1982
DOI: 10.1093/bja/54.11.1175
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Urinary Retention During I.M. And Extradural Morphine Analgesia

Abstract: In the postoperative period fifty-six healthy patients undergoing cholecystectomy or operations for duodenal ulcer, received, in a randomized order, i.m., "high-level" or "low-level" extradural morphine. Thirty-five per cent in the i.m. group, 33% in the high-level group and 50% in the low-level group suffered urinary retention, in all cases within the first 24 h. The mean cumulative dose of morphine necessary for pain relief was in the same range (13.4-16.5 mg) during the first 2 h of therapy for all groups, … Show more

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Cited by 45 publications
(17 citation statements)
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“…The urodynamic effects of intrathecal opioid are mainly caused by the action on the opioid receptors in the spinal cord (l and d receptors) that decrease the parasympathetic firing in the sacral region and decrease the afferent inputs from the bladder to the spinal cord, and the rostral spread of opioid through the cerebrospinal fluid to the pontine micturition center [15]. Opioids interrupt the micturition reflex by several mechanisms, opioid analgesics reduce parasympathetic tone within the bladder, decreasing detrusor tone and permitting passive filling, They also impair perception of bladder fullness and the urge to void, decrease activity in the pelvic nerves by depressing preganglionic neurons in the sacral parasympathetic nucleus, cause detrusor-sphincter dyssynergy secondary to failure of sphincter relaxation [16], Opioid-mediated depression of bladder motility is largely secondary to action at the m-opioid receptor, and can be reversed by intravenous naloxone, which promotes detrusor contraction and sphincter relaxation [15].…”
Section: Discussionmentioning
confidence: 99%
“…The urodynamic effects of intrathecal opioid are mainly caused by the action on the opioid receptors in the spinal cord (l and d receptors) that decrease the parasympathetic firing in the sacral region and decrease the afferent inputs from the bladder to the spinal cord, and the rostral spread of opioid through the cerebrospinal fluid to the pontine micturition center [15]. Opioids interrupt the micturition reflex by several mechanisms, opioid analgesics reduce parasympathetic tone within the bladder, decreasing detrusor tone and permitting passive filling, They also impair perception of bladder fullness and the urge to void, decrease activity in the pelvic nerves by depressing preganglionic neurons in the sacral parasympathetic nucleus, cause detrusor-sphincter dyssynergy secondary to failure of sphincter relaxation [16], Opioid-mediated depression of bladder motility is largely secondary to action at the m-opioid receptor, and can be reversed by intravenous naloxone, which promotes detrusor contraction and sphincter relaxation [15].…”
Section: Discussionmentioning
confidence: 99%
“…3~ Urinary retention following intrathecal and epidural opioids is much more common than after intravenous or intramuscular administration of equivalent doses of opioid. [55][56][57] Urinary retention induced by intrathecal and epidural opioids is likely related to interaction with opioid receptors located in the sacral spinal cord. 55 This interaction promotes inhibition of sacral parasympathetic nervous system outflow which causes detntsor muscle relaxation and an increase in maximal bladder capacity leading to urinary retention.…”
Section: Urinary Retentionmentioning
confidence: 99%
“…According to Wall et al14 pain may be a contributory factor. Post‐delivery pain effects include an inability to contract the perineum and also to mount a detrusor contraction as well as the effects of a pain relief associated with the use of opiates on suppression of the parasympathetic nerve supply 15…”
Section: Pathophysiology and Consequencesmentioning
confidence: 99%