Chronic painful cystitis and ureteric stricture following long term recreational Ketamine use
Chronic painful cystitis and ureteric stricture following long term recreational Ketamine use
Bhavana Shyamanur, Siva Muthukumarasamy
Ketamine, an N–methyl–D–aspartate receptor antagonist used as general anaesthetic, has increasingly grown in popularity for recreational use due to its dissociative, hallucinogenic side effects(1). Long term use causes multisystem damage however the high prevalence of lower urinary symptoms in patients has been widely documented in the literature since the first case of ketamine induced ulcerative cystitis described in 2007 (2–4). The spectrum of urinary tract side effects includes urethral inflammation, cystitis, permanent bladder fibrosis, renal papillary necrosis and ureteric obstruction(5). We present a case of ketamine induced bladder fibrosis and ureteric stricture.
A young female patient presented with symptoms of chronic painful cystitis due to long-term Ketamine use; dysuria, increased urinary frequency, inability to fill the bladder and blood-stained urethral discharge. She was investigated with ultrasound, CT, MRI and cystoscopy. Following persistent, debilitating symptoms she underwent cystectomy and orthotopic neobladder formation which improved her quality of life. Subsequent development of loin pain and renal obstruction diagnosed on nuclear medicine renogram required further urointervention.
Figure 1: MRI pelvis: Non-specific diffuse thickening of the urethral complex.
Figure 2: CT abdomen and pelvis: bilateral moderate hydronephrosis with urothelial thickening and hyperenhancement. Distended neobladder in the pelvis.
Figure 3: Nuclear Medicine Renogram shows that the left kidney is significantly larger than the right and contributes 80% function. Tracer uptake is in keeping with the known mild hydronephrosis and the renogram curve continues to rise for approximately 20 minutes and then plateaus. Appearances of the renogram indicate obstruction and the patient went on to have antegrade ureteric stent insertion on the left.
Initial imaging was non-specific. Ultrasound showed an underfilled urinary bladder, while MRI pelvis and CT urinary tract demonstrated diffuse thickening of the urethra and a thick walled, collapsed urinary bladder (Figure 1). Intravesical Botox injections offered initial relief however she eventually underwent cystectomy and neobladder formation with confirmation of diagnosis on histopathology. Histology demonstrated extensively ulcerated bladder mucosa with granulation tissue and mixed inflammatory cell infiltrate typical of ketamine related chronic ulcerative cystitis. She continued to have recurrent urinary tract infections and chronic bilateral flank pain. In the 3rd postoperative year, contrast enhanced CT abdomen demonstrated bilateral moderate hydronephrosis with urothelial thickening and hyperenhancement (Figure 2). A nuclear medicine renogram was performed to investigate further and diagnosed an asymmetrically enlarged left kidney contributing 80% of renal function. The left kidney demonstrated a rising renogram curve which plateaued, indicating renal obstruction (Figure 3). This was thought to be likely to ureteric stricture and was managed with left antegrade ureteric stent insertion. 6 months later she developed contralateral abdominal pain and nuclear medicine renogram confirmed an obstructed renogram curve of the right kidney. The left kidney showed normal excretion, with resolution of obstruction following previous stent insertion (Figure 4). Right nephrostomy and ureteric stenting were subsequently performed (Figure 5).
Figure 4: Nuclear Medicine Renogram shows abnormal split function, with the left kidney contributing 72% and right kidney 28% of renal function. The right kidney now shows an obstructed renogram curve with prompt tracer uptake with a prominent renal pelvis and a flat non-draining renogram curve. Normal excretion from the left kidney, improved following stent insertion.
Figure 5: Eventual placement of bilateral ureteric stents following progressive bilateral ureteric stricture and renal obstruction. The distal aspects of the stents terminate in the orthotopic neobladder.
Ketamine abuse is an important diagnosis to consider in young patients presenting with lower urinary tract symptoms and the corresponding urinary tract findings on imaging. Early diagnosis and drug cessation may halt disease progression while end stage disease is irreversible with a severe detriment to quality of life, requiring renal dialysis or extensive surgical intervention. References: 1. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-. Ketamine. [Updated 2018 Apr 25]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK548337 2. Cottrell AM, Gillatt DA. Ketamine-associated urinary tract pathology: The tip of the iceberg for Urologists? British Journal of Medical and Surgical Urology. 2008;1(3):136–8. doi:10.1016/j.bjmsu.2008.08.005 3. Chu, P.S.-K. et al. (2008) ‘The destruction of the lower urinary tract by ketamine abuse: A new syndrome?’, BJU International, 102(11), pp. 1616–1622. doi:10.1111/j.1464-410x.2008.07920.x. 4. Cottrell, A.M. et al. (2008) ‘Urinary tract disease associated with chronic ketamine use’, BMJ, 336(7651). doi:10.1136/bmj.39562.711713.80. 5. Srirangam, S. and Mercer, J. (2012) ‘Ketamine bladder syndrome: An important differential diagnosis when assessing a patient with persistent lower urinary tract symptoms’, Case Reports, 2012(sep26 1). doi:10.1136/bcr-2012-006447.