Urinary Care Reference Material

Prostate Cancer and Prostatic Diseases (2004) 7, 32–37 & 2004 Nature Publishing Group All rights reserved 1365-7852/04 $25.00

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Review

Acute Urinary Retention: a review of the aetiology and management K Thomas1*, K Chow1 & RS Kirby1 1

Urology Department, St George’s Hospital, London, UK

Acute retention of urine (AUR) is a common urological emergency characterised by a sudden inability to pass urine associated with lower abdominal pain. In recent years, the natural history and incidence of AUR has become better understood, however, further research into methods to prevent it and evaluation of the impact an episode of AUR has on the patient is required. This review provides an overview of the current management of AUR in men and the impact of the condition on patients’ quality of life.

Prostate Cancer and Prostatic Diseases (2004) 7, 32–37. doi:10.1038/sj.pcan.4500700

Keywords: acute urinary retention; catheterisation; quality of life; benign prostatic hyperplasia

Introduction Acute retention of urine (AUR) is a common urological condition that often presents as an emergency with a sudden inability to pass urine associated with lower abdominal pain.1,2 The reported incidence varies between studies from a 4 to 73% 10-year risk of AUR.3,4 One of the most common causes of acute urinary retention is benign prostatic hyperplasia (BPH), which with an ageing population is likely to increase. It may be anticipated, therefore, that the incidence of AUR will also rise, unless preventative measures are taken for the treatment of BPH.5 The immediate management of this condition varies between institutions, but usually involves placement of a urinary catheter either, supra-pubic or urethral, medical therapy and either immediate admission to hospital or discharge home with outpatient follow-up.6,7 In recent years, the natural history and incidence of AUR has become better understood, however, further research into methods to prevent it and evaluation of the impact an episode of AUR has on the patient is required. This review provides an overview of the current management of AUR in men and the impact of the condition on patients’ quality of life.

Search methods A Medline search using databases from 1966 to 2003 was conducted using the words acute AND retention AND *Correspondence: K Thomas, Urology Department, Ashford Hospital, Middlesex, UK. E-mail: specialkthomas@hotmail.com Received 28 August 2001; revised 9 October 2003; accepted 20 October 2003

urin* in the title, limited to English language. From this search 465 records were identified. Further information was gathered from related references within the articles identified and by hand searching recent abstracts at urological scientific meetings. Of the 465 records identified, 121 were case reports of unusual cases of AUR.

Aetiology The precise aetiological factors responsible for the development of AUR are still unproven but the main mechanisms postulated are (Table 1): (1) increased resistance to flow of urine via mechanical or dynamic means8 (2) interruption of sensory innervation or motor supply to detrusor muscle9 (3) overdistension of the bladder.1,2,10 Increased resistance to the flow of urine can occur secondary to a mechanical obstruction such as stricture or prostatic enlargement, or less commonly an increase in either the smooth or striated muscle tone. Interruption of the sensory or motor nerve supply to the detrusor muscle is caused by a variety of pathologies, for example, spinal cord lesion (traumatic or neurological), diabetic neuropathy, cerebrovascular accident. Overdistension of the bladder is seen after a general anaesthetic or a large fluid challenge (often with alcohol). Postoperative AUR occurs during a prolonged procedure with the patient uncatheterised and in men who have had mild symptoms of BPH preoperatively. It is also exacerbated by the use of opiates, concomitant anticholinergic administration and the generalised increase in alpha-adrenergic activity that exists after surgery.11

Acute urinary retention K Thomas et al Table 1 Pathogenesis of AUR Pathogenesis

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Table 2 Potential neuromodulators in the bladder Example

Increased resistance to flow

Prostatic hyperplasia Urethral stricture Detrusor sphincter dysynergia

Interruption of sensory or motor innervation to detrusor

Spinal cord lesion Cerebrovascular lesion Diabetes mellitus

Overdistension

Postoperative Opiate analgesia Large volume alcohol consumption

A scientific explanation for the clinically observed aetiologies has been explored, with the following processes thought to be involved; 1. prostatic infarction.12–14 2. neurotransmitter modulation.15,16 3. stromal epithelial tissue ratio.17,18 Prostatic infarction has been discussed as a potential cause for AUR by several authors.12–14 Spiro et al evaluated the potential role of prostatic infarction as a cause of AUR by examining open prostatectomy specimens of 200 patients. The first 100 patients had large prostates and AUR, while the second group of 100 patients had elective surgery for BPH. In all, 85% of the AUR group had histological evidence prostatic infarction compared with 3% of the elective group. It has also been proposed that the elevated prostate-specific antigen (PSA) found in patients with AUR is secondary to prostatic infarction.14 Experimental work in animals has suggested that there may be multiple neuromodulators affecting the nerves that supply the bladder and urethra (Table 2).15,16 Reversible and irreversible changes are seen when AUR is induced experimentally in animals. In particular, changes in the nonadrenergic, noncholinergic neurotransmitters have been reported in rats. It has been shown that if the episode of AUR is not relieved, cell death in ganglia in the bladder wall can occur within 24 h and is well established by 48 h.

A retrospective study in a small number of patients (10) found that the ratio of stromal to epithelial tissue was decreased in patients with AUR compared with agematched controls.17 This finding was confirmed by another group, who conducted a prospective study of the TURP specimens of 70 patients (35 with AUR and 35 with symptomatic BPH). The AUR group had a significantly higher epithelial component 71%, compared with the BPH group 60% (Po0.01).18 The cause for this observation is uncertain, but it may explain why finasteride, which acts on the epithelial component, is effective in the prevention of AUR.

Identification of risk factors The exact aetiology of AUR is still unclear, however, there are studies that have identified risk factors for AUR in men and calculated the overall risk at 5–7/1000 year (Table 3).

Acetylcholine (ACh) Noradrenaline (NAd) Vasoactive polypeptide (VIP) Neuropeptide Y (NYP) Substance P (SP) Enkephaline Somatostatin Nitric oxide (NO)

Table 3 Risk factors for AUR Risk factor

Parameter

Agea Symptomsa Prostate volumea Flow ratea

470 y IPSS47 430 ml o12 ml/s

7.8 3.2 3.0 3.9

Risk factor

Parameter

Area under the curve

PSAb Transition zone indexc

42.5 40.65

Relative risk

Confidence interval 3.7–16.4 1.9–5.4 1.0–9.0 2.3–6.6

0.70 0.924

a

Jacobsen et al.19 Roehrborn et al.22 c Kurita et al.25 b

The most comprehensive of these is the Olmstead County trial, which identified a cohort of men in the general population aged between 40 and 79 y.19 Those with previous history of prostatectomy, prostate cancer or any other condition except benign prostatic hyperplasia were excluded from the study. The 2115 men recruited underwent an interview, completed a questionnaire and had their flow rate measured. Of these, 537 (25%) were randomly selected for a clinical examination, PSA measurement and trans-rectal ultrasound (TRUS) of the prostate. The men were followed up for a median average of 50 months. The risk of AUR was shown to be increased with age, from 1.6% risk at 5 y for men aged 40–49 y to 10% for men aged between 70–79 y. The symptom correlation was also found as men with moderate to severe symptoms had three times the risk of AUR compared with those with none to mild symptoms. In younger men, symptoms of double voiding and stopping and starting appeared most significant. A single peak flow rate measure of o12 ml/s correlated with a four times risk of AUR and a prostate volume 430 ml was associated with a threefold increase in risk. Potential limitations of this study were the retrospective collection of follow-up data, the ethnic and socio-economic status of the population studied, who were mostly white, middle class men.

Also, the age range of the men was below that of most patients admitted with acute retention in the UK and elsewhere.20 These factors mean that caution should be taken in extrapolating the findings to hospital practice elsewhere in the world.

The risk factors discussed have also been identified in other studies. In a population-based study of 6100 male health professionals aged between 45 and 82 y, it was found that older age (470 y), moderate or severe lower urinary tract symptoms and the use of medications with Prostate Cancer and Prostatic Diseases

Acute urinary retention K Thomas et al

34

adrenergic or anticholinergic side effects significantly increased the risk of AUR. 21 The placebo arms of trials of pharmaceutical treatments for BPH provide useful epidemiological data and have demonstrated that PSA, prostate volume and symptom severity significantly affect the risk of AUR.22–24 With increased use of TRUS, the transition zone index (TZI ¼ transition zone volume/total prostate volume) has recently been suggested as a predictor for acute retention.25

Treatment Catheterisation The initial management of AUR of urine is prompt relief of retention and pain by catheterisation of the bladder.

This can be achieved via the urethral or supra-pubic route, each of which has its merits. Depending on the cause of the episode of AUR, local policy, the patient’s physical condition and social circumstances they may be discharged with the catheter or admitted into hospital.

Urethral catheterisation is performed more commonly than supra-pubic because of concern regarding the potential complications of inserting a supra-pubic catheter and that the personnel (ie accident and emergency staff, family practitioners) who first see patients with AUR are generally more familiar with this method.26,27 A prospective study of 86 patients with AUR catheterised described a significantly lower incidence of urinary tract infection (18 vs 40%) and stricture formation (0 vs 16.7%) with supra-pubic vs urethral catheters.28 It was also commented that trial without catheter was easier as it merely required clamping and unclamping of the supra-pubic catheter. The relatively high stricture rate may be explained in part by the now outdated use of latex catheters by this group; however, the incidence is still likely to be higher than when the supra-pubic route is used. The lower infection rate with supra-pubic catheterisation was also reported by a group, who randomised patients to urethral vs suprapubic catheterisation.29 Also, it was noted that patients found the supra-pubic catheter was more comfortable and easier to manage. Despite these findings the majority of patients with AUR are still managed with a urethral catheter, probably due to the continuing perception of supra-pubic catheterisation as a potentially hazardous procedure.30 A novel suggestion recently by one group is that patients with AUR can be managed by clean intermittent self-catheterisation (CISC).31 The authors found that the CISC group had a higher rate of spontaneous voiding (56 vs 25%) and lower infection rate (32 vs 75%) compared with the indwelling catheter group. They concluded that patients found CISC acceptable and manageable and experienced fewer complications than those with an indwelling catheter do.

An area of debate is the timing of the removal of a catheter (trial without catheter or TWOC). While some have found no difference in success rates at 24 and 48 h,32 others have suggested a benefit to waiting longer, particularly in men with large residual volumes 41 l.33 It has recently been suggested that prostate size 427.5 g, residual volume 41 l and age 475 y may reduce the Prostate Cancer and Prostatic Diseases

chance of successfully voiding after a TWOC.34 It has also been suggested that the use of an alpha blocker may improve the success rate of a TWOC.35

Pharmacotherapy There has been an increasing trend towards the use of drugs in both the prevention and treatment of AUR due to prostatic obstruction. The two main classes of drugs used are alpha blockers and 5 alpha-reductase inhibitors.

