Sacral neuromodulation for Organophosphate-induced delayed neuropathy neurogenic lower urinary tract dysfunction: a case report

Sacral neuromodulation for Organophosphate-induced delayed neuropathy neurogenic lower urinary tract dysfunction: a case report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Sacral neuromodulation for Organophosphate-induced delayed neuropathy neurogenic lower urinary tract dysfunction: a case report Junjie Han, Dingliang Zhao, Shuqiang Feng, Xuesong Yang, Yinchun Wang, and 5 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-4439399/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 04 Oct, 2024 Read the published version in BMC Urology → Version 1 posted 11 You are reading this latest preprint version Abstract Background : Organophosphate-Induced Delayed Neuropathy (OPIDN) is a rare neurological disorder triggered by exposure to organophosphorus compounds. These compounds exert their neurotoxic effects by impacting the nervous system, leading to systemic manifestations. Urinary system symptoms are infrequently observed in clinical settings. Currently, effective therapeutic interventions for OPIDN-related urinary symptoms are lacking. Sacral nerve modulation therapy, an FDA-approved approach for managing lower urinary tract symptomatology, presents as a promising way. Herein, we present a case of OPIDN-induced lower urinary tract obstruction successfully treated with sacral nerve modulation therapy, resulting in substantial symptom relief. Case report : a 27-year-old male patient. He presented with severe bilateral hydronephrosis, attributed to low bladder compliance and accompanied by a fever persisting for 6 days. The patient's medical history revealed accidental ingestion of organophosphate pesticide (Dimethoate) with no concomitant underlying diseases. In consideration of the potential for OPIDN, surgical intervention in the form of sacral nerve I modulation was undertaken. Subsequent evaluation one month post-surgery revealed notable improvements in both bladder compliance and bilateral hydronephrosis, necessitating sacral nerve II surgery. Presently, following a 5-month follow-up period, the patient remains asymptomatic and in favorable health. Conclusion : This patient achieved long-term relief using Sacral neuromodulation. Organophosphate-induced delayed neuropathy (OPIDN) Sacral neuromodulation Neurogenic bladder Organophosphorus compounds Peripheral nerve axons Figures Figure 1 Figure 2 Figure 3 Figure 4 Background Organophosphorus compounds are a category of chemical substances widely utilized in agricultural and industrial sectors, garnering significant attention due to their inherent toxicity. Organophosphate poisoning manifests in both acute cholinergic crisis and an intermediate phase, with specific individuals vulnerable to organophosphate-induced delayed neuropathy (OPIDN). This neuropathy, triggered by organophosphorus compounds, entails neural damage extending beyond the confines of the central nervous system, implicating the peripheral nervous system as well. The regulation of lower urinary tract function primarily hinges on three sets of peripheral nerves, and any impairment or affliction of the nervous system can lead to lower urinary tract dysfunction. In the presented case, sacral nerve modulation effectively facilitated the transition of the patient's small-capacity, high-pressure bladder into a large-capacity, low-pressure bladder, thereby alleviating the patient's symptoms. Currently, research on organophosphate-induced delayed neuropathy concerning the urinary system remains relatively limited. This paper aims to provide additional insights into understanding and addressing this clinical challenge, while also fostering advancements in related research endeavors geared towards enhancing the quality of life for affected individuals. Case report A 27-year-old male, presented with intermittent low back pain and fever persisting for six days. Six days earlier, the patient had undergone a CT scan of the upper abdomen, along with routine blood and urine tests at a local hospital, due to back pain and fever. The results indicated severe hydronephrosis with ureteral dilatation in both kidneys, alongside elevated leukocyte counts. The diagnosis was bilateral hydronephrosis accompanied by a urinary tract infection. Despite receiving anti-infection treatment, the patient's symptoms persisted, necessitating admission to our hospital. Upon admission, the patient was administered anti-inflammatory treatment and fitted with an indwelling catheter for one week. One week later, a follow-up urologic CT examination revealed persistent hydronephrosis in both kidneys and the bilateral ureters, along with bladder wall thickening(Fig. 1 ). Further urodynamic examination identified multiple issues, including heightened bladder sensitivity, reduced compliance, a strong urge to urinate at a bladder volume of 140 ml, diminished contraction of the urethral sphincter, abdominal pressure-assisted voiding, a maximum urinary flow rate of 8 ml/s, and a residual urine volume of 300 ml. Urethrocystography revealed a characteristic "pear-shaped" bladder pattern (Fig. 2 ). The physical examination did not reveal any specific signs. The patient's medical history was not reported. At age 14, the patient accidentally ingested a poison known as Dimethoate and underwent dialysis treatment at a local hospital. Currently, the patient's renal function is normal. Based on medical history and auxiliary