Rapid and complete decompression of chronic urinary retention: a safe and effective practice

Introduction

Urinary retention represents a clinical state in which the amount of urine, drained or measured using ultrasound, in the urinary bladder of a patient who is either unable to void or the post void residual (PVR) urine after voiding is about, or greater than, the bladder capacity. The International Continence Society defines chronic retention as a non-painful bladder which remains palpable or percussible after the patient has passed urine. Such patients may be incontinent. ¹ Chronic urinary retention occurs insidiously and is not usually associated with pain. Patients are usually able to pass urine, although with variable degrees of difficulty or may be incontinent. ² Occasionally, these patients also develop an inability to void and this is known as acute-on-chronic retention. There is no consensus on the cut-off urine volume that is diagnostic of urinary retention, However, a cut-off of 300 mL has been typically used arbitrarily and it is thought to correspond to the volume at which the bladder is palpable par abdomen. ³ It has also been suggested that drained volumes between 500 mL-800 mL are typical of acute retention while >800 mL is suggestive of either chronic or acute-on-chronic retention. ⁴ In chronic retention, urine volumes above 4 L (4000 mL) have been described. ⁵

Treatment begins with prompt bladder drainage via urethral catheterization. If this fails drainage should be via suprapubic cystostomy. In patients with a deranged renal function, close monitoring for post-obstructive diuresis, haematuria from hyperaemia or rupture of distended veins and the risk of further progression of the impaired kidney function is important. In order to reduce the risk of these complications it was advocated that the bladder should be decompressed slowly in all patients with chronic urinary retention.^6–8 In theory, slow decompression should relieve the sudden engorgement of the bladder mucosa and the development of petechial haemorrhages. The traditional slow decompression of the bladder by gradually releasing a gate clip on the drainage tube, or by removing small quantities of urine at regular intervals, does not achieve its aim of gradual reduction in intravesical pressure^7,9–13 George et al. ¹⁴ have shown from isotope renography that there is a dramatic change in isotope washout from the upper urinary tract as the bladder pressure diminishes and that there seems to be no justification for delaying this improvement by slow decompression. ¹⁴

Patients and methods

We carried out a prospective study of patients who presented with chronic urinary retention over a period of 2 years (January 2010 to December 2011). Ethical approval was sought and obtained. All consenting consecutive patients who presented to our accident and emergency unit or to the urology clinic with features suggestive of chronic urinary retention were enrolled in the study. There were no additional expenses borne by the patient for the purposes of this study other than the routine.

The diagnosis of chronic urinary retention and the presence or absence of complications were established by obtaining detailed history and a physical examination and were confirmed by investigations. The information sought included: age; sex; lower urinary tract symptoms (LUTS); duration of symptoms; history of a likely primary pathology; medication; lower limbs oedema; and a review of other systems. The investigations undertaken included: abdominopelvic ultrasound scan; renal function assessment by measurement of serum creatinine; electrolytes, urea and haemoglobin concentration.

Urinary retention was relieved using a protocol of rapid and complete decompression of the bladder. The method of relief of retention (urethral catheterization or suprapubic cystostomy) and the total volume of urine drained were documented. Patients were closely monitored for post-obstructive complications (post-obstructive diuresis, haematuria, hypotension and worsening renal function). Post-obstructive diuresis was defined as urine output > 3 L/day or >200 mL/h on consecutive measurements. Impaired renal function was defined by serum creatinine > 120 μmol/L. Patients who remained stable were discharged after a 24 h observation. The data obtained were analysed using tables, charts and percentages.

