Retrospective study to characterize post-obstructive diuresis in cats with urethral obstruction

Abstract

Urethral obstruction is a common medical emergency in cats. Frequency of post-obstruction diuresis in cats following resolution of urethral obstruction is unknown. The objective of this study was to document frequency and associated clinical features of post-obstruction diuresis in cats. The records of 32 cats undergoing 33 admissions to the Colorado State University Veterinary Hospital for urethral obstruction were reviewed. Signalment, admission blood values, fluid therapy, and urine output were recorded. Diuresis was defined as urine output greater than 2 ml/kg/h. Post-obstructive diuresis occurred in 46% (13/28) of cats within the first 6 h of treatment. Occurrence of post-obstructive diuresis was statistically more likely in cats with venous pH<7.35 on admission. Urine production following resolution of urethral obstruction should be monitored so that fluid therapy can be adjusted to the individual patient, as many cats will have a higher fluid requirement secondary to post-obstruction diuresis.

Urethral obstruction is a medical emergency, often accompanied by post-renal azotemia and uremia. ¹ Cats may also have cardiovascular signs resulting from fluid and electrolyte disturbances. ² In a recent study of cats with urethral obstruction, 97% of cats underwent urethral catheterization for at least 24 h following unblocking. ² Although temporary catheterization is not a benign therapy (it carries risks of infection and further trauma), careful maintenance of a urinary catheter may be required in some cats for 1–7 days following resolution of urethral obstruction. Subsequent urine output measurements may assist in the management of these cases where an indwelling urinary catheter is maintained, especially in those cats undergoing post-obstructive diuresis.

The hallmark sign of post-obstructive diuresis is increased urine production. Post-obstruction diuresis probably results from a combination of physiologic factors. ³ Following resolution of urinary obstruction, glomerular filtration rate and renal blood flow are reduced. ^3,4 Therefore, diuresis in the post-obstruction period is secondary to impaired tubular reabsorption of glomerular filtrate. ³ Impaired tubular absorption may result from urea osmotic diuresis, expansion of extracellular fluid volume, altered intrarenal physical factors secondary to elevated intrarenal pressure, vasopressin insensitivity, and alterations in other natriuretic factors yet to be defined. ^3–6

While there are many theories as to the etiology of post-obstructive diuresis, the prevalence and contributing risk factors have not been reported. The objectives of this study were to describe the frequency of post-obstructive diuresis following urethral obstruction in cats and to identify factors associated with its occurrence. We hypothesized that onset of diuresis in the post-obstruction period might be associated with the magnitude of acid–base disturbance, hyperglycemia, calculated plasma osmolality, and/or azotemia on admission.

Materials and Methods

Records were identified by computerized medical record search from 12/01/2002 to 12/01/2007 and cats were included if they were admitted for hospitalization due to urethral obstruction and underwent laboratory blood analysis, urinary catheterization, and urine output monitoring. Cats were excluded from analysis if urinary obstruction was secondary to trauma.

Medical records were reviewed for cat signalment, body weight, presenting clinical signs, and vital parameters (temperature, pulse and respiration). Admission venous blood pH, glucose, bicarbonate, and creatinine concentrations were recorded. Blood pH was defined as acidotic if <7.35 [reference interval (RI) 7.33–7.44], hyperglycemia was defined at >168 mg/dl (9.32 mmol/l; RI 3.82–7.55 mmol/l), and bicarbonate concentration was defined as low if <14 mEq/l (<14 mmol/l; RI 13–22 mmol/l). Plasma osmolality was calculated by the following equation where BUN is blood urea nitrogen: 1.86(Na+K)+BUN/2.8+glucose/18 and considered elevated if >316 mOsm/kg. Decreased renal function was described as serum creatinine concentration >2.0 mg/dl (177 μmol/l; RI 88.4–203 μmol/l). An indwelling urinary catheter was maintained in all cats. The urinary catheter was connected to a sterile closed collection system to keep the bladder empty and to quantify urine production. Urine was measured every 6 h following relief of urinary obstruction. The urinary bladder was emptied at time 0 immediately after urethral flushing and prior to the start of monitored collection. If a technical issue was encountered with the urinary catheter during a time interval, such as dislodging of the catheter or disconnection of the closed collection system, it was corrected and that time point was excluded from analysis. Diuresis was defined as a urine output of >2 ml/kg/h. Cats were concurrently treated with intravenous fluid therapy at rates higher than maintenance to match rate of output following initiation of treatment. Rate and type of fluid therapy were recorded.

Continuous data were tested for normality using the Shapiro–Wilk W test and reported as mean and 95% confidence interval (CI) or median and interquartile range (IQR) as dictated by distribution. Bivariable regression analysis using a generalized estimating equation method was used to investigate if there was an association between time interval and diuresis. Repeated measurements performed on the same cat were taken into account for the bivariable and multivariable regression analysis. Multivariable regression analysis using a generalized estimating equation method with binary distribution and logit link was used to evaluate the association between baseline acid–base derangement parameters and diuresis and between baseline azotemia, elevated osmolality and diuresis. The crystalloid fluid rate was included in the model to account for the impact of fluid rate on diuresis. Statistical analysis was performed with commercial software (SAS version 9.1, SAS Incorporated, Cary, NC). Statistical analyses were considered significant at a P value of <0.05.

