Urinary and liver toxicity
Urinary toxicity occurs primarily in people who use large amounts of ketamine routinely, with 20–30% of frequent users having bladder complaints. It includes a range of disorders from cystitis to hydronephrosis to kidney failure. The typical symptoms of ketamine-induced cystitis are frequent urination, dysuria, and urinary urgency sometimes accompanied by pain during urination and blood in urine. The damage to the bladder wall has similarities to both interstitial and eosinophilic cystitis. The wall is thickened and the functional bladder capacity is as low as 10–150 mL.Management of ketamine-induced cystitis involves ketamine cessation as the first step. This is followed by NSAIDs and anticholinergics and, if the response is insufficient, by tramadol. The second line treatments are epithelium-protective agents such as oral pentosan polysulfate or intravesical (intra-bladder) instillation of hyaluronic acid. Intravesical botulinum toxin is also useful.Liver toxicity of ketamine involves higher doses and repeated administration. In a group of chronic high dose ketamine users, the frequency of liver injury was reported to be about 10%. There are case reports of increased liver enzymes involving ketamine treatment of chronic pain. Dependence and tolerance
Although the incidence of ketamine dependence is unknown, some people who regularly use ketamine develop ketamine dependence. Animal experiments also confirm the risk of misuse. Additionally, the rapid onset of effects following insufflation may increase potential use as a recreational drug. The short duration of effects promotes bingeing. Ketamine tolerance rapidly develops, even with repeated medical use, prompting the use of higher doses.
It is often recommended that patients being started on immunosuppression be screened for chronic strongyloidiasis; however, this is often impractical (screen tests are often unavailable) and in developed countries, the prevalence of chronic strongyloidiasis is very small, so screening is usually not cost-effective, except in endemic areas. The reality of global travel and need for modern advanced healthcare, even in the so-called "developed world", necessitates that in non-endemic areas there is easily accessible testing and screening for neglected tropical diseases such as strongyloidiasis.It is important to note that there is not necessarily any eosinophilia in the disseminated disease. Absence of eosinophilia in an infection limited to the gastrointestinal tract may indicate poor prognosis. Eosinophilia is often absent in disseminated infection. Steroids will also suppress eosinophilia, while leading to dissemination and potential hyperinfection.Escalated disseminated infections caused by immunosuppression can result in a wide variety and variable degree of disparate symptoms depending on the condition and other biological aspects of the individual, that may emulate other diseases or diagnoses. In addition to the many palpable gastrointestinal and varied other symptoms drastic cachexia amidst lassitude is often present, although severe disseminated infections can occur in individuals without weight loss regardless of body mass index. Diagnosis
Diagnosis rests on the microscopic identification of larvae (rhabditiform and occasionally filariform) in the stool or duodenal fluid. Examination of many samples may be necessary, and not always sufficient, because direct stool examination is relatively insensitive, with a single sample only able to detect larvae in about 25% of cases.