Alpha blockers act by relaxing the smooth muscle in the bladder neck and prostate thereby decreasing the resistance to urinary flow. The potential role of alpha blockers in the treatment and prevention of AUR was first described 25 y ago.36 Since then different types of alpha blockers have been produced and reported to have differing side effect profiles.37 The impact of some of these in the prevention of AUR has been compared against placebo. A double-blind study of 2084 patients randomised to terazosin or placebo, reported no difference in the incidence of AUR in each group during the 1 y follow-up period.38 In contrast, a study of 81 patients with AUR randomised to receive either alfuzosin or placebo for 48 h prior to trial without catheter after 24 h showed that those patients on alfuzosin had a significantly increased chance of passing a trial without catheter, 55 vs 28% (P ¼ 0.03). This effect was sustained over 18 months of follow-up.39 Finasteride was until recently the only 5 alphareductase inhibitor available, although now a newer agent, dutasteride, is available.40,41 They act by selective inhibition of 5 alpha-reductase responsible for the conversion of testosterone to dihydrotestosterone.42 In a large double-blind randomised placebo-controlled trial, 3040 men with moderate to severe lower urinary tract symptoms and enlarged prostates were recruited.43 Over a 4 y period, they were treated daily with either 5 mg finasteride or placebo. AUR developed in 99 (7%) men in the placebo group vs 42 (3%) in the finasteride group. This represents over a 50% risk reduction for developing AUR. However, because of the relatively rarity of AUR, 15 men would have to be treated for 4 y to avoid one episode of AUR. Similar reductions in the risk of events such as heart attack or stroke occur with statins and antihypertensive medication.44 A pooled analyses of three randomised trials comprising 4222 men with moderately symptomatic BPH treated with either finasteride or placebo for 2 y reported 81 episodes of AUR (24/2113 finasteride group, 57/2109 placebo group).42 The hazard ratio for the occurrence of AUR was consistent among the studies with a 57% decrease in the hazard rate for patients treated with finasteride compared with placebo (Po0.001).

Combination therapy Prevention of the progression of BPH and in particular AUR has been studied using the combination of an alpha-blocker and a 5 alpha-reductase inhibitor by several investigators.45–47 Two four-arm randomised placebo-controlled trials compared placebo with an alpha-blocker, finasteride and combination therapy. Lepor et al used terazosin, whereas

Acute urinary retention K Thomas et al

the Kirby group used doxazosin with similar results.

Both groups found that the alpha-blocker was an effective treatment for BPH and that over the study period of 1 y, finasteride or combination therapy was no more effective than an alpha-blocker alone.

The medical therapy of prostatic symptoms (MTOPS) study, a 5-y multicentre clinical trial evaluated whether the treatment with doxazosin and finasteride was more effective than using either drug alone in preventing the clinical progression of BPH.47 One of the endpoints for establishing the progression of BPH was AUR. The combination therapy and finasteride significantly reduced the long-term risk of AUR (crude rate per 100 patient years; placebo 0.6, doxazosin 0.4, finasteride 0.2, combination therapy 0.1). It was also noted that men in the placebo group with higher baseline serum PSA, prostate volumes and ages and lower flow rate were significantly more likely to progress.

Surgical intervention At present, TURP still remains the ‘gold standard’ surgical treatment for patients with AUR. It reduces the risk of developing AUR by a factor of eight.48 It is not without risk, however, and if patients who have had an episode of AUR have a TURP they are at a higher risk of per-operative complications.49 The National Prostatectomy Audit found that men undergoing a TURP within 30 days of an episode of AUR had an excess risk of death (relative risk 26.6, CI 2.5–7.6).20 With greater insight into the potential morbidity and occasional mortality associated with this procedure, alternatives have been sought in the form of pharmacotherapy and minimally invasive techniques. Most of these new technologies are still based on the endoscopic removal or ablation of prostatic tissue; Electrovaporisation, laser resection (holmium, Nd-YAG, ELAP, interstitial), interstitial radiofrequency (TUNA) and microwave thermotherapy (TUMT).50–52 Temporary or permanent urethral stents are available to keep the prostatic urethra open, but only provide modest improvements in symptoms with a high incidence of complications such as migration, infection, encrustation, obstruction secondary to prostatic ‘ingrowth’ and calculus formation.51 These problems have limited their current use to elderly infirm patients unfit for surgery.53,54 Some patients may still be unable to void after a TURP.55 Urodynamic evaluation has not been shown to predict this in patients under the age of 80 y as detrusor failure may recover postoperatively.33 Therefore, urodynamics are not recommended for routine preoperative evaluation in this age group. The presence of residual volume 41500 ml, lack of detrusor instability, detrusor pressure at maximum fill of o9 cm water and maximal detrusor pressure o28 cm water were all found to predict treatment failure.

Quality of life As AUR usually involves an emergency admission to hospital and insertion of a catheter, it is perhaps not surprising that some patients may find the event

traumatic. There have been a few studies, that have looked at the impact of an episode of AUR on the patient, but this has remained a relatively neglected aspect of the management of this condition. A recent retrospective study of the management of patients with AUR in one surgeon’s practice over a 23 y period showed that 90% of patients were discharged home with a catheter to await surgery.56 While at home 72% of patients experienced some complication, 69% found the catheter uncomfortable and 65% found it inconvenient particularly with respect to finding adequate toilet facilities. Another group prospectively evaluated the impact of discharging patients with AUR home with a catheter by means of a self-completion questionnaire.57 A total of 101 patients were seen with AUR and discharged home immediately with a catheter. In all, 93% of the questionnaires were completed. Unlike the previous group, the majority of patients (87%) did not find that the catheter limited their activities in anyway, although all of them had experienced at least one complication. The questionnaire used was not a validated measure, however, it did show that despite having complications from the catheter most of the patients still found having a catheter at home acceptable. This study challenges the perception of most clinicians that patients do not like having a catheter.

Further work is required using validated questionnaires, a longer follow-up period and a broader evaluation of all aspects of quality of life to define the impact of AUR and having a catheter at home on patients.

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Future research There are various aspects of the management of AUR that should be targeted in the future: (1) (2) (3) (4)

catheters minimally invasive therapy medical therapy quality of life

Catheters are crucial in the management of AUR. The ideal catheter material would be inert, malleable, biocompatible and be resistant to colonisation with bacteria. In the future, newer technology in catheter design should make some of these properties possible and, therefore, reduce some of the complications associated with having a catheter.

Evolution of minimally invasive techniques will make daycase treatment of BPH feasible, which should reduce the time patients spend at home with a catheter following an episode of AUR. As discussed previously, the use of combination therapy for the treatment of BPH offers the opportunity to prevent the progression of BPH and, therefore, episodes of AUR. Newer agents are under development and may prove to be even more effective than the current formulations.

An episode of AUR can have an adverse effect on a patient’s quality of life, which is further exacerbated by delay in treatment and, prolonged period of catheterisation. Awareness of the impact of AUR on a patient and streamlining of the treatment of AUR so that prompt effective care is delivered would reduce the impact it has on the patients, quality of life.

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Acute urinary retention K Thomas et al

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Discussion Although AUR is an age-old condition, it remains a modern day management problem. As demonstrated by Modi et al, treatment of patients with AUR may be considered to be regressing rather than progressing.56 New pharmacological agents will emerge over then next few years as will variations on TURP using modern methods of tissue ablation. However, as clinicians we must not lose sight of the impact of these treatments on our patients. When introducing new therapies in the future the effect of these on the patients’ quality of life in addition to their clinical effectiveness must be evaluated if we are to improve our management of this common and disturbing condition.

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2 Choong S, Emberton M. Acute urinary retention. Br J Urol 2000; 85: 186–201.

3 Ball A, Feneley R, Abrahams P. The natural history of untreated ‘‘prostatism’’. Br J Urol 1981; 53: 613–616.

4 Birkhoff J, Wiederhorn A, Hamilton M, Zinsser H. Natural history of benign prostatic hypertrophy and acute urinary retention. Urology 1976; 7: 48–52.

5 McConnell JD. The long term effects of medical therapy on the progression of BPH. Results from the MTOPS trial. J Urol 2002; 167, Abstract 1042.

6 Beard R, Hindley R, Borley N, Cox C The management of acute urinary retention in the South Thames Region. South Thames Health Authorities Urology Audit, 2001.

7 Higgins PM, Karia SJ, Mehta. The management of acute retention of urine. Br J Urol 1981; 53: 344–348.

8 Powell PH, Smith PJB, Feneley RCL. The identification of patients at risk from acute retention. Br J Urol 1980; 52: 520–522.

9 Murray K, Massey A, Feneley RCL. Acute urinary retention—a urodynamic assessment. Br J Urol 1984; 56: 468–473.

10 Waterhouse N et al. Urinary retention after total hip replacement.

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11 Raz S, Zeigler M, Caine M. Pharmacological receptors in the prostate. Br J Urol 1973; 45: 663.

12 Spiro LH, Labay G, Orkin LA. Prostatic infarction. Role in acute urinary retention. Urology 1974; 3: 345–347.

13 Strachan JR, Corbishley CM, Shearer RJ. Post-operative retention associated with acute prostatic infarction. Br J Urol 1993; 72: 311–313.

14 McNeill SA et al. Serum PSA levels and histological changes associated with acute urinary retention. BJU Int 2000; 83 (Suppl 4): Abstract P65.

15 Zhou Y, Ling EA. Effects of acute complete outlet obstruction on the NADPH-diaphorase reactivity in the intra-mural ganglis of the guinea pig urinary bladder: light and electron microscopic studies. J Urol 1997; 158: 916–923.

16 Crowe R, Haven AJ, Burnstock G. Intramural neurons of the guinea pig urinary bladder: histochemical localisation of putative neurotransmitters in cultures and newborn animals.

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17 Abehouse BS. Infarct of the prostate. J Urol 1933; 3: 345–347.

18 Saboorian MH et al. Morphometric analysis of pathological specimens in men undergoing prostate surgery for acute retention or symptoms of BPH only. J Urol 1998; 159, Abstract 417.

19 Jacobsen SJ et al. Natural history of prostatism: risk factors for acute urinary retention. J Urol 1997; 158: 481–487.

20 Pickard R et al. The management of men with acute urinary retention. Br J Urol 1998; 81: 712–720.

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21 Meigs JB et al. Incidence rates and risk factors for acute urinary retention: the health professionals follow up study. J Urol 1999; 162: 376–382.