Results

A total of 22 patients met the inclusion criteria during the period of the study. The mean age was 53 years with a range of 18–78 years. More than 60% of the patients were aged 50 years or older and they were all male and all had experienced LUTS at one time with varying degrees of severity but had not sought treatment until they perceived it to be significant: 68.2% presented because of bothersome LUTS alone but others also had pedal oedema, fatigue and other general symptoms. Up to 25.5% had overflow incontinence. Abdominopelvic ultrasound scans showed some degree of upper urinary tract dilatation in all the patients. The primary aetiology of the urinary retention was predominantly benign prostatic hyperplasia (BPH; 45.5%), the other causes are shown in Figure 1. Urinary retention was relieved by urethral catheterization in 72.7% and the remainder who could not be catheterized had suprapubic cystostomy. The mean volume of drained urine was ∼1500 mL, range 800–4200 mL. Post-obstructive complications included diuresis, haematuria and hypotension as summarized in Table 1. All patients who developed post-obstructive diuresis had a drained urine volume in excess of 2000 mL. Those who developed post-obstructive diuresis were managed, preferably by oral fluid administration, while intravenous fluid administration with careful monitoring of hydration status was reserved for patients with significant haemodynamic instability. Once stable, all were maintained on an oral fluid intake as thirst demanded. Post-obstructive haematuria occurred in more than half (54.5%) but it resolved completely within 24 h without the need for blood transfusion. 59.1% had impaired renal function and all those who developed diuresis had impairment of renal function. Renal impairment either resolved completely following drainage in 81.8% or improved significantly at follow up.

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Table 1

Frequency of post-obstructive complications

Post-obstructive complication	Yes (%)	No (%)	Normal (%)	Impaired (%)	Improved (%)
Post-obstructive diuresis	18.2	81.8	–	–	–
Post-obstructive haematuria	54.5	45.5	–	–	–
Post-obstructive hypotension	9.1	90.9	–	–	–
Baseline renal function	–	–	40.9	59.1	–
Follow-up renal function	–	–	81.8	9.1	9.1

Discussion

The International Continence Society defines chronic retention as a non-painful bladder which remains palpable or percussible after the patient has passed urine and such patients may be incontinent. ¹ Chronic urinary retention occurs insidiously and is not usually associated with pain - patients are still able to void, although with variable degree of difficulty, or may develop late unset enuresis. Urinary retention is a common urological problem and occurs predominantly in the elderly. It commonly results from mechanical obstruction to bladder outlet by BPH^14–16 while less common causes include: carcinoma of the prostate; urethral stricture; and from neurogenic and myogenic bladder dysfunction. In our study, BPH was the most common cause of obstruction (45.5%) followed by urethral stricture (22%) and others as shown in Table 1.

The pathophysiological mechanism of chronic urinary retention is commonly due to increased bladder outlet resistance as seen in patients with bladder outlet obstruction (BOO) manifesting with high pressure chronic retention (HPCR) while vesical myogenic, or neurogenic dysfunction, leads to low pressure chronic retention (LPCR)^14,16,17. The prolonged increased voiding pressure and progressively PVR urine eventually leads to bladder dysfunction and may manifest as detrusor instability with decreased compliance and compromise of the storage function worsening LUTS. Such a dysfunctional bladder can decompensate insidiously with progressive distension of the bladder, resulting in chronic retention. Chronic retention may be high pressure (intra vesical pressure ≥30 cm of H₂O) or low pressure when less than 30 cm of H₂O. The bladder becomes insensitive, hypocontractile, allowing distension beyond its capacity that may present as overflow incontinence or nocturnal enuresis. In high pressure retention, bladder changes may also result in functional failure of ureterotrigonal complex resulting in vesicoureteric reflux and hydronephosis.^3,17 With time, this may lead to nephron loss, impaired glomerular function and eventual chronic renal failure. This may further be complicated by calculi formation and urinary tract infection.

The majority of our patients had LUTS which were, however, not bothersome enough to necessitate earlier presentation and up to 25.5% presented with incontinence which is consistent with findings in other studies. ¹⁵ Chronic urinary retention usually progress insidiously, unnoticed by most patients, and they are usually still able to pass urine with or without minimal difficulty except that they develop acute-on-chronic retention. Others present with features of impaired renal function such as pedal oedema, fatigue and hypertension.^4,8,18,19 All our patients had some degree of upper tract dilatation on an abdominopelvic ultrasound which is a common finding in patients with HPCR.^14,16,20 However, only 59.1% had impaired renal function based on elevated serum creatinine (>120 μmol/L); 81.8% had complete recovery of renal function at 2 weeks follow-up after initial decompression; 9.1% had marked improvement; and another 9.1% had persistent impairment of renal function. The later had probably developed irreversible renal damage that may require renal replacement therapy at some future date.

