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. 2023 Jun 13;35(3):205-212.
doi: 10.4103/tcmj.tcmj_94_23. eCollection 2023 Jul-Sep.

Pathophysiology, clinical presentation, and management of ketamine-induced cystitis

Jia-Fong Jhang  1 , Lori A Birder  2 , Hann-Chorng Kuo  1
Affiliations

Pathophysiology, clinical presentation, and management of ketamine-induced cystitis

Jia-Fong Jhang et al. Tzu Chi Med J. .

Abstract

Ketamine is illegally used as a recreational drug in many Asian countries. Long-term ketamine abusers often develop irritable bladder symptoms that gradually develop into more severe urinary frequency and urgency and eventually into a painful ulcerated bladder. These patients typically have reduced functional bladder capacity, increased bladder sensation, detrusor overactivity, severe urgency, urinary incontinence, and bladder contracture. Ketamine metabolites can cause severe inflammation of the urothelium, urothelial barrier deficits, vascular endothelial fibrinoid changes, increased oxidative stress, and bladder wall fibrosis. A decrease in bladder compliance, urinary tract infection, severe bladder pain with a full bladder, and painful micturition are also common symptoms. Finally, with continued abuse of ketamine, hydronephrosis, ureteral stricture, vesicoureteral reflux, and renal failure may develop. Cessation of ketamine is the mainstay of treatment. Lower urinary tract symptoms usually relapse if patients reuse ketamine after stopping. In cases of severe ketamine cystitis, only augmentation enterocystoplasty can relieve bladder pain and restore normal lower urinary tract function. This article reviews the underlying pathophysiology, clinical characteristics, and management of ketamine cystitis.

Keywords: Augmentation; contracted bladder; cystitis; ketamine; treatment.

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Conflict of interest statement

Dr. Hann-Chorng Kuo, the editorial board member at Tzu Chi Medical Journal, played no role in the peer review process or decision to publish this article. The other authors declared no conflicts of interest in writing this paper.

Figures

Figure 1
Figure 1
Videourodynamic study of a patient with ketamine cystitis. Detrusor overactivity (arrow 1), decreased bladder compliance (arrow 2), high and rapidly increasing detrusor pressure (arrow 3), dyssynergic external sphincter (arrow 4), and grade 3 left vesicoureteral reflux (arrow 5) are noted
Figure 2
Figure 2
Typical intravenous urography findings in a patient with (a) mild ketamine cystitis with contracted bladder and ureteral stricture (arrow), and (b) severe ketamine cystitis and bilateral obstructive uropathy (arrows)
Figure 3
Figure 3
Bladder computerized tomography of ketamine cystitis (KC, a) and Hunner’s ulcer interstitial cystitis (HIC, b) reveals more perivesical infiltration (arrows) in KC than in HIC
Figure 4
Figure 4
Pathological findings of ketamine cystitis: (a) fibrinoid necrosis of arterioles, (b) focal calcification, (c) eosinophil-predominant inflammation, (d) fibrinoid necrosis of arterioles [14]
Figure 5
Figure 5
(a) Severe mucosal denudation and (b) diffused hemorrhage from a patient with ketamine cystitis during cystoscopy and after hydrodistention. Histopathology findings revealed (c) severe inflammation and fibrosis of the suburothelium of the bladder and (d) the ureter wall [14]
Figure 6
Figure 6
Histopathological finding of ketamine cystitis shows thickening of the endothelial basement membrane (arrow), chronic inflammation, interstitial fibrosis, and fibrinoid necrosis within small- and medium-sized arterioles [26]
Figure 7
Figure 7
Urinary tract changes after augmentation enterocystoplasty: (a) upper and middle ureteral stricture (arrow) after the operation, (b) severe ureteral stricture (arrow) and hydronephrosis worsen after surgery, (c) persistent bilateral vesicoureteral reflux (arrows) after augmentation enterocystoplasty without concomitant ureteral reimplantation
See this image and copyright information in PMC

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