22 Roehrborn CG et al. Serum prostate-speific antigen concentration is a powerful predictor of acute urinary retention and need for surgery in men with clinical benign prostatic hyperplasia.

Urology 1999; 53: 473–479.

23 Lieber M et al. PSA is the strongest predictor of BPH related outcomes: results of a 4 year placebo controlled trial. J Urol 1998; 159: 104.

24 Rhodes T et al. Serum PSA levels predict acute urinary retention in 40-79 year old community men in Olmsted county. J Urol 2000; 161 (Suppl 4): Abstract 1118.

25 Kurita Y et al. Transition zone index as a risk factor for acute urinary retention in benign prostatic hyperplasia. Urology 1998; 51: 595–600.

26 Allardice JT et al. Acute urinary retention: which catheter? Ann R Coll Surg Engl 1988; 70: 366–368.

27 Webb VJ, Booth CM. Cutting the cost of catheterisation for acute retention – a hospital or domiciliary procedure? Br J Urol 1995; 76: 443–445.

28 Horgan AF, Prasad B, Waldron DJ, O’Sullivan DC. Acute urinary retention. Comparison of supra-pubic and urethral catheterisation. Br J Urol 1992; 70: 149–151.

29 Ischan J, Hunt DR. Suprapubic catheters: a comparison of suprapubic versus urethral catheters in the treatment of acute urinary retention. Aust N Z Surg 1987; 57: 33–36.

30 Abrahams PH et al. Role of suprapubic catheterisation in the retention of urine. J R Soc Med 1980; 73: 845–848.

31 Patel MI, Watts W, Grant A. The optimal form of urinary drainage after acute retention of urine. Br J Urol Int 2001; 88: 26–29.

32 Taube M, Gajraj H. Trial without catheter following acute retention of urine. Br J Urol 1989; 63: 180–182.

33 Djavan B, Madersbacher S, Klinger C, Marberger M. Urodynamic assessment of patients with acute urinary retention: is treatment failure after prostatectomy predictable? J Urol 1997; 158: 1829–1833.

34 Kumar V, Marr C, Bhuvangiri A, Irwin P. A prospective study of conservatively managed acute urinary retention: prostate size matters. Br J Urol 2000; 86: 816–819.

35 McNeill AS et al. Long term follow up following presentation with first episode of acute urinary retention. J Urol 2000; 163 (Suppl 4): Abstract 1366.

36 Caine M, Pfau A, Perlberg S. The use of alpha-adrenergic blockers in benign prostatic obstruction. Br J Urol 1976; 48: 255–263.

37 De Mey. Alpha blockers for BPH: are there differences? Eur Urol 1999; 36: 52–63.

38 Somers WJ, Mora MJ, Mason MF, Padley RJ. The natural history of benign prostatic hypertrophy: incidence of urinary retention and significance of AUA symptom score. J Urol 1996; 155: 586A Abstract 1102.

39 McNeill SA et al. Sustained-release alfuzosin and trial without catheter after acute urinary retention: a prospective, placebocontrolled trial. Br J Urol 1999; 84: 622–627.

40 Clark RV et al. Effective suppression of dihydrotestosterone (DHT) by G1198745, a novel, dual 5 alpha-reductase inhibitor.

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41 Roehrborn CG et al. Efficacy and safety of a dual inhibitor of 5 alpha reductase types 1 and 2 (dutasteride) in men with benign prostatic hyperplasia. Urology 2002; 60: 434–441.

42 Andersen JT et al. Finasteride significantly reduces acute urinary retention and need for surgery in patients with symptomatic benign prostatic hyperplasia. Urology 1997; 49: 839–845.

43 Mc Connell JD et al. The effect of finasteride on the risk of acute urinary retention and the need for surgical treatment among men with benign prostatic enlargement. New Engl J Med 1998; 338: 557–563.

44 Byington RP et al. Reduction in cardiovascular events during pravastatin therapy. Pooled analysis of clinical events of the Pravastatin Atherosclerosis Intervention Program. Circulation 1995; 92: 2419–2425.

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46 Kirby RS et al. Results of the PREDICT (prospective European doxazosin and combination therapy) trial. J Urol 1999; 161: Abstract 266.

47 McConnell JD. The long term effects of medical therapy on the progression of BPH. Results from the MTOPS trial. J Urol 2002; 167: Abstract 1042.

48 Wasson JH et al. A comparison of transurethral surgery with watchful waiting for moderate symptoms of benign prostatic hyperplaia. N Engl J Med 1995; 332: 75–79.

49 Higgins PM, French ME, Chadalavada SR. Management of acute retention of urine: a reappraisal. Br J Urol 1990; 67: 365–368.

50 Kabalin JN et al. Holmium: YAG laser resection of prostate (HoLRP) for patients in urinary retention. J Endourol 1997; 11: 291–293.

51 Isotalo T et al. A pilot study of a bioabsorbable self-reinforced poly L-lactic acid urethral stent combined with finasteride in the

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Reproduced with permission of the copyright owner. Further reproduction prohibited without permission.

0022-5347/99/1616-1781/0 THE JOURNAL OF UROLOGY Copyright © 1999 by AMERICAN UROLOGICAL ASSOCIATION, INC.

Vol. 161, 1781–1785, June 1999 Printed in U.S.A.

PROTEINURIA AND RENAL FUNCTION DURING AND AFTER ACUTE URINARY RETENTION SIRKKU MUSTONEN, ILPO ALA-HOUHALA

AND

TEUVO L. J. TAMMELA

From the Division of Urology and Department of Medicine, Tampere University Hospital, Tampere, Finland

ABSTRACT

Purpose: Benign prostatic hyperplasia is the most common neoplasm as well as the main cause of bladder outlet obstruction in men. It may progress to involve a risk of urinary retention. We investigated the effects of acute urinary retention on renal function.

Materials and Methods: We evaluated renal function using biochemical markers in 25 men with a mean age of 69 years in whom an episode of acute urinary retention a mean of 31 hours in duration was due to bladder outlet obstruction. Patients were followed for 6 months after acute retention was relieved. Patients were not known to have had any renal disease previously.

Results: During acute urinary retention at presentation, and after 1 and 6 months we noted albuminuria in 100, 92 and 54% of patients, elevated a1-microglobulin excretion in 54, 39 and 58%, and elevated b2-microglobulin excretion in 17, 19 and 9%. Serum creatinine or creatinine clearance did not predict proteinuria. All parameters became normal at 6 months in only 2 cases.

Conclusions: Acute urinary retention affects glomerular and tubular renal function. After acute urinary retention was relieved increased glomerular permeability and tubular damage persisted in the majority of patients. This condition may have been partially due to previous long-term bladder outlet obstruction. Our findings stress the importance of the rapid recognition and treatment of acute urinary retention.

KEY WORDS: prostate, prostatic hyperplasia, bladder, urinary retention

Acute urinary retention in men is most often caused by benign prostatic enlargement. Other common causes are urethral stricture, bladder neck obstruction and prostate cancer.

Kidney obstruction leads to terminal kidney failure within a few years but even short-term urinary obstruction affects renal function. In newborns and infants renal function returns to normal within 14 days after obstructive uropathy resolves.1 In dogs there is a certain degree of renal dysfunction after 2 months of complete renal obstruction.2 Renal tubular defects resulting in water and salt depletion are particularly characteristic of obstructive nephropathy.

Hyperchloremic acidosis, often with hyperkalemia (type 4 distal renal tubular acidosis), may also result from distal nephron or collecting duct damage.3 Distal renal tubular acidosis is associated with hypocitruria.4 Hypophosphatemia due to the inappropriately high urinary excretion of phosphate has been reported during diuresis after resolution of bilateral obstruction in humans and animals.3 Urinalysis may be normal in acute or chronic urinary tract obstruction. In most cases proteinuria is absent or mild (less than 1.5 gm./24 hours).3 However, transient severe proteinuria has also been reported.5 Glomerular and tubular dysfunction may cause proteinuria.6 Even a small increase in the urinary level of albumin signifies glomerular dysfunction of clinical significance.7, 8 Tubular function has been followed by measuring the urinary level of b2-microglobulin. Nearly all b2-microglobulin filtered by the glomerulus is normally reabsorbed by the proximal tubule.9 Although measuring b2-microglobulin is difficult because it is unstable at room temperature and low pH, increased urinary excretion of this low molecular weight plasma protein signifies malfunction in

the proximal portion of the renal tubule.10 Urinary excretion of a1-microglobulin is a clinically useful index of proximal tubular function since it is more stable in urine than b2microglobulin.11 Urinary excretion of albumin and b2-microglobulin increases 0 to 24 hours after extracorporeal shock wave lithotripsy for renal stones.9 To our knowledge no previous studies have been done of glomerular and tubular proteinuria after acute urinary retention due to infravesical obstruction.

We investigate abnormalities in renal function and proteinuria during and after an episode of acute urinary retention by monitoring urinary biochemical markers.

MATERIALS AND METHODS

We evaluated 25 consecutive men 50 to 87 years old (mean age 69) who presented to the emergency department at our hospital in acute urinary retention, defined as painful and subjectively abolished voiding ability. Acute retention was confirmed by the mechanical emptying of at least 400 ml. of urine. Mean duration of retention was 31 hours (range 7 to 96) and mean retained urine volume was 1,135 ml. (range 400 to 3,080, table 1).

Most patients had a history of lower urinary tract symptoms. A provoking factor was identified in 13 cases, including alcohol consumption in 5, urinary tract infection in 3, medical examination in 2, and minor trauma, constipation and furosemide administration in 1 each. Patients were in good general health. In 8 patients with hypertension treatment involved b-blockers in 4, thiazide diuretics in 2, furosemide in 1 and ramipril in 1. No patient was known to have had previous renal dysfunction or diabetes. One patient died of heart infarction 2 months after the acute urinary retention episode. The study was performed according to good clinical practice and the principles of the Declaration of Helsinki. All patients provided informed consent and the study was approved by the ethics committee at our hospital.

Accepted for publication December 11, 1998.

Supported by a grant from the Research Foundation of Tampere University Hospital.

Editor’s Note: This article is the second of 5 published in this issue for which category 1 CME credits can be earned.

Instructions for obtaining credits are given with the questions on pages 1958 and 1959.

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PROTEINURIA AND RENAL FUNCTION DURING AND AFTER ACUTE URINARY RETENTION TABLE 1. Clinical data of study patients

Pt. Age No.—(yrs.)

