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Anesthesiology:
doi: 10.1097/ALN.0b013e31819f7aea
Review Articles

Postoperative Urinary Retention: Anesthetic and Perioperative Considerations

Baldini, Gabriele M.D.*; Bagry, Hema M.D., F.R.C.A., F.R.C.P.C.*; Aprikian, Armen M.D., F.R.C.S.C.†; Carli, Franco M.D., M.Phil., F.R.C.A., F.R.C.P.C.‡
Section Editor(s): Warner, David S. M.D.; Warner, Mark A. M.D., Editors

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Abstract

Urinary retention is common after anesthesia and surgery, reported incidence of between 5% and 70%. Comorbidities, type of surgery, and type of anesthesia influence the development of postoperative urinary retention (POUR). The authors review the overall incidence and mechanisms of POUR associated with surgery, anesthesia and analgesia. Ultrasound has been shown to provide an accurate assessment of urinary bladder volume and a guide to the management of POUR. Recommendations for urinary catheterization in the perioperative setting vary widely, influenced by many factors, including surgical factors, type of anesthesia, comorbidities, local policies, and personal preferences. Inappropriate management of POUR may be responsible for bladder overdistension, urinary tract infection, and catheter-related complications. An evidence-based approach to prevention and management of POUR during the perioperative period is proposed.
BLADDER catheterization is a common procedure during inpatient major surgery that allows monitoring of urine output, guides volume resuscitation, and serves as a surrogate marker of hemodynamic stability. With an increase in outpatient and fast-track surgical procedures, perurethral catheterization is restricted to fewer procedures and for a limited time. Awareness and identification of patients at risk of developing postoperative urinary retention (POUR) thus assumes greater significance. POUR has been defined as the inability to void in the presence of a full bladder. The widely varying reported incidence of POUR reflects its multifactorial etiology and the lack of uniform defining criteria. This paper reviews the physiology of micturition and analyzes the perioperative factors that contribute to POUR. Evidence-based guidelines for the management of POUR are also provided.
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Mechanism of Micturition

The bladder is composed of a body formed by the detrusor muscle and a funnel-shaped neck. The neck has an internal layer of smooth muscle that surrounds the internal meatus of the bladder—the internal urethral sphincter (IUS). The external urethral sphincter is formed collectively by the overlying striated muscle fibers of the pelvic floor. The adult urinary bladder has a capacity of 400 to 600 ml. The bladder is innervated by efferent somatic, sympathetic, and parasympathetic fibers, whereas the visceral afferent fibers (Aδ and C) arise from the bladder wall (stretch receptors). The parasympathetic fibers cause contraction of the detrusor and relaxation of the neck, permitting micturition. The sympathetic fibers, in contrast, influence the relaxation of the detrusor and close the internal urethral sphincter. These two systems are governed by spinal reflexes, which are regulated by two pontine brainstem centers, the Pontine Storage Centre and the Pontine Micturition Centre. The voluntary control of the bladder becomes fully developed by the first few years of life and involves the coordination among the frontal cortex, the pontine centers, and the spinal segments influencing bladder control. During micturition, two phases can be distinguished, the storage phase and the emptying phase.
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Table 1
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The high compliant bladder allows for storage of a large volume of urine without an increase in the intravesical pressure. The first urge to void is felt at a bladder volume of 150 ml. The tension receptors in the bladder wall are activated at a volume of approximately 300 ml, creating the sense of fullness. The activation of the tension receptors propagates signals through Aδ and C fibers that travel through the pelvic sensory nerves, arriving at the spinal cord, where they activate parasympathetic neurons. Activation of the parasympathetic neuron stimulates efferent pelvic nerves that lead to contraction of the detrusor muscle. Detrusor contractions last only a few seconds, substantially raising the intravesical pressure from a resting pressure of 40 mm H2O to a few hundred mm H2O. When the intravesical pressure reaches the voiding threshold, the detrusor contractions increase in intensity, frequency, and duration. This creates a complete and synchronous contraction of the detrusor muscle, allowing the bladder to empty quickly and efficiently. If micturition is not desired or is inconvenient, afferent stimuli from the stretch receptors of the bladder along with the proprioceptive afferents of the urethra, penis, vagina, rectum perineum, and anal sphincters activate the sympathetic system and external urethral sphincter motor neurons and simultaneously inhibit the parasympathetic system. The final effect is to prevent micturition through the contraction of the sphincters and the relaxation of detrusor muscle. Furthermore cerebral input from the frontal cortex and the pontine centers also aids in inhibiting the parasympathetic neurons and activating the sympathetic pathways. A schematic illustration of the anatomical structures and reflexes involved in the storage phase and emptying phase is summarized in figure 1 and table 1.1,2
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Diagnosis of POUR

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Three methods have been used to diagnose POUR: history and physical examination, the need for bladder catheterization, and, more recently, ultrasonographic assessment (table 2).
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Clinical Examination
Pain and discomfort in the lower part of the abdomen have been used as conventional indicators of POUR. However, these symptoms may be masked by regional anesthesia, comorbidities including patients with spinal cord injury or stroke or sedated patients who are unable to effectively communicate their symptoms.3
Clinical assessment by palpation and percussion in the suprapubic area is another commonly used method for diagnosis of POUR. This method however lacks the sensitivity to provide an accurate measure of the residual urinary volume. Dullness of the bladder to the level of the umbilicus provides a rough estimate of at least 500 ml of urine, but it can vary as much as 1,000 ml with dullness extending above the umbilicus.3 Deep palpation of the bladder is not recommended because it can produce significant discomfort and can elicit vagal reflexes evoked by pain. In addition, clinical evaluation has been shown to overestimate the bladder volume compared to ultrasound.4
Pavlin et al. showed that 61% of day-case surgical patients admitted to the postanesthesia care unit after general anesthesia did not report any symptoms of bladder distension, despite a bladder volume greater than 600 ml as measured by ultrasonography.5 Similar findings were reported by Stallard et al.6 Lamonerie found that almost a quarter of inpatients evaluated for POUR with ultrasound had overdistended bladder, even in absence of clinical symptoms, and were unable to void at the time of discharge from the recovery room.7
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Bladder Catheterization
Bladder catheterization is used both as a diagnostic tool and as treatment for POUR. The inability to void in the postoperative period could be multifactorial, including inadequate perioperative fluids. It is imperative to evaluate and treat the underlying cause before making the diagnosis of POUR and proceeding with catheterization. Catheterization is an invasive procedure with the potential to cause complications, including catheter-related infections, urethral trauma, prostatitis, and patient discomfort.8
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Ultrasound Assessment
Although ultrasound has been used as an imaging modality to evaluate bladder function, its use in the perioperative period as a diagnostic tool for POUR has gained popularity only in the past decade.9–15 Several studies have shown good correlation between the volumes measured by bladder catheterization and by ultrasound4,16; in women, however, ultrasound can slightly underestimate bladder volume.9,16 When ultrasound is performed by the same individual, the difference between urinary volume measured by the ultrasound and by catheterization varies minimally, indicating the need for operator consistency.15 During laparoscopic cholecystectomy, Greig et al. showed that ultrasound monitoring of the bladder before the procedure was more accurate than clinical examination, especially in obese patients and in those with previous lower abdominal surgery.17 Both the times to void and to discharge from hospital were reduced by using ultrasound in patients considered to be at a high risk of developing POUR.17 However, this has not been demonstrated in patients considered to be at a low risk of developing POUR.4 Ultrasound is also useful to monitor bladder volume before it becomes excessively large. Pavlin et al. showed that patients at high-risk of POUR can have a postresidual volume greater than 600 ml, even though they were able to void. By identifying these patients at risk of having an overdistended bladder, intravenous fluids can be monitored, and inappropriate early discharge can be avoided.5
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Perioperative Risk Factors for POUR