examinations, the patient was diagnosed with neurogenic bladder, low-compliance bladder, and vesicoureteral reflux. To resolve the patient's bilateral hydronephrosis, it was necessary to improve bladder compliance. In July 2023, our institution performed a phase I (test phase) sacral nerve electrical stimulation implantation on the patient(Fig. 3 ). Postoperative parameters recorded included a pulse width of 210 µs, voltage of 0.5 V, and frequency of 14 Hz. One month later, imaging and urodynamic studies showed an increase in bladder capacity from 150 ml before the test to 320 ml after the test, with no evidence of ureteral reflux. The maximum urinary flow rate improved from 8 ml/s before the test to 16 ml/s after the test, with a residual bladder volume of 5 ml. A comparison of cystography and urological CT findings indicated a reduction in bladder wall thickness and significant increases in bladder capacity and compliance post-test. Additionally, the characteristic 'pear-shaped' bladder morphology was no longer present(Fig. 4 ). The patient experienced significant symptomatic relief following the evaluation and was referred for the second stage of permanent stimulator implantation. As of now, after five months of follow-up, the patient has shown symptom improvement and positive outcomes. Discussion Organophosphate-induced delayed neuropathy (OPIDN) is a neurological disorder induced by exposure to organophosphorus compounds. The pathogenesis of delayed-onset peripheral neuropathy remains incompletely understood. Some researchers propose that exposure to organophosphorus compounds inhibits neurotoxic esterase (NTE) activity in axons, leading to their aging and disrupted energy metabolism in axonal transport. This disruption can impair transport, induce degenerative changes in axons, and potentially cause demyelinating disease[ 1 ]. Additionally, organophosphorus compounds are thought to disrupt calcium ion/calmodulin kinase II activity, resulting in disturbed calcium homeostasis and the degeneration of peripheral nerve axons[ 2 ]. Research indicates that exposure to organophosphorus compounds may result in peripheral nerve damage, manifesting after a latency period of 1–8 weeks as chronic progressive lesions[ 3 ]. A cohort epidemiological study using vibration sensitivity testing found that motor nerve conduction velocity (NCV) decreases following exposure to organophosphorus compounds[ 4 ], before the appearance of clinical signs of peripheral neuropathy or muscle weakness. The literature suggests that OPIDN begins with a latency period of 1 to 3 weeks, leading to a progressive phase characterized by motor-sensory neuropathy. This phase involves motor or sensory-motor weakness in the lower extremities. Subsequently, a resting phase occurs, allowing for partial recovery of motor functions. Ultimately, symptoms indicating the involvement of cones and the central nervous system intensify. Although less frequently discussed[ 5 ], OPIDN can also impact the urinary system. Urine storage and release are dependent on the activity of smooth and striated muscles in the bladder, urethra, and external urethral sphincter[ 6 ]. However, the coordination of these functions is regulated by a complex neural control system in the brain, spinal cord, and peripheral ganglia[ 7 ]. Regulation of these muscles is primarily managed by three groups of peripheral nerves: sacral parasympathetic, thoracolumbar sympathetic, and somatic nerves distributed bilaterally. Lower urinary tract dysfunction can result from nervous system injuries or diseases[ 8 ]. Urinary function is susceptible to a range of injuries, diseases, and chemicals impacting the nervous system[ 9 ]. Bladder dysfunction is often attributed to the degeneration of axons in peripheral and central nerves[ 10 ]. Thus, neurological mechanisms must be considered in the diagnosis and treatment of voiding disorders. The patient had a history of Dimethoate usage. Cystoscopy revealed no bladder outlet obstruction or other underlying conditions. Despite the absence of overt clinical symptoms, imaging findings indicated a chronic progression. Consequently, the patient's condition was deemed closely associated with Dimethoate use. The patient displayed high bladder pressure during storage and low urine flow rate during voiding, typical of a neurogenic bladder. Sacral neuromodulation, involving electrode placement in the S3 or S4 sacral foramen and continuous low-frequency electrical stimulation of the sacral nerves, is a therapeutic technique leading to the denervation of the bladder, urethral sphincter, and pelvic floor muscles[ 11 ]. It is currently FDA-approved for treating refractory overactive bladder (OAB), non-obstructive urinary retention (NOR), and fecal incontinence[ 12 ], and has shown effectiveness in treating neurogenic lower urinary tract dysfunction (NLUTD), interstitial cystitis, bladder pain syndrome (IC/BPS), and other bowel dysfunctions[ 13 , 14 ]. Neurogenic bladder, however, is a complex syndrome with various etiologies and factors, leading to diverse urodynamic and clinical manifestations. Thus, a thorough preoperative evaluation of neurogenic bladder across different clinical manifestations is crucial for positive postoperative outcomes. The primary goal in treating neurogenic bladder is to preserve upper urinary tract function[ 15 ]. Consequently, the main treatment objective was to enhance bladder compliance. In this instance, severe bladder hypo-compliance resulted in