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Current approaches for the treatment of ketamine-induced cystitis

期刊

NEUROUROLOGY AND URODYNAMICS
卷 42, 期 3, 页码 680-689

出版社

WILEY
DOI: 10.1002/nau.25148

关键词

cystitis; inflammation; ketamine; pain

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Ketamine is a dissociative anesthetic commonly used for anesthesia. Chronic abuse of ketamine can lead to urinary system complications, such as ketamine-induced cystitis. Treatment involves cessation of ketamine use and individualized plans based on symptoms and disease progression.
AimsKetamine is a dissociative anesthetic, historically used in a clinical setting for the induction and maintenance of anesthesia. Ketamine usage can produce undesirable psychological manifestations including hallucinations and long-term psychotomimetic effects. As a results of its fast onset and short period of action, ketamine is widely used as a recreational drug. Chronic abuse of ketamine can lead to significant urinary system complications including ketamine-induced cystitis (KIC). Common side effects of chronic ketamine abuse are urinary pain and discomfort and decreased bladder compliance and voiding pressure. Cessation of ketamine use is associated with improvement of symptoms however the exact pathophysiology of KIC remains unknown, complicating the ability of clinicians to treat this condition. MethodA literature search was performed using the National Center for Biotechnology Information (NCBI) Pubmed database up to May 2021. ResultsAnimal models of KIC are necessary to further our understanding of KIC pathophysiology and explore potential treatment options. In all cases, cessation of ketamine use is the first line of treatment and is most effective in managing KIC. In addition to cessation, treatment plans must be tailored to the individual, based on the severity of symptoms and disease progression, and include options such as: oral anti-inflammatories, intravesical treatment and in the most severe cases, surgical intervention. ConclusionKIC is a painful condition that currently lacks standardized treatment methods. Both animal models of KIC and clinical trials to further elucidate the mechanism of KIC pathophysiology must be explored to create targeted treatment plans.

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