Age and Gender
POUR has been shown to increase with age, with the risk increasing by 2.4 times in patients over 50 yr of age.8,18–22
A higher incidence of POUR has been reported in men (4.7%) compared to women (2.9%).8,23 Possible reasons for such age and gender influences include age-related progressive neuronal degeneration leading to bladder dysfunction19 and gender-specific pathologies such as benign prostatic hypertrophy among others.8,18,20,21
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Type of Surgery
The incidence of POUR varies according to the type of surgery. Although the incidence of POUR in general surgical population is around 3.8%,8,23 the incidence in joint arthroplasty varies widely (10.7–84%).24–27 The incidence of POUR after anorectal surgery ranges between 1 and 52%.22,28–31 Injury to the pelvic nerves and pain evoked reflex increase in the tone of the internal sphincter explains the high incidence of POUR in patients undergoing anorectal surgery.32–37 After hernia repair, the incidence of POUR ranges between 5.9% and 38%.18,22,38 POUR has also been reported after gynecological surgery, but with conflicting results. Pavlin found that none of the patients undergoing routine outpatient gynecologic surgery developed POUR, probably because over 90% of these patients had been catheterized during the operation and arrived in postanesthesia care unit with an empty bladder.5 Previous pelvic surgery can increase the risk of POUR, probably as a result of direct damage to the nerves innervating the lower urinary tract.8
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Comorbidities
Concurrent neurologic diseases such as stroke, poliomyelitis, cerebral palsy, multiple sclerosis, spinal lesions, and diabetic and alcoholic neuropathy are predisposing factors to the development of urinary retention.8,31
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Drugs
Medications commonly used in the perioperative period, such as anticholinergic agents, ß-blockers, and sympathomimetics, can interfere with the bladder function.
Administration of muscarinic agonists such as carbachol and bethanecol in animals and humans causes an increase in intravescical pressure, leading to hyperactive detrusor contractions.39,40 Anticholinergic drugs such as atropine and glycopyrrolate block detrusor contractions and cause bladder hypotonia, also resulting in urinary retention.8,18
α2 agonists and antagonists alter bladder function by acting on the α-receptors of the smooth muscle cells in the upper and lower urinary tracts.39,41–45 In a randomized double-blind study, Gentili et al. studied the effect of intrathecal clonidine, an α2 agonist, on bladder function and found clonidine caused less POUR when compared to morphine.44 Although systemic administration of clonidine causes an increase in urethral resistance,39 its intrathecal injection is devoid of any peripheral effect. Possible mechanisms of clonidine have been proposed including: a decrease in spinal cord sympathetic outflow lowering the tone of IUS,44 and a supraspinal inhibitory effect on IUS tone and a diuretic effect.45
Prazosin, an α1 antagonist, decreases the peristaltic movements in the ureter, the amplitude of detrusor contractions, the urethral opening pressure, and the frequency of micturition.42 Stimulation of α1 receptors by sympathomimetic agents increases the tone of IUS, thus increasing the risk of developing POUR.8,18
When ephinephrine is injected intraperitoneally in rats, the intravescical pressure increases without raising urine output, suggesting that ephinephrine increases IUS tone by acting on α receptors in the bladder neck.39 ß-adrenergic receptors are located in the smooth muscle cells of the detrusor and in minor concentration in the bladder outlet.46 In animals, stimulation of ß-adrenergic receptors causes relaxation of the detrusor and reduces sphincter tone.39,46,47 In contrast, ß-adrenergic antagonists may cause urinary retention.8
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Intravenous Fluids
The amount of intravenous fluids may influence the development of POUR. In patients undergoing hernia repair and anorectal surgery, intravenous administration of more than 750 ml of fluids during the perioperative period increased the risk of POUR by 2.3 times compared to other surgeries.8,18,19,28,31,48–50 POUR has not been reported in low-risk surgery and in patients without history of urinary retention.20,21,51 Excessive infusion of intravenous fluids can lead to overdistension of the bladder,37 especially in patients under spinal anesthesia whose bladder filling perception is abolished.52 Overdistension inhibits detrusor function, and the normal micturition reflex cannot be restored even after emptying the urinary bladder with a catheter.28,50 Therefore, bladder volume greater than 270 ml represents a risk factor for POUR.19
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Duration of Surgery
Prolonged duration of surgery can cause POUR.4,53 In patients undergoing ambulatory surgery under central neuraxial technique, the time to void was shown to be directly proportional to the total duration of anesthesia.53 These findings could be explained by the variation in the volume of intravenous fluids administered during surgery of varying lengths. In fact, Pavlin et al. found a significant correlation between bladder volume and the duration of surgery but failed to show a relationship between the bladder volume and the total amount of fluids administered.4 In contrast, Peterson did not find any causal relationship between the duration of surgery and the risk of POUR.54
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Effects of Anesthesia and Analgesia
Impact of the Anesthetic and Analgesic Techniques on the Incidence of POUR.
In this section, we have examined the evidence from published data with regard to the effects of anesthetic and analgesic techniques on the development of POUR.
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A MEDLINE search of clinical trials, published in English, relating to the incidence and the management of POUR was conducted. The computerized search identified key words such as urinary retention, POUR, void dysfunction, micturition dysfunction, opioids and POUR, local anesthetic and POUR, anesthesia and POUR, analgesia and POUR, and surgery and POUR in the title, abstract, and Medical Subject Headings. POUR was defined on the basis of the three methods used in clinical practice, such as clinical examination, the need for bladder catheterization, and ultrasound assessment (table 2). Most of the studies did not specify the criteria to define POUR, reporting only whether it was present or not. The search was amplified to include relevant articles identified by cross-referencing (fig. 2). We included, as selection criteria, clinical trials relating to POUR after cardiothoracic, abdominal, obstetric, gynecologic, and orthopedic surgeries. We excluded articles related to pediatric and urology surgeries, reviews, editorial letters, and case reports. Studies that reported incidence of POUR and those from which it was possible to calculate incidence of POUR were grouped by method of anesthesia and by method of analgesia. The mean percentage reporting the overall incidence of POUR was determined by the method of weighted mean with weighting by the number of subjects in the group. There was considerable variability in the criteria used to define POUR. Variability was minimized by subgrouping the incidence of POUR by the diagnostic method used to define it.55 When the 95% confidence intervals (CI) fell within the same distribution, the mean incidences of POUR were compared using a chi-square test.
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Table 10
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A total of 190 studies were identified as suitable for analysis. There were 86 randomized controlled trials, 21 prospective studies, 23 retrospective studies, 57 clinical and experimental trials, 2 meta-analyses, and 1 review. POUR was the primary outcome in 50 studies and secondary outcome in 58. When patients were grouped by method of anesthesia or analgesia, some studies contributed subjects to more than one group. In 26 studies, 5,268 patients received general anesthesia (table 3), whereas 5,105 patients received intraoperative conduction blockade (spinal, epidural and combined spinal-epidural anesthesia) in 34 studies (table 4). There were 26 studies with a total of 4,870 patients receiving epidural analgesia either as continuous infusion or as single/intermittent bolus or patient-controlled epidural analgesia (table 5), and there were 27 studies with a total of 4,360 patients who received either patient-controlled anesthesia (PCA) or parenteral morphine with or without nonsteroidal antiinflammatory drugs (table 6). In 9 studies, 292 patients received peripheral nerve blocks, (table 7) and 2,141 patients received infiltrations of local anesthetics in 10 studies (table 8). The overall incidence of POUR after general anesthesia was found to be significantly lower in comparison with conduction blockade, whereas the overall incidence of POUR after epidural analgesia was found to be not significantly different in comparison with systemic analgesia (table 9). Similar incidence was found when the criteria to diagnose POUR were unspecified or based on the need for catheterization (table 10). In contrast, when clinical criteria were used to define POUR, the incidence after general anesthesia and systemic analgesia were significantly higher then with regional anesthesia and epidural analgesia, respectively (P < 0.001 [OR = 1.20] and P < 0.001 [OR = 1.76], respectively) (table 10). Such discrepancy can be explained by the fact that most of the studies analyzed were retrospective in nature, with the data obtained from the clinical charts. Furthermore, the clinical criteria used to define POUR differed widely and were often subjective (table 2). Due to the relative paucity of studies using ultrasound assessment, it was not possible to make meaningful comparisons.
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Effect of the Anesthetic and Analgesic Techniques on Bladder Function.
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General Anesthetic Agents.
General anesthetic agents cause bladder atony by interfering with the autonomic nervous system. Studies in rats and dogs have shown that sedative-hypnotic agents and volatile anesthetics suppress micturition reflex.56,57 Diazepam, pentobarbital, and propofol all decrease detrusor contractions, and isoflurane, methoxyflurane, and halothane suppress detrusor contractions. Halothane also increases bladder capacity.56 The urodynamic effects caused by volatile anesthetics and sedative-hypnotic agents appear to be caused by inhibition of pontine micturition center and the voluntary control of the cortex on the bladder.56,57 In a retrospective study by Petros,20 duration of surgery was found to be significantly associated with POUR, suggesting that urinary retention was more the result of high cumulative doses of halothane administered and not necessarily the length of exposure.
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Conduction Blockade.
Spinal Local Anesthetics.
Intrathecal local anesthetics act on the neurons of the sacral spinal cord segments (S2–S4) by blocking the transmission of the afferent and efferent action potentials on the nervous fibers from and to the bladder.52,58 The sensation of urgency to void disappears 30–60 s after intrathecal injection of local anesthetics, but a dull feeling of tension on maximal filling of the bladder persists. Bladder analgesia is due to the block of the transmission of the afferent nerve fibers from the bladder to the micturition center in the brain. The detrusor contraction (detrusor block) is completely abolished 2–5 min after the injection of spinal anesthesia, and its recovery depends on the duration of sensory block above the S2 and S3 sacral segments.
Time for sensory block to regress to S3 is 7–8 h after spinal injection of isobaric bupivacaine (20 mg), hyperbaric bupivacaine (21.5 mg), and hyperbaric tetracaine (7.5 mg) without significant difference between the three local anesthetics. Fifteen minutes after the level of analgesia regressed to L5 or lower (S2–S3), the strength of detrusor starts to return to normal values, allowing the patient to void.58 Complete normalization of detrusor strength occurs 1–3.5 h after ambulation.58
The use of long-acting local anesthetics is related to a higher incidence of POUR.52,53,59,60 In contrast, time to void after ambulatory surgery with short-acting and low-dose local anesthetics is shorter as a result of faster regression of sensory and motor block leading to a rapid recovery of bladder function.61–64 Also, unilateral spinal anesthesia with hyperbaric bupivacaine for knee arthroscopy is associated with lower incidence of POUR and shorter time to void.65,66 To our knowledge, no studies comparing the effect of the baricity of local anesthetics on bladder function have been conducted. According to the distribution of local anesthetics in the cerebrospinal fluid, the concentration of the hyperbaric local anesthetics in the sacral segments (S2–S3) is greater than that caused by an isobaric solution, suggesting that isobaric solutions a similar dose of a hyperbaric drug. In patients undergoing lumbar spine surgery, the incidence of POUR is lower when intrathecal local anesthetics are administered without opioids.67,68
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Spinal opioids.
Several studies on animals and on humans have consistently shown that spinal opioids influence bladder functions and cause urinary retention.54,64,67–75 In rats, intrathecal and intracerebro ventricular morphine inhibits spontaneous bladder contractions and increases bladder capacity.39,76 The block of micturition contraction occurs approximately 16 min after intrathecal morphine and lasts between 250 and 350 min. Reappearance of the micturition reflex corresponds with the return of the nociceptive response.39 In dogs, intrathecal fentanyl decreases bladder compliance and causes relaxation of internal urethral sphincter.70 In humans, intrathecal opioids decrease the urge sensation and detrusor contraction, increasing the bladder capacity and the residual volume, altering sphincter function, and resulting in impaired coordination between the detrusor contraction and internal urethral sphincter relaxation.71,72,76 The onset time and the duration of the these effects on bladder function depend on the type and the dose of opioid used, with a large variability in the recovery time.71 In healthy volunteers, inhibition of the bladder occurred within 1 h after intrathecal morphine and sufentanil and lasted approximately 24 h. Morphine decreased the urge to void to a lesser degree than sufentanil. These effects were dose-dependent, and the recovery time of the functions of the bladder was shorter with sufentanil than with morphine. In a study conducted in subjects with spinal lesions up to the sacral region, intrathecal morphine reversed the urodynamic effects that the spinal lesion caused on bladder function.72 These subjects had detrusor hypereflexia (uninhibited detrusor contractions), vesicosphincter dysfunction, and vesicosomatic reflexes. Intrathecal morphine has been shown to enhance bladder capacity by increasing detrusor contractions and decrease vesicosomatic reactions.72 The urodynamic effects of intrathecal opioids are mainly caused by the action on the opioid receptors in the spinal cord71 and in the cerebral structures.73 The rostral spread of opioids through the cerebrospinal fluid to the pontine micturition center has also been hypothesized as a possible mechanism of action of intrathecal opioids, but the rapid onset of the urodynamic effects with the concomitant onset of analgesia after intrathecal opioid injection and the reversal of the effects by intrathecal naloxone suggest a spinal site of action.71 In support of this hypothesis, intrathecal naloxone in rats has been shown to reverse the urodynamic effects of systemic morphine at doses that were ineffective systemically.76
The opioids receptors involved in the urodynamic effects are μ and δ.70,74–76 Buprenorphine, a partial agonist with poor affinity for μ and δ, has poor effect on the detrusor contraction and on the urethral sphincter.70 Intrathecal opioids acting on opioid receptors in the spinal cord decrease the parasympathetic firing in the sacral region and decrease the afferent inputs from the bladder to the spinal cord.39 De Groat et al. demonstrated that the axons of parasympathetic preganglionic neurons contain enkephalins that are transported in the parasympathetic ganglia.77 These enkephalins seem to have an inhibitory modulating effect on the release of acetylcholine that causes detrusor contractions.77 Intrathecal fentanyl prolongs the duration of sensory block of spinal anesthesia with short-acting and long-acting local anesthetic without affecting the ability to void.78,79 In outpatients, low-dose (20 mg) spinal lidocaine with small doses (25 μg) of fentanyl decreases the duration of sensory block and the time to void when compared with high-dose (50 mg) spinal lidocaine without fentanyl (130 vs. 162 min, respectively).80 These results suggest that a low dose of local anesthetic alone66,78,79 or in combination with a low dose of an opiate such as fentanyl78–79 may be a better way to minimize POUR and facilitate discharge of ambulatory patients without voiding.80,82 Intrathecal morphine has a poor effect on the urethral sphincter,71 whereas intrathecal fentanyl causes its relaxation.70 This effect might be explained by the potent inhibitory property of fentanyl on the sympathetic fibers (T10-L2) that would otherwise increase the tone of the urethral sphincter.70
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Epidural Local Anesthetics.
Similar to intrathecal local anesthetic, epidural local anesthetics act on the sacral and lumbar nerve fibers, blocking the transmission of afferent and efferent nervous impulses from and to the bladder. The onset and the duration of the block would depend on the pharmacokinetic properties of the local anesthetic used. The incidence of POUR with epidural local anesthetics for inguinal herniorrhaphy has been shown to be lower than with spinal anesthesia.83 Postoperative epidural ropivacaine 0.2% at different infusion rates was studied in a group of patients who underwent anterior cruciate ligament repair, and it was found that high infusion rate was associated with greater incidence of POUR and motor block.84 Similarly, by using different concentrations (0.06% and 0.12%) of bupivacaine with sufentanil in patients receiving patient-controlled epidural analgesia after orthopedic surgery, there was a direct positive relationship between incidence of POUR and concentration of epidural bupivacaine.85 POUR has also been reported after thoracic surgery patients receiving thoracic epidural analgesia with local anesthetic.86
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Epidural Opioids.
The urodynamic effects of epidural opioids have been studied extensively.56,57,84–109 In a nationwide follow-up survey in Sweden, anesthesiologists reported a greater incidence of POUR with epidural morphine (38%) compared with intrathecal morphine (13%).95 However, at close analysis, the patients that developed POUR had bladder catheterization as a result of the type and the duration of surgery, making assessment of POUR more difficult. The incidence of POUR after epidural opioids may also be related to the level at which opioids are injected. Administration of opioids in the lumbar epidural space is associated with higher rate of urinary retention compared to thoracic.97
Detrusor strength starts to decrease within 5–15 min after 4 mg of epidural morphine, its maximum effect reached between 30 and 120 min and lasting 10–15 h.69,98 A supraspinal effect due to the rostral spread of opioids in the cerebrospinal fluid toward the pontine micturition center, where opioids receptors are placed, could poorly contribute to the development of POUR, as the onset of analgesia corresponds to the beginning of bladder relaxation and to the loss of detrusor strength.69,71
Naloxone per se has no effect on normal bladder function; however, it has been shown to reverse the urodynamic effects associated with epidural opioids.69,90 By increasing the dose of IV naloxone, it is possible to prevent the decrease of detrusor contractions and the increase in bladder capacity.69 Because of the short half-life of naloxone (t1/2 = 1–1.5 h), the reversal effect on POUR could resolve before the effects of long-lasting opioids on the bladder. The urodynamic effects are not dose-dependent as shown for intrathecal opioids.69,71,99,100 The reason for this difference could be explained by the different route of administration, as spinal opioids suppress polysynaptic reflexes in a dose-dependent manner.71
Different epidural opioids have different urodynamic effects depending on their pharmacokinetic properties and receptor selectivity.97 In a study by Kim et al., patients undergoing gastric bypass surgery receiving postoperative thoracic epidural with either ropivacaine and sufentanil or ropivacaine and morphine in equipotent doses, the incidence of POUR was greater with the latter mixture.101 In another study on postpartum urinary retention, the incidence of POUR after epidural bupivacaine and epinephrine was less than epidural bupivacaine and sufentanil.89 Sufentanil and fentanyl are more lipophilic than morphine and undergo greater systemic uptake; as a result, there is less rostral spread in the central nervous system and less influence on the urodynamics.110 In contract, the hydrophilic nature of morphine delays its systemic uptake; more morphine is therefore available at the lumbar region, directly inhibiting the neurons controlling the bladder. For similar reasons, the incidence of POUR was also found to be less with epidural buprenorphine as compared with epidural morphine.102 In addition, buprenorphine, a partial agonist with poor affinity for μ and δ receptors, has minimal effect on the detrusor contraction and on the urethral sphincter.70 Also epidural methadone and meperidine were shown to be associated with less incidence of POUR.108,111
Although it has been suggested that the dose of epidural opioid may influence the incidence of POUR, this has yet been not confirmed or corroborated in the literature. Rucci et al. studied the side effects of epidural bupivacaine alone and with varying doses of fentanyl (50 to 200 μg) to bupivacaine in the lumbar epidural space in patients undergoing lower abdominal surgery. Micturition abnormalities were observed in all the groups, without significant differences, but the patients that received fentanyl needed catheterization.103
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Opioids and Epinephrine as Adjuvants.
The addition of opioids to epidural local anesthetics increases the risk of POUR and urinary tract complications, such as renal failure and cystitis by 8%.96 The incidence of POUR is 5 to 20% higher in patients with continuous epidural infusion or patient-controlled epidural analgesia compared with PCA,112–118 13.1% with continuous epidural infusion and 5.2% with patient-controlled epidural analgesia.119 Ephinephrine is used as adjuvant to prolong the effect of neuraxial anesthesia,88,104,105 resulting in longer recovery of sensory and motor block with possible consequences on bladder function.120–122
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Postpartum Urinary Retention and Epidural Anesthesia-Analgesia.
Postpartum urinary retention is a frequent complication and this appears to be the result of the pressure from the uterus on the body of the bladder.89 Urodynamic studies have shown that 85% of parturients investigated had bladder hypotonia after delivery with a consequent increase in bladder volume.89 Epidural anesthesia-analgesia, which is often used during labor and delivery, has been shown to cause postpartum urinary retention.123 Olofsson et al. observed a significantly higher incidence of postpartum urinary retention in parturients that received epidural with two different epidural mixtures (bupivacaine 0.25% with adrenaline 1:200,000 or bupivacaine 0.125% with 10 μg of sufentanil) than women who did not receive epidural. At a close analysis, those women receiving epidural anesthesia had higher incidence of instrumental deliveries and difficult labor. Therefore, it is not clear whether the effect on postpartum urinary retention was a direct effect of epidural blockade or resulted from the instrumentation and difficult labor. No difference in urinary retention was found when either epinephrine or sufentanil was added to bupivacaine.89 In contrast, Evron et al. observed less incidence of urinary retention when epidural methadone was used after Cesarean section.111
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Systemic Analgesia.
Systemic opioids both by the IV and intramuscular routes have a direct effect on bladder function40,57,69,92–94,111,124,125 via their action on spinal cord receptors. This effect is reversed by intrathecal naloxone.76,77 Systemic opioids cause POUR by inhibiting the release of acetylcholine from the parasympathetic sacral neurons that control detrusor contractility.20,21 In patients undergoing cholecystectomy and appendectomy the incidence of POUR has been shown to be directly related to the amount of systemic opioids used in the postoperative period. Furthermore, the incidence of POUR was greater if patients received intravenous PCA technique instead of intramuscular morphine or meperidine, suggesting that the steadier/steady plasma opioid concentration obtained with PCA was indirectly responsible for prolonging the effect on bladder function. Ketamine, nonsteroidal antiinflammatory drugs, and proparacetamol used together with morphine (delivered by PCA) have a morphine-sparing effect and have shown to decrease the incidence of POUR by 20%.52,126–131
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Peripheral Nerve Block.
POUR has not been reported with interscalene block.132 Paravertebral block and intercostal block in patients undergoing thoracotomy and cholecystectomy, respectively, were associated with less incidence of POUR compared to epidural or PCA.106,133,134 Capdevilla et al. and Singelyn et al., comparing the efficacy and the side effects of three analgesic techniques for major knee surgery, found the incidence of POUR significantly lower in those patients receiving peripheral nerve block compared with epidural and PCA.117,118 In patients undergoing anorectal surgery, bilateral pudendal block decreases also the incidence of POUR.135
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Infiltration of Local Anesthetics.
Field block or infiltration technique is commonly used for herniorraphy and anorectal surgery. Pain is an important factor found in the development of POUR after herniorrhaphy, and local anesthetic infiltration has been shown to decrease analgesic requirements and the risk of POUR.136–139 Similarly, perineal pain and tension in the anal canal after anorectal surgery cause sphincter spasm and detrusor relaxation.140 In a randomized study of patients undergoing anorectal surgery, Li et al. found no difference in the incidence of POUR among the patients who received either general anesthesia or regional anesthesia or local infiltration. However, at a close analysis, the two former groups had the anorectal area infiltrated with local anesthetic, making it difficult to identify whether general and regional anesthesia influenced POUR.141 In contrast with these findings, a prospective study by Fleischer et al. showed that patients undergoing anorectal surgical procedures under local anesthesia had less urinary retention then patients who received spinal anesthesia.142 Cataldo et al. and Ryan et al. reported a higher incidence of POUR after local infiltration in patients undergoing anorectal surgery (49%) and herniorraphy (17.9%).32,59 However, all patients received spinal or epidural anesthesia for surgery, rendering it difficult to assess the potential benefits of local anesthetic infiltration on POUR. Long-acting local anesthetics are advocated for herniorraphy. The reduction in acute postoperative pain afforded by the long-acting local anesthetics may potentially attenuate the inhibition of bladder reflexes that increase the risk of POUR.59,60,143,144 Furthermore, long-acting local anesthetics could facilitate, in the absence of motor block, early postoperative mobilization; allowing the patient to contract the abdominal muscles and to stand up to facilitate the emptying of the bladder.143 Paravertebral nerve block for herniorrhaphy has also been found to be associated with lower incidence of POUR.145
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Complications/Adverse Effects Associated With POUR