reduced bladder capacity and the development of bilateral hydronephrosis. The study noted an increase in maximum bladder capacity from 150 ml to 320 ml pre- and post-test period. Additionally, there was an 8 ml/s increase in the maximum urinary flow rate pre- and post-test period. CT scans demonstrated a significant reduction in bilateral hydronephrosis pre- and post-test periods. Bladder elasticity significantly improved, with no ureteral reflux observed. Consequently, progression to the second stage of permanent stimulator implantation was warranted. Ensuring treatment longevity necessitates strict management of the post-sacral neurotomy regimen. While there was an increase in bladder capacity and a decrease in residual urine volume post-test, studies indicate that patients previously experiencing chronic urinary retention, despite spontaneous urination post-implantation, continue to depend on abdominal pressure to void and remain at risk for hydronephrosis and vesicoureteral reflux[ 16 ]. Post-operatively, patients were advised to consume 1500 ml of water daily, maintain a urinary voiding diary, and undergo regular follow-ups and urodynamic evaluations. To prevent transient ureteric reflux, intermittent catheterization was recommended. Follow-up results were positively noted. Conclusion In this instance of OPIDN presenting as a neurogenic lower urinary tract disorder, sacral neuromodulation (SNM) effectively transformed the patient's small, high-pressure bladder into one with a larger capacity and lower pressure. This outcome, in conjunction with postoperative management, mitigated the patient's bilateral renal and ureteral hydronephrosis caused by reflux, thereby safeguarding the upper urinary tract. Consequently, SNM proves to be a safe and efficacious therapy for neurogenic bladder under these circumstances. Abbreviations OPIDN Organophosphate-Induced Delayed Neuropathy FDA Food and Drug Administration CT Computed tomography ML Milliliter US Microsecond V Volt HZ Hertz NTE Neurotoxic esterase NCV Nerve conduction velocity NOR Non-obstructive urinary retention NLUTD Neurogenic lower urinary tract dysfunction IC/BPS Interstitial cystitis/Bladder pain syndrome SNM Sacral neuromodulation Declarations Acknowledgements Thank for the patients in this research, thank for all the scholars in this article. Thank for all the teammates for supporting this research. We are also particularly grateful to our colleagues in The Second Affiliated Hospital of Jilin University for their contributions. Author contributions JJH, DLZ, ZHD: preparing manuscript. JJH, XSY, YCW, ZS, ZYD: patient management, providing diagnostic and treatment results. SQF, YZ: providing diagnostic and treatment results. RWL: Article Guidance. All authors contributed to the article and approved the submitted version. Funding Not applicable. Availability of data and materials All data generated or analyzed during this study are included in this published article. Ethics approval and consent to participate The study was conducted according to the guidelines of the Declaration of Helsinki and approved by the Ethics Committee of The Second Hospital of Jilin University (Changchun, China). Written informed consent was obtained from the patient. Consent for publication Written informed consent was obtained from the patient for publication of the data and images in this case report. Competing interests The authors declare that they have no competing interests. Publisher’s note All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. References Richardson RJ, Fink JK, Glynn P, Hufnagel RB, Makhaeva GF, Wijeyesakere SJ. Neuropathy target esterase (NTE/PNPLA6) and organophosphorus compound-induced delayed neurotoxicity (OPIDN). Adv Neurotoxicol. 2020;4:1–78. Ding Q, Fang S, Chen X, Wang Y, Li J, Tian F, et al. TRPA1 channel mediates organophosphate-induced delayed neuropathy. Cell Discovery. 2017;3:17024. Mendes PA, Pereira TC, Pina R, Santos R. Chlorpyrifos-induced delayed neurotoxicity with a rare presentation of flaccid quadriplegia: a diagnostic challenge. Eur J Case Rep Intern Med. 2018;5:751. Pannu AK, Bhalla A, Vishnu RI, Dhibar DP, Sharma N, Vijayvergiya R. Organophosphate induced delayed neuropathy after an acute cholinergic crisis in self-poisoning. Clin Toxicol (Phila Pa). 2021;59:488–92. Nayak P, Mallick AK, Mishra S, Panigrahy D. Organophosphorus-induced toxic myeloneuropathy: series of three adolescent patients with short review. J Pediatr Neurosci. 2019;14:42–5. Panicker JN, Fowler CJ, Kessler TM. Lower urinary tract dysfunction in the neurological patient: clinical assessment and management. Lancet Neurol. 2015;14:720–32. Tudor KI, Sakakibara R, Panicker JN. Neurogenic lower urinary tract dysfunction: evaluation and management. J Neurol. 2016;263:2555–64. Podnar S, Vodušek DB. Lower urinary tract dysfunction in patients with peripheral nervous system lesions. Handb Clin Neurol. 2015;130:203–24. New frontiers of basic science research in. neurogenic lower urinary tract dysfunction - PubMed. https://pubmed.ncbi.nlm.nih.gov/28716328/ . Accessed 13 Apr 2024. Smith PP, DeAngelis A, Kuchel GA. Detrusor expulsive strength is preserved, but responsiveness to bladder filling and urinary sensitivity is diminished in the aging mouse. Am J Physiol Regul Integr Comp Physiol. 2012;302:R577–586. Barboglio Romo PG, Gupta P. Peripheral and sacral neuromodulation in the treatment of neurogenic lower urinary tract dysfunction. Urol Clin N Am. 2017;44:453–61. Tanagho EA, Schmidt RA. Bladder pacemaker: scientific basis and clinical future. Urology. 