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Patients with a spinal cord injury above the 6th thoracic vertebrae may be prone to autonomic dysreflexia (AD) in response to bladder stimulus associated with a urodynamics investigation. It is essential that these patients are managed carefully in the urodynamics clinic in order to prevent life-threatening hypertension and bradycardia. Part of this management is the measurement and manual recording of pulse rate (PR) and non-invasive blood pressure (NIBP), alongside the standard urodynamics data set. The purpose of recording these additional data is to identify the characteristic drop in PR and rise in NIBP that indicates the onset of AD. This technical note describes the development of a novel, in-house constructed interface that allows PR and NIBP to be recorded alongside the standard urodynamics data set, using a commonly available vital signs monitor and urodynamics workstation. [ABSTRACT FROM AUTHOR]

Objective: To establish whether the urothelial ulceration observed in ketamine-induced cystitis is triggered by urinary or systemic factors. This was achieved with a rare case where an urachal cyst was found near the bladder dome in a patient undergoing cystectomy for unremitting pain following ketamine abuse.Methods: Clinical investigations included cystoscopy, video urodynamic investigation, and computed tomography of the kidneys, ureters, and bladder. Histological staining was combined with immunoperoxidase labeling for markers of transitional epithelial differentiation.Results: The urachus found near the dome of the bladder was observed to be a separate cyst, with no evidence of patency found during surgery or video urodynamic investigation. The urachus was lined by a mildly reactive metaplastic epithelium of mixed transitional and columnar morphologies. Evidence of widespread cytokeratin 13, basal p75(NTR), and sparse superficial uroplakin 3a immunoreactivity suggested the urachal epithelium was fundamentally transitional in nature. Near total loss of bladder urothelium was observed from regions in contact with urine, whereas the urachal epithelium (not exposed to urine) remained healthy.Conclusion: This study supports the hypothesis that urinary (and not systemic) factors are the main driver of urothelial ulceration in ketamine-induced cystitis. The most likely excreted factors responsible are ketamine and potentially its metabolites. This study reinforces the importance of complete cessation of ketamine use in patients with ketamine-induced cystitis. [ABSTRACT FROM AUTHOR]

Background: There is an emerging association between ketamine abuse and the development of urological symptoms including dysuria, frequency and urgency, which have a neurological component. In addition, extreme cases are associated with severe unresolving bladder pain in conjunction with a thickened, contracted bladder and an ulcerated/absent urothelium. Here we report on unusual neuropathological features seen by immunohistology in ketamine cystitis., Results: In all cases, the lamina propria was replete with fine neurofilament protein (NFP+) nerve fibres and in most patients (20/21), there was prominent peripheral nerve fascicle hyperplasia that showed particular resemblance to Morton's neuroma. The nerve fascicles, which were positive for NFP, S100 and the p75 low-affinity nerve growth factor receptor (NGFR), were generally associated with a well-developed and in places, prominent, epithelial membrane antigen+/NGFR+ perineurium. This peripheral nerve fascicle hyperplasia is likely to account for the extreme pain experienced by ketamine cystitis patients. Urothelial damage was a notable feature of all ketamine cystitis specimens and where urothelium remained, increased NGFR expression was observed, with expansion from a basal-restricted normal pattern of expression into the suprabasal urothelium., Conclusions: The histological findings were distinguishing features of ketamine cystitis and were not present in other painful bladder conditions. Ketamine cystitis afflicts predominantly young patients, with unknown long-term consequences, and requires a strategy to control severe bladder pain in order to remove a dependency on the causative agent. Our study indicates that the development of pain in ketamine cystitis is mediated through a specific neurogenic mechanism that may also implicate the urothelium.