The term "ket" carries multiple meanings across various fields, from linguistics to physics and medicine. This article will explore the different definitions and applications of the word "ket," providing a comprehensive overview of its diverse usage.
Etymology and Linguistic Usage
In linguistics, "ket" has several interesting facets. It is related to the Icelandic word "kjöt," meaning "flesh," and akin to Swedish "kött," Danish "kød," and Norwegian "kjøtt." This connection highlights the shared linguistic roots across Germanic languages.
In other languages, such as Breton, "ket" functions as a particle. The phrase "N'ouzon ket petra eo" translates to "I don't know what it is." It also appears in the structure "ne … ket," mirroring the French "ne … pas." Additionally, "ket" can be a noun, specifically referring to a member of the Ket people, an Indigenous group residing in central Siberia along the Yenisei River tributaries. Their language, also called Ket, belongs to the Yeniseian language family.
Physics and Quantum Mechanics
In the realm of physics, particularly quantum mechanics, a "ket" is a column vector in Hilbert space. It represents the state of a quantum mechanical system. It is also the complex conjugate transpose of a bra (a row vector). A specific ket, denoted as |⟩, can be represented by a particular column vector.
Medical and Pharmaceutical Context: Ketamine
The term "ket" is also frequently used as a shortened, informal name for the drug ketamine. Ketamine is a chiral compound, a mixture of equal amounts of two enantiomers: esketamine and arketamine.
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Ketamine: Synthesis and Approval
Ketamine was first synthesized in 1962 by Calvin L. Stevens, a professor of chemistry at Wayne State University and a Parke-Davis consultant. Initially known by the developmental code name CI-581, it was tested in human prisoners in 1964 after promising preclinical research in animals. These early investigations highlighted ketamine's short duration of action and reduced behavioral toxicity compared to phencyclidine (PCP), making it a more favorable anesthetic option. It was approved for use in the United States in 1970.
Anesthetic and Clinical Applications
At anesthetic doses, ketamine induces dissociative anesthesia, a trance-like state characterized by pain relief, sedation, and amnesia. A distinguishing feature of ketamine as an anesthetic is that it preserves breathing and airway reflexes, stimulates heart function (leading to increased blood pressure), and causes moderate bronchodilation. It is often used in trauma, emergency, and pediatric cases. The use of ketamine in anesthesia reflects its characteristics. It is a drug of choice for short-term procedures when muscle relaxation is not required. The effect of ketamine on the respiratory and circulatory systems is different from that of other anesthetics.
Ketamine infusions are used for acute pain treatment in emergency departments and in the perioperative period for individuals with refractory or intractable pain. These infusions involve lower, sub-anesthetic doses. Ketamine, either as an adjunct to morphine or on its own, can reduce morphine use, pain levels, nausea, and vomiting after surgery. For chronic pain, ketamine is used as an intravenous analgesic, mainly if the pain is neuropathic. It has the added benefit of counteracting spinal sensitization or wind-up phenomena experienced with chronic pain.
In multiple clinical trials, ketamine infusions have delivered short-term pain relief in neuropathic pain diagnoses, pain after a traumatic spine injury, fibromyalgia, and complex regional pain syndrome (CRPS). However, the 2018 consensus guidelines on chronic pain concluded that, overall, there is only weak evidence in favor of ketamine use in spinal injury pain, moderate evidence in favor of ketamine for CRPS, and weak or no evidence for ketamine in mixed neuropathic pain, fibromyalgia, and cancer pain.
Ketamine as an Antidepressant
Ketamine is also recognized as a rapid-acting antidepressant, though its effects are transient. Intravenous ketamine infusion in treatment-resistant depression may result in improved mood within 4 hours, reaching its peak at 24 hours. A single dose of intravenous ketamine has shown a response rate greater than 60% as early as 4.5 hours after the dose (with a sustained effect after 24 hours) and greater than 40% after 7 days. Evidence suggests that a 0.5 mg/kg dose injected over 40 minutes gives an optimal outcome. The antidepressant effect of ketamine is diminished at 7 days, and most people relapse within 10 days. One of the main challenges with ketamine treatment can be the length of time that the antidepressant effects last after finishing a course of treatment.