1982;20:614–9. Hanno PM, Erickson D, Moldwin R, Faraday MM, American Urological Association. Diagnosis and treatment of interstitial cystitis/bladder pain syndrome: AUA guideline amendment. J Urol. 2015;193:1545–53. Moore CK, Rueb JJ, Derisavifard S. What is new in neuromodulation? Curr Urol Rep. 2019;20:55. Wiener JS, Chaudhry R. Neurogenic lower urinary tract dysfunction. Urol Clin N Am. 2023;50:415–32. Chen G, Liao L, Deng H. The effect of sacral neuromodulation in ambulatory spina bifida patients with neurogenic bladder and bowel dysfunction. Urology. 2021;153:345–50. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Published Journal Publication published 04 Oct, 2024 Read the published version in BMC Urology → Version 1 posted Editorial decision: Revision requested 19 Aug, 2024 Reviews received at journal 18 Aug, 2024 Reviewers agreed at journal 18 Aug, 2024 Reviews received at journal 08 Jun, 2024 Reviewers agreed at journal 29 May, 2024 Reviewers agreed at journal 28 May, 2024 Reviewers invited by journal 28 May, 2024 Editor invited by journal 27 May, 2024 Submission checks completed at journal 27 May, 2024 Editor assigned by journal 27 May, 2024 First submitted to journal 18 May, 2024 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-4439399","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":312051218,"identity":"25d8a0cb-4c8d-4c5f-87d2-e5400989af0e","order_by":0,"name":"Junjie Han","email":"","orcid":"","institution":"The Second Hospital of Jilin University","correspondingAuthor":false,"prefix":"","firstName":"Junjie","middleName":"","lastName":"Han","suffix":""},{"id":312051219,"identity":"5ec706c6-051e-49fc-ae82-ad1e2871937e","order_by":1,"name":"Dingliang Zhao","email":"","orcid":"","institution":"The First Hospital of Jilin 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reduction\u003cstrong\u003e(B)\u003c/strong\u003e\u003c/p\u003e","description":"","filename":"OnlineFig.1.png","url":"https://assets-eu.researchsquare.com/files/rs-4439399/v1/c79a2ebb2463a64c9d7b72e7.png"},{"id":58223632,"identity":"c498ae4d-09c3-41d4-88a1-0df104eef53c","added_by":"auto","created_at":"2024-06-12 17:25:23","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":1371798,"visible":true,"origin":"","legend":"\u003cp\u003eCystography demonstrating pear bladder\u003c/p\u003e","description":"","filename":"OnlineFig.2.png","url":"https://assets-eu.researchsquare.com/files/rs-4439399/v1/686b0f0b9443eecc4a85a190.png"},{"id":58223635,"identity":"d649d60a-9041-4182-80ab-8b4db492959b","added_by":"auto","created_at":"2024-06-12 17:25:23","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":2834500,"visible":true,"origin":"","legend":"\u003cp\u003eAfter electrical stimulation of sacral nerve implantation\u003c/p\u003e","description":"","filename":"OnlineFig.3.png","url":"https://assets-eu.researchsquare.com/files/rs-4439399/v1/049af0b9b60597c729f0e36b.png"},{"id":58223634,"identity":"c5dce4e3-2908-4400-b800-26f833639f25","added_by":"auto","created_at":"2024-06-12 17:25:23","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":2503847,"visible":true,"origin":"","legend":"\u003cp\u003ePosttreatment CT-Abdomen demonstrating hydronephrosis relief in both\u003c/p\u003e\n\u003cp\u003ekidneys and the bilateral ureters \u003cstrong\u003e(A)\u003c/strong\u003e and bladder wall thinning and bladder capacity\u003c/p\u003e\n\u003cp\u003eexpanding\u003cstrong\u003e(B)\u003c/strong\u003e. Cystography demonstrating pear bladder disappeared\u003cstrong\u003e(C)\u003c/strong\u003e\u003c/p\u003e","description":"","filename":"OnlineFig.4.png","url":"https://assets-eu.researchsquare.com/files/rs-4439399/v1/24eb1cf9f6b30c8f22a7eebf.png"},{"id":66097015,"identity":"887ef6ef-923e-4e53-871b-9f606ec68a96","added_by":"auto","created_at":"2024-10-07 16:12:40","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1419357,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-4439399/v1/81d5ec60-5486-4b1a-9f0b-fe99467f2bd4.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Sacral neuromodulation for Organophosphate-induced delayed neuropathy neurogenic lower urinary tract dysfunction: a case report","fulltext":[{"header":"Background","content":"\u003cp\u003eOrganophosphorus compounds are a category of chemical substances widely utilized in agricultural and industrial sectors, garnering significant attention due to their inherent toxicity. Organophosphate poisoning manifests in both acute cholinergic crisis and an intermediate phase, with specific individuals vulnerable to organophosphate-induced delayed neuropathy (OPIDN). This neuropathy, triggered by organophosphorus compounds, entails neural damage extending beyond the confines of the central nervous system, implicating the peripheral nervous system as well. The regulation of lower urinary tract function primarily hinges on three sets of peripheral nerves, and any impairment or affliction of the nervous system can lead to lower urinary tract dysfunction.\u003c/p\u003e \u003cp\u003eIn the presented case, sacral nerve modulation effectively facilitated the transition of the patient's small-capacity, high-pressure bladder into a large-capacity, low-pressure bladder, thereby alleviating the patient's symptoms. Currently, research on organophosphate-induced delayed neuropathy concerning the urinary system remains relatively limited. This paper aims to provide additional insights into understanding and addressing this clinical challenge, while also fostering advancements in related research endeavors geared towards enhancing the quality of life for affected individuals.