1—64 2—76 3—76 4—60 5—69 6—71 7—64 8—56 9—74 10—59 11—58 12—66 13—83 14—67 15—74 16—54 17—80 18—75 19—67 20—50 21—65 22—87 23—73 24—65 25—82

Retention Hrs.

Ml.

Cause

72 96 24 24 24 24 48 24 72 72 24 24 24 48 12 10 12 24 7 10 11 9 24 24 24

3,080 1,200 900 1,000 1,000 550 1,400 1,100 1,700 1,000 800 1,250 1,400 1,000 1,000 1,250 900 1,050 800 400 1,300 800 1,100 1,000 1,400

Benign prostatic enlargement Benign prostatic enlargement Benign prostatic enlargement Benign prostatic enlargement Benign prostatic enlargement Benign prostatic enlargement Benign prostatic enlargement Benign prostatic enlargement Benign prostatic enlargement Bladder neck obstruction Benign prostatic enlargement Benign prostatic enlargement Benign prostatic enlargement Benign prostatic enlargement Benign prostatic enlargement Benign prostatic enlargement Benign prostatic enlargement Benign prostatic enlargement Urethral stricture Urethral stricture Benign prostatic enlargement Bladder neck obstruction Benign prostatic enlargement Benign prostatic enlargement Benign prostatic enlargement

Acute urinary retention was relieved by inserting a suprapubic catheter. The volume of urinary retention was measured and blood samples were immediately obtained. Urinary collection was then initiated for 8 hours and kidney ultrasound was performed. None of the patients had macroscopic hematuria after the suprapubic catheter was inserted. Patients were hospitalized overnight and discharged home the next day with an indwelling suprapubic catheter, which remained open to guarantee free bladder drainage until the initial 1-month followup visit. During this hospital visit the cause of urinary retention was clarified as benign prostatic enlargement in 21 cases, bladder neck obstruction in 2 and urethral stricture in 2. All but 2 patients underwent surgery after the 1-month followup to resolve infravesical obstruction, after which all voided normally (table 1). Two patients with benign prostatic enlargement who voided normally at 1 month required no surgical procedure. This status was verified at the 6-month followup.

At followup 1 and 6 months after the episode of acute urinary retention patients provided an overnight urine collection with the time of collection documented. Blood samples were then obtained. Another urine sample was provided to analyze b2-microglobulin. Because b2-microglobulin is rapidly destroyed in an acid medium, each urine specimen was placed in a tube containing sodium carbonate. Blood and urine samples were stored at 270C until assayed. Serum and urinary creatinine, urea and electrolytes were measured by conventional quality control methods in the clinical chemistry department at our hospital. Serum and urinary b2microglobulin was measured by radioimmunoassay, while albumin and a1-microglobulin were measured in urine using a Behring Nephelometer.* Values are presented as the mean plus or minus standard deviation or the median and range.

For statistical analysis we performed Wilcoxon9s nonparametic test and Student9s t test for paired comparisons.

Provocative Factors

Ultrasound Prostate Vol. (ml.)

None Trauma None Alcohol Alcohol Medical examination None Urinary tract infection Dementia None Urinary tract infection None Urinary tract infection None None Alcohol Medical examination Furosemide None None Alcohol None Alcohol None Obstipation

51 24 54 32 52 54 41 31 27 17 64 77 71 21 40 56 25 99 Not available 20 54 15 88 43 37

after acute urinary retention. During retention average creatinine (normal 115 mmol./l. or less) was slightly elevated. It became normal during followup but the improvement was not statistically significant. Average blood urea nitrogen (BUN) (normal 3 to 8.5 mmol./l.), uric acid (normal 0.16 to 0.45 mmol./l.), phosphorus (normal 0.8 to 1.4 mmol./l.), albumin (normal 36.1 to 47.5 gm./l.), b2-microglobulin (normal 1 to 2.5 mg./l.) and lysozyme (normal 0.9 to 2.1 mg./l.) values were within normal limits during acute retention and followup. The difference during retention and followup was statistically significant only for BUN. Table 3 lists the changes in glomerular and tubular proteinuria markers. Urinary excretion of albumin (normal less than 11 mg. per minute) and a1-microglobulin (normal less than 7 mg. per minute) was elevated but that of b2microglobulin (normal less than 400 mg./l.) was normal during acute urinary retention. Albuminuria improved during followup but median a1-microglobulin excretion remained increased 6 months after acute retention was relieved. In collected and individual urine samples median b2microglobulin excretion was normal during acute retention and 6 months later but it was higher in the individual specimen. There was a difference in the percentage of abnormal values in b2-microglobulin excretion in collected and individual urinary specimens at the 6-month followup (9 and 21%, respectively, table 4).

Table 5 shows the changes in other urinary biochemical markers during acute urinary retention and followup. Average creatinine clearance (normal greater than 1.4 ml. per

TABLE 2. Serum renal function parameters during and after acute urinary retention Av. During Retention 6 SD

RESULTS

Ultrasound showed hydronephrosis in 3 patients, including 1 with hydroureters, but renal parenchyma and kidney size were normal in all. After retention was relieved 5 patients had polyuria (20%). Table 2 shows average serum parameters plus or minus standard deviation during and * Behringwerke AG, Marburg, Germany.

Creatinine (mmol./l.)

BUN (mmol./l.)

Uric acid (mmol./l.)

Phosphorus (mmol./l.)

Albumin (gm./l.) b2-microglobulin (mg./l.)

Lysozyme (mg./l.) * p ,0.05 t test.

128 6 102 8.6 6 4.8 0.3 6 0.08 1 6 0.4 42.4 6 6.4 2.0 6 0.6 1.5 6 0.5

Av. After Retention 6 SD 1 Mo.

6 Mos.

97 6 25 98 6 19 5.9 6 1.7* 6.3 6 1.6* 0.3 6 0.08 0.3 6 0.06 1 6 0.2 0.9 6 0.1 42.2 6 8.3 41.8 6 3.9 2.1 6 0.8 2.2 6 0.7 1.5 6 0.6 1.4 6 0.3

PROTEINURIA AND RENAL FUNCTION DURING AND AFTER ACUTE URINARY RETENTION TABLE 3. Proteinuria during and after acute urinary retention Median During Median After Retention (range) Retention (range) 1 Mo. 6 Mos. 238 (12–7,292) 72 (4–1,746)* 12 (2–135)* Albumin excretion (mg./min.)

7.7 (2–175) 6.4 (1–43) 9.8 (2–47) a1-Microglobulin excretion (mg./min.) b2-Microglobulin 154 (100–19,000) 135 (100–2,000) 126 (28–800) excretion (mg./l.)

225 (100–12,200) 238 (100–2,000) 211 (28–1,363) b2-Microglobulin after urine collection (mg./l.) * p ,0.01 Wilcoxon signed rank test.

TABLE 4. Proportion of abnormal urinary values during and after acute urinary retention

Albumin a1-Microglobulin b2-Microglobulin b2-Microglobulin* Creatinine clearance Phosphorus Uric acid Citrate * Separate sample.

% After Retention

% During Retention

1 Mo.

6 Mos.

100 54 17 21 65 14 8 24

92 39 19 18 48 8 4 28

54 58 9 21 42 13 13 17

second per 1.73 m.2) was decreased during retention but it became normal during followup. Average urinary excretion of phosphorus (normal 14 to 35 mmol. per minute), uric acid (normal 2 to 4.1 mmol. per minute) and citrate (normal greater than 1 mmol. per minute) was within the normal range during acute retention and followup. There were statistically significant differences in creatinine clearance and urinary phosphorus excretion during retention and after 6 months.

Table 4 lists the proportions of abnormal values in urinary renal function parameters. Albuminuria persisted in 54% of the patients, 58% had elevated a1-microglobulin excretion and creatinine clearance was decreased in 42% 6 months after acute urinary retention was relieved. Although mean urinary uric acid excretion was normal, there was abnormally low uric acid excretion during retention in 29% of the patients, after 1 month in 56% and after 6 months in 46%. All urinary renal function parameters were normal in only 2 patients 6 months after acute urinary retention was relieved.

DISCUSSION

Benign prostatic enlargement, which is common in older men, is the main cause of bladder outlet obstruction, and it may progress and cause a risk of urinary retention.12 Although many men with mild to moderate symptoms do well without therapy, others who have gradually increasing symptoms require therapy.13 Oesterling estimated that the lifetime incidence of surgical or medical intervention for beTABLE 5. Renal function parameters during and after acute urinary retention Av. During Retention 6 SD Creatinine clearance (ml./sec./1.73 m.2) Phosphorus excretion (mmol./min.)

Uric acid excretion (mmol./min.)

Citrate excretion (mmol./min.) * p ,0.05 t test.

Av. After Retention 6 SD 1 Mo.

6 Mos.

1.2 6 0.5

1.4 6 0.5

1.7 6 0.6*

24 6 9.9

24 6 9.4

30 6 17.1*

2.7 6 1.8

2.1 6 0.8

2.4 6 1.4

1.7 6 1

1.6 6 1

2.2 6 1.8

1783

nign prostatic enlargement is 35% in 50-year-old men.14 In the recent 4-year study of McConnell et al acute urinary retention developed in 7% of patients with moderate to severe lower urinary tract symptoms.15 Most often acute urinary retention is treated with mechanical bladder emptying and the patient is discharged home. However, Breum et al reported that retention recurred in 70% of their patients within a week and voiding was unaffected in only 16% during 5 years of observation.16 Therefore, acute urinary retention is considered to be a powerful indication for definitive treatment in prostatic disorders. Simple mechanical emptying of the bladder is unacceptable without subsequent observation.

All but 2 of our patients needed surgery to normalize voiding, which may be explained by the fact that in the majority spontaneous acute urinary retention developed without provocative factors. In addition, Higgins et al showed that there is significantly higher mortality after prostate surgery in patients with than without acute urinary retention.17 Little is known about the effects of acute urinary retention on renal function. Because most patients with acute retention have chronic obstruction, a suprapubic catheter remained indwelling for 1 month in all of our patients to guarantee free drainage before surgery to relieve obstruction, permitting the recovery of renal function. Only a small amount of serum spilling into the urinary tract would explain the elevated albumin excretion in our cases. However, none of our patients had macroscopic hematuria after the suprapubic catheter was inserted. In addition, urinary collection was not started until after bladder emptying, and at 1 and 6 months of followup there was no hematuria. Therefore, it seems unlikely that suprapubic catheter insertion, an indwelling catheter or the subsequent surgical procedure significantly contributed to urinary collection findings.

