Ketamine

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. /Ketamine hydrochloride/

Advice for firefighters: Wear self contained breathing apparatus for fire fighting if necessary. /Ketamine hydrochloride/

Keep container tightly closed in a dry and well-ventilated place. Recommended storage temperature: 2-8 °C. /Ketamine hydrochloride/

Store in a tightly sealed container, protected from light, and at room temperature.

Store at 20 to 25 °C (68 to 77 °F).

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal. /Ketamine hydrochloride/

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber; Contaminated packaging: Dispose of as unused product. /Ketamine hydrochloride/

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Do not let product enter drains. /Ketamine hydrochloride/

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Provide appropriate exhaust ventilation at places where dust is formed. Normal measures for preventive fire protection. /Ketamine hydrochloride/

Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday. /Ketamine hydrochloride/

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands. /Ketamine hydrochloride/

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

Eye/face protection: Safety glasses with side-shields conforming to EN166. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU). /Ketamine hydrochloride/

Skin protection: Handle with gloves. /Ketamine hydrochloride/

Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace. /Ketamine hydrochloride/

Respiratory protection: For nuisance exposures use type P95 (US) or type P1 (EU EN 143) particle respirator. For higher level protection use type OV/AG/P99 (US) or type ABEK-P2 (EU EN 143) respirator cartridges. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU). /Ketamine hydrochloride/

/The study objective was/ to determine the effects of ketamine-diazepam and ketamine-acepromazine combinations on intraocular pressure (IOP) in rabbits. /This was a/ randomized clinical trial. Sixteen adult New Zealand white rabbits approximately one year old, weighing 2.3 +/- 0.2 kg were used in this study. The animals were randomly divided into two groups of eight each (KA and KD). The pre-treatment IOPs were recorded in both groups (T0). All rabbits in group KA received intramuscular ketamine-acepromazine (ketamine 30 mg/kg + acepromazine 0.5 mg/kg). Ketamine-diazepam (ketamine 30 mg/kg + diazepam 1 mg/kg) was administered intramuscularly in members of group KD. The IOP values were measured at 5 (T(5)), 15 (T(15)), and 20 (T(20)) minutes after drug administration in both treatment groups. Significant increases in IOP values were observed in both treatment groups at T(5,) T(15), and T(20) in comparison to the baseline values. In group KA the mean +/- SD IOP at T(5,) T(15), and T(20) were 37 +/- 13 (p < 0.001), 35 +/- 4 (p < 0.001) and 34 +/- 4 mmHg (p < 0.001). The post-treatment mean +/- sd values in group KD were 23 +/- 8 (p = 0.002), 23 +/- 5 (p < 0.001) and 23 +/- 6 mmHg (p = 0.001) at 5, 15, and 20 minutes respectively. Both ketamine-diazepam and ketamine-acepromazine combinations increased IOP after intramuscular administration in rabbits.

Prolonged recovery time may occur if barbiturates and/or /CNS depressants/ are used concurrently with ketamine.

Retrospective analysis was conducted of patients with super-refractory status epilepticus (SRSE) who were treated simultaneously with propofol and ketamine. Sixty-seven patients were identified from 2012 to 2015, and outcomes documented were resolution and mortality. The duration of combined ketamine and propofol use ranged from 1 to 28 days (mean - 3.6 days). Infusion rates ranged up to 145 and 175 ug/kg/min. Vasopressors were used in 53 patients (79%), and were given within the first 5 days of the ICU admission in 48 (91%) patients. The overall SRSE resolution rate was 91%, and the overall mortality including patients with anoxic brain injury was 39%. Of the 13 patients with SRSE as a result of anoxic brain injury, SRSE was controlled in 5 (56%). The primary determinant of mortality was family withdrawing care related to the presence of severe medical/neurological diseases.

