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ANALGESIA

The Effects of Spinal Anesthesia with Lidocaine and Sufentanil on Lower Urinary Tract Functions

Ed T. Kamphuis, MD, PhD^*, Peter W. Kuipers, MD, Ger E. van Venrooij, PhD, and Cor J. Kalkman, MD, PhD

From the *Department of Anesthesiology, Rijnstate Ziekenhuis, Arnhem; Department of Anesthesiology, Gelre Ziekenhuizen, Apeldoorn; Departments of Urology (GE van Vanrooij former fellow); and Anesthesiology, University Medical Center, Utrecht, The Netherlands.

Address correspondence and reprint requests to Ed T. Kamphuis, MD, PhD, Department of Anesthesiology, Rijnstate Ziekenhuis, Postbus 9555, 6800 TA Arnhem, The Netherlands. Address e-mail to ed.kamphuis{at}planet.nl.

Abstract

BACKGROUND: Spinal local anesthetics interrupt the micturition reflex; bladder function remains impaired until sensory block had regressed to the S3 segment. Intrathecal opioids cause dose-dependent suppression of detrusor contractility. We studied the effects of spinal anesthesia with a combination of lidocaine and sufentanil on lower urinary tract function.

METHODS: Filling cystometry was performed in 10 healthy young male patients undergoing elective lower limb orthopedic surgery. After baseline recordings, each patient received spinal anesthesia with 100 mg hyperbaric lidocaine combined with 20 µg sufentanil. In the postoperative phase, regressions of sensory and motor block were recorded and urodynamic measurements continued until the patient could void spontaneously without residual volume in the bladder.

RESULTS: The mean (sd) time to recovery of urge was 240 (37) min after spinal injection, but no patient was able to void at that time. Six patients experienced urge at the previously observed maximum bladder capacity when the sensory block had regressed to the second sacral segment (S2), in four patients to S3. Despite this urge, no detrusor contraction was recorded. The patients were able to completely empty the bladder 332 (52) min after spinal injection. The average time difference between recovery of urge and return of normal bladder emptying was 90 min.

CONCLUSION: Bladder contractility returns much later than recovery of sensory function in sacral dermatomes (S3) when hyperbaric lidocaine combined with sufentanil is used for spinal anesthesia.

Postoperative urinary retention occurs frequently after spinal anesthesia, with a reported incidence between 3% and 42%.1–6 Urinary retention is benign if the ability to void returns before the bladder becomes excessively distended.

In a study evaluating the effects of spinal anesthesia with 100 mg hyperbaric lidocaine or 10 mg hyperbaric bupivacaine on the storage and emptying functions of the lower urinary tract, the authors noted that detrusor functions (urge with spontaneous voiding without residual volumes) remained impaired until sensory blockade had regressed to the S3 segment.7

In a separate study investigating the effects of intrathecal morphine and sufentanil on functions of the lower urinary tract, it was noted that both opioids decreased bladder function by a dose-dependent effect on spinal receptors, which leads to suppression of detrusor contractility and decreased sensation of urge.8

Adding an opioid to the local anesthetic can adapt the spinal anesthetic to a specific type and duration of surgery. By using the synergistic analgestic effect of the opioid it is possible to create adequate spinal anesthesia for surgery with normally subtherapeutic doses of local anesthetics.9 However, urinary retention is a potentially harmful side effect of intrathecal opioids.10 The present study investigated the effects of spinal anesthesia with hyperbaric lidocaine combined with sufentanil on the storage and emptying functions of the lower urinary tract to evaluate recovery of the lower urinary tract function.

METHODS

After obtaining approval from the Committee on Medical Ethics of the University Medical Centre, Utrecht, and written informed consent, 10 male patients, aged 22 to 47 yr, classified as ASA I physical status, scheduled for elective minor orthopedic surgery of the lower limb using spinal anesthesia in ambulatory surgery settings were enrolled. No premedication was administered.

For the preanesthetic urodynamic examination the patients were transported to the urodynamic room where baseline electrocardiogram, arterial blood pressure and Spo₂ were recorded and cystometry catheters were placed.