Esketamine, an enantiomer of ketamine, was approved as an antidepressant by the European Medicines Agency in 2019. Esketamine was approved as a nasal spray for treatment-resistant depression in the United States and elsewhere in 2019. A Cochrane review of randomized controlled trials in adults with major depressive disorder found that when compared with placebo, people treated with either ketamine or esketamine experienced reduction or remission of symptoms lasting 1 to 7 days. There were 18.7% (4.1 to 40.4%) more people reporting some benefit and 9.6% (0.2 to 39.4%) more who achieved remission within 24 hours of ketamine treatment. Among people receiving esketamine, 12.1% (2.5 to 24.4%) encountered some relief at 24 hours, and 10.3% (4.5 to 18.2%) had few or no symptoms. Ketamine may partially improve depressive symptoms among people with bipolar depression at 24 hours after treatment, but not three or more days.
Adverse Effects and Contraindications
Ketamine use is associated with several potential adverse effects. At anesthetic doses, 10-20% of adults and 1-2% of children experience adverse psychiatric reactions that occur during emergence from anesthesia, ranging from dreams and dysphoria to hallucinations and emergence delirium. Psychotomimetic effects can be counteracted by pretreatment with a benzodiazepine or propofol. Ketamine anesthesia commonly causes tonic-clonic movements (greater than 10% of people) and rarely hypertonia. Vomiting can be expected in 5-15% of the patients; pretreatment with propofol mitigates it as well. Laryngospasm occurs only rarely with ketamine.
At lower sub-anesthetic doses, psychiatric side effects are prominent. The most common psychiatric side effects are dissociation, visual distortions, and numbness. Also common (20-50%) are difficulty speaking, confusion, euphoria, drowsiness, and difficulty concentrating. Hallucinations are described by 6-10% of people. Dizziness, blurred vision, dry mouth, hypertension, nausea, increased or decreased body temperature, or flushing are the common (>10%) non-psychiatric side effects.
Ketamine is contraindicated in individuals with severe heart or liver disease and uncontrolled psychosis.
Recreational Use and Long-Term Effects
Ketamine is also used recreationally for its hallucinogenic and dissociative effects. When used recreationally, it is found both in crystalline powder and liquid form, and is often referred to by users as "Ket", "Special K" or simply "K". The long-term effects of repeated use are largely unknown and are an area of active investigation. Liver and urinary toxicity have been reported among regular users of high doses of ketamine for recreational purposes. 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.
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. 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 instillation of hyaluronic acid. Liver toxicity of ketamine involves higher doses and repeated administration.
Dependence and Tolerance
Although the incidence of ketamine dependence is unknown, some people who regularly use ketamine develop ketamine dependence. Ketamine tolerance rapidly develops, even with repeated medical use, prompting the use of higher doses.
Mechanism of Action
The mechanism of action of ketamine in alleviating depression is not well understood, but it is an area of active investigation. Ketamine principally acts as a pore blocker of the NMDA receptor, an ionotropic glutamate receptor. The S-(+) and R-(-) stereoisomers of ketamine bind to the dizocilpine site of the NMDA receptor with different affinities, the former showing approximately 3- to 4-fold greater affinity for the receptor than the latter. Whether ketamine is an agonist of D2 receptors is controversial.
Pharmacokinetics
Ketamine can be absorbed by many different routes due to its water and lipid solubility. In the body, ketamine undergoes extensive metabolism. After an intravenous injection of tritium-labelled ketamine, 91% of the radioactivity is recovered from urine and 3% from feces. The medication is excreted mostly in the form of metabolites, with only 2% remaining unchanged.
Detection
Ketamine may be quantified in blood or plasma to confirm a diagnosis of poisoning in hospitalized people, provide evidence in an impaired driving arrest, or assist in a medicolegal death investigation. Blood or plasma ketamine concentrations are usually in a range of 0.5-5.0 mg/L in persons receiving the drug therapeutically (during general anesthesia), 1-2 mg/L in those arrested for impaired driving, and 3-20 mg/L in victims of acute fatal overdosage. Urine is often the preferred specimen for routine drug use monitoring purposes.
Veterinary Use
In veterinary anesthesia, ketamine is often used for its anesthetic and analgesic effects on cats, dogs, rabbits, rats, and other small animals. It is frequently used in induction and anesthetic maintenance in horses. It is an important part of the "rodent cocktail", a mixture of drugs used for anesthetising rodents. Veterinarians often use ketamine with sedative drugs to produce balanced anesthesia and analgesia, and as a constant-rate infusion to help prevent pain wind-up. Ketamine is also used to manage pain among large animals. Ketamine appears not to produce sedation or anesthesia in snails.
Dissociative Effects
At sub-anesthetic doses, ketamine produces a dissociative state, 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 dissociation with visual and auditory hallucination.
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