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Ketamine

Pronunciation

Pronunciation

(KEET a meen)

Index Terms

  • Ketamine HCl
  • Ketamine Hydrochloride

Dosage Forms

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Solution, Injection:

Ketalar: 10 mg/mL (20 mL); 50 mg/mL (10 mL); 100 mg/mL (5 mL)

Generic: 10 mg/mL (20 mL); 50 mg/mL (10 mL); 100 mg/mL (5 mL, 10 mL)

Brand Names: U.S.

  • Ketalar

Pharmacologic Category

  • General Anesthetic

Pharmacology

Produces a cataleptic-like state in which the patient is dissociated from the surrounding environment by direct action on the cortex and limbic system. Ketamine is a noncompetitive NMDA receptor antagonist that blocks glutamate. Low (subanesthetic) doses produce analgesia, and modulate central sensitization, hyperalgesia and opioid tolerance. Reduces polysynaptic spinal reflexes.

Distribution

Vdss: 2.4 L/kg (Wagner 1997)

Metabolism

Hepatic via N-dealkylation (metabolite I [norketamine]), hydroxylation of the cyclohexone ring (metabolites III and IV), conjugation with glucuronic acid and dehydration of the hydroxylated metabolites to form the cyclohexene derivative (metabolite II); metabolite I (norketamine) is 33% as potent as parent compound. When administered orally, norketamine concentrations are higher compared to other routes of administration due to extensive first-pass metabolism in the liver (Blonk 2010; Soto 2012).

Excretion

Urine (91%); feces (3%) (Ghoneim 1977)

Onset of Action

IV: Anesthetic effect: Within 30 seconds

IM: Anesthetic effect: 3 to 4 minutes; Analgesia: Within 10 to 15 minutes

Intranasal: Analgesic effect: Within 10 minutes (Carr 2004); Sedation: Children 2 to 6 years: 5 to 8 minutes (Bahetwar 2011)

Oral: Analgesia: Within 30 minutes; Sedation: Children 2 to 8 years (Turhanoglu 2003):

4 mg/kg/dose: 12.9 ± 1.9 minutes

6 mg/kg/dose: 10.4 ± 2.9 minutes

8 mg/kg/dose: 9.5 ± 1.9 minutes

Time to Peak

Plasma:

IM: 5 to 30 minutes (Clements 1982)

Intranasal: 10 to 14 minutes (Huge 2010); Children 2 to 9 years: ~20 minutes (Malinovsky 1996)

Oral: ~30 minutes (Soto 2012)

Rectal: Children 2 to 9 years: ~45 minutes (Malinovsky 1996)

Duration of Action

IV: Anesthetic effect: 5 to 10 minutes; Recovery: 1 to 2 hours

IM: Anesthetic effect: 12 to 25 minutes; Analgesia: 15 to 30 minutes; Recovery: 3 to 4 hours

Intranasal: Analgesic effect: Up to 60 minutes (Carr 2004); Recovery: Children 2 to 6 years: 34 to 46 minutes (Bahetwar 2011)

Half-Life Elimination

Alpha: 10 to 15 minutes; Beta: 2.5 hours

Protein Binding

27% (Brunton 2006)

Use: Labeled Indications

Anesthesia: Induction and maintenance of general anesthesia

Use: Unlabeled

Analgesia, sedation

Contraindications

Hypersensitivity to ketamine or any component of the formulation; conditions in which an increase in blood pressure would be hazardous

Note: In the emergency department, the following additional absolute contraindications according to the American College of Emergency Physicians have been asserted (ACEP [Green 2011]): Infants <3 months of age; known or suspected schizophrenia (even if currently stable or controlled with medications)

Dosing: Adult

May administer atropine, scopolamine, or another drying agent prior to induction and at appropriate intervals to decrease hypersalivation. Note: Titrate dose for desired effect.

Anesthesia:

Induction of anesthesia:

Manufacturer's labeling:

IM: 6.5 to 13 mg/kg

IV: 1 to 4.5 mg/kg

Alternate recommendations (off-label dosing): Note: lower doses may be used if adjuvant drugs (eg, midazolam) are administered (Miller 2010)

IM: 4 to 10 mg/kg (Green 1990; Miller 2010; White 1982)

IV: 0.5 to 2 mg/kg (Miller 2010; White 1982)

Maintenance of anesthesia: May administer supplemental doses of one-half to the full induction dose or a continuous infusion of 0.1 to 0.5 mg/minute (per manufacturer). Note: To maintain an adequate concentration of ketamine for maintenance of anesthesia, 1 to 2 mg/minute has been recommended (White 1982); doses in the range of 15 to 90 mcg/kg/minute (~1 to 6 mg/minute in a 70-kg patient) have also been suggested (Miller 2010). Concurrent use of nitrous oxide reduces ketamine requirements. Recent laboratory/clinical studies support the use of low-dose ketamine to improve postoperative analgesia/outcome (Adam 2005; Menigaux 2000).

