Characterization and treatment of acid-base and renal defects due to urethral obstruction in cats.
In 23 cats, urinary obstruction of 24 to 48 hours' duration caused marked azotemia, hyperphosphatemia, hyperkalemia, and metabolic acidosis. The metabolic acidosis was a consistent finding and was severe in all cats (venous pH, 7.11 +/- 0.09). Serum sodium and chloride were normal. Glycosuria was found in 17 (74%) of the cats. There was no clear difference in blood pH, serum chemical values, or electrolyte concentrations between cats obstructed 24 hours and those obstructed 48 hours or longer. At a mean of 8.4 hours after relief of obstruction, acid-base status was corrected to normal, using fluid replacement and sodium bicarbonate therapy. Blood urea nitrogen serum creatinine, and serum inorganic phosphorus improved significantly (P less than 0.01) at a mean of 19.5 hours after treatment. Variation in azotemia after fluid replacement suggested variable decreases in glomerular filtration rate after relief of obstruction. Hypokalemia occasionally developed after relief of obstruction during the postobstructive diuresis. It was concluded that fluid and electrolyte therapy must be regulated in response to the postobstructive diuresis, to ensure proper medical management.
D000137:Acid-Base Imbalance / Q000209:etiology / Q000662:veterinary*; D000138:Acidosis / Q000662:veterinary; D000818:Animals; D001639:Bicarbonates / Q000627:therapeutic use; D002371:Cat Diseases / Q000378:metabolism / Q000628:therapy; D002415:Cats; D007263:Infusions, Parenteral / Q000662:veterinary; D007668:Kidney / Q000503:physiopathology*; D008297:Male; D011507:Proteinuria / Q000662:veterinary; D014522:Urethral Diseases / Q000378:metabolism / Q000628:therapy / Q000662:veterinary*
D001639:Bicarbonates