The non-competitive N-methyl-D-aspartate receptor antagonist ketamine leads to transient psychosis-like symptoms and impairments in oculomotor performance in healthy volunteers. This study examined whether the adverse effects of ketamine on oculomotor performance can be reversed by the atypical antipsychotic risperidone. In this randomized double-blind, placebo-controlled study, 72 healthy participants performed smooth pursuit eye movements (SPEM), prosaccades (PS) and antisaccades (AS) while being randomly assigned to one of four drug groups (intravenous 100 ng/mL ketamine, 2 mg oral risperidone, 100 ng/mL ketamine plus 2 mg oral risperidone, placebo). Drug administration did not lead to harmful adverse events. Ketamine increased saccadic frequency and decreased velocity gain of SPEM (all P < 0.01) but had no significant effects on PS or AS (all P > or = 0.07). An effect of risperidone was observed for amplitude gain and peak velocity of PS and AS, indicating hypometric gain and slower velocities compared with placebo (both P < or = 0.04). No ketamine by risperidone interactions were found (all P > or = 0.26). The results confirm that the administration of ketamine produces oculomotor performance deficits similar in part to those seen in schizophrenia. The atypical antipsychotic risperidone did not reverse ketamine-induced deteriorations. These findings do not support the cognitive enhancing potential of risperidone on oculomotor biomarkers in this model system of schizophrenia and point towards the importance of developing alternative performance-enhancing compounds to optimize pharmacological treatment of schizophrenia.

For more Interactions (Complete) data for Ketamine (17 total), please visit the HSDB record page.

Short term use of ketamine for anesthesia has been associated with rare instances of serum enzyme elevations, but not with clinically apparent liver injury. With chronic or intermittent use, however, unusual biliary and hepatic complications have been described. In a manner similar to its effects on the urinary tract, ketamine can also cause abnormalities in the biliary system with dilation and irregularity of the intra- and extra-hepatic bile ducts. Patients typically developed right upper quadrant pain and tenderness associated with elevations in serum alkaline phosphatase and aminotransferase levels, with minimal or no increase in bilirubin (Case 1). Biliary imaging may reveal dilation and irregularity of the intra- and extra-hepatic bile ducts with fusiform dilation of the common bile duct suggestive of choledochal cysts. Liver biopsy demonstrates changes suggestive of chronic liver obstruction or sclerosing cholangitis. Discontinuation of ketamine is usually followed by slow improvement and the abnormalities found on biliary imaging may no longer be demonstrable several months later.

TERRESTRIAL FATE: Based on a classification scheme(1), a reported log Koc value of 3.062(2), indicates that ketamine is expected to have low mobility in soil(SRC). The pKa of ketamine is 7.5(3), indicating that this compound will exist partially in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization of the cation from moist soil is not expected because cations do not volatilize(SRC). Volatilization of neutral ketamine from moist soil surfaces is not expected(SRC) given an estimated Henry's Law constant of 1.4X10-8 atm-cu m/mole(SRC), using a fragment constant estimation method(5). Ketamine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 5.2X10-5 mm Hg at 25 °C(SRC), determined from a fragment constant method(5). Ketamine was found to be highly stable to degradation in two studies in sewage with <10% transformation at pH 7.5 at 20 °C(6) suggesting that biodegradation is not an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), a reported log Koc value of 3.062(2), indicates that ketamine is expected to adsorb to suspended solids and sediment(SRC). A pKa of 7.5(3) indicates ketamine will exist partially in the cation form at pH values of 5 to 9 and, therefore, volatilization of the cation from water surfaces is not expected(SRC). Volatilization from water surfaces of the neutral ketamine is not expected(4) based upon an estimated Henry's Law constant of 1.4X10-8 atm-cu m/mole(SRC), developed using a fragment constant estimation method(5). Ketamine is not expected to undergo hydrolysis in the environment due to the lacks of functional groups that hydrolyze under environmental conditions(4). According to a classification scheme(6), an estimated BCF of 13(SRC), from its log Kow of 2.18(7) and a regression-derived equation(5), suggests the potential for bioconcentration in aquatic organisms is low. Ketamine was found to be highly stable to degradation in two studies in sewage with <10% transformation at pH 7.5 at 20 °C(1). Ketamine was found to be highly stable to degradation in two studies in sewage with <10% transformation at pH 7.5 at 20 °C(8) suggesting that biodegradation is not an important environmental fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), ketamine, which has an estimated vapor pressure of 5.2X10-5 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase ketamine is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 5 hours(SRC), calculated from its rate constant of 7.7X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(2). Particulate-phase ketamine may be removed from the air by wet or dry deposition(SRC). Ketamine contains chromophores that absorb at wavelengths >290 nm(3) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

The most common adverse drug reactions associated with ketamine are nausea, vomiting, dizziness, diplopia, drowsiness, dysphoria, and confusion. Reports of the emergence phenomenon exist for approximately 6% to 12% of patients. The common adverse drug reactions of ketamine are listed below.