Analgesia (subanesthetic dosing) (off-label use):

Acute pain: Intranasal (off-label route): 0.5 to 1 mg/kg; may repeat in 10 to 15 minutes with 0.25 to 0.5 mg/kg if necessary (Andolfatto 2013; Corrigan 2015; Yeaman 2014)

Chronic pain:

Intranasal (off-label route): 10 mg every 90 seconds as needed until a maximum total dose of 50 mg is reached or pain relieved (Carr 2004).

IV: Note: Various dosing protocols have been utilized. One suggested inpatient protocol is presented. Consider the concomitant use of a benzodiazepine (eg, lorazepam) to prevent or reduce psychotomimetic effects and glycopyrrolate for excessive salivation or lacrimation.

Initial: IV infusion: 0.5 mg/kg over 6 hours. If pain improved by 50% or more after completion of initial dose, then continue infusion at 1.5 mg/kg/24 hours for 48 hours. If pain not improved after completion of initial dose, increase to 2 mg/kg over 12 hours. If pain recurs after initial improvement, titrate upwards by 50% to 100% every 24 hours as needed. Discontinue infusion if pulse >110 bpm, SBP increases >25% of baseline, sustained respiratory rate <7, agitation or severe psychotomimetic effects (Okon 2007).

Oral (off-label route): Initial: 0.5 mg/kg as a single dose to evaluate effect on pain and duration of effect; may increase dose in increments of 0.5 mg/kg as appropriate. For a continuous analgesic effect, may administer 3 to 4 times daily (Blonk 2010).

Acute on chronic episodes of neuropathic pain, severe: Continuous IV or SubQ (off-label route) infusion: 2.3 to 6.7 mcg/kg/minute (equivalent to 0.14 to 0.4 mg/kg/hour) (Hocking 2003).

Postoperative opioid sparing:

IM: 2 to 4 mg/kg (Miller 2010; White 1982); may follow with a continuous infusion if necessary.

IV: 0.2 to 0.8 mg/kg bolus (Miller 2010; Remérand 2009; White 1982; Zakine 2008); a maximum bolus dose of 50 mg was used in one study (Remérand 2009). May follow bolus dose with a continuous infusion if necessary.

Continuous IV infusion: 2 mcg/kg/minute (equivalent to 0.12 mg/kg/hour) (Remérand 2009; Zakine 2008)

Critically ill patients (as an adjunct to an opioid analgesic for non-neuropathic pain): IV: Initial: 0.1 to 0.5 mg/kg bolus; followed by a continuous infusion of 0.83 to 6.7 mcg/kg/minute (equivalent to 0.05 to 0.4 mg/kg/hour) (SCCM [Barr 2013])

Procedural sedation/analgesia (off-label use):

IM: The IV route is preferred; however if IV route unavailable, may administer 4 to 5 mg/kg IM as a single dose; may give a repeat dose (range: 2 to 5 mg/kg) if sedation inadequate after 5 to 10 minutes or if additional doses are required. May consider prophylactic use of a benzodiazepine (eg, midazolam) before ketamine administration to reduce the risk of emergence reactions (ACEP [Green 2011]).

IV: 1 to 2 mg/kg (usual adult dose: 100 mg) over 1 to 2 minutes; may consider prophylactic use of a benzodiazepine (eg, midazolam) before ketamine administration to reduce the risk of emergence reactions (ACEP [Green 2011]; Chudnofsky 2000; Green 2000). If initial sedation inadequate or repeated doses are necessary to accomplish a longer procedure, may administer incremental doses of 0.5 to 1 mg/kg every 5 to 15 minutes as needed (ACEP [Green 2011]).

Dosing: Geriatric

Refer to adult dosing.

Dosing: Pediatric

May administer atropine, scopolamine, or another drying agent prior to induction and at appropriate intervals to decrease hypersalivation.

Anesthesia: Adolescents ≥16 years:

Induction of anesthesia:

IM: 6.5 to 13 mg/kg

IV: 1 to 4.5 mg/kg

Maintenance of anesthesia: May administer supplemental doses of one-half to the full induction dose as needed.

Procedural sedation/analgesia (off-label use): Infants >3 months, Children, and Adolescents:

IM: 4 to 5 mg/kg as a single dose; may give a repeat dose (range: 2 to 5 mg/kg) if sedation inadequate after 5 to 10 minutes or if additional doses are required (ACEP [Green 2011]). Some have recommended smaller doses (2 to 2.5 mg/kg) for minor procedures (eg, wound suture with local anesthetic) (McGlone 2004).

IV: 1.5 to 2 mg/kg over 30 to 60 seconds. If initial sedation inadequate or repeated doses are necessary to accomplish a longer procedure, may administer additional doses of 0.5 to 1 mg/kg every 5 to 15 minutes as needed (ACEP [Green 2011]).

Oral: 6 to 10 mg/kg for 1 dose (mixed in cola or other beverage) 30 minutes before the procedure (Funk 2000; Gutstein 1992; Rosenberg 1991; Stewart 1990)

Dosing: Renal Impairment

There are no dosage adjustments provided in the manufacturer’s labeling.

Dosing: Hepatic Impairment

There are no dosage adjustments provided in the manufacturer’s labeling.