\u003c/p\u003e"},{"header":"Case report","content":"\u003cp\u003eA 27-year-old male, presented with intermittent low back pain and fever persisting for six days. Six days earlier, the patient had undergone a CT scan of the upper abdomen, along with routine blood and urine tests at a local hospital, due to back pain and fever. The results indicated severe hydronephrosis with ureteral dilatation in both kidneys, alongside elevated leukocyte counts. The diagnosis was bilateral hydronephrosis accompanied by a urinary tract infection. Despite receiving anti-infection treatment, the patient's symptoms persisted, necessitating admission to our hospital. Upon admission, the patient was administered anti-inflammatory treatment and fitted with an indwelling catheter for one week. One week later, a follow-up urologic CT examination revealed persistent hydronephrosis in both kidneys and the bilateral ureters, along with bladder wall thickening(Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e). Further urodynamic examination identified multiple issues, including heightened bladder sensitivity, reduced compliance, a strong urge to urinate at a bladder volume of 140 ml, diminished contraction of the urethral sphincter, abdominal pressure-assisted voiding, a maximum urinary flow rate of 8 ml/s, and a residual urine volume of 300 ml. Urethrocystography revealed a characteristic \"pear-shaped\" bladder pattern (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). The physical examination did not reveal any specific signs. The patient's medical history was not reported. At age 14, the patient accidentally ingested a poison known as Dimethoate and underwent dialysis treatment at a local hospital. Currently, the patient's renal function is normal.\u003c/p\u003e \u003cp\u003eBased on medical history and auxiliary examinations, the patient was diagnosed with neurogenic bladder, low-compliance bladder, and vesicoureteral reflux. To resolve the patient's bilateral hydronephrosis, it was necessary to improve bladder compliance. In July 2023, our institution performed a phase I (test phase) sacral nerve electrical stimulation implantation on the patient(Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e). Postoperative parameters recorded included a pulse width of 210 \u0026micro;s, voltage of 0.5 V, and frequency of 14 Hz. One month later, imaging and urodynamic studies showed an increase in bladder capacity from 150 ml before the test to 320 ml after the test, with no evidence of ureteral reflux. The maximum urinary flow rate improved from 8 ml/s before the test to 16 ml/s after the test, with a residual bladder volume of 5 ml. A comparison of cystography and urological CT findings indicated a reduction in bladder wall thickness and significant increases in bladder capacity and compliance post-test. Additionally, the characteristic 'pear-shaped' bladder morphology was no longer present(Fig.\u0026nbsp;\u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003e). The patient experienced significant symptomatic relief following the evaluation and was referred for the second stage of permanent stimulator implantation. As of now, after five months of follow-up, the patient has shown symptom improvement and positive outcomes.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eOrganophosphate-induced delayed neuropathy (OPIDN) is a neurological disorder induced by exposure to organophosphorus compounds. The pathogenesis of delayed-onset peripheral neuropathy remains incompletely understood. Some researchers propose that exposure to organophosphorus compounds inhibits neurotoxic esterase (NTE) activity in axons, leading to their aging and disrupted energy metabolism in axonal transport. This disruption can impair transport, induce degenerative changes in axons, and potentially cause demyelinating disease[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Additionally, organophosphorus compounds are thought to disrupt calcium ion/calmodulin kinase II activity, resulting in disturbed calcium homeostasis and the degeneration of peripheral nerve axons[\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eResearch indicates that exposure to organophosphorus compounds may result in peripheral nerve damage, manifesting after a latency period of 1\u0026ndash;8 weeks as chronic progressive lesions[\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. A cohort epidemiological study using vibration sensitivity testing found that motor nerve conduction velocity (NCV) decreases following exposure to organophosphorus compounds[\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e], before the appearance of clinical signs of peripheral neuropathy or muscle weakness. The literature suggests that OPIDN begins with a latency period of 1 to 3 weeks, leading to a progressive phase characterized by motor-sensory neuropathy. This phase involves motor or sensory-motor weakness in the lower extremities. Subsequently, a resting phase occurs, allowing for partial recovery of motor functions. Ultimately, symptoms indicating the involvement of cones and the central nervous system intensify. Although less frequently discussed[\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e], OPIDN can also impact the urinary system.