Recreational use of ketamine
Ketamine is a prescription anesthetic that is federally regulated (e.g., U.S. Schedule III, U.K. Class B) that functions as a dissociative anesthetic, and so has seen use as a recreational drug. Originating in the United States in the 1970s, the recreational use of ketamine has since spread to Europe, Canada, Asia, and Australia. Attempts are made to use the drug at sub-anesthetic doses; contexts for use include both private settings and at club venues (raves and parties), where it initially gained popularity. Despite its emergence as a club drug, users may eventually relegate their use to more private settings
Ketamine interacts with a variety of other drugs, most pronounced with alcohol, opioids (potentiation), and barbiturates, and with drugs that increase blood pressure (e.g., stimulants, SNRI antidepressants, and especially MAOIs). The latter may have an additive effect on the user’s blood pressure, causing tachycardia, palpitations and potentially serious arrhythmias.[not verified in body] Ketamine use as a recreational drug has been implicated in a small but greatly exaggerated number of annual deaths, the majority of which are youth or young adults, which have, taken together, led to increasing stringency of its regulation worldwide.
As a consequence of its drug interactions and adverse effects, including the ability to cause confusion and amnesia, and adverse reactions that occur during emergence from anaesthesia, some cases are known from the media that involved irresponsibly high dosages and accidents in people who were not prepared for the experience and/or took other drugs at the same time, despite ketamine being a physically very safe substance in comparison to other psychoactives like opioids or even alcohol. But ketamine can leave users vulnerable to date rape (i.e., because of the associated confusion and amnesia).
Due to the complexity of its chemical synthesis, ketamine supplies for recreation use must be diverted from licit medical sources, though there have been reports of industrial-scale illicit ketamine manufacture in China and India.
Ketamine’s use as a recreational drug has contributed to more than 90 fatalities—the majority among young adults—in England and Wales in the years of 2005-2013, including accidental poisonings, drownings, and traffic accidents. This has led to its increasingly stringent regulation (e.g., upgrading ketamine from a Class C to a Class B banned substance in the U.K.).
Ketamine may increase the effects of other sedatives, including, but not limited to: alcohols, benzodiazepines, opioids, and barbiturates. Other drugs which increase blood pressure may interact with ketamine, having an additive effect on blood pressure; such agents include stimulants, SNRI antidepressants, and MAOIs. Increase blood pressure and heart rate, palpitations, and arrhythmias may be potential effects.
Ketamine is generally safe even for those critically ill, when administered by trained medical professionals. The dosages used recreationally are somewhat lower than a fully anaesthetic dosage, making the substance physically relatively safe in comparison to other psychoactive drugs. Still, even in these cases, there are known side effects that include one or more of the following:
- Cardiovascular: abnormal heart rhythms, slow heart rate or fast heart rate, high blood pressure or low blood pressure; and
- Central nervous system: increased intracranial pressure (ICP), leading to intracranial hypertension.
In addition there are dermatologic adverse reactions (ARs; transient erythema, transient morbilliform rash), gastrointestinal ARs (anorexia, nausea, increased salivation, vomiting), neuromuscular and skeletal ARs (Increased skeletal muscle tone, i.e., tonic-clonic movements), ocular ARs (double vision, increased intraocular pressure, nystagmus), respiratory ARs (airway obstruction, apnea, increased bronchial secretions, respiratory depression, laryngospasm), as well as local pain or exanthema (e.g., at injection sites) and possible anaphylaxis and dependence.
In 10-20% of patients at anesthetic doses, adverse reactions are experienced that occur during emergence from anesthesia, reactions that can manifest as seriously as hallucinations and delirium. These reactions may be less common in some patients subpopulations, and when administered intramuscularly, and can occur up to 24 hours postoperatively; the chance of this occurring can be reduced by minimizing stimulation to the patient during recovery and pretreating with a benzodiazepine, alongside a lower dose of ketamine. Patients who experience severe reactions may require treatment with a small dose of a short- or ultrashort-acting barbiturate.
