Treatment strategies for hyperkalemia secondary to urethral obstruction in 50 male cats: 2002–2017

Abstract

Objectives The aims of this study were: to describe the potassium-lowering treatment strategies used to manage moderate-to-severe hyperkalemia in male cats with urethral obstruction (UO); to determine how much dextrose was required per unit of insulin to prevent hypoglycemia; to determine whether early initiation of a dextrose continuous rate infusion (CRI) prevented hypoglycemia; and to determine whether in-hospital mortality was associated with presenting plasma potassium concentration ([K+]). Methods The medical records of male cats presenting with a [K+] ⩾7.0 mEq/l due to UO that had another [K+] measured within 6 h were reviewed retrospectively. All [K+] values within the first 6 h, blood glucose concentrations, treatments for hyperkalemia and survival to discharge were recorded. Analyses were performed to test for associations between dextrose:insulin ratios or method of dextrose administration and the development of hypoglycemia; and for presenting [K+] and mortality. Normally distributed groups of continuous data were compared with a t-test and categorical data were compared with a Fisher’s exact test. Results Fifty cats were included. Mean presenting [K+] was 8.9 ± 1.0 mEq/l, while the mean final [K+] within 6 h was 6.6 ± 1.4 mEq/l. Forty-two (84%) cats were treated with intravenous fluids and 40 (80%) were treated with dextrose and insulin. Median dextrose:insulin ratio was 2 g/u (range 0.4–100). No dextrose:insulin ratio was found to protect against hypoglycemia, and 3/8 cats that became hypoglycemic had received ⩾2 g dextrose per unit of insulin. There was no association between the early initiation of a dextrose-containing CRI and avoidance of hypoglycemia. No association was found between presenting [K+] and mortality. Conclusions and relevance While no specific dextrose:insulin ratio was found to protect against hypoglycemia, there is evidence that the commonly recommended dextrose:insulin ratio of 2 g/u may be inadequate in preventing hypoglycemia in every cat. Severity of hyperkalemia was not associated with mortality.

Ventricular fibrillation in a dog with refractory hyperkalaemia due to uroabdomen following extradural anaesthesia

“…2 Sodium bicarbonate also produces an alkalosis that drives potassium into cells, indirectly activates the aforementioned pump and enhances kaliuresis within 15 minutes. 2,23,24 Terbutaline exerts its potassium-reducing effect in twice this time. 25 However, potassium concentrations did not decrease significantly until over 60 minutes after terbutaline and 30 minutes after bicarbonate administration in the presented case.…”

“…Alkalinising solutions, such as Hartmann's, are further beneficial in shifting potassium into cells. 2,23 A total of 70 mL/kg of Hartmann's solution was administered in boluses of 10-30 mL/kg before arrest of the patient, alongside continuous infusions of Hartmann's and 2.5% glucose. At this point, the patient was not clinically responsive to fluid challenges that were primarily administered to induce kaliuresis.…”

“…These agents all cause an intracellular shift of potassium by stimulating the sodium–potassium–ATPase pump 2 . Sodium bicarbonate also produces an alkalosis that drives potassium into cells, indirectly activates the aforementioned pump and enhances kaliuresis within 15 minutes 2,23,24 . Terbutaline exerts its potassium‐reducing effect in twice this time 25 .…”

“…Successful fluid resuscitation is critical to maintain perfusion, oxygen delivery to tissues and glomerular filtration rate (GFR), enhancing renal excretion of potassium. Alkalinising solutions, such as Hartmann's, are further beneficial in shifting potassium into cells 2,23 . A total of 70 mL/kg of Hartmann's solution was administered in boluses of 10–30 mL/kg before arrest of the patient, alongside continuous infusions of Hartmann's and 2.5% glucose.…”

Fatores De Risco Anestésicos Associados a Felinos Com Obstrução Uretral: Revisão De Literatura

“…CREEDON; EPSTEIN, 2022). Ademais, promove juntamente com a acidose metabólica uma hipotensão grave, com pressão arterial média menor que 60 mmHg, que associado a agentes anestésicos pode agravar a depressão cardiovascular e culminar em parada cardiorrespiratória (PYPENDOP; ILKIW, 2015;ROBERTSON et al, 2018).…”