Some diseases, such as hypertension and diabetes, and drugs, such as diuretics, angiotensin converting enzyme inhibitors and nonsteroidal anti-inflammatory analgesics, may cause renal damage or affect other mechanisms of proteinuria. In our current study we noted no difference in serum or urinary renal function parameters in our 8 patients with hypertension, or in the 4 on diuretics or angiotensin converting enzyme inhibitor compared with the others. Ureteral reflux is a known predisposing factor for proteinuria and focal glomerulosclerosis. However, in our study ultrasound showed hydronephrosis in only 3 patients at the time urinary retention was relieved. Previous chronic obstruction may have had an effect on renal function that was not currently evaluated. Ultrasound revealed normal renal parenchyma and normal sized kidneys in the 5 patients with polyuria after bladder drainage, which suggests the acute nature of retention.

Renal function is most commonly monitored by serum creatinine, whereas creatinine clearance, urinary excretion of albumin, b2-microglobulin and a1-microglobulin are seldom determined because they require urinary collection, which is not always possible. Robert18 and Parkin19 et al indicated that serum creatinine is accurate enough to measure renal function. In our study 6 patients had elevated serum creatinine during acute urinary retention and 65% had decreased creatinine clearance, although all had albuminuria. Thus, serum creatinine and creatinine clearance did not predict proteinuria. Hypocitruria, and excessive excretion of phosphate and urate in post-obstructive diuresis have been described but our study did not confirm these findings. BUN was elevated in patients with elevated serum creatinine.

Serum uric acid, phosphorus, albumin, b2-microglobulin and lysozyme were randomly high and low during acute urinary retention and followup. These parameters seemed to provide no information on possible renal dysfunction in patients with urinary retention.

Proteinuria was common in our cases. Elevated urinary albumin excretion noted during acute urinary retention re-

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PROTEINURIA AND RENAL FUNCTION DURING AND AFTER ACUTE URINARY RETENTION

flected increased glomerular permeability. Patients with albuminuria also had elevated a1-microglobulin and b2microglobulin excretion, which improved as albuminuria resolved. Although it is difficult to measure b2-microglobulin because of its instability, we used b2-microglobulin and a1microglobulin to provide more reliable data on tubular function. Urinary b2-microglobulin excretion was elevated in only a few patients with elevated urinary a1-microglobulin excretion. There was a difference in the excretion of b2microglobulin at 1 and 6 months, as measured in collected and individual specimens. This finding confirms that b2microglobulin is unstable in the bladder and it is not a reliable parameter of tubular dysfunction.

Immediately after acute urinary retention was relieved glomerular and tubular renal function was impaired but partially recovered during the initial month of free bladder drainage.

Glomerular damage presenting as albuminuria and tubular damage presenting as increased a1-microglobulin excretion also persisted at the 6-month followup in approximately half of our cases and, thus, it was most probably permanent. Mean duration of acute urinary retention was 31 hours, which may explain why glomerular and tubular function was damaged.

This observation stresses the importance of rapid recognition and treatment of acute urinary retention.

12.

13.

14.

15.

16.

17.

18.

CONCLUSIONS

Acute urinary retention affects glomerular and tubular renal function. All of our patients had albuminuria and many had elevated a1-microglobulin excretion during retention.

Although these parameters improved after acute urinary retention was relieved, glomerular and tubular damage persisted, possibly due partially to previous long-term bladder outlet obstruction. Acute urinary retention should be prevented by promptly treating obstructive prostatic enlargement. If acute urinary retention presents, it should be recognized and treated without delay.

REFERENCES

1. Kallerhoff, M., Munz, D. L., Osmers, R., Söllick, S., Weber, M. H., Weigel, W., Zappel, H., Zöller, G. and Ringert, R. H.: Bildgebende und funktionelle Parameter in der Diagnostik der obstruktiven Nephropathie. Urologe, 31: 354, 1992.

2. Baker, L. R. I. and Whitfield, H.: N.: The patient with urinary tract obstruction. In: Oxford Textbook of Clinical Nephrology.

Edited by S. Cameron, A. M. Davison, J.-P. Grünfeld, D. Kerr, and E. Ritz. Oxford: Oxford University Press, vol. 3, chapt.

16.2, pp. 2002-2022, 1992.

3. Wilson, D. R.: Urinary tract obstruction. In: Diseases of the Kidney. Boston: Little, Brown and Co., vol. 1, chapt. 23, pp.

715-746, 1992.

4. Eriksson, P., Denneberg, T., Larsson, L. and Lindström, F.: Biochemical markers of renal disease in primary Sjögren’s syndrome. Scand. J. Urol. Nephrol., 29: 383, 1995.

5. Jones, B. F. and Nandra, R. S.: Post-obstructive diuresis. Aust.

New Zeal. J. Med., 13: 519, 1983.

6. Guder, W. G. and Hofmann, W.: Markers for the diagnosis and monitoring of renal tubular lesions. Clin. Nephrol., suppl., 38: S3, 1992.

7. Nergelius, G., Vinge, E., Grubb, A. and Lidgren, L.: Renal impairment after hip or knee arthroplasty. Urinary excretion of protein markers studied in 59 patients. Acta Orthopaed.

Scand., 68: 34, 1997.

8. Recker, F., Hofmann, W., Bex, A. and Tscholl, R.: Quantitative determination of urinary marker proteins: a model to detect intrarenal bioeffects after extracorporeal lithotripsy. J. Urol., 148: 1000, 1992.

9. Karlsen, S. J. and Berg, K. J.: Acute changes in kidney function following extracorporeal shock wave lithotripsy for renal stones. Brit. J. Urol., 67: 241, 1991.

10. Flynn, F. V.: Assessment of renal function: selected developments. Clin. Biochem., 23: 49, 1990.

11. Tsukahara, H., Hiraoka, M., Kuriyama, M., Haruki, S.,

19.

Nakamura, K., Suehiro, F. and Sudo, M.: Evaluation of proximal tubular function in preterm infants by urinary a1microglobulin. Acta Paed. Jap., 35: 127, 1993.

Girman, C. J., Epstein, R. S., Jacobsen, S. J., Guess, H. A., Panser, L. A., Oesterling, J. E. and Lieber, M. M.: Natural history of prostatism: impact of urinary symptoms on quality of life in 2115 randomly selected community men. Urology, 44: 825, 1994.

McConnell, J. D., Barry, M. J., Bruskewitz, R. C. and the Agency for Health Care Policy and Research: Benign prostatic hyperplasia: diagnosis and treatment. Clin. Pract. Guide., 8: 1, 1994.

Osterling, J. E.: Benign prostatic hyperplasia: review of its histogenesis and natural history. Prostate, suppl., 6: 67, 1996.

McConnell, J. D., Bruskewitz, R., Walsh, P., Andriole, G., Lieber, M., Holtgrewe, H. L., Albertsen, P., Roehrborn, C. G., Nickel, J. C., Wang, D. Z., Taylor, A. M. and Waldstreicher, J.: The effect of finasteride on the risk of acute urinary retention and the need for surgical treatment among men with benign prostatic hyperplasia. New Engl. J. Med., 338: 557, 1998.

Breum, L., Klarskov, P., Munck, L. K., Nielsen, T. H. and Norgestgaard, A. G.: Significance of acute urinary retention due to infravesical obstruction. Scand. J. Urol. Nephrol., 16: 21, 1982.

Higgins, P. M., French, M. E. and Chadalavada, V. S. R.: Management of acute retention of urine: a reappraisal. Brit.

J. Urol., 67: 365, 1991.

Robert, S., Zarowitz, B. J., Peterson, E. L. and Dumler, F.: Predictability of creatinine clearance estimates in critically ill patients. Crit. Care Med., 21: 1487, 1993.

Parkin, A., Smith, H. C. and Brocklebank, J. T.: Which routine test for kidney function? Arch. Dis. Child., 64: 1261, 1989.

EDITORIAL COMMENT

The authors conclude that acute urinary retention causes increased glomerular permeability and renal tubular damage, the relief of acute urinary retention only partially allows increased glomerular permeability and tubular damage to return to normal, increased glomerular permeability and tubular damage are clinically significant, and more rapid treatment of acute urinary retention would partially prevent increased glomerular permeability and tubular damage. Immediately after relieving acute urinary retention with a suprapubic tube the median spilling of albumin into the urine was elevated. However, no pre-retention measurements were made to record whether these 25 men 50 to 87 years old, a third of whom were being treated for hypertension, had normal glomerular permeability before retention. Although aging alone is reported not to increase albuminuria in normal elderly humans, in the more carefully studied rat model aging alone causes increased albuminuria.1 The trauma of the suprapubic tube is unknown, although none of the subjects had gross hematuria at the time of urine collection.

Spillage of only a small amount of serum (5 cc) into the urine collection in 24 hours is enough to cause the observed differences in albuminuria. The relief of outlet obstruction seemed to decrease the percentage of men with albuminuria. Of men 65 to 84 years old 37% have proteinuria,2 which is probably not significantly different than the 54% of patients in this study who had albuminuria after relief of retention. Tubular damage due to acute urinary retention approximates the upper limits of normal, and is probably not statistically significantly different than in the normal population. Interestingly tubular damage, which one would expect to heal with relief of obstruction, did not improve after 6 months.

Is increased glomerular permeability with acute retention clinically significant? In humans with diabetes, as long as albuminuria is less than 30 mg. per minute, clinically important medical renal disease develops in few (4%) in the long term.3 The data in this study are not presented in a manner that assesses this question but it appears that most patients with acute urinary retention had a level of glomerular injury that if maintained would put them at long-term risk. The relief of retention within 72 hours removed such risk for the most part.

Obviously we want to believe that rapid relief of retention is important. However, the important controls of renal parameters before retention and suprapubic tube alone without retention are

PROTEINURIA AND RENAL FUNCTION DURING AND AFTER ACUTE URINARY RETENTION missing in this study. Therefore, the conclusion that retention should be recognized and treated without delay to preserve renal function is not warranted.

Stephen C. Jacobs Division of Urology University of Maryland Hospital Baltimore, Maryland 1. Lopez-Novoa, J. M. and Montanes, I.: Changes in renal function and morphology in aging laboratory animals. In: Renal Func-

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tion and Disease in the Elderly. Edited by J. F. M. MaciasNunez and J. S. Cameron. London: Butterworths, pp. 162–183, 1987.

2. Mimica, M., Durakovic, P. L. and Bule, L. J.: Proteinuria in samples of younger and older persons in the population. Acta Med. Yugoslav., 35: 165, 1981.

3. Viberti, G. C., Jarrett, R. J. Mahmud, U., Hill, R. D., Argyropoulos, A. and Keen, H.: Microalbuminuria as predictor of clinical nephropathy in insulin-dependent diabetes mellitus.