\u003c/p\u003e \u003cp\u003eUrine storage and release are dependent on the activity of smooth and striated muscles in the bladder, urethra, and external urethral sphincter[\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. However, the coordination of these functions is regulated by a complex neural control system in the brain, spinal cord, and peripheral ganglia[\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. Regulation of these muscles is primarily managed by three groups of peripheral nerves: sacral parasympathetic, thoracolumbar sympathetic, and somatic nerves distributed bilaterally. Lower urinary tract dysfunction can result from nervous system injuries or diseases[\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. Urinary function is susceptible to a range of injuries, diseases, and chemicals impacting the nervous system[\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. Bladder dysfunction is often attributed to the degeneration of axons in peripheral and central nerves[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. Thus, neurological mechanisms must be considered in the diagnosis and treatment of voiding disorders.\u003c/p\u003e \u003cp\u003eThe patient had a history of Dimethoate usage. Cystoscopy revealed no bladder outlet obstruction or other underlying conditions. Despite the absence of overt clinical symptoms, imaging findings indicated a chronic progression. Consequently, the patient's condition was deemed closely associated with Dimethoate use. The patient displayed high bladder pressure during storage and low urine flow rate during voiding, typical of a neurogenic bladder.\u003c/p\u003e \u003cp\u003eSacral neuromodulation, involving electrode placement in the S3 or S4 sacral foramen and continuous low-frequency electrical stimulation of the sacral nerves, is a therapeutic technique leading to the denervation of the bladder, urethral sphincter, and pelvic floor muscles[\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]. It is currently FDA-approved for treating refractory overactive bladder (OAB), non-obstructive urinary retention (NOR), and fecal incontinence[\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e], and has shown effectiveness in treating neurogenic lower urinary tract dysfunction (NLUTD), interstitial cystitis, bladder pain syndrome (IC/BPS), and other bowel dysfunctions[\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e, \u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e]. Neurogenic bladder, however, is a complex syndrome with various etiologies and factors, leading to diverse urodynamic and clinical manifestations. Thus, a thorough preoperative evaluation of neurogenic bladder across different clinical manifestations is crucial for positive postoperative outcomes. The primary goal in treating neurogenic bladder is to preserve upper urinary tract function[\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e]. Consequently, the main treatment objective was to enhance bladder compliance. In this instance, severe bladder hypo-compliance resulted in reduced bladder capacity and the development of bilateral hydronephrosis. The study noted an increase in maximum bladder capacity from 150 ml to 320 ml pre- and post-test period. Additionally, there was an 8 ml/s increase in the maximum urinary flow rate pre- and post-test period. CT scans demonstrated a significant reduction in bilateral hydronephrosis pre- and post-test periods. Bladder elasticity significantly improved, with no ureteral reflux observed. Consequently, progression to the second stage of permanent stimulator implantation was warranted.\u003c/p\u003e \u003cp\u003eEnsuring treatment longevity necessitates strict management of the post-sacral neurotomy regimen. While there was an increase in bladder capacity and a decrease in residual urine volume post-test, studies indicate that patients previously experiencing chronic urinary retention, despite spontaneous urination post-implantation, continue to depend on abdominal pressure to void and remain at risk for hydronephrosis and vesicoureteral reflux[\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]. Post-operatively, patients were advised to consume 1500 ml of water daily, maintain a urinary voiding diary, and undergo regular follow-ups and urodynamic evaluations. To prevent transient ureteric reflux, intermittent catheterization was recommended. Follow-up results were positively noted.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eIn this instance of OPIDN presenting as a neurogenic lower urinary tract disorder, sacral neuromodulation (SNM) effectively transformed the patient's small, high-pressure bladder into one with a larger capacity and lower pressure. This outcome, in conjunction with postoperative management, mitigated the patient's bilateral renal and ureteral hydronephrosis caused by reflux, thereby safeguarding the upper urinary tract. Consequently, SNM proves to be a safe and efficacious therapy for neurogenic bladder under these circumstances.