Autonomic Response
Painful stimulation resulting from an overdistended bladder can cause vomiting, bradycardia, hypotension, hypertension, cardiac dysrhythmias, or even asystole.52 POUR has been shown to prolong hospital stay in patients undergoing elective cholecystectomy20 and increase the discharge time in 19% of outpatients.146,147
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Infection
Urinary infection can be a direct complication of persistent POUR (consequence of bladder hypotonia and the inability to completely empty the bladder) or an indirect complication of bladder catheterization.148 Higher mortality rate has been reported in hospitalized patients who developed nosocomial urinary tract infection after indwelling bladder catheterization.149 The incidence of bactremia after single catheterization has been reported to be as high as 8%.150 Akthar et al. found that 21% of women undergoing laparoscopic surgery that had been catheterized before the procedure had bacteriuria 6 days later.151 The use of an indwelling catheter after total joint replacement surgery for 24 h or less decreased the incidence of POUR without increasing the incidence of urinary tract infections.152 Complications have also been reported with in-out and intermittent catheterization techniques.153
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Bladder Overdistension and Adverse Effects on Urodynamics
Bladder overdistension is a potentially serious adverse effect associated with POUR, and it has a reported incidence of 44%.7 In a study by Pavlin et al., 20.5% of outpatients had a bladder volume greater than 500 ml.4 Mulroy et al. set up a target volume of 400 ml in a study of outpatients undergoing ambulatory surgery under spinal and epidural anesthesia. Eighteen percent of the patients assessed with ultrasound had a bladder volume greater than 400 ml, and only 13% of these patients required catheterization due to inability to void.53 On the basis of animal studies, bladder ischemia may be responsible for the persistent dysfunction after bladder over distension.154 Furthermore, Katida et al. observed that, if the rabbit bladder was overdistended for a period of time between 4 and 24 h, the concentration of muscarinic receptors decreased, resulting in reduced detrusor contractility.154 Transient filling volume between 500 and 1,000 ml is not harmful if it is diagnosed and treated early within 1 to 2 h.4 Tammela showed in patients undergoing inpatient surgery that an initial volume over 500 ml detected by in-out bladder catheterization, increased the incidence of persistent POUR when compared with an initial volume below 500 ml. However 51% of these patient were catheterized after 12 h, and 38% had a bladder volume greater than 1,000 ml, suggesting that an early catheterization could have decreased the incidence of prolonged micturition difficulties.23 It is thus logical to investigate further and establish safe bladder volume ranges to avoid bladder overdistention and persistent bladder dysfunction.
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Clinical Management of POUR