Urodynamic Measurements
Cystometry is a method by which the pressure– volume relation of the bladder is measured and used to assess detrusor activity, urge sensation, bladder capacity and compliance. Before cystometry, a urethral catheter is placed and residual volume is measured. A residual volume over 10% of the cystometric capacity is defined as significant. The bladder is then filled. Bladder sensation is difficult to evaluate because of its subjective nature. It is usually assessed by questioning the patient in relation to the fullness of the bladder during cystometry, according to definitions of the urodynamic studies. Commonly used descriptive terms include the following: First desire to void. Normal desire to void—this is defined as the feeling that leads the patient to pass urine at the next convenient moment. Strong desire to void—this is defined as a persistent desire to void without the fear of leakage. Urgency—this is defined as a strong desire to void accompanied by a fear of leakage or fear of pain. Pain—pain during bladder filling or micturition is abnormal.

To measure the pressure in the abdomen, a catheter is inserted in the rectum. In clinical practice, intrarectal pressure appears to be a fair approximation of abdominal pressure. During filling and voiding, the pressure in the bladder (intravesical pressure) is measured using a separate urethral catheter. The detrusor pressure is that component of intravesical pressure that is created by forces in the bladder wall. It is estimated by subtracting abdominal pressure (rectal pressure) from intravesical pressure. During voiding the urethra opens to allow the bladder to empty. The urethra is fully relaxed and the urethral resistance is then at its lowest.

The urinary flow rate during voiding is defined as the volume of fluid expelled via the urethra per unit of time and is expressed in milliliters per second. Urinary flow rate is measured using a rotating disk uroflowmeter (standard equipment in general urologic practice). Flow rate is registered simultaneously with the pressures, Fig. 1. The maximum flow rate is the maximum measured value of the flow rate during voiding.11

View larger version (24K): [in this window] [in a new window]   Figure 1. The intravesical pressure (Pi) is the pressure within the bladder. The rectal pressure represents abdominal pressure (Pa). The detrusor pressure (Pd) is the intravesical pressure (Pi) minus the abdominal pressure (Pa): (Pd = Pi – Pa). The urinary flow rate during voiding is defined as the volume of fluid expelled via the urethra per unit of time and is expressed as milliliters per second.

In this study, bladder pressure was measured using a 5-French open ended urethral catheter and rectal pressure was measured using a 14-French open ended catheter. Both were expressed as centimeters of water. After emptying via the catheter, the bladder was filled with saline at 37°C, through a second 5-French urethral catheter, at a constant rate of 50 mL/min with the patient in the supine position. Filling was stopped when the patient had a strong desire to void without the fear of leakage. The volume in the bladder at this point was defined as the cystometric capacity and recorded. Voiding with simultaneous recording of pressures and flow was then performed in the standing position. The patient urinated around the catheters in the uroflowmeter. From the recordings, maximum urinary flow rate and detrusor pressure at maximum flow rate were estimated. The catheters in the bladder and rectum remained in situ until complete recovery of bladder function. Based on urodynamic data, we calculated detrusor contraction strength and urethral resistance factor when urinary flow was present and artifact-free tracings were available using the urethral resistance factor algorithm of Griffiths et al.12 The methods, definitions, and units of the urodynamic studies used were those proposed by the International Continence Society, except when specifically noted.11

After baseline cystometry was completed, the patients were transported to the adjacent orthopedic room. An IV cannula for infusion was inserted. A colloid solution (Gelofusine®), 6 mL/kg, was rapidly administered IV to prevent hypotension. The skin was swabbed with tincture of iodine and sterile drapes were applied. Dural puncture was performed with the patient in the sitting position at the L3-4 interspace by a midline approach using a 25-gauge pencil-point needle with the orifice directed cephalad. Spinal anesthesia was induced by injection of 2 mL 5% hyperbaric plain lidocaine combined with 20 µg sufentanil (0.4 mL of sufentanil 50 µg/mL) in 10 s. Subsequently, the patient was returned to the supine position.

The segmental level of sensory block to pinprick was assessed after 15 and 30 min. as well as lower extremity motor blockade. The pinprick sensation was tested on the trunk in the mid-axillary line and on the lower limb according to the lumbar and sacral dermatomes. The pinprick sensation was compared with a control stimulus on the upper chest just below the clavicle. Motor blockade was tested according to the Bromage score. (0: no motor blockade; 1: inability to raise the extended leg; 2: inability to flex the knee; 3: inability to flex the ankle). The gelofusine infusion was reduced to a rate of 1 mL · kg^–1 · h^–1 and allowed to infuse until the end of the operation.

When patients were unable to experience pain by testing the surgical field with a tweezers, spinal anesthesia was considered to be sufficient and the operation was started. Heart rate, arterial blood pressure, and Spo₂ were recorded at 5 min intervals.