Relief of retention can be achieved by either rapid and complete or slow decompression. Advocates of slow bladder decompression claim that not only does it reduce the incidence of post-obstructive haematuria but it also prevents the occurrence of tubular necrosis of the kidney and post-obstructive diuresis. In theory, the traditional slow decompression should relieve the sudden engorgement of the bladder mucosa and the development of pethechial haemorrhages. However, slow decompression of the bladder by gradually releasing a gate clip on the drainage tube, or by removing small quantities of urine at regular intervals, does not achieve its aim of gradual reduction of intravesical pressure.^7,9–13 George et al. ¹⁴ have shown from isotope renography that there is a dramatic change in isotope washout from the upper urinary tract as the bladder pressure diminishes and that there seems no justification for delaying this improvement by slow decompression. ¹⁴ Slow decompression has been shown to have several disadvantages. Firstly, the intended slow and gradual reduction of intravesical pressure is not usually achievable because withdrawal of as little as 50 mL of urine from a tensely distended inelastic bladder leads to close to 50% reduction in vesical pressure. Secondly, prolonged drainage of stagnant urine at high pressure with an indwelling catheter predisposes to urinary tract infection which may worsen the already compromised renal function. Thirdly it is time-consuming and labourintensive. ^4,6,7,13 Recently Perry et al. ²¹ suggested using slow decompression of the bladder with a suprapubic intravenous fluid giving-set. However, this is also susceptible to the same disadvantages detailed above.

In this study, rapid and complete bladder decompression was adopted for all patients. Bladder drainage was done as soon as the diagnosis was established and investigations completed. The mean drained urine volume was 1.5 L with a range 800–4200 mL. This is consistent with earlier studies. O'Reilly et al. ¹⁶ reported a mean residual urine volume of 2.4 L in 36 patients while Abrams et al. ³ and Bishop ¹⁵ reported 1.4 L and 1.43 L, respectively, in 55 patients each. The reported incidence of postoperative diuresis has a wide variation ranging from as low as 0.5% and to as high as 78%.^8,15 O'Reilly et al. had a 78% incidence of postobstructive diuresis while Bishop reported diuresis in 27 of the 47 patients (57%) with elevated plasma creatinine (>120 μmol/L). Although all the patients studied by O'Reilly et al. had elevated plasma creatinine, only 57% developed post-obstructive diuresis following rapid bladder decompression. Thus, post-obstructive diuresis has not been shown to correlate with the degree of plasma creatinine elevation or extent of renal impairment.

Studies that directly compared slow versus rapid bladder decompression found no significant difference in the incidence of complications.^{7,10,12,13,22} We found an 18.2% incidence of post-obstructive diuresis, all the patients that developed post-obstructive diuresis had some degree of renal function impairment and drained urine volumes 2000 mL or more. However, not all the patients with impaired renal function developed post-obstructive diuresis. Therefore, it might be safe to postulate that post-obstructive diuresis is more likely to occur in patients with impaired renal function and, thus, such patients should be closely monitored at the outset and the possibility of diuresis anticipated.

Post-obstructive haematuria is thought to be a common complication and advocates of slow bladder decompression are quick to name the sudden decompression of the bladder and subsequent engorgement of the vesical veins and their rupture as the cause. However, they fail to take into account the contribution of urinary tract infection and the trauma of catheterization. Studies have shown that the incidence of haematuria, when it does occur, is low and is often variable and usually mild, inconsequential, resolves within 24–48 h and rarely requires blood transfusion. ^2,6,9,12,19 The largest study that specifically looked at the incidence of haematuria following rapid bladder decompression was reported by Glahn et al. ¹² They studied 300 patients and found a 16% incidence of haematuria. We recorded an incidence of 54.5% which is much higher than most reports. However, we did not exclude patients who had bladder decompression via suprapubic cystostomy in which the trauma from the procedure may have caused the haematuria. Thus, the actual incidence is likely to be much lower. Other complications, such as hypotension and urinary tract infection, were not significant.

Conclusion

The traditional dangers attributed to rapid and complete bladder decompression of the chronically obstructed bladder remain a myth and are, at best, merely theoretical. The complications are mild and of no clinical significance. However, patients with impaired renal function drained urine volumes ≥2000 mL are most at risk of developing post-obstructive diuresis and should be closely monitored. Thus, rapid and complete decompression of the chronically obstructed urinary bladder not only saves time but is safe and effective and should be adopted as the standard practice.