Transcript Ketamine bladder

Carmel Ramage
19th October 2012
Case Presentation
 24 year old woman
 Complaining of
 Urinary frequency
 Urgency
 Pain
 Dysuria - shooting and leads to poor flow because tenses up
 post micturation pain
 Symptoms of recurrent UTI but one proven UTI
 Jelly like urethral discharge
 Deep dyspareunia
History
 P 1+4
 No significant medical history
 Smoker
 Social alcohol intake
 NKDA
 10 stone – lost weight but normal appetite
 LFT – only raised gamma GT
Examination
 Pelvic examination – normal
 Urethra –no discharge
 Attempted cystoscopy in OPD – very tender and in
severe discomfort
 Cystoscopy under GA
Cystoscopy
 Severe haematuria
 Unable to visualise any
anatomy
 No response to saline washout
 Indwelling catheter left in situ
 USS organised
Further investigations
 USS – fluid in POD, catheter
in bladder
 Discussed with Urologists
 CT recommended
 Free fluid confirmed in pelvis and
abdomen
 Bladder abnormally thick walled and
small
 Plan
 Catheter in for 2 weeks
 Cystogram
Diagnosis
 Re-interviewed following initial USS and CT
 Admitted to Ketamine use for 4 years
 Several times a week for a year
 Stopped during pregnancy (2008)
 Now once / twice monthly
 Previous hospital admission (November 2010) with
severe abdominal pain following sniffing ketamine
 Managed conservatively
 Treated for UTI
 Readmission 4 months later with upper abdominal
pain
 Gastroscopy
 Abdominal USS
 Renal USS )
)
)
NAD
Cystogram
 Small volume bladder (20mls)
and patient unable to tolerate
 CT
 No further fluid in pelvis and
abdomen
 contrast in uterus and vagina –
suspicion of vesico-uterine fistula
 Repeat cystogram 3 weeks later
 Severe pain on distending bladder
 No extravasation seen
Ongoing Management
 Continued with indwelling catheter
 Started on Solifenacin
 Cystistat bladder installations
 Aware that symptoms may not settle due to
irreversible bladder fibrosis
 May need Augmentation cystoplasty
Current Update
 Cystistat bladder instillations for 8 months
 Symptoms
 Daytime frequency – 3 hourly
 Nightime – 6 hourly
 Full bladder without urgency
 No bladder pain
 No Haematuria
 No UTI
 No need for reconstructive bladder surgery
Ketamine
 Fastest growing "party drug" among 16-24 year olds
 Also known as
 Special K
 Kit-Kat
 Ket
 Cat valium
 Vitamin K
 Estimated 125,000 users in the UK
 More users than crack and heroin combined in UK and
Wales
History
 Developed by Parke-Davis in 1962
 First given to American soldiers during the Vietnam
War
 Battlefield / emergency anaesthetic
 Short duration of action
 Dissociative anaesthesia
 Muscle paralysis
 Increase in illicit use in USA during 1990’s
 Class C drug (January 2006)
 Possession - 2 years
 Supply - 14 years
 Unlimited fine
Ketamine effects
 Floating feeling
 may feel completely detached from body and surroundings
 Dissociative paralysis – “entering the K-hole”
 Change in perception
 Hallucinations
 ‘Trip’ for up to an hour
 After effects may take several hours to wear off
 Confusion
 Panic attacks
 Depression
 Exacerbation of any pre-existing mental health problems
Ketamine Use




Sold in either powdered or liquid form
Inhaled as snuff
Injected
Orally
 Bitter taste
 Slower onset of action
 Ecstasy Tablets known as "Strawberry“
and "Sitting Duck" contained
Ketamine
 >80% ketamine seized in the US is of
Mexican origin
Ketamine Detection
 Urine
 Blood/ plasma
 Norketamine
 Pharmacologically-active
metabolite
 Plasma levels:
 Therapeutic - 0.5-5.0 mg/L
 Arrested for impaired driving –
1–2 mg/L
 Acute fatal overdose - 3–20 mg/L
Ketamine and Urinary system
 “Bristol bladder”
 described in 20081
 frequency, haematuria, incontinence and dysuria
associated with ketamine use*
 Scarred thickened shrunken bladder
 Erythema with contact bleeding
 Severe ulcerative cystitis
 Can ascend to ureters and kidneys
 Symptomatic relief
 Cessation of Ketamine use2
 Pentosan Polysulphate
1Cottrell et al 2008. BMJ 336: 973
2Shahani
et al 2007 Urology 69 (5)
Presentation
 “K cramps”
 Severe long lasting abdominal pain
 Cause unknown
 Usually limited to users of >1 g / day
 Hepatic damage
 Urinary tract
 Overactive bladder syndrome
 Painful bladder symptoms
 Incontinence
 Upper tract obstruction
 Renal papillary necrosis
 Patients erroneously treated for recurrent UTI’s/ painful
bladder syndrome
Ketamine and Bladder damage


Causal link
Precise mechanism unclear
 Direct toxicity of Ketamine or its metabolites (supported
by animal models)
 Microvascular damage
 Autoimmune reaction triggered by circulating or urinary
ketamine
 Unrecognised bacteruria

Toxicity receptor mediated
 No NDMA receptors in bladder
Diagnosis of Ketamine Bladder
 Cystoscopy
 Denuded urothelium
 Can slough off as intact sheets of cells
 Histology
 Absence of urothelium
 Eosinophilia in blood vessels
 Lymphocytic infiltration
 mast cells
 Cell Markers
 P53 (assoc. with cell death)– high
 Ki07 (assoc. with cell growth) - very low
 CK20 (assoc with Ca in situ)– absent
Wood et al 2011; BJUI 107:1881-1884
How to make the Diagnosis
 Good history of recreational drug abuse
 MSU for C&S
 Cystoscopy and biopsy
 Renal function tests
 CT urogram for extent of disease
Treatment
 Stop ketamine
 Involve
 drug support agencies
 GP
 National Club Drug Clinic London (Chelsea and Westminister)
 Liaise with chronic pain team
 Medication
 Bupenorphine patches
 Co-codamol
 Amytriptylline at night (Bristol)
 Anticholinergics
 Intra-vesical installations
 Bladder augmentation / urinary diversion +/- cystectomy
Future
 Awareness and Education of Clinical Staff
 Education and Support for ketamine users
 Effects on the urinary tract
 Where to seek help
 Liaison with pain services, psychiatry, social services
Summary
 Increasing Ketamine use
 May cause significant
urinary tract damage
 Be aware of potential
diagnosis in young
patients with severe
painful bladders