Fig. 3
Fig. 3
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Fig. 4
Fig. 4
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Prevention of POUR requires the identification of patients with perioperative risk factors (fig. 3). Pharmacological strategies have been used as an attempt to prevent or to treat persistent POUR (fig. 4). Systemic phentolamine has been shown to decrease the resistance of IUS in rats,155 whereas phenoxybenzamine reduces the time to first void and the incidence of bladder catheterization.41,43 In a prospective randomized study Goldman et al. showed that phenoxybenzamine was effective in preventing and treating POUR in patients undergoing inguinal hernioplasty.156 Similar effect was shown in different types of surgery157 and in patients with prostate enlargement undergoing anorectal surgery.158 In contrast, phenoxybenzamine failed to prevent POUR after anorectal surgery.32 In conclusion, the use of phenoxybenzamine remains controversial.
Postoperative pain, rectal distension, and anal dilatation increase sympathetic tone. The resultant stimulation of the α-receptors in the IUS leads to increased pressure on the bladder neck and potentially to POUR. It has been hypothesized that this physiologic mechanism could explain urinary retention after anorectal surgery. Therefore, the use of α-antagonists in patients with postoperative pain after anorectal surgery could decrease the incidence of POUR.32 Further studies are needed to establish the role of these agents in the prevention of POUR among patients undergoing anorectal surgery.
In the following section, practical guidelines addressing clinical questions are proposed on the basis of a literature review and documented findings.
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Role of Bladder Catheterization
Bladder catheterization is the standard treatment of POUR. Although in-out and indwelling urinary catheterization remain the standard therapy to treat POUR, it is not known which patients require catheterization, and the duration of catheterization and bladder volume thresholds are also unknown. Some of these issues are addressed on the basis of currently available evidence.
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When and in Whom Should the Bladder Be Catheterized?
By selecting patients who need a bladder catheter, the likelihood of urinary complications may be potentially minimized. Bladder catheterization, while preventing persistent voiding dysfunction secondary to bladder overdistension, may be associated with urinary tract infections, urethral trauma, and patient discomfort.8 Ultrasound assessment of bladder volume remains an accurate method.9–15 The bladder volume at which one may decide to catheterize depends on the preoperative bladder functional capacity and the ability to void. Normal bladder capacity ranges between 400 to 600 ml.7,52 To easily measure functional bladder capacity to avoid invasive methods, Brouwer et al. suggest holding the urine until the desire to void is uncomfortable and then measuring the urinary volume that the patient voids.9 If POUR is diagnosed early (within 1–2 h), transient bladder distention with 500 to 1,000 ml volume may not have adverse effects on voiding function. At a volume 600 ml, catheterization is recommended.4 This volume is slightly higher than the maximum bladder volume of 400–500 ml recommended in the adult population.15
Fig. 5
Fig. 5
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In summary, low-risk outpatients may be discharged without void, and bladder catheterization is advised in high-risk subjects when the bladder volume is greater than 600 ml over a minimum period of 2 h (fig. 5).
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How Long Must Surgical Patients Need Keep the Bladder Catheter?
Catheterization of the bladder is required for monitoring urinary output after major surgery, guiding volume resuscitation and preventing POUR. However, both intermittent and indwelling bladder catheterization have been associated with urinary tract infections.148,149,159,160 Aseptic techniques during the placement of bladder catheter and antibiotic prophylaxis have been reported to reduce the incidence of urinary tract infections.161,162 POUR in ambulatory surgery is commonly treated with in-out catheterization. For in-hospital patients, the optimal duration of bladder catheterization remains controversial. In a heterogenous surgical population, in-out catheterization was compared to indwelling catheterization for 24 h. No differences in terms of recatheterization and urinary tract infections were found between the two strategies, but indwelling catheterization increased hospital stay by 1 day.22 For anorectal surgery, most authors suggest 5 days with a range between 3 and 10 days.35,163–165 The incidence of urinary tract infections after anorectal surgery and 5 days of catheterization ranges between 42% and 60%.33,36,165 The incidence of POUR after anorectal surgery was similar whether patients had an indwelling catheter for either 1 day or 5 days, but a lower incidence of urinary tract infections was reported in the 1-day group. Preoperative dysuria and metastatic lymph node disease in patients with rectal cancer were identified as risk factors of POUR. The recommendations are that patients undergoing anorectal surgery with no other risk factors for POUR should keep the catheter for 1 day to reduce the risk of urinary tract infections, whereas patients at high risk (rectal cancer, preoperative dysuria, and metastatic lymph nodes) should keep the catheter for 5 days.36 Basse et al. studied the incidence of POUR, urinary tract infections, and permanent voiding dysfunction after colonic resection in 102 patients, catheterized for only 24 h, and continuous epidural bupivacaine-morphine infusion. These authors reported a low incidence of POUR (9%) and urinary tract infections (4%). None of the patients had long-term voiding dysfunction.166 However, because of the absence of a control group and the absence in literature of large prospective randomized studies, further investigations are needed to establish the optimal duration and the necessity of bladder catheterization during continuous epidural analgesia. Removal of the bladder catheter after abdominal or vaginal hysterectomy and vaginal prolapse surgery either immediately167,168 or within the first 24 h has been shown to decrease the incidence of postoperative urinary infections and duration of hospitalization without increasing the risk of bladder dysfunction.167,169–171
In summary, the results of a few randomized studies suggest that intermittent catheterization is adequate for outpatient surgery. For major uncomplicated surgery with or without epidural anesthesia/analgesia, bladder catheterization may be limited to a period of 24 h. Ultrasound may be used to guide catheterization if urine volume exceeds 600 ml and in-out catheterization technique may be preferable. For major complicated surgery and with extensive perineal and rectal dissection, bladder catheterization is required for a longer period of time according to clinical indications.
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Is Bladder Catheterization Necessary for Surgical Patients Undergoing Lower Limb Joint Surgery?
Urinary tract infection related to bladder catheterization is a well known postoperative complication in patients undergoing orthopedic surgery.150,172–175 Hematogenous spread from the urinary tract could potentially infect the prosthetic joint or disseminate systemically, causing severe complications, including sepsis.173,175–179 Postoperative bacteriuria has been shown to increase 3 to 6 times the risk of prosthetic infection,178,180,181 with male patients at higher risk of developing POUR.174,175,182,183 Epidural morphine is associated with an incidence of 62% of POUR compared with 24% when systemic opioids are used.183 Some data seem to indicate that indwelling bladder catheter in patients at risk of POUR might be advantageous over intermittent catheterization with less POUR and no change in incidence of urinary tract infection.25,152,184–186 No difference in urinary tract infections has been found when either an indwelling bladder catheterization for 24 h or intermittent catheterization techniques were used.187 With regard to the latter, an increased risk of undiagnosed bladder overdistension resulting in risk of permanent bladder dysfunction and secondary urinary tract infections has to be considered. Short-term antibiotic prophylaxis, limited to one dose of cefazolin before the surgery, is associated with less bacteriuria with intermittent bladder catheterization than with indwelling catheterization.188 Currently, bacterial resistance and increased costs are the main reasons for the choice of short-term antibiotic prophylaxis in patients undergoing total joint replacement.181,189 This approach does not cover the period of indwelling bladder catheterization; therefore, it may increase the risk of urinary tract infections.188 Although POUR after total joint arthroplasty has been shown to occur frequently (67%) in patients who receive intermittent catheterization as necessary, routine preoperative catheterization may not be warranted, except when high risk factors for POUR are present.187,190 If POUR occurs and catheterization is required, intermittent catheterization is the preferable choice, and it has been shown to be more cost-effective than indwelling catheterization.187,190
In summary, bladder catheterization is not required in low-risk patients receiving neuraxial lipohilic opioids, whereas bladder catheterization is recommended in high-risk patients for 24 h under adequate anthibiotic prophylaxis. Subsequent in-out catheterization should be guided by ultrasound.
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Must Outpatients Void before Being Discharged?
Ability to void has always been considered as one of the criteria to discharge outpatients. By stratifying preoperative risk for POUR, selected patients could be discharged without voiding.4,5,53 In two prospective studies by Pavlin et al., outpatients were classified as low-risk for POUR if they had general anesthesia or nonpelvic surgery and high-risk if they had hernia/anal surgery or spinal/epidural anesthesia.4,5 In low-risk outpatients, the incidence of POUR (defined as the inability to void with a bladder volume greater than 600 ml detected by ultrasound) was less than 1% compared to 15% in the high-risk group. Of 227 low-risk patients, 1 patient had POUR. The others voided approximately 75 min after surgery and were discharged without voiding. In the high-risk patients, the incidence of POUR was 5%; when they were catheterized (in-out catheterization at a bladder volume greater than 600 ml), the incidence of urinary retention was high (25%). According to these published findings, low-risk patients undergoing ambulatory surgery could be discharged without voiding, whereas high-risk patients who have been catheterized before discharge may require medical assistance if not able to void spontaneously within 8 h from surgery. If ultrasound equipment is not available and high-risk patients do not void before discharge, then they should be catheterized.5 Ultrasound remains a useful instrument in high-risk patients not only because it measures bladder volume; it also guides timing of the catheterization and thus avoids unnecessary bladder and catheter-related complications and delayed disharges (fig. 5).
In summary, outpatients in the low-risk category group can be sent home without voiding, but those in the high-risk group can be catheterized under ultrasound guidance and then sent home with medical assistance.
In conclusion, several anesthetic and nonanesthetic factors contribute to the development of POUR in the surgical patient. The diagnosis of POUR is often arbitrary, and its true incidence is unknown due to lack of defining criteria. By carefully identifying patients at risk, adopting appropriate anesthetic techniques and perioperative care principles and accurately monitoring bladder volume by ultrasound, POUR may be prevented and the associated morbidity minimized. Hence it becomes imperative to evaluate the true incidence and consequences of POUR in large prospective clinical trials.
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References

