Ketamine bladder treatment

Added: Adekunle Royston - Date: 11.02.2022 15:22 - Views: 48801 - Clicks: 500

Current Issue. Past Issues. Online First. For Authors. Submit an Article. Corresponding author: Prof CF Ng ngcf surgery. Ketamine is an N-methyl-d-aspartate receptor antagonist, a dissociative anaesthetic agent and a treatment option for major depression, treatment-resistant depression, and bipolar disorder.

Its strong psychostimulant properties and easy absorption make it a favourable candidate for substance abuse. Ketamine entered Hong Kong as a Ketamine bladder treatment drug in and the first local report of ketamine-associated urinary cystitis was published in Ketamine-associated lower—urinary tract symptoms include frequency, urgency, nocturia, dysuria, urge incontinence, and occasionally painful haematuria. The exact prevalence of ketamine-associated urinary cystitis is difficult to assess because the abuse itself and many of the associated symptoms often go unnoticed until a very late stage.

Additionally, upper—urinary tract pathology, such as hydronephrosis, and other complications involving neuropsychiatric, hepatobiliary, and gastrointestinal systems have also been reported. Gradual improvement can be expected after abstinence from ketamine Ketamine bladder treatment. Sustained abstinence is the key to recovery, as relapse usually le to recurrence of symptoms. Both medical and surgical management Ketamine bladder treatment be used. The Youth Urological Treatment Centre at the Prince of Wales Hospital, Hong Kong, has developed a four-tier treatment protocol with initial non-invasive investigation and management for these patients.

Multidisciplinary care is essential given the complex and diverse psychological factors and sociological background that underlie ketamine abuse and abstinence status. Ketamine is an N-methyl-d-aspartate NMDA receptor antagonist, a dissociative anaesthetic agent that was first synthesised in the United States in It has been widely used in both human and veterinary medicine since It has also been used as a treatment for major depression, treatment-resistant depression, and bipolar disorder. Ketamine abuse has become increasingly common over the past two decades.

Ketamine remained the most popular psychotropic substance abused from to Fig 1. Figure 1. The abuse of ketamine and its popularity nonetheless created a new medical entity. The first report of ketamine-associated urinary cystitis in Hong Kong was published in This understanding spans from pathology to clinical management, from urological complications to upper-gastrointestinal GI complications, and from a mouse model to humans. We have also explored holistic ways to manage this condition in the long term, such as helping young adults to have a fresh start while living with potentially irreversible complications.

This article reviews the evolution of local clinical awareness and management of these complications, with a particular focus on the work and contributions of local researchers.

Ketamine bladder treatment

Chu et al 5 reported the first local case series of ketamine-associated bladder dysfunction in Ketamine-associated lower—urinary tract symptoms LUTS include frequency, urgency, nocturia, dysuria, urge incontinence, and occasionally painful haematuria. The exact prevalence of ketamine-associated Ketamine bladder treatment cystitis is difficult to assess because ketamine abuse and many of the associated symptoms often go unnoticed until a very late stage. A survey among 12 local secondary school students revealed that InYee et al 8 reported the largest available cohort of both active and past ketamine users who had ketamine-associated uropathy.

The PUF score is initially used to assess interstitial cystitis, and a higher PUF score correlates with worse symptoms. Among active ketamine users, a higher PUF score was found to correlate with a poorer quality of life and a smaller functional bladder capacity. As well as bladder involvement, upper—urinary tract pathology presenting as hydronephrosis and flank pain has also been reported Fig 2. Hydronephrosis was frequently accompanied by ureteral lesions, ureteral wall thickening, or vesicoureteral vesicoureteric reflux.

Figure 2. Intravenous urogram of a year-old female in Prince of Wales Hospital showing bilateral hydronephrosis and small bladder. Although the exact mechanism of ketamine-associated cystitis remains to be explored, there is evidence that ketamine metabolites in the urine induce chemical irritation of the urothelium, thereby causing an inflammatory response. Vesicoureteral reflux or urinary stasis in the ureter may occur, causing chronic ureteral inflammation and ureteral stricture.