Ketamine produces effects similar to phencyclidine (PCP) and dextromethorphan (DXM). Unlike these other well-known dissociatives, ketamine is very short-acting, its hallucinatory effects lasting tens of minutes when inhaled (insufflated) or injected, and hours when ingested. With ketamine, intensities of hallucinations are dose-dependent. Like other dissociative anaesthetics, hallucinations caused by ketamine are fundamentally different from those caused by serotonergic psychedelic (classic) hallucinogens.
The specific dissociative state produced by ketamine is characterised by a sense of detachment from one’s physical body and the external world that is known as depersonalization and derealization. At sufficiently high doses, users may experience what is called the “K-hole”, a state of extreme dissociation with phenomenology of schizophrenia (e.g., visual and auditory hallucinations).
John C. Lilly, Marcia Moore and D. M. Turner (amongst others) have written extensively about their own entheogenic use of and psychonautic experiences with ketamine. Both Moore and Turner died prematurely (due to hypothermia and drowning respectively) during presumed unsupervised ketamine use.
As the recreational dosages used are always below the fully anaesthetic threshold and thus lower than those medically administered, the term ‘overdose’ needs to be seen a bit differentiated from other drugs. While with continued use, people may build up some degree of tolerance, leading to the use of higher dosages than medically advised, it is technically somewhat difficult to overdose on ketamine. An even higher dosage will just lead to full anaesthesia, amnesia, but no physical danger from the drug itself as long as the environment isn’t dangerous. The user will become catatonic when fully dissociated, not experiencing any pain but also unable to move his/her body.
There is no known effective antidote used to treat ketamine overdose, and treatment generally focuses on the maintenance of respiratory and circulatory function until the patient is capable of breathing under their own power and all cardiac abnormalities have subsided. Unlike many other anaesthetics, ketamine has a minimal effect on respiratory drive and tidal volume; while pulse oximetry is always essential it rarely drops enough to require mechanical ventilation or supplemental oxygen, except in the most massive of overdoses and in cases of mixed-drug-overdose.
Verbal reassurance and a calming environment (i.e. dim lights, calming music, and the presence of supportive individuals in the room) should be provided when possible to calm the patient and/or prophylacticly to prevent agitation. Occasionally it may become necessary to restrain highly agitated patients during recovery should they become violent, experience panic attacks, or otherwise present a threat to themselves or others.
Even after all vital signs have normalized and the patient appears functional it is advised to require the patient to be driven home as residual impairment of motor skills may persist for up to a day after apparent resolution.
Ketamine’s potential for dependence has been established in various operant conditioning paradigms, including conditioned place preference and self-administration; further, rats demonstrate locomotor sensitization following repeated exposure to ketamine. Increased subjective feelings of ‘high’ have been observed in healthy human volunteers exposed to ketamine. Additionally, the rapid onset of effects following smoking, insufflation, and/or intramuscular injection is thought to increase the drug’s recreational use potential. The short duration of effects promotes bingeing, tolerance can develop, and withdrawal symptoms, including anxiety, shaking, and palpitations, may be present in some daily users following cessation of use.
Due to its primary NMDA-antagonist effect, sudden withdrawal in severely addicted users will result in overexcitability, manifesting as increased sensitivity to stress, anxiety and pain. There are speculations about possible excitotoxicity resulting from the rebound surge in glutamate, but this has not yet been proven or disproven in humans and it doesn’t seem to be a huge concern in healthy adults. Unlike GABAergic sedatives however, overexcitation secondary to ketamine withdrawal is not life-threatening as long as no underlying seizure disorders are present and even very tolerant users will likely suffer, at worst, only minor neurological sequela following the abrupt discontinuation of the drug. Some titration or the administration of anti-excitatory agents like memantine could be of benefit.
Ketamine can cause a variety of urinary tract problems that are more likely to occur with heavier and/or higher dosed use, especially in those not watching for a healthy lifestyle, according to a UK study.
See also: K-Hole (“K-hole” is a slang term for the subjective state of dissociation from the body commonly experienced after sufficiently high doses of the dissociative anesthetic ketamine. This state may mimic the experiences such as catatonic schizophrenia, out-of-body experiences (OBEs) or near-death experiences (NDEs), and is often accompanied by feelings of extreme derealization, depersonalization and disorientation, as well as temporary memory loss and vivid hallucinations.)