1. Yoshimura N, Chancellor MB: Physiology and pharmacology of the bladder and urethra, Campbell-Walsh Urology, 9th edition. Edited by Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peters CA. Philadelphia, Elsevier, 2006, pp 1922–79

2. Hall JE: Urine formation by the kidneys, Textbook of Medical Physiology, 11th edition. Edited by Guyton AC, Hall JE. Philadelphia, Saunders Elsevier, 2006, pp 307–14

3. Kemp D, Tabaka N: Postoperative urinary retention: Part II–A retrospective study. J Post Anesth Nurs 1990; 5:397–400

4. Pavlin DJ, Pavlin EG, Gunn HC, Taraday JK, Koerschgen ME: Voiding in patients managed with or without ultrasound monitoring of bladder volume after outpatient surgery. Anesth Analg 1999; 89:90–7

5. Pavlin DJ, Pavlin EG, Fitzgibbon DR, Koerschgen ME, Plitt TM: Management of bladder function after outpatient surgery. Anesthesiology 1999; 91:42–50

6. Stallard S, Prescott S: Postoperative urinary retention in general surgical patients. Br J Surg 1988; 75:1141–3

7. Lamonerie L, Marret E, Deleuze A, Lembert N, Dupont M, Bonnet F: Prevalence of postoperative bladder distension and urinary retention detected by ultrasound measurement. Br J Anaesth 2004; 92:544–6

8. Tammela T, Kontturi M, Lukkarinen O: Postoperative urinary retention. I. Incidence and predisposing factors. Scand J Urol Nephrol 1986; 20:197–201

9. Brouwer TA, Eindhoven BG, Epema AH, Henning RH: Validation of an ultrasound scanner for determing urinary volumes in surgical patients and volunteers. J Clin Monit Comput 1999; 15:379–85

10. Griffiths CJ, Murray A, Ramsden PD: Accuracy and repeatability of bladder volume measurement using ultrasonic imaging. J Urol 1986; 136:808–12

11. Massagli TL, Cardenas DD, Kelly EW: Experience with portable ultrasound equipment and measurement of urine volumes: Inter-user reliability and factors of patient position. J Urol 1989; 142:969–71

12. Topper AK, Holliday PJ, Fernie GR: Bladder volume estimation in the elderly using a portable ultrasound-based measurement device. J Med Eng Technol 1993; 17:99–103

13. Revord JP, Opitz JL, Murtaugh P, Harrison J: Determining residual urine volumes using a portable ultrasonographic device. Arch Phys Med Rehabil 1993; 74:457–62

14. Ding YY, Sahadevan S, Pang WS, Choo PW: Clinical utility of a portable ultrasound scanner in the measurement of residual urine volume. Singapore Med J 1996; 37:365–8

15. Coombes GM, Millard RJ: The accuracy of portable ultrasound scanning in the measurement of residual urine volume. J Urol 1994; 152:2083–5

16. Rosseland LA, Stubhaug A, Breivik H: Detecting postoperative urinary retention with an ultrasound scanner. Acta Anaesthesiol Scand 2002; 46:279–82

17. Greig JD, Mahadaven M, John TG, Garden OJ: Comparison of manual and ultrasonographic evaluation of bladder size in patients prior to laparoscopy. Surg Endosc 1996; 10:432–3

18. Petros JG, Rimm EB, Robillard RJ, Argy O: Factors influencing postoperative urinary retention in patients undergoing elective inguinal herniorrhaphy. Am J Surg 1991; 161:431–3

19. Keita H, Diouf E, Tubach F, Brouwer T, Dahmani S, Mantz J, Desmonts JM: Predictive factors of early postoperative urinary retention in the postanesthesia care unit. Anesth Analg 2005; 101:592–6

20. Petros JG, Rimm EB, Robillard RJ: Factors influencing urinary tract retention after elective open cholecystectomy. Surg Gynecol Obstet 1992; 174:497–500

21. Petros JG, Mallen JK, Howe K, Rimm EB, Robillard RJ: Patient-controlled analgesia and postoperative urinary retention after open appendectomy. Surg Gynecol Obstet 1993; 177:172–5

22. Lau H, Lam B: Management of postoperative urinary retention: A randomized trial of in-out versus overnight catheterization. ANZ J Surg 2004; 74:658–61

23. Tammela T, Kontturi M, Lukkarinen O: Postoperative urinary retention. II. Micturition problems after the first catheterization. Scand J Urol Nephrol 1986; 20:257–60

24. Waterhouse N, Beaumont AR, Murray K, Staniforth P, Stone MH: Urinary retention after total hip replacement. A prospective study. J Bone Joint Surg Br 1987; 69:64–6

25. Oishi CS, Williams VJ, Hanson PB, Schneider JE, Colwell CW Jr, Walker RH: Perioperative bladder management after primary total hip arthroplasty. J Arthroplasty 1995; 10:732–6

26. Lingaraj K, Ruben M, Chan YH, Das SD: Identification of risk factors for urinary retention following total knee arthroplasty: A Singapore hospital experience. Singapore Med J 2007; 48:213–6

27. O’Riordan JA, Hopkins PM, Ravenscroft A, Stevens JD: Patient-controlled analgesia and urinary retention following lower limb joint replacement: Prospective audit and logistic regression analysis. Eur J Anaesthesiol 2000; 17:431–5

28. Zaheer S, Reilly WT, Pemberton JH, Ilstrup D: Urinary retention after operations for benign anorectal diseases. Dis Colon Rectum 1998; 41:696–704

29. Salvati EP, Kleckner MS: Urinary retention in anorectal and colonic surgery. Am J Surg 1957; 94:114–7

30. Scoma JA: Catheterization in anorectal surgery. Arch Surg 1975; 110:1506

31. Toyonaga T, Matsushima M, Sogawa N, Jiang SF, Matsumura N, Shimojima Y, Tanaka Y, Suzuki K, Masuda J, Tanaka M: Postoperative urinary retention after surgery for benign anorectal disease: Potential risk factors and strategy for prevention. Int J Colorectal Dis 2006; 21:676–82

32. Cataldo PA, Senagore AJ: Does alpha sympathetic blockade prevent urinary retention following anorectal surgery? Dis Colon Rectum 1991; 34:1113–6

33. Zanolla R, Torelli T, Campo B, Ordesi G: Micturitional dysfunction after anterior resection for rectal cancer. Rehabilitative treatment. Dis Colon Rectum 1988; 31:707–9

34. Burgos FJ, Romero J, Fernandez E, Perales L, Tallada M: Risk factors for developing voiding dysfunction after abdominoperineal resection for adenocarcinoma of the rectum. Dis Colon Rectum 1988; 31:682–5

35. Hojo K, Vernava AM 3rd, Sugihara K, Katumata K: Preservation of urine voiding and sexual function after rectal cancer surgery. Dis Colon Rectum 1991; 34:532–9

36. Benoist S, Panis Y, Denet C, Mauvais F, Mariani P, Valleur P: Optimal duration of urinary drainage after rectal resection: A randomized controlled trial. Surgery 1999; 125:135–41

37. Gerstenberg TC, Nielsen ML, Clausen S, Blaabjerg J, Lindenberg J: Bladder function after abdominoperineal resection of the rectum for anorectal cancer. Urodynamic investigation before and after operative in a consecutive series. Ann Surg 1980; 191:81–6

38. Gonullu NN, Gonullu M, Utkan NZ, Dulger M, Gokgoz S, Karsli B: Postoperative retention of urine in general surgical patients. Eur J Surg 1993; 159:145–7

39. Durant PA, Yaksh TL: Drug effects on urinary bladder tone during spinal morphine-induced inhibition of the micturition reflex in unanesthetized rats. Anesthesiology 1988; 68:325–34

40. Bromage PR, Camporesi EM, Durant PA, Nielsen CH: Nonrespiratory side effects of epidural morphine. Anesth Analg 1982; 61:490–5

41. Evron S, Samueloff A, Sadovsky E, Berger M, Magora F: The effect of phenoxybenzamine on postoperative urinary complications during extradural morphine analgesia. Eur J Anaesthesiol 1984; 1:45–54

42. Lee JZ, Tillig B, Perkash I, Constantinou CE: Effect of alpha1 adrenoceptor antagonist on the urodynamics of the upper and lower urinary tract of the male rat. Neurourol Urodyn 1998; 17:213–29

43. Evron S, Magora F, Sadovsky E: Prevention of urinary retention with phenoxybenzamine during epidural morphine. BMJ (Clin Res Ed) 1984; 288:190