After surgery, the patient was returned to the urodynamic room. Sensory segmental analgesia and lower extremity motor blockade were recorded every 30 min. When the sensory segmental analgesia had regressed to the L5 segment, the sensation of urge at previously recorded cystometric capacity was again studied with interval cystometrograms. Every 30 min, before filling the bladder with saline, the volume of urine accumulated in the bladder was estimated by emptying the bladder via the catheter. The urinary bladder was then refilled to the cystometric capacity, the sensation of urge was estimated and compared with the preanesthetic strong desire to void and spontaneous voiding of the bladder was attempted. If the urodynamic variables had not returned to baseline values, the urethral resistance factor and detrusor contractility, according to Griffiths et al.,12 were calculated and compared with the baseline values.

The duration of motor blockade was defined as the time from the spinal injection until total recovery of hip, knee, and ankle motility. Duration of detrusor blockade was defined as the time from spinal injection until complete recovery of bladder function (i.e., return of urge at cystometric capacity together with the ability to completely empty the bladder using the detrusor muscle exclusively).

After surgery, all patients were allowed free oral fluids, and both intake and urine production were recorded. The volume of urine accumulated in the bladder as measured before refilling the bladder every 30 min, plus the difference between emptied volume and filling volume at these time points, were recorded as the total volume of urine produced by the patient during the detrusor block.

Statistical Analysis
Results are expressed as mean (sd). Nonparametric Wilcoxon Ranks test was used to compare the differences. Probability values <0.05 were considered significant.

RESULTS

Demographic data with regard to age, height, and weight were 34 (9) yr, 182 (6) cm, and 82 (10) kg, respectively. All patients had a normal baseline electrocardiogram, arterial blood pressure, and Spo₂. No patient had residual volume in the bladder after the preanesthetic urodynamic examination. Spinal anesthesia was satisfactory for the performance of the surgical procedure in all patients. During the study, bradycardia, arterial hypotension, nausea or respiratory depression was not observed in any patient. Eight of the 10 patients developed mild pruritus. There was no need for additive analgesic or sedative drugs. Lower extremity motor function returned after 124 (40) min and the patients were able to ambulate at that time.

Detrusor pressure at maximum flow and maximum flow (mL/s) were similar to baseline values at return of the detrusor function (Table 1). The mean time of recovery of the urge sensation, strong desire to void, was 240 (37) minutes after injection of lidocaine and sufentanil (Table 2). However, no patient was able to void at that time. Despite a strong desire to void, no detrusor contractility was recorded. Six patients, in whom the sensory block had regressed to the second sacral segment, experienced strong desire to void at cystometric capacity. The remaining four patients experienced strong desire to void when the sensory block had regressed to the third sacral segment. The patients were able to completely empty the bladder 332 (52) min after spinal injection (Table 2). The difference in time between the recovery of the urge sensation and recovered emptying function of the detrusor was on average 91.6 (44) minutes (P = 0.005). In four patients we observed no detrusor contractility during this period, followed by return to preanesthetic contractility. In the remaining six patients, three phases were recorded in the following sequence: no detrusor contractility, reduced contractility and return to preanesthetic contractility (Fig. 2). In four of these six patients we were able to calculate urethral resistance factor and detrusor contraction strength at peak flow during the reduced detrusor contractility period and compared the responses to preanesthetic values (Table 3). In the remaining two patients, urethral resistance factor could not be calculated, due to extreme abdominal straining during the voiding efforts. This resulted in high abdominal pressures and expulsion of the urethral catheters and the necessity for replacement to allow further measurements for estimation of residual urine after every voiding attempt. The urethral resistance factor at peak flow was only slightly higher than the resistance factor at peak flow before anesthesia. However, the differences in detrusor contractility at peak flow between preanesthetic values and after administration of lidocaine and sufentanil were obvious (Table 3). As long as the urodynamic variables had not returned to baseline, all patients had residual urine in the bladder after every voiding attempt.

View larger version (10K): [in this window] [in a new window]   Figure 2. Recordings of intravesical pressure, abdominal pressure, detrusor pressure (intravesical pressure minus abdominal pressure), flow rate in one representative patient before and after spinal injection of lidocaine and sufentanil. A, Pressure flow study before anesthesia. B, T1= 0. Pressure flow study on attaining normal sensation at S3. The patient experiences urge, but is not able to void. There is no detrusor pressure. C, T2 = 30 min after T1. The patient experiences urge and is able to void with an intermittent flow. The detrusor pressure is low and there is residual urine. D, T3 = 60 min after T1. The patient experiences urge and is able to void with a continuous flow. The detrusor pressure is still low and the voiding time is longer than before anesthesia; also residual urine occurs. E, T4 = 90 min after T1. The urodynamic parameters have returned to baseline values. The pressure, flow and voiding time have returned to preoperative values, and there is no residual urine in the bladder.