There is also evidence that both systemic and local inflammatory markers are elevated in ketamine users. As ketamine is a psychostimulant, it is not Ketamine bladder treatment that it is associated with long-term neurocognitive problems.

Chan et al 14 found that when ketamine users were compared with healthy controls, they had impaired verbal fluency, cognitive processing speed, and verbal learning. Heavy ketamine use correlated with deficits in verbal memory and visual recognition memory.

Liang et al 15 also identified Ketamine bladder treatment verbal and visual memory impairment in ketamine poly-drug users.

Ketamine bladder treatment

Unfortunately, Ketamine bladder treatment deficits persisted in ex-users. A much higher incidence of psychiatric co-morbidities, including psychosis, depression, and anxiety, was observed among ketamine users. Structural brain damage associated with ketamine abuse was supported by magnetic resonance imaging MRI by Wang et al. Cortical atrophy was also found in the frontal, parietal, or occipital cortices of addicts. Reduced grey- and white-matter volumes were noted in the bilateral orbitofrontal cortex, right medial prefrontal cortex, and bilateral hippocampi.

There was also ificantly decreased connectivity inside the brain in chronic ketamine abusers. A series of studies on the neurotoxicity of ketamine suggested that ketamine could cause apoptosis of neuronal cells in both in-vitro and in-vivo models. InWong et al 23 reported ketamine-associated hepatobiliary complications for the first time. Three ketamine abusers presented with recurrent epigastric pain and dilated bile ducts mimicking choledochal cysts.

Ketamine bladder treatment

Subsequently, more similar cases were identified. Fusiform dilatation of the common bile duct was also observed. A study of chronic ketamine abusers with urinary tract dysfunction showed that the prevalence of liver injury was 9. The exact Ketamine bladder treatment of ketamine-associated bile injury is still unknown. The associated rise in C-reactive protein suggests a possible inflammatory process in the liver parenchyma, including or excluding the bile duct. In addition to urological complaints, GI problems are also frequently the symptoms for which ketamine abusers seek medical help.

A review of ketamine-related visits to accident and emergency departments found that 49 Liu et al 30 found that about a quarter ; The majority of the symptoms reported were epigastric pain and recurrent vomiting. Nearly three-quarters of patients required hospitalisation for acute or chronic upper-GI symptoms.

With the exception of acid reflux and perforated peptic ulcer, the prevalence of all the above-mentioned symptoms and hospitalisation rates were statistically ificantly higher in ketamine users than in non-ketamine users. All patients using ketamine had undergone oesophagogastroduodenoscopy during which biopsies were taken. Pathological findings ranged from gastritis to gastroduodenal erosions, peptic ulceration, and intestinal metaplasia. Patients developed upper-GI symptoms after a mean standard deviation of 5. Ketamine bladder treatment difference may provide an opportunity to identify hidden ketamine abuse when assessing young patients with epigastric symptoms.

The identification of ketamine use is important, as cessation of use can greatly improve GI symptoms. The exact pathophysiological mechanism by which ketamine produces upper-GI toxicity remains unknown but Ketamine bladder treatment are several postulations. First, ketamine, as an NMDA antagonist, might act on local smooth muscle or the central nervous system, thereby affecting gastric motility and leading to cramping pain. Second, microvascular damage by ketamine and its metabolites, which was believed to be a possible cause of ketamine uropathy, might also cause similar microvascular damage in the stomach and duodenum, leading to ischaemic pain and inflammation.

Likewise, circulating ketamine might also trigger some unknown autoimmune responses, and thus induce interstitial inflammation in the urinary and GI tracts. Finally, as many ketamine abusers like to swallow the nasal drips occurring from ketamine inhalation, the swallowed ketamine might also induce direct cytotoxic injury to the vulnerable GI tract. As in the management of other substance abuse, abstinence is the key to success in overall management of ketamine use.