44. Gentili M, Bonnet F: Spinal clonidine produces less urinary retention than spinal morphine. Br J Anaesth 1996; 76:872–3

45. Hamaya Y, Nishikawa T, Dohi S: Diuretic effect of clonidine during isoflurane, nitrous oxide, and oxygen anesthesia. Anesthesiology 1994; 81:811–9

46. Gregg RA, Boyarsky S, Labay P, Levie BB: Presence of beta-adrenergic receptors in urinary bladder of dog and cat: Response to isoproterenol. Arch Phys Med Rehabil 1970; 51:88–94

47. Nergardh A: The functional role of adrenergic receptors in the outlet region of the urinary bladder. An in vitro and in vivo study in the cat. Scand J Urol Nephrol 1974; 8:100–7

48. Bailey HR, Ferguson JA: Prevention of urinary retention by fluid restriction following anorectal operations. Dis Colon Rectum 1976; 19:250–2

49. Kozol RA, Mason K, McGee K: Post-herniorrhaphy urinary retention: A randomized prospective study. J Surg Res 1992; 52:111–2

50. Petros JG, Bradley TM: Factors influencing postoperative urinary retention in patients undergoing surgery for benign anorectal disease. Am J Surg 1990; 159:374–6

51. Petros JG, Alameddine F, Testa E, Rimm EB, Robillard RJ: Patient-controlled analgesia and postoperative urinary retention after hysterectomy for benign disease. J Am Coll Surg 1994; 179:663–7

52. Kamphuis ET, Ionescu TI, Kuipers PW, de Gier J, van Venrooij GE, Boon TA: Recovery of storage and emptying functions of the urinary bladder after spinal anesthesia with lidocaine and with bupivacaine in men. Anesthesiology 1998; 88:310–6

53. Mulroy MF, Salinas FV, Larkin KL, Polissar NL: Ambulatory surgery patients may be discharged before voiding after short-acting spinal and epidural anesthesia. Anesthesiology 2002; 97:315–9

54. Petersen MS, Collins DN, Selakovich WG, Finkbeiner AE: Postoperative urinary retention associated with total hip and total knee arthroplasties. Clin Orthop Relat Res 1991; 269:102–8

55. Cashman JN, Dolin SJ: Respiratory and haemodynamic effects of acute postoperative pain management: Evidence from published data. Br J Anaesth 2004; 93:212–23

56. Matsuura S, Downie JW: Effect of anesthetics on reflex micturition in the chronic cannula-implanted rat. Neurourol Urodyn 2000; 19:87–99

57. Combrisson H, Robain G, Cotard JP: Comparative effects of xylazine and propofol on the urethral pressure profile of healthy dogs. Am J Vet Res 1993; 54:1986–9

58. Axelsson K, Mollefors K, Olsson JO, Lingardh G, Widman B: Bladder function in spinal anaesthesia. Acta Anaesthesiol Scand 1985; 29:315–21

59. Ryan JA Jr, Adye BA, Jolly PC, Mulroy MF 2nd: Outpatient inguinal herniorrhaphy with both regional and local anesthesia. Am J Surg 1984; 148:313–6

60. Bowen JR, Thompson WR, Dorman BA, Soderberg CH Jr, Shahinian TK: Change in the management of adult groin hernia. Am J Surg 1978; 135:564–9

61. Gupta A, Axelsson K, Thorn SE, Matthiessen P, Larsson LG, Holmstrom B, Wattwil M: Low-dose bupivacaine plus fentanyl for spinal anesthesia during ambulatory inguinal herniorrhaphy: A comparison between 6 mg and 7. 5 mg of bupivacaine. Acta Anaesthesiol Scand 2003; 47:13–9

62. Pawlowski J, Sukhani R, Pappas AL, Kim KM, Lurie J, Gunnerson H, Corsino A, Frey K, Tonino P: The anesthetic and recovery profile of two doses (60 and 80 mg) of plain mepivacaine for ambulatory spinal anesthesia. Anesth Analg 2000; 91:580–4

63. Liu SS, Ware PD, Allen HW, Neal JM, Pollock JE: Dose-response characteristics of spinal bupivacaine in volunteers. Clinical implications for ambulatory anesthesia. Anesthesiology 1996; 85:729–36

64. Ben-David B, Levin H, Solomon E, Admoni H, Vaida S: Spinal bupivacaine in ambulatory surgery: The effect of saline dilution. Anesth Analg 1996; 83:716–20

65. Esmaoglu A, Karaoglu S, Mizrak A, Boyaci A: Bilateral versus unilateral spinal anesthesia for outpatient knee arthroscopies. Knee Surg Sports Traumatol Arthrosc 2004; 12:155–8

66. Valanne JV, Korhonen AM, Jokela RM, Ravaska P, Korttila KK: Selective spinal anesthesia: A comparison of hyperbaric bupivacaine 4 mg versus 6 mg for outpatient knee arthroscopy. Anesth Analg 2001; 93:1377–9

67. Jellish WS, Thalji Z, Stevenson K, Shea J: A prospective randomized study comparing short- and intermediate-term perioperative outcome variables after spinal or general anesthesia for lumbar disk and laminectomy surgery. Anesth Analg 1996; 83:559–64

68. McLain RF, Kalfas I, Bell GR, Tetzlaff JE, Yoon HJ, Rana M: Comparison of spinal and general anesthesia in lumbar laminectomy surgery: A case-controlled analysis of 400 patients. J Neurosurg Spine 2005; 2:17–22

69. Rawal N, Mollefors K, Axelsson K, Lingardh G, Widman B: An experimental study of urodynamic effects of epidural morphine and of naloxone reversal. Anesth Analg 1983; 62:641–7

70. Drenger B, Magora F: Urodynamic studies after intrathecal fentanyl and buprenorphine in the dog. Anesth Analg 1989; 69:348–53

71. Kuipers PW, Kamphuis ET, van Venrooij GE, van Roy JP, Ionescu TI, Knape JT, Kalkman CJ: Intrathecal opioids and lower urinary tract function: A urodynamic evaluation. Anesthesiology 2004; 100:1497–503

72. Herman RM, Wainberg MC, del Giudice PF, Willscher MK: The effect of a low dose of intrathecal morphine on impaired micturition reflexes in human subjects with spinal cord lesions. Anesthesiology 1988; 69:313–8

73. Dray A, Metsch R: Morphine and the centrally-mediated inhibition of urinary bladder motility in the rat. Brain Res 1984; 297:191–5

74. Dray A, Metsch R: Opioid receptor subtypes involved in the central inhibition of urinary bladder motility. Eur J Pharmacol 1984; 104:47–53

75. Dray A, Metsch R: Spinal opioid receptors and inhibition of urinary bladder motility in vivo. Neurosci Lett 1984; 47:81–4

76. Dray A, Metsch R: Inhibition of urinary bladder contractions by a spinal action of morphine and other opioids. J Pharmacol Exp Ther 1984; 231:254–60

77. De Groat WC, Booth AM, Milne RJ, Roppolo JR: Parasympathetic preganglionic neurons in the sacral spinal cord. J Auton Nerv Syst 1982; 5:23–43

78. Ben-David B, Solomon E, Levin H, Admoni H, Goldik Z: Intrathecal fentanyl with small-dose dilute bupivacaine: Better anesthesia without prolonging recovery. Anesth Analg 1997; 85:560–5

79. Liu S, Chiu AA, Carpenter RL, Mulroy MF, Allen HW, Neal JM, Pollock JE: Fentanyl prolongs lidocaine spinal anesthesia without prolonging recovery. Anesth Analg 1995; 80:730–4

80. Ben-David B, Maryanovsky M, Gurevitch A, Lucyk C, Solosko D, Frankel R, Volpin G, DeMeo PJ: A comparison of minidose lidocaine-fentanyl and conventional-dose lidocaine spinal anesthesia. Anesth Analg 2000; 91:865–70

81. Mulroy MF, Larkin KL, Hodgson PS, Helman JD, Pollock JE, Liu SS: A comparison of spinal, epidural, and general anesthesia for outpatient knee arthroscopy. Anesth Analg 2000; 91:860–4

82. Korhonen AM, Valanne JV, Jokela RM, Ravaska P, Korttila K: Intrathecal hyperbaric bupivacaine 3 mg + fentanyl 10 microg for outpatient knee arthroscopy with tourniquet. Acta Anaesthesiol Scand 2003; 47:342–6

83. Faas CL, Acosta FJ, Campbell MD, O’Hagan CE, Newton SE, Zagalaniczny K: The effects of spinal anesthesia versus epidural anesthesia on 3 potential postoperative complications: Pain, urinary retention, and mobility following inguinal herniorrhaphy. Aana J 2002; 70:441–7

84. Turner G, Blake D, Buckland M, Chamley D, Dawson P, Goodchild C, Mezzatesta J, Scott D, Sultana A, Walker S, Hendrata M, Mooney P, Armstrong M: Continuous extradural infusion of ropivacaine for prevention of postoperative pain after major orthopaedic surgery. Br J Anaesth 1996; 76:606–10

85. Vercauteren MP, Van Den Bergh L, Kartawiadi SL, Van Boxem K, Hoffmann VL: Addition of bupivacaine to sufentanil in patient-controlled epidural analgesia after lower limb surgery in young adults: Effect on analgesia and micturition. Reg Anesth Pain Med 1998; 23:182–8

86. Conacher ID, Paes ML, Jacobson L, Phillips PD, Heaviside DW: Epidural analgesia following thoracic surgery. A review of two years’ experience. Anaesthesia 1983; 38:546–51

87. Bigler D, Dirkes W, Hansen R, Rosenberg J, Kehlet H: Effects of thoracic paravertebral block with bupivacaine versus combined thoracic epidural block with bupivacaine and morphine on pain and pulmonary function after cholecystectomy. Acta Anaesthesiol Scand 1989; 33:561–4

88. Leicht CH, Carlson SA: Prolongation of lidocaine spinal anesthesia with epinephrine and phenylephrine. Anesth Analg 1986; 65:365–9

89. Olofsson CI, Ekblom AO, Ekman-Ordeberg GE, Irestedt LE: Post-partum urinary retention: A comparison between two methods of epidural analgesia. Eur J Obstet Gynecol Reprod Biol 1997; 71:31–4

90. Husted S, Djurhuus JC, Husegaard HC, Jepsen J, Mortensen J: Effect of postoperative extradural morphine on lower urinary tract function. Acta Anaesthesiol Scand 1985; 29:183–5