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eOPIDN\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Organophosphate-Induced Delayed Neuropathy\u003c/p\u003e\n\u003cp\u003eFDA\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Food and Drug Administration\u003c/p\u003e\n\u003cp\u003eCT\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Computed tomography\u003c/p\u003e\n\u003cp\u003eML\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Milliliter\u003c/p\u003e\n\u003cp\u003eUS\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Microsecond\u003c/p\u003e\n\u003cp\u003eV\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Volt\u003c/p\u003e\n\u003cp\u003eHZ\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Hertz\u003c/p\u003e\n\u003cp\u003eNTE\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Neurotoxic esterase\u003c/p\u003e\n\u003cp\u003eNCV\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Nerve conduction velocity\u003c/p\u003e\n\u003cp\u003eNOR\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Non-obstructive urinary retention\u003c/p\u003e\n\u003cp\u003eNLUTD\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Neurogenic lower urinary tract dysfunction\u003c/p\u003e\n\u003cp\u003eIC/BPS\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Interstitial cystitis/Bladder pain syndrome\u003c/p\u003e\n\u003cp\u003eSNM \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; Sacral neuromodulation\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003eAcknowledgements\u003c/p\u003e\n\u003cp\u003eThank for the patients in this research, thank for all the scholars in this article. Thank for all the teammates for supporting this research. We are also particularly grateful to our colleagues in The Second Affiliated Hospital of Jilin University for their contributions.\u003c/p\u003e\n\u003cp\u003eAuthor contributions\u003c/p\u003e\n\u003cp\u003eJJH, DLZ, ZHD: preparing manuscript. JJH, XSY, YCW, ZS, ZYD: patient management, providing diagnostic and treatment results. SQF, YZ: providing diagnostic and treatment results. RWL: Article Guidance. All authors contributed to the article and approved the submitted version.\u003c/p\u003e\n\u003cp\u003eFunding\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003eAvailability of data and materials\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eAll data generated or analyzed during this study are included in this published article.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eEthics approval and consent to participate\u003c/p\u003e\n\u003cp\u003eThe study was conducted according to the guidelines of the Declaration of Helsinki and approved by the Ethics Committee of The Second Hospital of Jilin University (Changchun, China). Written informed consent was obtained from the patient.\u003c/p\u003e\n\u003cp\u003eConsent for publication\u003c/p\u003e\n\u003cp\u003eWritten informed consent was obtained from the patient for publication of the data and images in this case report.\u003c/p\u003e\n\u003cp\u003eCompeting interests\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003ePublisher\u0026rsquo;s note\u003c/p\u003e\n\u003cp\u003eAll claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eRichardson RJ, Fink JK, Glynn P, Hufnagel RB, Makhaeva GF, Wijeyesakere SJ. Neuropathy target esterase (NTE/PNPLA6) and organophosphorus compound-induced delayed neurotoxicity (OPIDN). Adv Neurotoxicol. 2020;4:1\u0026ndash;78.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDing Q, Fang S, Chen X, Wang Y, Li J, Tian F, et al. TRPA1 channel mediates organophosphate-induced delayed neuropathy. Cell Discovery. 2017;3:17024.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMendes PA, Pereira TC, Pina R, Santos R. Chlorpyrifos-induced delayed neurotoxicity with a rare presentation of flaccid quadriplegia: a diagnostic challenge. Eur J Case Rep Intern Med. 2018;5:751.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePannu AK, Bhalla A, Vishnu RI, Dhibar DP, Sharma N, Vijayvergiya R. Organophosphate induced delayed neuropathy after an acute cholinergic crisis in self-poisoning. Clin Toxicol (Phila Pa). 2021;59:488\u0026ndash;92.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNayak P, Mallick AK, Mishra S, Panigrahy D. Organophosphorus-induced toxic myeloneuropathy: series of three adolescent patients with short review. J Pediatr Neurosci. 2019;14:42\u0026ndash;5.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePanicker JN, Fowler CJ, Kessler TM. Lower urinary tract dysfunction in the neurological patient: clinical assessment and management. Lancet Neurol. 2015;14:720\u0026ndash;32.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTudor KI, Sakakibara R, Panicker JN. Neurogenic lower urinary tract dysfunction: evaluation and management. J Neurol. 2016;263:2555\u0026ndash;64.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePodnar S, Vodušek DB. Lower urinary tract dysfunction in patients with peripheral nervous system lesions. Handb Clin Neurol. 2015;130:203\u0026ndash;24.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNew frontiers of basic science research in. neurogenic lower urinary tract dysfunction - PubMed. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://pubmed.ncbi.nlm.nih.gov/28716328/\u003c/span\u003e\u003cspan address=\"https://pubmed.ncbi.nlm.nih.gov/28716328/\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e. Accessed 13 Apr 2024.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSmith PP, DeAngelis A, Kuchel GA. Detrusor expulsive strength is preserved, but responsiveness to bladder filling and urinary sensitivity is diminished in the aging mouse. Am J Physiol Regul Integr Comp Physiol. 2012;302:R577\u0026ndash;586.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBarboglio Romo PG, Gupta P. Peripheral and sacral neuromodulation in the treatment of neurogenic lower urinary tract dysfunction. Urol Clin N Am. 2017;44:453\u0026ndash;61.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTanagho EA, Schmidt RA. Bladder pacemaker: scientific basis and clinical future. Urology. 