IDENTIFICATION AND USE: Ketamine is a cyclohexanone derivative used as an anesthetic agent in human and veterinary procedures. Ketamine hydrochloride injection, USP is indicated as the sole anesthetic agent for diagnostic and surgical procedures that do not require skeletal muscle relaxation. HUMAN STUDIES: Ketamine is a unique anesthetic because it has both hypnotic and analgesic effects and also potential hallucinogenic side effects. Lack of cardiopulmonary depression makes the drug a popular choice for anesthesia in the prehospital setting. In recent years ketamine has been found to have anti-hyperalgesic and opioid saving effects, opening to new ways of managing post-operative and chronic pain states. Ketamine has been used as a drug of abuse. Ketamine produces a variety of symptoms including, but not limited to, anxiety, dysphoria, disorientation, insomnia, flashbacks, hallucinations, and psychotic episodes. Ketamine dependence and tolerance are possible following prolonged administration. A withdrawal syndrome with psychotic features has been described following discontinuation of long-term ketamine use. Frequent recreational users of ketamine have been found to have impaired memory 3 days after their last dose, compared with infrequent users. Flashbacks have also been reported. Frequent use result in tolerance and the need to increase the dose in order to maintain similar effects. Respiratory depression may occur with overdosage or too rapid a rate of administration of ketamine, in which case supportive ventilation should be employed. Mechanical support of respiration is preferred to administration of analeptics. ANIMAL STUDIES: Ketamine hydrochloride administration altered the hemogram of rhesus monkeys when compared to physical restraint for venipuncture. The alterations were decreases in the leukocyte count, total plasma proteins, and hematocrit. The decrease in the leukocyte count was due primarily to a decrease in lymphocytes with a smaller decrease in neutrophils. Ketamine decreased locomotor activity and increased cell death in the prefrontal cortex of monkeys with 6 months of ketamine treatment when compared with the control monkeys. Such decreases were not found in the 1-month ketamine-treated group. Pre- or post-training systemic administration of ketamine (0.3, 1 and 3 mg/kg ip) in a dose-dependent manner disrupted rats performance in spatial and non-spatial recognition memory tests, suggesting that ketamine affected pre- and post-training memory components. Intraperitoneal injections of ketamine 75 mg/kg in rats of both sexes (age 1-16 weeks) revealed a significant relationship between increased age and decreased duration of sleeping time for both sexes during the first 3 weeks of age. This decrease in sleeping time seemed to be associated with the increased production of the cyclohexanone oxidation metabolite of ketamine. After 3 weeks of age there was a greater sleeping time in the female rat than the male and this seemed to be associated with a greater ability of the male to produce the cyclohexanone oxidation metabolite. In rats, ketamine, or its urinary metabolites, disrupted the proliferation of bladder epithelial cells, resulting in defected bladder epithelial barrier. A single 24-hr episode of ketamine anesthesia, occurring during a sensitive period of brain development, resulted in very long-lasting deficits in brain function in rhesus monkeys. The pattern of neurodegeneration induced by ketamine in fetuses was different from that in neonates, and loss of neurons attributable to ketamine exposure was 2.2 times greater in the fetal than neonatal brains. A subanesthetic dose of ketamine increased exploratory locomotion in one strain of mice, but decreased it in another strain of mice. Therefore, hereditary factors may play an important role in ketamine-induced responses. Epidural ketamine injection was associated with caudal anti-nociception, sedation and ataxia in the dromedary camels. Published animal studies demonstrate that the administration of anesthetic and sedation drugs that block NMDA receptors and/or potentiate GABA activity increase neuronal apoptosis in the developing brain and result in long-term cognitive deficits when used for longer than 3 hours.

EPA has released the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays/[USEPA; ICSS Dashboard Application; Available from, as of November 16, 2017: http://actor.epa.gov/dashboard/]

The following link will take the user to the National Toxicology Program (NTP) Test Status of Agents Search page, which tabulates the results and current status of tests such as "Short-Term Toxicity Studies", "Long-term Carcinogenicity Studies", "Developmental Studies", "Genetic Toxicology Studies", etc., performed with this chemical. Testing status for ketamine hydrochloride is available.[Available from, as of August 24, 2017: https://ntpsearch.niehs.nih.gov/?e=True&ContentType=Testing+Status]

Raw wastewater samples collected 2008-2014 from sewage treatment plants in 17 Italian cities contained ketamine as follows(1):[Table#3905]