91. Izard JP, Sowery RD, Jaeger MT, Siemens DR: Parameters affecting urologic complications after major joint replacement surgery. Can J Urol 2006; 13:3158–63

92. Bromage PR, Camporesi EM, Durant PA, Nielsen CH: Rostral spread of epidural morphine. Anesthesiology 1982; 56:431–6

93. Gustafsson LL, Friberg-Nielsen S, Garle M, Mohall A, Rane A, Schildt B, Symreng T: Extradural and parenteral morphine: Kinetics and effects in postoperative pain. A controlled clinical study. Br J Anaesth 1982; 54:1167–74

94. Reiz S, Ahlin J, Ahrenfeldt B, Andersson M, Andersson S: Epidural morphine for postoperative pain relief. Acta Anaesthesiol Scand 1981; 25:111–4

95. Rawal N, Arner S, Gustafsson LL, Allvin R: Present state of extradural and intrathecal opioid analgesia in Sweden. A nationwide follow-up survey. Br J Anaesth 1987; 59:791–9

96. Finucane BT, Ganapathy S, Carli F, Pridham JN, Ong BY, Shukla RC, Kristoffersson AH, Huizar KM, Nevin K, Ahlen KG: Prolonged epidural infusions of ropivacaine (2 mg/mL) after colonic surgery: The impact of adding fentanyl. Anesth Analg 2001; 92:1276–85

97. Torda TA, Pybus DA: Comparison of four narcotic analgesics for extradural analgesia. Br J Anaesth 1982; 54:291–5

98. Rawal N, Mollefors K, Axelsson K, Lingardh G, Widman B: Naloxone reversal of urinary retention after epidural morphine. Lancet 1981; 2:1411

99. Martin R, Salbaing J, Blaise G, Tetrault JP, Tetreault L: Epidural morphine for postoperative pain relief: A dose-response curve. Anesthesiology 1982; 56:423–6

100. Stenseth R, Sellevold O, Breivik H: Epidural morphine for postoperative pain: Experience with 1,085 patients. Acta Anaesthesiol Scand 1985; 29:148–56

101. Kim JY, Lee SJ, Koo BN, Noh SH, Kil HK, Kim HS, Ban SY: The effect of epidural sufentanil in ropivacaine on urinary retention in patients undergoing gastrectomy. Br J Anaesth 2006; 97:414–8

102. Lanz E, Simko G, Theiss D, Glocke MH: Epidural buprenorphine: A double-blind study of postoperative analgesia and side effects. Anesth Analg 1984; 63:593–8

103. Rucci FS, Cardamone M, Migliori P: Fentanyl and bupivacaine mixtures for extradural blockade. Br J Anaesth 1985; 57:275–84

104. Niemi L, Pitkanen M, Tuominen M, Rosenberg PH: Technical problems and side effects associated with continuous intrathecal or epidural post-operative analgesia in patients undergoing hip arthroplasty. Eur J Anaesthesiol 1994; 11:469–74

105. Niemi G, Breivik H: Epinephrine markedly improves thoracic epidural analgesia produced by a small-dose infusion of ropivacaine, fentanyl, and epinephrine after major thoracic or abdominal surgery: A randomized, double-blinded crossover study with and without epinephrine. Anesth Analg 2002; 94:1598–605

106. Asantila R, Rosenberg PH, Scheinin B: Comparison of different methods of postoperative analgesia after thoracotomy. Acta Anaesthesiol Scand 1986; 30:421–5

107. Gurel A, Unal N, Elevli M, Eren A: Epidural morphine for postoperative pain relief in anorectal surgery. Anesth Analg 1986; 65:499–502

108. Gedney JA, Liu EH: Side-effects of epidural infusions of opioid bupivacaine mixtures. Anaesthesia 1998; 53:1148–55

109. Reiz S, Westberg M: Side-effects of epidural morphine. Lancet 1980; 2:203–4

110. Ahuja BR, Strunin L: Respiratory effects of epidural fentanyl. Changes in end-tidal CO2 and respiratory rate following single doses and continuous infusions of epidural fentanyl. Anaesthesia 1985; 40:949–55

111. Evron S, Samueloff A, Simon A, Drenger B, Magora F: Urinary function during epidural analgesia with methadone and morphine in post-cesarean section patients. Pain 1985; 23:135–44

112. Paulsen EK, Porter MG, Helmer SD, Linhardt PW, Kliewer ML: Thoracic epidural versus patient-controlled analgesia in elective bowel resections. Am J Surg 2001; 182:570–7

113. Blanco J, Blanco E, Rodriguez G, Castro A, Alvarez J: One year’s experience with an acute pain service in a Spanish University Clinic hospital. Eur J Anaesthesiol 1994; 11:417–21

114. Barretto de Carvalho Fernandes Mdo C, Vieira da Costa V, Saraiva RA: Postoperative urinary retention: Evaluation of patients using opioids analgesic. Rev Lat Am Enfermagem 2007; 15:318–22

115. Carli F, Mayo N, Klubien K, Schricker T, Trudel J, Belliveau P: Epidural analgesia enhances functional exercise capacity and health-related quality of life after colonic surgery: Results of a randomized trial. Anesthesiology 2002; 97:540–9

116. Senagore AJ, Delaney CP, Mekhail N, Dugan A, Fazio VW: Randomized clinical trial comparing epidural anaesthesia and patient-controlled analgesia after laparoscopic segmental colectomy. Br J Surg 2003; 90:1195–9

117. Singelyn FJ, Ferrant T, Malisse MF, Joris D: Effects of intravenous patient-controlled analgesia with morphine, continuous epidural analgesia, and continuous femoral nerve sheath block on rehabilitation after unilateral total-hip arthroplasty. Reg Anesth Pain Med 2005; 30:452–7

118. Capdevila X, Barthelet Y, Biboulet P, Ryckwaert Y: Effects of perioperative analgesic technique on the surgical outcome and duration of rehabilitation after major knee surgery. Anesthesiology 1999;91:8–15

119. Wu CL, Cohen SR, Richman JM, Rowlingson AJ, Courpas GE, Cheung K, Lin EE, Liu SS: Efficacy of postoperative patient-controlled and continuous infusion epidural analgesia versus intravenous patient-controlled analgesia with opioids: A meta-analysis. Anesthesiology 2005; 103:1079–88

120. Moore JM, Liu SS, Pollock JE, Neal JM, Knab JH: The effect of epinephrine on small-dose hyperbaric bupivacaine spinal anesthesia: Clinical implications for ambulatory surgery. Anesth Analg 1998; 86:973–7

121. Chiu AA, Liu S, Carpenter RL, Kasman GS, Pollock JE, Neal JM: The effects of epinephrine on lidocaine spinal anesthesia: A cross-over study. Anesth Analg 1995; 80:735–9

122. Baron CM, Kowalski SE, Greengrass R, Horan TA, Unruh HW, Baron CL: Epinephrine decreases postoperative requirements for continuous thoracic epidural fentanyl infusions. Anesth Analg 1996; 82:760–5

123. Musselwhite KL, Faris P, Moore K, Berci D, King KM: Use of epidural anesthesia and the risk of acute postpartum urinary retention. Am J Obstet Gynecol 2007; 196:472.e1–5

124. Lanz E, Theiss D, Riess W, Sommer U: Epidural morphine for postoperative analgesia: A double-blind study. Anesth Analg 1982; 61:236–40

125. Malinovsky JM, Le Normand L, Lepage JY, Malinge M, Cozian A, Pinaud M, Buzelin JM: The urodynamic effects of intravenous opioids and ketoprofen in humans. Anesth Analg 1998; 87:456–61

126. Javery KB, Ussery TW, Steger HG, Colclough GW: Comparison of morphine and morphine with ketamine for postoperative analgesia. Can J Anaesth 1996; 43:212–5

127. Fletcher D, Negre I, Barbin C, Francois A, Carreres C, Falgueirettes C, Barboteu A, Samii K: Postoperative analgesia with i.v. propacetamol and ketoprofen combination after disc surgery. Can J Anaesth 1997; 44:479–85

128. Varrassi G, Panella L, Piroli A, Marinangeli F, Varrassi S, Wolman I, Niv D: The effects of perioperative ketorolac infusion on postoperative pain and endocrine-metabolic response. Anesth Analg 1994; 78:514–9

129. Etches RC, Warriner CB, Badner N, Buckley DN, Beattie WS, Chan VW, Parsons D, Girard M: Continuous intravenous administration of ketorolac reduces pain and morphine consumption after total hip or knee arthroplasty. Anesth Analg 1995; 81:1175–80

130. Hernandez-Palazon J, Tortosa JA, Martinez-Lage JF, Perez-Flores D: Intravenous administration of propacetamol reduces morphine consumption after spinal fusion surgery. Anesth Analg 2001; 92:1473–6

131. Peduto VA, Ballabio M, Stefanini S: Efficacy of propacetamol in the treatment of postoperative pain. Morphine-sparing effect in orthopedic surgery. Italian Collaborative Group on Propacetamol. Acta Anaesthesiol Scand 1998; 42:293–8

132. Brown AR, Weiss R, Greenberg C, Flatow EL, Bigliani LU: Interscalene block for shoulder arthroscopy: Comparison with general anesthesia. Arthroscopy 1993; 9:295–300

133. Matthews PJ, Govenden V: Comparison of continuous paravertebral and extradural infusions of bupivacaine for pain relief after thoracotomy. Br J Anaesth 1989; 62:204–5

134. Marret E, Bazelly B, Taylor G, Lembert N, Deleuze A, Mazoit JX, Bonnet FJ: Paravertebral block with ropivacaine 0.5% versus systemic analgesia for pain relief after thoracotomy. Ann Thorac Surg 2005; 79:2109–13

135. Imbelloni LE, Vieira EM, Gouveia MA, Netinho JG, Spirandelli LD, Cordeiro JA: Pudendal block with bupivacaine for postoperative pain relief. Dis Colon Rectum 2007; 50:1656–61

136. Sanjay P, Woodward A: Inguinal hernia repair: Local or general anaesthesia? Ann R Coll Surg Engl 2007; 89:497–503

137. Young DV: Comparison of local, spinal, and general anesthesia for inguinal herniorrhaphy. Am J Surg 1987; 153:560–3

138. Peiper C, Tons C, Schippers E, Busch F, Schumpelick V: Local versus general anesthesia for Shouldice repair of the inguinal hernia. World J Surg 1994; 18:912–5

139. Jensen P, Mikkelsen T, Kehlet H: Postherniorrhaphy urinary retention–effect of local, regional, and general anesthesia: A review. Reg Anesth Pain Med 2002; 27:612–7