1982;20:614\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHanno PM, Erickson D, Moldwin R, Faraday MM, American Urological Association. Diagnosis and treatment of interstitial cystitis/bladder pain syndrome: AUA guideline amendment. J Urol. 2015;193:1545\u0026ndash;53.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMoore CK, Rueb JJ, Derisavifard S. What is new in neuromodulation? Curr Urol Rep. 2019;20:55.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWiener JS, Chaudhry R. Neurogenic lower urinary tract dysfunction. Urol Clin N Am. 2023;50:415\u0026ndash;32.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eChen G, Liao L, Deng H. The effect of sacral neuromodulation in ambulatory spina bifida patients with neurogenic bladder and bowel dysfunction. Urology. 2021;153:345\u0026ndash;50.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-urology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"buro","sideBox":"Learn more about [BMC Urology](http://bmcurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/buro/default.aspx","title":"BMC Urology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Organophosphate-induced delayed neuropathy (OPIDN), Sacral neuromodulation, Neurogenic bladder, Organophosphorus compounds, Peripheral nerve axons","lastPublishedDoi":"10.21203/rs.3.rs-4439399/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-4439399/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground\u003c/strong\u003e: Organophosphate-Induced Delayed Neuropathy (OPIDN) is a rare neurological disorder triggered by exposure to organophosphorus compounds. These compounds exert their neurotoxic effects by impacting the nervous system, leading to systemic manifestations. Urinary system symptoms are infrequently observed in clinical settings. Currently, effective therapeutic interventions for OPIDN-related urinary symptoms are lacking. Sacral nerve modulation therapy, an FDA-approved approach for managing lower urinary tract symptomatology, presents as a promising way. Herein, we present a case of OPIDN-induced lower urinary tract obstruction successfully treated with sacral nerve modulation therapy, resulting in substantial symptom relief.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCase report\u003c/strong\u003e: a 27-year-old male patient. He presented with severe bilateral hydronephrosis, attributed to low bladder compliance and accompanied by a fever persisting for 6 days. The patient's medical history revealed accidental ingestion of organophosphate pesticide (Dimethoate) with no concomitant underlying diseases. In consideration of the potential for OPIDN, surgical intervention in the form of sacral nerve I modulation was undertaken. Subsequent evaluation one month post-surgery revealed notable improvements in both bladder compliance and bilateral hydronephrosis, necessitating sacral nerve II surgery. Presently, following a 5-month follow-up period, the patient remains asymptomatic and in favorable health.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusion\u003c/strong\u003e: This patient achieved long-term relief using Sacral neuromodulation.\u003c/p\u003e","manuscriptTitle":"Sacral neuromodulation for Organophosphate-induced delayed neuropathy neurogenic lower urinary tract dysfunction: a case report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2024-06-12 17:25:18","doi":"10.21203/rs.3.rs-4439399/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2024-08-19T15:08:47+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2024-08-18T14:06:19+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"176261782168777148929711565141068903512","date":"2024-08-18T14:01:15+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2024-06-08T09:56:34+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"206709157819474193647576335885909890662","date":"2024-05-29T08:57:28+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"145898395300601883596203539899167345839","date":"2024-05-28T13:48:02+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2024-05-28T13:43:13+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2024-05-27T16:33:19+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2024-05-27T16:32:06+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2024-05-27T16:32:06+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Urology","date":"2024-05-18T04:51:34+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-urology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"buro","sideBox":"Learn more about [BMC Urology](http://bmcurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/buro/default.aspx","title":"BMC Urology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"3d846321-bb37-4b3d-8342-0386056e5671","owner":[],"postedDate":"June 12th, 2024","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[],"tags":[],"updatedAt":"2024-10-07T16:05:33+00:00","versionOfRecord":{"articleIdentity":"rs-4439399","link":"https://doi.org/10.1186/s12894-024-01600-x","journal":{"identity":"bmc-urology","isVorOnly":false,"title":"BMC Urology"},"publishedOn":"2024-10-04 15:58:17","publishedOnDateReadable":"October 4th, 2024"},"versionCreatedAt":"2024-06-12 17:25:18","video":"","vorDoi":"10.1186/s12894-024-01600-x","vorDoiUrl":"https://doi.org/10.1186/s12894-024-01600-x","workflowStages":[]},"version":"v1","identity":"rs-4439399","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-4439399","identity":"rs-4439399","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}