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Published on: January 7, 2019
Clinical Outcome of Augmentation Enterocystoplasty for Patients with Ketamine-induced Cystitis
Yu Khun Lee1, Jia-Fong Jhang2, Hann-Chorng Kuo1
1Buddhist Tzu Chi General Hospital and Tzu Chi University, Hualien, Taiwan.
Background:
Ketamine abuse has become a global phenomenon in recent years. Ketamine-induced cystitis (KC) is a new clinical syndrome which can result in severely inflamed bladder and intractable bladder pain. Currently there is no guideline for managing patients with KC.
Objectives:
To analyze the clinical outcome of patients with KC managed with augmentation enterocystoplasty (AE).
Study Design:
Retrospective interventional study.
Setting:
A tertiary teaching hospital, Hualien Tzu Chi Hospital.
Methods:
We retrospectively collected and analyzed the medical records and video-urodynamic (VUD) test results of 26 patients who underwent AE as treatment for refractory KC during the period 2009 - 2014. All of these patients abused ketamine with nasal snorting, at least 3 grams per dose, twice per week for 6 months. Data from VUD studies performed before AE and 3 - 6 months after surgery that were analyzed in this study included cystometric bladder capacity (CBC), post-void residual (PVR) urine volume, maximum urinary flow rate (Qmax), voided volume, and bladder compliance. A self-report questionnaire was used to assess patient satisfaction with AE.
Results:
Patients included 14 women and 12 men aged 20 - 43 years (mean age, 28.5 years) with an average duration of ketamine abuse of 4.7 years (range, 1 - 10 years). All patients had contracted bladder, 9 had hydronephrosis, and 10 had vesicoureteral reflux (VUR). There was significant improvement in CBC (52.7 ± 29.7 v 327 ± 69.4 mL, P < 0.0001), Qmax (6.94 ± 4.32 v 13.7 ± 4.96 mL/s, P < 0.0001), PVR (8.08 ± 19.2 v 82.6 ± 91.5 mL, P < 0.0001), voided volume (44.1 ± 28.3 v 250.7 ± 133.4 mL, P < 0.0001), and bladder compliance (11.1 ± 11.9 v 54 ± 43, P < 0.0001) after AE. Hydronephrosis resolved in 7 patients after AE and VUR resolved in all patients who underwent AE with ureteral reimplantation. All patients who stopped using ketamine were free of bladder pain postoperatively. However, 10 patients who reused ketamine had recurrent bladder pain and recurrent urinary tract infection.
Limitations:
Small number of patients limits scope of study.
Conclusions:
AE is effective at treating KC-induced bladder pain and restoring normal lower urinary tract function. However, absolute cessation of ketamine is the key to success in KC treatment.Key words: Ketamine-induced cystitis, augmentation enterocystoplasty, bladder pain, contracted bladder, inflammation, surgery.
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