140. Weiss H, Badlani G: Effects of anesthesia on micturition and urodynamics. Int Anesthesiol Clin 1993; 31:1–24

141. Li S, Coloma M, White PF, Watcha MF, Chiu JW, Li H, Huber PJ Jr: Comparison of the costs and recovery profiles of three anesthetic techniques for ambulatory anorectal surgery. Anesthesiology 2000; 93:1225–30

142. Fleischer M, Marini CP, Statman R, Capella J, Shevde K: Local anesthesia is superior to spinal anesthesia for anorectal surgical procedures. Am Surg 1994; 60:812–5

143. Song D, Greilich NB, White PF, Watcha MF, Tongier WK: Recovery profiles and costs of anesthesia for outpatient unilateral inguinal herniorrhaphy. Anesth Analg 2000; 91:876–81

144. Finley RK Jr, Miller SF, Jones LM: Elimination of urinary retention following inguinal herniorrhaphy. Am Surg 1991; 57:486–8

145. Klein SM, Greengrass RA, Weltz C, Warner DS: Paravertebral somatic nerve block for outpatient inguinal herniorrhaphy: An expanded case report of 22 patients. Reg Anesth Pain Med 1998; 23:306–10

146. Chung F: Recovery pattern and home-readiness after ambulatory surgery. Anesth Analg 1995; 80:896–902

147. Pavlin DJ, Rapp SE, Polissar NL, Malmgren JA, Koerschgen M, Keyes H: Factors affecting discharge time in adult outpatients. Anesth Analg 1998; 87:816–26

148. Martinez OV, Civetta JM, Anderson K, Roger S, Murtha M, Malinin TI: Bacteriuria in the catheterized surgical intensive care patient. Crit Care Med 1986; 14:188–91

149. Platt R, Polk BF, Murdock B, Rosner B: Mortality associated with nosocomial urinary-tract infection. N Engl J Med 1982; 307:637–42

150. Sullivan NM, Sutter VL, Mims MM, Marsh VH, Finegold SM: Clinical aspects of bacteremia after manipulation of the genitourinary tract. J Infect Dis 1973; 127:49–55

151. Akhtar MS, Beere DM, Wright JT, MacRae KD: Is bladder catheterization really necessary before laparoscopy? Br J Obstet Gynaecol 1985; 92:1176–8

152. Michelson JD, Lotke PA, Steinberg ME: Urinary-bladder management after total joint-replacement surgery. N Engl J Med 1988; 319:321–6

153. Dobbs SP, Jackson SR, Wilson AM, Maplethorpe RP, Hammond RH: A prospective, randomized trial comparing continuous bladder drainage with catheterization at abdominal hysterectomy. Br J Urol 1997; 80:554–6

154. Kitada S, Wein AJ, Kato K, Levin RM: Effect of acute complete obstruction on the rabbit urinary bladder. J Urol 1989; 141:166–9

155. Yamanishi T, Yasuda K, Kamai T, Tsujii T, Sakakibara R, Uchiyama T, Yoshida K: Combination of a cholinergic drug and an alpha-blocker is more effective than monotherapy for the treatment of voiding difficulty in patients with underactive detrusor. Int J Urol 2004; 11:88–96

156. Goldman G, Leviav A, Mazor A, Kashtan H, Aladgem D, Greenstein A, Wiznitzer T: Alpha-adrenergic blocker for posthernioplasty urinary retention. Prevention and treatment. Arch Surg 1988; 123:35–6

157. Leventhal A, Pfau A: Pharmacologic management of postoperative overdistention of the bladder. Surg Gynecol Obstet 1978; 146:347–8

158. Goldman G, Kahn PJ, Kashtan H, Stadler J, Wiznitzer T: Prevention and treatment of urinary retention and infection after surgical treatment of the colon and rectum with alpha adrenergic blockers. Surg Gynecol Obstet 1988; 166:447–50

159. Shapiro J, Hoffmann J, Jersky J: A comparison of suprapubic and transurethral drainage for postoperative urinary retention in general surgical patients. Acta Chir Scand 1982; 148:323–7

160. David TS, Vrahas MS: Perioperative lower urinary tract infections and deep sepsis in patients undergoing total joint arthroplasty. J Am Acad Orthop Surg 2000; 8:66–74

161. Wille JC, Blusse van Oud Alblas A, Thewessen EA: Nosocomial catheter-associated bacteriuria: A clinical trial comparing two closed urinary drainage systems. J Hosp Infect 1993; 25:191–8

162. van der Wall E, Verkooyen RP, Mintjes-de Groot J, Oostinga J, van Dijk A, Hustinx WN, Verbrugh HA: Prophylactic ciprofloxacin for catheter-associated urinary-tract infection. Lancet 1992; 339:946–51

163. Hallbook O, Pahlman L, Krog M, Wexner SD, Sjodahl R: Randomized comparison of straight and colonic J pouch anastomosis after low anterior resection. Ann Surg 1996; 224:58–65

164. Ratnaval CD, Renwick P, Farouk R, Monson JR, Lee PW: Suprapubic versus transurethral catheterisation of males undergoing pelvic colorectal surgery. Int J Colorectal Dis 1996; 11:177–9

165. Sethia KK, Selkon JB, Berry AR, Turner CM, Kettlewell MG, Gough MH: Prospective randomized controlled trial of urethral versus suprapubic catheterization. Br J Surg 1987; 74:624–5

166. Basse L, Werner M, Kehlet H: Is urinary drainage necessary during continuous epidural analgesia after colonic resection? Reg Anesth Pain Med 2000; 25:498–501

167. Dunn TS, Shlay J, Forshner D: Are in-dwelling catheters necessary for 24 hours after hysterectomy? Am J Obstet Gynecol 2003; 189:435–7

168. Summitt RL Jr, Stovall TG, Bran DF: Prospective comparison of indwelling bladder catheter drainage versus no catheter after vaginal hysterectomy. Am J Obstet Gynecol 1994; 170:1815–8

169. Alessandri F, Mistrangelo E, Lijoi D, Ferrero S, Ragni N: A prospective, randomized trial comparing immediate versus delayed catheter removal following hysterectomy. Acta Obstet Gynecol Scand 2006; 85:716–20

170. Hakvoort RA, Elberink R, Vollebregt A, Ploeg T, Emanuel MH: How long should urinary bladder catheterisation be continued after vaginal prolapse surgery? A randomised controlled trial comparing short term versus long term catheterisation after vaginal prolapse surgery. BJOG 2004; 111:828–30

171. Chamberlain DH, Hopkins MP, Roberts JA, McGuire EJ, Morley GW, Wang CC: The effects of early removal of indwelling urinary catheter after radical hysterectomy. Gynecol Oncol 1991; 43:98–102

172. Coventry MB, Beckenbaugh RD, Nolan DR, Ilstrup DM: 2,012 total hip arthroplasties. A study of postoperative course and early complications. J Bone Joint Surg Am 1974; 56:273–84

173. Donovan TL, Gordon RO, Nagel DA: Urinary infections in total hip arthroplasty. Influences of prophylactic cephalosporins and catheterization. J Bone Joint Surg Am 1976; 58:1134–7

174. Eftekhar NS, Kiernan HA Jr, Stinchfield FE: Systemic and local complications following low-friction arthroplasty of the hip joint. A study of 800 consecutive operations. Arch Surg 1976; 111:150–5

175. Wroblewski BM, del Sel HJ: Urethral instrumentation and deep sepsis in total hip replacement. Clin Orthop Relat Res 1980; 146:209–12

176. Cruess RL, Bickel WS, von Kessler KL: Infections in total hips secondary to a primary source elsewhere. Clin Orthop Relat Res 1975; 106:99–101

177. Irvine R, Johnson BL Jr, Amstutz HC: The relationship of genitourinary tract procedures and deep sepsis after total hip replacements. Surg Gynecol Obstet 1974; 139:701–6

178. Ritter MA, Faris PM, Keating EM: Urinary tract catheterization protocols following total joint arthroplasty. Orthopedics 1989; 12:1085–7

179. Wilson JN: The treatment of pathological fractures with special reference to the use of major prosthetic replacement of bone. Ital J Orthop Traumatol 1975; Suppl 1:180–4

180. Surin VV, Sundholm K, Backman L: Infection after total hip replacement. With special reference to a discharge from the wound. J Bone Joint Surg Br 1983; 65:412–8

181. Wymenga AB, van Horn JR, Theeuwes A, Muytjens HL, Slooff TJ: Perioperative factors associated with septic arthritis after arthroplasty. Prospective multicenter study of 362 knee and 2,651 hip operations. Acta Orthop Scand 1992; 63:665–71

182. Redfern TR, Machin DG, Parsons KF, Owen R: Urinary retention in men after total hip arthroplasty. J Bone Joint Surg Am 1986; 68:1435–8

183. Walts LF, Kaufman RD, Moreland JR, Weiskopf M: Total hip arthroplasty. An investigation of factors related to postoperative urinary retention. Clin Orthop Relat Res 1985; 194:280–2

184. Kumar P, Mannan K, Chowdhury AM, Kong KC, Pati J: Urinary retention and the role of indwelling catheterization following total knee arthroplasty. Int Braz J Urol 2006; 32:31–4

185. Knight RM, Pellegrini VD Jr: Bladder management after total joint arthroplasty. J Arthroplasty 1996; 11:882–8

186. Carpiniello VL, Cendron M, Altman HG, Malloy TR, Booth R: Treatment of urinary complications after total joint replacement in elderly females. Urology 1988; 32:186–8

187. Iorio R, Whang W, Healy WL, Patch DA, Najibi S, Appleby D: The utility of bladder catheterization in total hip arthroplasty. Clin Orthop Relat Res 2005; 432:148–52

188. van den Brand IC, Castelein RM: Total joint arthroplasty and incidence of postoperative bacteriuria with an indwelling catheter or intermittent catheterization with one-dose antibiotic prophylaxis: A prospective randomized trial. J Arthroplasty 2001; 16:850–5

189. Mauerhan DR, Nelson CL, Smith DL, Fitzgerald RH Jr, Slama TG, Petty RW, Jones RE, Evans RP: Prophylaxis against infection in total joint arthroplasty. One day of cefuroxime compared with three days of cefazolin. J Bone Joint Surg Am 1994; 76:39–45

190. Iorio R, Healy WL, Patch DA, Appleby D: The role of bladder catheterization in total knee arthroplasty. Clin Orthop Relat Res 2000; 380:80–4

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