Lancet, 1: 1430, 1982.

0022-5347/04/1725-1911/0 THE JOURNAL OF UROLOGY® Copyright © 2004 by AMERICAN UROLOGICAL ASSOCIATION

Vol. 172, 1911–1914, November 2004 Printed in U.S.A.

DOI: 10.1097/01.ju.0000140502.34334.75

Voiding Dysfunction POST-VOID RESIDUAL URINE VOLUME IN WOMEN WITH OVERACTIVE BLADDER SYMPTOMS MARK MILLEMAN, PETER LANGENSTROER*

AND

MICHAEL L. GURALNICK† , ‡

From the Department of Urology, Medical College of Wisconsin, Milwaukee, Wisconsin

ABSTRACT

Purpose: Most patients with overactive bladder symptoms initially present to their primary care provider for treatment. It is currently recommended that post-void residual urine (PVR) should be measured during the assessment of women complaining of overactive bladder symptoms and anticholinergic medication should be used if PVR is low. However, many primary care providers are reluctant to measure PVR and, therefore, they may delay treatment or even inappropriately treat patients who have a high PVR. We identified clinical factors that are associated with increased PVR that could be used to select which patients are at risk for this.

Materials and Methods: The charts of women presenting to our clinic with complaints of urinary frequency, urgency and/or urge incontinence were retrospectively reviewed. Patient demographics, physical examination and PVR were analyzed to determine if any factor was associated with increased PVR (100 ml or greater).

Results: The charts of 201 patients with complete data were reviewed. Patient age was 20 to 90 years (mean 55). Overall 19% of patients were found to have elevated PVR. Univariate analysis identified that older age, prior incontinence surgery, history of multiple sclerosis, greater American Urological Association Symptom Score, vaginal parity greater than 2, greater pad use and stage 2 or greater vaginal prolapse were associated with elevated PVR. Multivariate analysis identified age older than 55 years, prior incontinence surgery, a history of multiple sclerosis and vaginal prolapse stage 2 or greater as independent predictors of elevated PVR. Conclusions: It is possible to identify patients with overactive bladder symptoms who are at risk for elevated PVR based on history and physical examination. This could result in fewer patients needing PVR measurement prior to initiating treatment.

KEY WORDS: bladder urination urinary incontinence

Overactive bladder (OAB) is defined as a complex of symptoms including the need to urinate frequently and urgently, with or without urge incontinence, in the absence of any identifiable pathological condition.1 It is becoming more prevalent as patient and physician awareness increases, and as such primary care providers can anticipate seeing increasing numbers of patients with this diagnosis. Initial treatment for OAB should consist of a combination of medical therapy in the form of anticholinergic medication and behavioral measures, such as pelvic floor exercises, timed voiding, and dietary and fluid modification. Prior to instituting this therapy the Agency for Health Care Policy and Research recommends that the basic evaluation for patients should include history, physical examination, measurement of post-void residual urine volume (PVR) and urinalysis.2 However, accurate measurement of PVR is obtainable only by catheterization or bladder ultrasound, which may be burdensome in a busy primary care setting. If Agency for Health Care Policy and

Research guidelines are to be adhered to, these patients may have to wait for specialist referral before appropriate treatment is begun. However, if one could identify clinical risk factors that portend an increased likelihood of detecting elevated PVR, one could selectively screen patients for increased PVR and be more comfortable treating patients deemed to be at low risk. We identified clinical factors in women presenting with symptoms of overactive bladder that can be used to predict who might be at risk for increased PVR.

METHODS

We performed a retrospective chart review of female patients attending our clinic with symptoms of overactive bladder (urinary frequency, urgency and/or urge incontinence).

Patients completed American Urological Association (AUA) Symptom Scores measuring storage and voiding urinary symptoms, and full medical histories were obtained. Notation was made of vaginal parity, pad use, any previous genitourinary tract surgery (eg, hysterectomy, anti-incontinence surgery, etc), neurological issues (eg multiple sclerosis [MS], stroke, etc), back surgery, diabetes and use of medications that affect bladder function (eg anticholinergic medications).

Patients underwent physical examination with a focus on the genitourinary tract, including an assessment of pelvic organ

Accepted for publication June 11, 2004. * Financial interest and/or other relationship with Pfizer, Bayer/ GlaxoSmithKline and Lilly/ICOS. † Correspondence: Department of Urology, Medical College of Wisconsin, 9200 West Wisconsin Ave., Milwaukee, Wisconsin 53226 (telephone: 414-456-6950; FAX: 414-456-6217; e-mail: mguralni@ mcw.edu). ‡ Financial interest and/or other relationship with Pfizer and Medtronic.

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POST-VOID RESIDUAL URINE AND OVERACTIVE BLADDER

prolapse using the Pelvic Organ Prolapse Quantification.3 Patients were examined while supine with the legs in stirrups and the head elevated off of the table to facilitate a Valsalva maneuver to assess vaginal prolapse. For study purposes we grouped patients into those with stage 2 or less and stage 2 or greater prolapse. Stage 2 or greater prolapse indicates that the greatest degree of vaginal wall descent is approximately to the level of the hymen, an observation that is easily made and recorded. Patients then provided a urine sample for analysis and PVR was measured by bladder ultrasound or a catheter. Increased PVR was defined as a volume of 100 ml or greater immediately following urination and patients were divided into 2 groups based on PVR (group 1—PVR less than 100 ml and group 2—PVR 100 ml or greater).

A logistic regression model was created to estimate the ability of selected demographic and clinical factors to predict PVR. Analysis of the variables was performed using univariate and multivariate tests. Variables showing p ⬍0.05 on univariate tests were included in the multivariate regression model. Analysis was done with SAS statistical software (SAS Institute, Cary, North Carolina).

RESULTS

A total of 201 patients were included in this review. Patient age was 20 to 90 years (mean 55). Table 1 lists patient demographics. Overall measured PVR was 0 to 997 ml (mean 60). Of the patients 163 (81%) had a PVR of less than 100 ml (mean 54) and were included in group 1, while 38 (19%) had a PVR of 100 ml or greater (mean 211, range 100 to 997) and were included in group 2. Table 2 shows factors found to be associated with increased PVR based on univariate analysis and factors not associated with increased PVR. Multivariate logistic regression analysis identified that 4 variables were independent predictors of increased PVR, namely age 55 years or older (OR 3.71, p ⫽ 0.007), a history of antiincontinence surgery (OR 4.32, p ⫽ 0.004), a history of multiple sclerosis (OR 15.32, p ⬍0.0001) and pelvic organ prolapse stage 2 or greater (OR 3.61, p ⫽ 0.008).

DISCUSSION

Technically to make the diagnosis of OAB it is necessary to exclude conditions such as urinary tract infection, bladder cancer, bladder stones, interstitial cystitis, etc. Therefore, standard evaluation in a patient complaining of overactive bladder symptoms should include urological history, focused physical examination and appropriate urine studies (urinalysis and culture).

Also, it would seem prudent to assess urine cytology in patients who may be at risk for bladder cancer (eg smokers and those with a history of bladder cancer). Another invaluable tool is a bladder diary, in which the patient records the number and volume of voids in a 24 to 72-hour period. This allows the exclusion of polyuria as a contributing cause to symptoms and it is useful for educating the patient about current voiding habits.

Furthermore, it may assist in the behavioral treatment of pa-

TABLE 1. Patient demographics No. pts No. prior hysterectomy (%) No. neurological disorder (%) No. MS (%) No. anticholinergic use: Current Prior No. prior anti-incontinence surgery (%) No. back surgery/trauma (%) No. DM (%) No. using pads for incontinence (%) Mean pad use daily (range)

201 79 45 20

(39) (22) (10)

54 (26) 14 (7) 37 (18) 29 (14) 17 (9) 91 (45) 1.9 (0–24)

TABLE 2. Univariate analysis of factors associated and not associated with increased PVR Factor Associated:* Mean age Mean pad use Mean AUA Symptom Score Mean voiding symptom score % Vaginal parity greater than 2 % Prior incontinence surgery % MS % Stage 2 prolapse or greater Not associated:† % Anticholinergic use Current Prior % Back surgery/trauma % Neurological disorder (nonMS) % DM * p ⬍0.05. † p ⬎0.05.

Less Than 100 Ml

Greater Than 100 Ml

54 1.7 18.4 8.5 24 15 6 27

60 2.9 21.2 10.4 40 34 26 50

25 33 15 12 5

34 37 13 13 8

tients with OAB, for example by helping to determine an appropriate timed voiding interval.

PVR represents the summation effect of the functions of the bladder and urethral sphincter mechanism. To empty with a low PVR patients must be able to relax the urethral sphincter and generate adequate intravesical pressure via bladder contractility and/or abdominal straining. OAB is presumed to result from bladder hyperactivity. It is treated with anticholinergic medications to relax the bladder and behavioral measures such as pelvic floor exercises and bladder retraining. However, patients may have an overactive bladder and one that does not completely empty, which raises a dilemma. Prescribing anticholinergic medications might actually worsen the ability to empty the bladder with the potential for urinary retention and the complications thereof (recurrent urinary tract infections, bladder calculi and hydronephrosis).

Increased PVR alone is not necessarily a problem. It can be associated with upper urinary tract problems such as hydronephrosis but usually this only occurs if retained urine is stored by the bladder at high pressure. Typically in women without neurological disease and no history of radiotherapy to the pelvis or other cause of bladder fibrosis the bladder is compliant and it can safely store large volumes at low pressure. However, increased PVR can be associated with recurrent urinary tract infections and bladder calculi, which are usually related to urine stagnation. Also, increased PVR may contribute to urinary frequency and nocturia because the bladder capacity is functionally decreased due to retained urine. The larger the volume of retained urine, the less time is needed for the bladder to achieve the capacity at which the patient feels the need to urinate. In this regard it seems prudent to rule out increased PVR in patients who complain of urinary frequency, urgency and nocturia. We sought to simplify matters for primary care givers to identify patients at risk for increased PVR. This might allow them to be more comfortable empirically treating women with OAB symptoms. However, this study cannot be used to predict which patients will have increased PVR following treatment with anticholinergic medications because that would require a prospective study. Furthermore, one cannot necessarily apply the results of this study to male patients since there are unique features of male voiding dysfunction (eg prostatic obstruction) that do not apply to females.