DISCUSSION

In this urodynamic study, healthy young male patients recovering from spinal anesthesia with a combination of lidocaine and sufentanil experienced a strong desire to void at cystometric capacity when the segmental sensory block had regressed to S2/3, but were still unable to void at that time. The average time until the patients were able to completely empty the bladder was more than 5 h after injection. It is of interest that the duration of the detrusor blockade was 90 min longer than the time for recovery of the urge sensation.

During voiding, the detrusor contracts and propels urine through the urethra. Within myogenic range, residual free emptying of the bladder is ensured, because the potential work increases with the filling volume. The detrusor does not generate a specific pressure or a specific flow rate during voiding, but provides mechanical power. The bladder outlet determines how this power is divided into pressure and rate. There is an inverse relation between pressure and flow rate. For a given power, a high pressure can occur only in combination with a low flow rate and visa versa.13

The observed urodynamic effects after intrathecal injection of a combination of opioids and local anesthetics may reflect an additive or synergistic effect of the drugs. During the interval between recovery of the urge sensation and the return to normal voiding, we observed a gradual recovery of the detrusor contractility in six patients. The detrusor pressure increased step by step and the detrusor contraction lasted longer than before anesthesia; also, a residual volume was present after every voiding attempt in this period (Figs. 2B–D). In the remaining four patients, the detrusor (Fig. 2B) did not contract after recovery of the sensation of urge, and approached preanesthetic values only later, but without an intermediate phase. Possibly we missed either a brief intermediate phase, as a result of our 30 min measuring intervals, or there was an abrupt change from an acontractile detrusor muscle to normal contractility. During the intermediate phase in the other patients, the urethral resistance factor was only slightly higher than the preanesthetic value (Table 3). Apparently, the relaxation of the urethral muscles was not significantly affected by sufentanil. This agrees with the findings of our previous study in volunteers.8 We also observed a decreased detrusor contraction in the recovery period (Table 3). Since hyperbaric lidocaine or bupivacaine alone did not produce an acontractile detrusor nor an intermediate phase7 in which patients experienced urge but had diminished contractile functions, it is likely that sufentanil was responsible for this intermediate phase of decreased detrusor contractility. The pathophysiologic mechanism may be either bladder afferent blockade or sacral parasympathetic motor outflow inhibition. Although the urge sensation, strong desire to void, is subjectively determined, it is likely that spinal sufentanil affects the bladder sensation. This is in keeping with our previous findings with sole intrathecal administration of opioids in male volunteers, where the sensory input recovered before the detrusor contraction strength had returned to baseline values.8

Because all patients experienced a strong desire to void at cystometric capacity, our results suggest that the afferent pathway of the micturition reflex had recovered. It is, therefore, reasonable to assume that the sacral parasympathetic inhibition by intrathecal sufentanil may be the source of the reduced detrusor contractility. The impairment of the detrusor contraction strength can be explained by the results of several animal studies demonstrating that enkephalins are transported intra-axonally via the S2 ventral root to the parasympathetic bladder ganglia.14–16 Intrathecal administration of enkephalins produced inhibition of micturition and naloxone injected intrathecally blocked the inhibitory effects of the opiate peptides.15–17 Thus the enkephalin system exerts an inhibitory modulating effect on the release of acetylcholine.16

A limitation of this observational study is that we studied a relatively small group of healthy male patients, which may decrease its generalizability. Nonetheless, this urodynamic study generated new knowledge regarding the time course of urodynamic disturbances caused by intrathecal administration of a local anesthetic/opioid combination. This information may be useful to clinicians when discussing optimization of bladder recovery management.

The observed effects of the intrathecal combination of lidocaine and sufentanil on lower urinary tract function may have clinical implications. Patients may experience urge but may still not be able to void. If voiding is not achieved and the bladder becomes excessively distended, bladder catheterization is indicated. Even when the patients are able to void, there still may be abnormal bladder function and large residual volume is possible.

In conclusion, bladder contractility returns much later than recovery of sensory function in sacral dermatomes (S3) after hyperbaric lidocaine combined with sufentanil. Adequate postoperative monitoring seems required until the patient can void without residual volume when this combination medications is used for spinal anesthesia.

Footnotes

Accepted for publication July 18, 2008.

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