Urethral obstruction is one of the most common emergencies involving the urinary tract in cats,1 and approximately 12% of feline patients with UO have life-threatening metabolic derangements.2 Cats with UO for more than 36 hours are considered to be severely affected.3 Death may occur as a result of cardiopulmonary failure, hydroelectrolytic imbalance, or acute renal failure.4 Hyperkalemia is considered to be the most common life-threatening complication associated with this condition2 because it impedes the myocardial resting membrane potential, thereby initiating a depolarization blockade effect and reducing the electrical conductivity.5,6
In cats with UO, it is recommended that administration of fluids is commenced as soon as possible to correct the hydroelectrolytic balance and replace urinary losses due to dehydration and postobstructive diuresis.1,7,8 Fluid therapy is the most important component involved in the stabilization of postrenal azotemia because it alleviates hyperkalemia, acidosis, and azotemia in most instances.8 Inadequate replacement of fluids during the postobstructive period can delay resolution of these electrolyte, acid-base, and uremic disturbances7 as well as cause development of renal lesions through hypoperfusion that results from hypovolemia.4 Several authors have indicated that the preferred electrolyte solution for treatment of hyperkalemic animals is PSS,7,9–12 despite its acidifying property. It is also recommended that use of LRS and other solutions that contain potassium should be avoided in patients with acute renal lesions because it is believed that their administration could cause or worsen hyperkalemia.13 This effect is improbable with the use of LRS because that solution contains a very small quantity of potassium (4 mEq/L), compared with the quantity stored in the body.13,14 In addition, the reestablishment of the urinary flow leads to a marked excretion of potassium, and the alkalinizing effect of LRS results in shift of K+ ions to the intracellular space.14
The alkalinizing effect of LRS is attributable to the presence of lactate buffer, which is biotransformed into bicarbonate in the liver and helps to stabilize the acid-base balance. Treatment of the UO-related acid-base disturbance with sodium bicarbonate should be carried out with caution because the increase in blood pH will cause more calcium to bind to negatively charged proteins, which may further decrease the concentration of its ionized form.2
Administration of PSS causes hyperchloremic metabolic acidosis15 and may cause renal vasoconstriction as a result of hyperchloremia16 and acidemia17; this leads to a decrease in the glomerular filtration rate, which may reduce urinary output as well as possibly induce hyperkalemia through the cation exchange with H+ ions.4,18
The purpose of the study reported here was to compare the renal and cardiorespiratory effects of IV treatment with LRS or PSS in severely decompensated cats with UO. Our hypothesis was that treatment with LRS would be more effective than treatment with PSS for stabilization of cats with UO during a 48-hour period following relief of obstruction.
Lactated Ringer's solution
Physiologie saline (0.9% NaCl) solution
Start of fluid therapy
Cloreto de sódio 0.9%, Texon, Viamäo, RS, Brazil.
Ringer com lactato de sódio, Aster Produtos Médicos Ltda, Sorocaba, Brazil.
Sovereign, 3.5 tom cat catheter, open end, Sherwood Medical, St Louis, Mo.
Sonda uretral, 04 F Mark Méd, Bragança Paulista, SP, Brazil.
Biovac, Bional Industria Biomédica, Recife, PE, Brazil.
GraphPad Prism 4, Graph Pad Software Inc, San Diego, Calif.
orta PVP. Clinical, laboratorial and electrocardiografic abnormalities in cats with urethral obstruction. MS thesis, Department of Veterinary Clinic, Säo Paulo University, Säo Paulo, Brazil, 2007.
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Drobatz KJ, Ward C, Graham P, et alSerum concentrations of parathyroid hormone and 25-OH vitamin D3 in cats with urethral obstruction. J Vet Emerg Crit Care 2005;15:179–184.
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