Ketamine was detected in 2 of 7 wastewater treatment plant influent samples at 16 and <5 ng/L; samples were collected from different regions of the US on unreported dates(1). Wastewater treatment plant influent and effluent concentrations of ketamine have been reported as 52-235 and 83-130 ng/L, respectively, in the UK(2). Ketamine was detected at 8033-138,000 and 4300-39,333 ng/L in influent and effluent wastewater treatment plant samples collected from Nanwan, respectively, and at respective concentrations of 44,333-92,667 and <2.5-9867 ng/L from a wastewater treatment plant in Kenting, Taiwan; samples were collected from Oct 2010 to Aug 2011(3). The mean concentration of ketamine in influent samples collected in 2015 from wastewater treatment plants in Beijing, China was reported as 6.63 ng/L(4). The mean wastewater effluent concentration of ketamine was <0.93 and 4.1 ng/L in samples collected Jan and June 2015, respectively from a treatment plant in southwest England(5). Based on studies, ketamine removal is about 23.4% in wastewater treatment plants(6).

The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Ketamine hydrochloride is included on this list. /Ketamine hydrochloride/

Schedule III shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. Each drug or substance has been assigned the DEA Controlled Substances Code Number set forth opposite it. Depressants. ... Unless specifically excepted or unless listed in another schedule, any material, compound, mixture, or preparation which contains any quantity of the following substances having a depressant effect on the central nervous system: Ketamine, its salts, isomers, and salts of isomers. DEA Code Number: 7285.

Implanatation or injectable dosage form new animal drugs. Ketamine. ... Federal law restricts this drug to use by or on the order of a licensed veterinarian. ... Conditions of use - (1) Cats ... Indications for use: For restraint or as the sole anesthetic agent in diagnostic or minor, brief surgical procedures that do not require skeletal muscle relaxation. (2) Subhuman primates ... Indications for use: For restraint.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including ketamine hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Ketamine hydrochloride/

The Generic Animal Drug and Patent Restoration act requires that each sponsor of an approved animal drug must submit to the FDA certain information regarding patents held for the animal drug or its method of use. The Act requires that this information, as well as a list of all animal drug products approved for safety and effectiveness, be made available to the public. Ketamine hydrochloride is included on this list. /Ketamine hydrochloride/

Ketamine, its salts, isomers, and salts of isomers (DEA Code Number: 7285) is a Schedule III controlled substance.

Schedule III Controlled Substance: (A) The drug or other substance has a potential for abuse less than the drugs or other substances in schedules I and II. (B) The drug or other substance has a currently accepted medical use in treatment in the United States. (C) Abuse of the drug or other substance may lead to moderate or low physical dependence or high psychological dependence.

Analgesics; Anesthetics, Dissociative; Excitatory Amino Acid Antagonists

MEDICATION

MEDICATION (VET)

Use (kg; approx.) in Germany (2009): >250

Preparation: C.L. Stevens, Belgium patent 634208; idem, United States of America patent 3254124 (1963, 1966 both to Parke, Davis).

... Prepared by bromination of o-chlorophenyl cyclopentyl ketone, which is then reacted with methylamine to give the methylimino alcohol. Thermolysis of the imino hydrochloride yields ketamine by ring expansion.

Trade Names. Ketanest (Parke-Davis); Ketaject (Bristol); Ketalar (Parke-Davis; Sankyo); Ketaset (Bristol); Vetalar (Parke-Davis, veterinary anesthetic).

Ketamine is supplied as a mixture of the R+ and S- isomers even though the S- isomer is more potent with fewer side effects. ... Ketamine is ... available as 10, 50, and 100 mg/mL solutions in sodium chloride plus the preservative benzethonium chloride.

Common street names include: Cat Tranquilizer, Cat Valium, Jet K, Kit Kat, Purple, Special K, Special La Coke, Super Acid, Super K, and Vitamin K.

Since the 1970s, ketamine has been marketed in the United States as an injectable, short-acting anesthetic for use in humans and animals. In 1999, ketamine including its salts, isomers and salts of isomers, became a Schedule III non-narcotic substance under the Controlled Substances Act.

Ketamine is produced commercially in a number of countries, including the United States. Most of the ketamine illegally distributed in the United States is diverted or stolen from legitimate sources, particularly veterinary clinics, or smuggled into the United States from Mexico.