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      Effectiveness of intramuscular neostigmine to accelerate bladder emptying after spinal anesthesia

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          Abstract

          Purpose

          Postoperative urinary retention (POUR) is one of the most common complications following spinal anesthesia. Spinal anesthesia may influence urinary bladder function due to interruption of the micturition reflex. Urinary catheterization is the standard treatment of POUR. Urinary catheter insertion is an invasive procedure, which is associated with catheter-related infections, urethral trauma, and patient discomfort. The purpose of this study was to determine the effectiveness of intramuscular (IM) neostigmine to accelerate bladder emptying after spinal anesthesia.

          Patients and methods

          A total of 36 patients undergoing lower abdominal (except for pelvic, urologic, anorectal, and hernia surgery) and lower extremity surgery under spinal anesthesia were divided into two groups randomly (n=18), to either neostigmine (N) group or control (C) group. Neostigmine 0.5 mg (N group) or NaCl 0.9% (C group) was administered intramuscularly when Bromage score 0 and sensory level sacral two have been achieved. The time to first voiding after IM injection and the time to first voiding after spinal anesthesia were measured.

          Results

          The time to first voiding after IM injection was significantly faster ( P≤0.05) in the N group than that in the C group, with median time as 40 minutes (20–70 minutes) and 75 minutes (55–135 minutes), respectively. Time to first voiding after spinal anesthesia was also significantly faster ( P≤0.05) in the N group than that in the C group (mean of 280.8±66.6 minutes and 364.2±77.3 minutes, respectively).

          Conclusion

          IM neostigmine effectively accelerates bladder emptying after spinal anesthesia.

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          Most cited references 16

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          Postoperative urinary retention: anesthetic and perioperative considerations.

          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.
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            Recovery of storage and emptying functions of the urinary bladder after spinal anesthesia with lidocaine and with bupivacaine in men.

            The aim of this study was to evaluate and compare the effects of spinal anesthesia with lidocaine and with bupivacaine on urinary bladder function in healthy men who were scheduled for minor orthopaedic surgical procedures. Twenty men were randomly allocated to receive either bupivacaine or lidocaine. Before spinal anesthesia, filling cystometry was performed with the patient in the supine position and a pressure flow study was done with the patient in the standing position. After operation, cystometric measurements were continued until the patient could void urine spontaneously. The levels of analgesia and of motor blockade were recorded. The urge to void disappeared immediately after injection of the local anesthetics. There was no difference in the duration of lower extremity motor blockade between bupivacaine and lidocaine. Detrusor blockade lasted significantly longer in the bupivacaine group (means +/- SD, 460 +/- 60 min) than in the lidocaine group (235 +/- 30 min). Total fluid intake and urine volume accumulated during the detrusor blockade were significantly higher in the bupivacaine group than in the lidocaine group. In the bupivacaine group, the total volume of accumulated urine (875 +/- 385 ml) was also significantly higher than cystometric bladder capacity (505 +/- 120 ml) with the risk of over distension of the bladder. Spontaneous voiding of urine did not occur until segmental sensory analgesia had regressed to the third sacral segment. Spinal anesthesia with lidocaine and with bupivacaine causes a clinically significant disturbance of bladder function due to interruption of the micturition reflex. The urge to void disappears quickly and bladder function remains impaired until the block has regressed to the third sacral segment in all patients. With long-acting local anesthetics, the volume of accumulated urine may exceed the cystometric bladder capacity. With respect to recovery of urinary bladder function, the use of short-acting local anesthetics for spinal anesthesia seems to be preferable.
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              Muscarinic receptor subtypes modulating smooth muscle contractility in the urinary bladder.

              Normal physiological voiding as well as generation of abnormal bladder contractions in diseased states is critically dependent on acetylcholine-induced stimulation of contractile muscarinic receptors on the smooth muscle (detrusor) of the urinary bladder. Muscarinic receptor antagonists are efficacious in treating the symptoms of bladder hyperactivity, such as urge incontinence, although the usefulness of available drugs is limited by undesirable side-effects. Detrusor smooth muscle is endowed principally with M2 and M3 muscarinic receptors with the former predominating in number. M3 muscarinic receptors, coupled to stimulation of phosphoinositide turnover, mediate the direct contractile effects of acetylcholine in the detrusor. Emerging evidence suggests that M2 muscarinic receptors, via inhibition of adenylyl cyclase, cause smooth muscle contraction indirectly by inhibiting sympathetically (beta-adrenoceptor)-mediated relaxation. In certain diseased states, M2 receptors may also contribute to direct smooth muscle contraction. Other contractile mechanisms involving M2 muscarinic receptors, such as activation of a non-specific cationic channel and inactivation of potassium channels, may also be operative in the bladder and requires further investigation. From a therapeutic standpoint, combined blockade of M2 and M3 muscarinic receptors would seem to be ideal since this approach would evoke complete inhibition of cholinergically-evoked smooth muscle contractions. However, if either the M2 or M3 receptor assumes a greater pathophysiological role in disease states, then selective antagonism of only one of the two receptors may be the more rational approach. The ultimate therapeutic strategy is also influenced by the extent to which pre-junctional M1 facilitatory and M2 inhibitory muscarinic receptors regulate acetylcholine release and also which subtypes mediate the undesirable effects of muscarinic receptor blockade such as dry mouth. Finally, the consequence of muscarinic receptor blockade in the central nervous system on the micturition reflex, an issue which is poorly studied and seldom taken into consideration, should not be ignored.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                2018
                11 September 2018
                : 14
                : 1685-1689
                Affiliations
                Department of Anesthesiology and Intensive Care, Sanglah Hospital, Faculty of Medicine, Udayana University, Denpasar, Bali, Indonesia, gungthey84@ 123456yahoo.com
                Author notes
                Correspondence: A A Gde Putra Semara Jaya, Department of Anesthesiology and Intensive Care, Sanglah Hospital, Faculty of Medicine, Udayana University, Diponegoro Street, Denpasar 80114, Bali, Indonesia, Tel +62 36 125 7361, Fax +62 36 123 5980, Email gungthey84@ 123456yahoo.com
                Article
                tcrm-14-1685
                10.2147/TCRM.S176281
                6140733
                © 2018 Senapathi et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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