We found several independent risk factors for increased PVR, including: older age, a history of anti-incontinence surgery or multiple sclerosis and stage 2 or greater vaginal prolapse (ie prolapse extending to the introitus with straining). These factors are easy to elicit and detect by a standard history and physical examination. Our results are similar to

POST-VOID RESIDUAL URINE AND OVERACTIVE BLADDER

those of Fitzgerald et al, who found that vaginal prolapse, symptoms of voiding difficulty and absent concomitant stress incontinence (incontinence secondary to increased intraabdominal pressure, such as coughing) were independent risk factors for increased PVR in women with OAB symptoms.4 In our study the symptoms of voiding difficulty (hesitancy, weak stream, need for straining and sensation of incomplete bladder emptying) as determined by the AUA symptom score were associated with increased PVR on univariate analysis but symptoms of voiding difficulty were not found to be independent risk factors on multivariate analysis. It is well known that lower urinary tract symptoms are not specific and the only way to make an accurate diagnosis of voiding dysfunction is with invasive urodynamic studies.5 Groutz et al found that 62% of women attending a urogynecology clinic had complaints of voiding difficulty, including urinary hesitancy, straining to void, weak stream, intermittent stream, double voiding or incomplete emptying, and yet only 21% had urodynamic evidence of true voiding difficulty, of which most was related to impaired bladder contractility.6 However, it would be these patients in whom one would be hesitant to prescribe anticholinergic medications because impaired bladder contractility could increase the risk of incomplete bladder emptying. Whether symptoms of voiding difficulty truly represent an increased risk for increased PVR, it is important to inquire about their presence. If they are significant, it would seem reasonable to consider evaluating PVR in those patients.

Unlike Fitzgerald et al,4 we found that a history of MS was a significant risk factor increased PVR. MS is known to cause significant lower urinary tract symptoms and the most common urodynamic finding in patients with MS is that of detrusor hyperactivity.7 However, MS can also cause detrusor hypocontractility/acontractility and bladder-sphincter dyssynergia, of which all can impair bladder emptying and result in increased PVR.7 The fact that Fitzgerald et al failed to find that MS is a significant risk factor for increased PVR may have simply been due to patient numbers.4 Only 8% of their patients had any underlying neurological disorder, which included diagnoses such as MS, stroke, etc, whereas 22% of our patients had an underlying neurological disorder, including 10% with MS. However, interestingly it was only MS and not any neurological disorder that increased the risk of increased PVR. Also, even a history of back surgery or trauma did not increase the risk increased PVR in our patients, which is consistent with the findings of Fitzgerald et al. While technically patients with neurological disorders known to cause bladder dysfunction should not be labeled as having OAB because by definition OAB represents the absence of an obvious cause, we elected to include these patients in our study because they still may complain of OAB symptoms and they are often treated the same way (eg medical and behavioral therapy).

We also identified previous anti-incontinence surgery as an independent risk factor for increased PVR, unlike Fitzgerald et al.4 Surgery to treat urinary incontinence by definition creates a new form of continence mechanism by repositioning the bladder neck to its proper intra-abdominal location and/or creating a backboard against which the urethra is compressed when intra-abdominal pressure increases (eg coughing or the Valsalva maneuver). Certain types of anti-incontinence surgeries, such as slings, cause a greater risk of postoperative voiding dysfunction/urinary retention than others, such as needle suspension. The fact that Fitzgerald et al did not identify prior incontinence surgery as a risk factor for increased PVR may simply have been due to the types of procedures that had been performed and they were not specified.4 Neither our review nor that of Fitzgerald et al4 showed that diabetes mellitus (DM) was significantly associated with increased PVR. It may be that there were too few patients in either study but it may also have been secondary to DM alone. Ali identified that objective evidence of neuropathy in

1913

insulin dependent and noninsulin dependent DM male patients was associated with increased PVR, whereas patients without objective evidence of neuropathy did not have PVR different from that of age matched controls.8 It is likely that our patients fit into the latter category. Typically patients with DM and neuropathy, and classic diabetic cystopathy have decreased bladder sensation, resulting in few voids daily. The absence of any frequency/urgency in these patients would have resulted in their exclusion from our study.

Our study clearly has limitations, including its retrospective nature and the fact that PVR was only assessed once. Studies have shown significant within patient variability in PVR measurements. Dunsmuir et al noted this variability in men and found that variability was greater when PVR was larger.9 Also, Griffiths et al found significant variability in PVR measurement depending on the time of day with the greatest volumes occurring in the morning.10 In our review we included only 1 PVR measurement and, therefore, it is possible that patients found to have increased PVR on 1 occasion might have had a normal result had they been measured on a different occasion. However, we wanted to try to reproduce what would most likely be noted in a primary care setting, that is a patient who complains of overactive bladder symptoms and desires treatment at that time. It might be reasonable to assess PVR at that visit but it would likely be too burdensome to have the patient return on several occasions for additional PVR measurements to confirm the finding.

Furthermore, one could question whether a threshold PVR of 100 ml or greater is truly problematic. Studies have shown that the majority of people appear to empty the bladder, such that usually less than 50 to 100 ml are retained.11 However, is a PVR of 110 ml that much worse than one of 80 ml? The answer is not known. Our choice of a cutoff of 100 ml is clearly arbitrary but consistent with that used by Fitzgerald et al.4 CONCLUSIONS

We identified certain clinical factors that are associated with an increased risk of increased PVR in women with overactive bladder symptoms. They include age older than 55 years, history of anti-incontinence surgery, history of multiple sclerosis and stage 2 or greater vaginal prolapse. Selective screening of women with these risk factors may result in fewer women needing PVRs assessment prior to initiating anticholinergic therapy to treat symptoms. This may facilitate the management of this condition by primary care givers.

H. J. Yun provided statistical support.

REFERENCES

1. Wein, A. J.: Diagnosis and treatment of the overactive bladder.

Urology, suppl., 62: 20, 2003 2. Fantl, J. A., Newman, D. K., Colling, J., DeLancey, O. L., Keeys, C., Loughery, R. et al: Urinary incontinence in adults: acute and chronic management. In: Clinical Practice Guideline. Rockville, Maryland: No. 2, 1996 update, Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, AHCPR Publication No. 96-0682 3. Bump, R. C., Mattiasson, A., Bo, K., Brubaker, L. P., DeLancey, J. O., Klarskov, P. et al: The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction.

Am J Obstet Gynecol, 175: 10, 1996 4. Fitzgerald, M. P., Jaffar, J. and Brubaker, L.: Risk factors for an elevated postvoid residual urine volume in women with symptoms of urinary urgency, frequency and urge incontinence. Int Urogynecol J Pelvic Floor Dysfunct, 12: 237, 2001 5. Webster, G. D. and Guralnick, M. L.: The neurourologic evaluation.

In: Campbell’s Urology, 8th ed. Edited by P. C. Walsh, A. B. Retik, E. D. Vaughan, Jr. and A. J. Wein. Philadelphia: W. B. Saunders Co., vol. 2, sect. V, chapt. 25, pp. 900–930, 2002 6. Groutz, A., Gordon, D., Lessing, J. B., Wolman, I., Jaffa, A. and David, M. P.: Prevalence and characteristics of voiding difficulties in women: are subjective symptoms substantiated by objective urodynamic data? Urology, 54: 268, 1999

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POST-VOID RESIDUAL URINE AND OVERACTIVE BLADDER

7. Hinson, J. L. and Boone, T. B.: Urodynamics and multiple sclerosis. Urol Clin North Am, 23: 475, 1996 8. Ali, S. T.: Measurement of the residual urine index in insulindependent and non-insulin dependent diabetic men with and without neuropathy. Acta Physiol Hung, 85: 243, 1997 9. Dunsmuir, W. D., Feneley, M., Corry, D. A., Bryan, J. and Kirby, R. S.: The day-to-day variation (test-retest reliability) of resid-

ual urine measurement. Br J Urol, 77: 192, 1996 10. Griffiths, D. J., Harrison, G., Moore, K. and McCracken, P.: Variability of post-void residual urine volume in the elderly.

Urol Res, 24: 23, 1996 11. Haylen, B. T., Law, M. G., Frazer, M. and Schulz, S.: Urine flow rates and residual urine volumes in urogynecology patients.

Int Urogynecol J Pelvic Floor Dysfunct, 10: 378, 1999

Australian and New Zealand Continence Journal

Guest Editorial

Management of the abnormal post void residual In this issue, the management of urinary retention in hospitalised adults is discussed 1. Guidelines are developed in the article, with the aid of existing research, to address this issue. Key to this endeavour is a greater understanding of an important measurement, the postvoid residual (PVR), defined as the volume of urine remaining in the bladder at the completion of micturition 2. It may be helpful, as a complement to that article, to revise what is known about normal and abnormal values of this parameter in both men and women, assess how retention might be defined, and establish some general guidelines for management of the abnormally high PVR. Men and women without lower urinary tract symptoms (asymptomatic) are both efficient at emptying their bladders.

If measured immediately postmicturition (ultrasound technique required), PVRs in asymptomatic men 3 and women 4 are almost identical – median 0mls (both sexes); mean 5.7mls (men) and 4.8mls (women); 95th centile 29mls (men) and 30mls (women).

Men and women do differ, however, in the rate of emptying 5.

The (maximum) urine flow rates of asymptomatic women are on average 0.19 times greater than those of asymptomatic younger men (up to 50 years) and 0.39 greater than asymptomatic older men (over 50 years), an intersex difference mainly related to urethral length (4cm vs 20cm).

Symptomatic women are also still reasonably efficient in bladder emptying. Their median immediate PVR is again 0mls with 81% PVRs 30mls or under 6, a level where recurrent urinary tract infections have been shown to significantly increase. Only 6% of their PVRs are over 100mls. Age and the presence of prolapse have the main bearing on higher PVRs in symptomatic women 6. Men tend to become significantly less efficient in bladder emptying as they develop symptoms of lower urinary tract dysfunction. This is because of their major diagnosis of bladder outflow obstruction.

There are no equivalent large PVR studies in symptomatic men.

However, in a limited study 7 of the immediate PVRs of 141 symptomatic men, the median PVRs were found to be 50mls (up to 50 years) and 93mls (over 50 years).

Many PVR studies to date involve ‘delayed’ measurement, i.e. by 5-10 minutes or more post micturition, a factor inherent to catheterisation techniques. This leads to significant inaccuracy

Bernard T Haylen Urogynaecologist St. Vincent’s Clinics & University of New South Wales, Sydney NSW

68

and wide variation in PVR measurement. For each minute between voiding and PVR measurement, there is additional renal input of 1-14ml/min as an automatic addition (error) to the PVR 8. In terms of the efficacy of the different catheters in completely draining the bladder, a short plastic female catheter will leave under 1ml in the female bladder after catheterisation, while a Foley will leave an average 77mls 8. There have been no equivalent studies of catheter efficacy in men.

