Burrows C F, Bovée K C
J Am Vet Med Assoc. 1978 Apr 1;172(7):801-5.
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.
在23只猫中，持续24至48小时的尿路梗阻导致明显的氮质血症、高磷血症、高钾血症和代谢性酸中毒。代谢性酸中毒是一个持续存在的发现，所有猫都很严重（静脉血pH值为7.11±0.09）。血清钠和氯正常。17只（74%）猫出现糖尿。梗阻24小时的猫与梗阻48小时或更长时间的猫之间，血液pH值、血清化学值或电解质浓度没有明显差异。在解除梗阻后的平均8.4小时，通过补液和碳酸氢钠治疗，酸碱状态恢复正常。治疗后平均19.5小时，血尿素氮、血清肌酐和血清无机磷显著改善（P<0.01）。补液后氮质血症的变化表明梗阻解除后肾小球滤过率有不同程度的降低。梗阻解除后在梗阻后利尿期间偶尔会出现低钾血症。结论是，必须根据梗阻后利尿情况调整液体和电解质治疗，以确保适当的医疗管理。