Results

The records of 32 cats undergoing 33 admissions for urethral obstruction were identified. All cats were castrated males and were classified as domestic shorthair or domestic longhair breeds. Mean body weight of cats (n=33) was 6.0 kg (95%CI: 5.4–6.6 kg). Median admission temperature (n=31) was 99.8F (IQR: 98.9–101.0F). One cat's temperature was too low to record. Mean admission heart rate (n=33) was 183 bpm (95%CI: 163–198 bpm). Median admission respiratory rate (n=30) was 38 bpm (IQR: 30–60 bpm).

Forty-six percent (13/28) of cats admitted for urethral obstruction developed post-obstruction diuresis during the first 6 h of urine collection and the percent of cats affected by diuresis continued to increase throughout the measurement period (see Table 1). The likelihood of developing diuresis was significantly higher during the time periods of 18–24 h (P=0.0006), 30–36 h (P=0.0044), 42–48 h (P=0.012), and >48 h (P=0.0023) post-obstruction when compared to the time period of 6–12 h post-obstruction. Median serum potassium concentration on admission (n=33) was 4.2 mEq/l (IQR: 3.8–7.6 mEq/l; RI 3.5–5.2 mEq/l). Mean ionized calcium concentration on admission (n=22) was 1.19 mmol/l (95%CI: 1.03–1.25 mmol/l; RI 1.3–1.4 mmol/l). Median venous pH on admission (n=20) was 7.32 (IQR: 7.26–7.37; RI 7.33–7.44). Baseline acidemia as defined by an admission blood pH<7.35 was significantly associated with diuresis (P=0.0084). Cats with urethral obstruction were five times more likely to be diuretic when they had concurrent acidemia. Median glucose concentration on admission (n=25) was 152 g/dl (IQR: 115–195 g/dl; RI 69–136 g/dl) [in SI units: 8.44 mmol/l (IQR: 6.38–10.82 mmol/l; RI 3.83–7.55 mmol/l)]. Mean bicarbonate concentration on admission (n=30) was 15.7 mEq/l (95%CI: 14.5–17.0 mEq/l; RI 13–22 mEq/l) [in SI units: 15.7 mmol/l (95%CI: 14.5–17.0 mmol/l; RI 13–22 mmol/l)]. Presence of hyperglycemia (P=0.29) and hypobicarbonatemia (P=0.53) were not associated with diuresis. Median serum creatinine concentration on admission (n=18) was 4.1 mg/dl (IQR: 1.6–11.9 mg/dl; RI 1.0–2.0 mg/dl) [in SI units: 360 μmol/l (IQR: 140–1050 μmol/l; RI 88–180 μmol/l)]. Baseline azotemia as defined by serum creatinine>2.0 mg/dl was not associated with diuresis (P=0.78). Mean plasma osmolality at admission (n=13) was 333 mOsm/kg (95%CI: 316–351 mOsm/kg). Elevated calculated osmolality defined as >316 mOsm/kg was also not associated with diuresis (P=0.76).

Table 1.

Frequency of post-obstruction diuresis by urine collection time period among cats admitted for urethral obstruction.

Cats post-obstruction	Urine collection time (h)
	6	12	18	24	30	36	42	48	54	60	66	72	78	84
Urine production <2 ml/kg/h	#	15	8	3	1	0	2	1	0	1	0	1	0	1	0
%	54	36	13	5	0	12	9	0	13	0	20	0	25	0
Urine production >2 ml/kg/h	#	13	14	20	19	13	15	10	9	7	6	4	3	3	3
%	46	64	87	95	100	88	91	100	88	100	80	100	75	100
Total		28	22	23	20	13	17	11	9	8	6	5	3	4	3

#=Number of cats where data were available at this time point.

Discussion

This study is the first to document the frequency of post-obstruction diuresis in cats with naturally occurring urethral obstruction. Most cats developed diuresis following non-surgical resolution of obstruction, with nearly half of cats displaying signs of diuresis within 6 h. Specific clinical variables associated with post-obstruction diuresis evaluated in this study were magnitude of acid–base disturbance, hyperglycemia, calculated plasma osmolality, and azotemia on admission. The admission variables evaluated were chosen as they clinically mirror disease severity. While serious electrolyte abnormalities like hypocalcemia and hyperkalemia are known to occur with urethral obstruction, ² only acidemia was significantly associated with onset of diuresis in this population. Acidemia has long been recognized as the primary acid–base disturbance associated with urethral obstruction in cats and as a marker for the severity of disease.7

Though this study contains relatively small numbers of cats, several of them displayed signs of diuresis for up to 84 h following resolution of urethral obstruction. Similarly, in an experimental model of urethral obstruction in the cat, urine output more than doubled following relief of obstruction and neared pre-obstruction amounts after 4 days regardless of the presence or absence of crystalloid treatment. ¹ These two studies support the conclusion that feline urethral obstruction may result in a significant period of post-obstruction diuresis. The length of diuresis may be more prolonged in cats undergoing naturally occurring urethral obstruction that have experienced preceding episodes of partial obstruction or have been obstructed for a longer time course, therefore, these cats should have urine output and fluid balance monitored closely. Intravenous fluid replacement at rates higher than normal maintenance may be necessary in these cats to prevent a negative fluid balance. Close attention to these parameters is especially important in cats with acidemia as low blood pH was significantly associated with diuresis. Other studies have documented variable times to resolution of azotemia following fluid replacement which they attributed to variable degrees of post-obstruction diuresis. ⁷ Inherent variability in the physiologic responses of cats with naturally occurring urethral obstruction underscores the need to monitor urine production, hydration, and body weight in order to individualize replacement fluid therapy to account for increased urinary losses.