Chronic urinary retention in women can be recognised as an (accurately measured) persistent (immediate) PVR over 200mls, prevalent in around 2.5% of women with symptoms of pelvic floor dysfunction 6. Acute urinary retention in women is a generally (but not always) painful, palpable bladder where little or no urine can be passed. Because of the longer urethra in men and the tendency for bladder outflow obstruction, the PVRs in men with lower urinary tract symptoms, as noted above, can be expected to be much higher than in symptomatic women.

Limited data 7 suggest that PVRs over 200mls in symptomatic men are present in 5% (up to 50 years old) and 28% (over 50 years). More research on PVRs in symptomatic men is needed.

Acute urinary retention requires urgent relief by catheterisation and an appropriate period of bladder ‘rest’ as one assesses the likely reason for the episode. This avoids possible post-renal failure or sepsis. Subject to that possible aetiology resolving, a ‘trial-of-voiding’ can be instituted with careful PVR monitoring.

If surgery is the respective aetiology, relevant postoperative catheterisation and PVR monitoring protocols should be in place. Postpartum urinary retention is not uncommon, requiring careful monitoring of voiding function and PVR in the 4-6 hours following delivery, particularly an operative delivery, or where a regional anaesthetic is involved. Delayed treatment of acute retention in any circumstance can result in longer-term bladder dysfunction.

PVR measurement is integral to the assessment of both men with symptoms of lower urinary tract dysfunction and women with any symptoms of pelvic floor dysfunction. Abnormal PVR readings confirmed by repeat measurement are one indicator of voiding dysfunction in women and bladder outflow obstruction in men. Correlation is necessary with other dysfunctions that might be present in either sex. Full urodynamics, including cystometry, is generally required to confirm a clear cause for an abnormal PVR. The study contained in this issue of the journal 1 looks more specifically at hospitalised older adults. While there is a higher prevalence of abnormal PVRs with age, an abnormal PVR

Vol. 14, No. 3 • Spring 2008

Australian and New Zealand Continence Journal

should not be regarded as a feature of ageing. A significantly higher prevalence of urinary retention is noted with men rather than women. The authors highlight an increasing risk of co-morbidities including diabetes, neurological disorders and impaired mobility with theoretical but unresearched impact on PVRs. The key point is that where there are relevant lower urinary tract symptoms with or without signs of urinary retention, a PVR by bladder scan or insertion of intermittent catheter should be performed. There should be no reason for hospitalised adults to have an undiagnosed chronic urinary retention. The guidelines should hopefully assist in focusing attention on this goal.

References 1. Ostaszkiewicz J, O’Connell B & Ski C. A guideline for the nursing assessment and management of urinary retention in elderly hospitalised patients. Aust NZ Cont J 2008; 76-83.

2. Abrams P, Cardozo L, Fall M et al. The standardisation of terminology of lower urinary tract function. Report from the standardisation subcommittee of the International Continence Society. Neurourol Urodyn 2002; 21:167-178.

3. Cerqui AJ & Haylen BT. Residual urine volumes in a normal male population. Urodinamica 2001; 11(1):9-12.

urinary tract dysfunction. Obstetric & Gynecol 2008; 111:13051312.

7. Parys BT & Haylen BT. Immediate postvoid residuals in men with symptoms of lower urinary tract dysfunction. 2008 (unpublished data).

8. Haylen BT & Lee J. The accuracy of postvoid residual measurement in women. Int Urogynecol J 2008; 19:603-606.

Nominations sought for Peer Review Panel Experts from the disciplines involved in continence treatment, management and promotion and those who are expert in research methods and statistical analysis are invited to nominate to join the Australian and New Zealand Continence Journal Peer Review Panel.

Peer review was introduced to the journal in 2004 and began an exciting new era in our publication. Peer review of articles is aimed to increase the calibre of academic and research papers published and to raise the standing of the journal.

4. Haylen BT. The residual urine volume in a normal female population – an application of transvaginal ultrasound. Br J Urol 1989; 64:347349.

The journal is proud to promote Australian and New Zealand scholarship.

5. Haylen BT, Yang V & Logan V. Uroflowmetry: its current clinical utility for women. Int Urogynecol J 2008; 19:899-903.

For details regarding the Peer Review Panel please email Jacinta Miller: jacmil@bigpond.com

6. Haylen BT, Lee J, Logan V, Husselbee S, Zhou J & Law M. Immediate postvoid residuals in women with symptoms of lower

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Vol. 14, No. 3 • Spring 2008

69

australian nursing federation anf guidelines

delegation by registered nurses and midwives The skill mix of staff working in nursing and midwifery settings necessitates a clear set of guidelines for registered nurses and midwives who delegate1 aspects of nursing and midwifery care to other registered nurses, registered midwives, enrolled nurses or to assistants in nursing or midwifery or other unlicensed workers (however titled).2 The practice of registered3 nurses and midwives and enrolled4 nurses is governed by nursing and midwifery Acts in each state and territory and nursing and midwifery regulatory authorities set up pursuant to those Acts and regulations. Assistants in nursing or midwifery and other unlicensed workers (however titled) are not licensed by nursing and midwifery regulatory authorities.

The purpose of these guidelines is to: â–Ş

clarify the role and obligation of registered nurses and midwives when delegating aspects of nursing and midwifery care;

â–Ş

guide registered nurses and midwives through the issues to be considered in delegating aspects of nursing and midwifery care; and

â–Ş

clarify the role and obligation of employers in the delegation of aspects of nursing and midwifery care by nurses and midwives.

The Australian Nursing Federation recommends the adoption of the following guidelines: 1.

Nursing and midwifery care needs of the client are assessed by registered nurses and midwives who develop a nursing or midwifery care plan, and make informed decisions relating to delegation within that nursing and midwifery care plan.

2.

The wishes, wellbeing and interests of the patient or client are central to the assessment and care delivery process developed by the registered nurse or midwife.

3.

A registered nurse or midwife must not require an assistant in nursing or midwifery or other unlicensed worker (however titled) to perform aspects of nursing or midwifery care where state or territory legislation expressly prohibits such delegation.

4.

Each registered nurse or midwife is responsible for their own practice and conduct. This responsibility includes an informed, responsible approach to delegation. The registered nurse or midwife remains accountable for delegated aspects of nursing or midwifery care.

5.

A registered nurse or midwife cannot assume that the policies, protocols and practices of the employer are always in accordance with legislative requirements. Registered nurses and midwives should seek advice or assistance from the ANF and other relevant organisations in matters relating to regulation and other legislation.

anf guidelines - delegation by registered nurses and midwives

anf guidelines delegation by registered nurses and midwives

6.

In accepting any delegated activity, the enrolled nurse or assistant in nursing or midwifery or other unlicensed worker (however titled) is making an undertaking to personally perform that activity. A delegated activity may not be re-delegated to another person by the person to whom the registered nurse or midwife has delegated the aspects of nursing or midwifery care.

7

Enrolled nurses are responsible for their own practice and conduct. In accepting delegated aspects of nursing or midwifery care, enrolled nurses are accepting responsibility and accountability for delivery of those aspects of nursing or midwifery care.

8

Enrolled nurses have a responsibility to advise the delegating registered nurse or midwife if they are not competent to provide the delegated care.

9

Assistants in nursing or midwifery or other unlicensed workers (however titled) assist registered nurses and midwives and enrolled nurses by providing delegated aspects of nursing or midwifery care within the limits specified by their education, training and experience, and in accordance with legislation.

10 Assistants in nursing or midwives or other unlicensed workers (however titled) work within a plan of care developed by registered nurses and midwives and under supervision at all times. This supervision may be direct or indirect.5 11 Assistants in nursing or midwifery and other unlicensed workers (however titled) are accountable for their own actions and are accountable to registered nurses or midwives for all delegated activities.

12 Employers are responsible for ensuring that all employees have the necessary competencies to carry out the role for which they have been employed.

13 Employers are responsible for ensuring that registered nurses and midwives have access to information regarding the current competencies of each assistant in nursing or midwife or other unlicensed worker (however titled) to whom they are likely to delegate aspects of nursing or midwifery care.

14 Employers are responsible for ensuring that registered nurses and midwives are not required to delegate aspects of nursing or midwifery care to assistants in nursing or midwifery or other unlicensed workers (however titled) where this is expressly prohibited by state or territory Acts or regulations or where the registered nurse or midwife considers that the assistant in nursing or midwifery or other unlicensed worker (however titled) is not competent to provide the delegated aspects of nursing or midwifery care.

15 Employers are responsible for ensuring that agency or workplace policies, protocols and practices in relation to delegation are in line with state and territory legislation and nursing and midwifery standards.

16 Employers must be cognisant of staffing levels, skills mix and level of nursing and midwifery care needs, as determined by nurses and midwives, when employing and allocating staff.

17 Employers are responsible for providing resources and infrastructure for the staff development of all staff involved in the delivery of care.

anf guidelines - delegation by registered nurses and midwives

anf guidelines delegation by registered nurses and midwives

checklist for delegation The following are examples of factors requiring consideration when delegating aspects of nursing or midwifery care: 

What is the client’s health status?



Has the care plan been recently evaluated and modified in line with changes in the client’s condition?



What co-morbidities and/or disabilities must be taken into account?



To what extent is the registered nurse or midwife required and/or able to supervise and monitor the activity being delegated?



What level of qualification, skill, knowledge and experience is required of the person to whom the activity is being delegated?



In what context is the delegated activity to be performed?



Is it reasonable to expect the person to accept the delegated activities?



Is the person able to manage the delegated activities within their current workload?



Is the activity within that person’s role?

endorsed november 2004 reviewed and re-endorsed december 2007

1 See

Delegation and Supervision for Nurses and Midwives (ANMC http://www.anmc.org.au/docs/May_06_Delegation_Supervision_for_Nurses_Midwives.pdf.

2006):

2 The

term assistant in nursing or mifwifery or other unlicensed worker (however titled), means a person who assists registered nurses and midwives and enrolled nurses in the delivery of nursing or midwifery care.

3 The

term registered nurse or midwife means a person who is registered and licensed to practice by an Australian nursing and midwifery regulatory authority. In Victoria, this refers to a Registered Nurse or Midwife Division 1.

4 The

term enrolled nurse means a person who is enrolled and licensed to practice by an Australian nursing and midwifery regulatory authority. In Victoria, this refers to a Registered Nurse Division 2.

5 Direct

supervision: the registered nurse or midwife is actually present, observes, works with and directs the person who is being supervised. Indirect supervision: the registered nurse or midwife is easily contactable but does not directly observe the activities.

anf guidelines - delegation by registered nurses and midwives