Ketamine bladder treatment

Whereas other treatment modalities may relieve symptoms and hasten the recovery process, many ketamine abusers have complicated underlying psychosocial problems and psychiatric co-morbidities. Long-term and consistent support and encouragement from doctors, nurses, social workers, family, and friends are vital for success. Recurrence of symptoms after resuming ketamine use highlights the importance of ketamine abstinence. Studies have shown that abstinence le to symptomatic improvement. Compared with active ketamine abusers, those who had abstained for 1 year had ificantly lower PUF scores and a larger voided volume.

There was a trend towards higher voided volumes and lower PUF scores as duration of ketamine cessation increased, although neither variable was statistically ificant. Nonetheless, abstinence does not lead to immediate and full recovery of symptoms. Gradual improvement can be expected but sustained abstinence is Ketamine bladder treatment key to recovery.

Ketamine bladder treatment

Patience and continuous support are of paramount importance. After having stopped using ketamine for 3 months or more, mean hour urinary frequency and mean UDI-6 and IIQ-7 scores decreased, and maximum voided volume increased.

Ketamine bladder treatment

These scores further improved after another 3 months, although this group continued to perform more poorly in all aspects compared with controls. Some of the clinical features share similarities with interstitial cystitis. Protocols are being developed to cater to the needs of patients in Hong Kong.

Ketamine bladder treatment

The standard treatment protocol involves four tiers of treatment, starting with an initial non-invasive investigative approach, including questionnaire assessment of Ketamine bladder treatment and calculation of 1 functional bladder capacity by measuring voided volume using uroflowmetry and 2 residual urine using ultrasound bladder scanning. Figure 3. Simple analgesics such as paracetamol and phenazopyridine are used for pain control. The Youth Urological Treatment Centre has reported the largest series of patients with ketamine-associated uropathy and their corresponding outcomes.

Of patients with ketamine cystitis who received first-line treatment, Functional bladder capacity was also shown to have improved. The opioid group of analgesics and pregabalin are used in the next tier of pain-control treatment when first-tier treatment is insufficient for symptom relief. Sixty-two patients received second-line treatment and 42 Third-tier treatment consists of a course of intravesical instillation of sodium hyaluronate 6-weekly instillations followed by 2-monthly instillations attempting to repair the glycosaminoglycan layer.

The drug Ketamine bladder treatment given to patients whose symptoms remain uncontrolled after second-tier treatment. Seventeen patients in the cohort received the third-tier treatment and eight completed the course. ificant improvement in voided volume was noted and five were able to reduce their oral medication usage after treatment. No ificant adverse effects were reported. Unfortunately, for a proportion of patients with extremely refractory symptoms, surgery becomes the fourth-tier treatment of choice.

In the Youth Urological Treatment Centre series, one patient in the cohort required hydrodistension and another underwent robotic-assisted laparoscopic augmentation cystoplasty. The patient with hydrodistension experienced a recurrence of symptoms post-treatment. Although they showed initial improvement, all patients relapsed and d ketamine use postoperatively. Therefore, patient selection, education, close follow-up, and support are vital to the success of augmentation cystoplasty.

Since the initial discovery of ketamine-associated uropathy, the impact of this disease entity has become more prominent in Asian countries. Thanks to the t efforts of urologists, gynaecologists, surgeons, psychiatrists, pathologists, and social workers, as well as the support of local government, the extent of medical complications has been revealed to also involve the brain, liver, and GI system. Clinicians must take the opportunity to identify hidden abusers when they consult for non-specific symptoms such as epigastric pain and LUTS.

Doing so will not only enable early diagnosis of ketamine-associated uropathy, but Ketamine bladder treatment will also help provide appropriate medical treatment in a timely manner. In addition to medical therapy, referral for appropriate psychosocial support is essential to sustain abstinence and manage underlying psychosocial problems. Hasselmann HW. Ketamine as antidepressant? Current state and future perspectives.

Curr Neuropharmacol ;

Ketamine bladder treatment

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Possible pathophysiology of ketamine-related cystitis and associated treatment strategies