Reconstitution

The 50 mg/mL and 100 mg/mL vials may be further diluted in D5W or NS to prepare a maintenance infusion with a final concentration of 1 mg/mL (or 2 mg/mL in patients with fluid restrictions); mix well. The 10 mg/mL vials are not recommended to be further diluted. Do not mix with barbiturates or diazepam (precipitation may occur). Note: The 100 mg/mL concentration should not be administered IV unless properly diluted with an equal volume of SWFI, NS, or D5W.

Administration

Oral: Mix the appropriate dose (using the injectable solution) in cola or other beverage; administer immediately after preparation (Gutstein 1992).

IM: Inject deep IM into large muscle mass.

IV: According to the manufacturer, administer bolus/induction doses over 1 minute or at a rate of 0.5 mg/kg/minute; more rapid administration may result in respiratory depression and enhanced pressor response. Some experts suggest administration over 2 to 3 minutes (Miller 2010). May also be administered as a continuous infusion.

Compatibility

Stable in D5W, NS.

Compatibility in syringe: Incompatible with amobarbital, diazepam, doxapram, methohexital, pentobarbital, phenobarbital.

Storage

Store at 20°C to 25°C (68°F to 77°F). Protect from light.

Drug Interactions

Alcohol (Ethyl): CNS Depressants may enhance the CNS depressant effect of Alcohol (Ethyl). Monitor therapy

Azelastine (Nasal): CNS Depressants may enhance the CNS depressant effect of Azelastine (Nasal). Avoid combination

Blonanserin: CNS Depressants may enhance the CNS depressant effect of Blonanserin. Consider therapy modification

Brimonidine (Topical): May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Buprenorphine: CNS Depressants may enhance the CNS depressant effect of Buprenorphine. Management: Consider reduced doses of other CNS depressants, and avoiding such drugs in patients at high risk of buprenorphine overuse/self-injection. Initiate buprenorphine patches (Butrans brand) at 5 mcg/hr in adults when used with other CNS depressants. Consider therapy modification

Cannabis: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

CNS Depressants: May enhance the adverse/toxic effect of other CNS Depressants. Monitor therapy

Conivaptan: May increase the serum concentration of CYP3A4 Substrates. Avoid combination

CYP2C9 Inducers (Strong): May increase the metabolism of CYP2C9 Substrates. Management: Consider an alternative for one of the interacting drugs. Some combinations may be specifically contraindicated. Consult appropriate manufacturer labeling. Consider therapy modification

CYP2C9 Inhibitors (Moderate): May decrease the metabolism of CYP2C9 Substrates. Monitor therapy

CYP2C9 Inhibitors (Strong): May decrease the metabolism of CYP2C9 Substrates. Consider therapy modification

CYP3A4 Inhibitors (Moderate): May decrease the metabolism of CYP3A4 Substrates. Monitor therapy

CYP3A4 Inhibitors (Strong): May decrease the metabolism of CYP3A4 Substrates. Consider therapy modification

Dabrafenib: May decrease the serum concentration of CYP2C9 Substrates. Management: Seek alternatives to the CYP2C9 substrate when possible. If concomitant therapy cannot be avoided, monitor clinical effects of the substrate closely (particularly therapeutic effects). Consider therapy modification

Dasatinib: May increase the serum concentration of CYP3A4 Substrates. Monitor therapy

Dimethindene: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Doxylamine: May enhance the CNS depressant effect of CNS Depressants. Management: The manufacturer of Diclegis (doxylamine/pyridoxine), intended for use in pregnancy, specifically states that use with other CNS depressants is not recommended. Monitor therapy

Dronabinol: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Droperidol: May enhance the CNS depressant effect of CNS Depressants. Management: Consider dose reductions of droperidol or of other CNS agents (e.g., opioids, barbiturates) with concomitant use. Consider therapy modification

Enzalutamide: May decrease the serum concentration of CYP2C9 Substrates. Management: Concurrent use of enzalutamide with CYP2C9 substrates that have a narrow therapeutic index should be avoided. Use of enzalutamide and any other CYP2C9 substrate should be performed with caution and close monitoring. Consider therapy modification

Flunitrazepam: CNS Depressants may enhance the CNS depressant effect of Flunitrazepam. Consider therapy modification

Fosaprepitant: May increase the serum concentration of CYP3A4 Substrates. Monitor therapy

Fusidic Acid (Systemic): May increase the serum concentration of CYP3A4 Substrates. Avoid combination

HYDROcodone: CNS Depressants may enhance the CNS depressant effect of HYDROcodone. Management: Consider starting with a 20% to 30% lower hydrocodone dose when using together with any other CNS depressant. Dose reductions in the other CNS depressant may also be warranted. Consider therapy modification

HydrOXYzine: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Idelalisib: May increase the serum concentration of CYP3A4 Substrates. Avoid combination

Ivacaftor: May increase the serum concentration of CYP3A4 Substrates. Monitor therapy

Kava Kava: May enhance the adverse/toxic effect of CNS Depressants. Monitor therapy

Luliconazole: May increase the serum concentration of CYP3A4 Substrates. Monitor therapy

Lumacaftor: May decrease the serum concentration of CYP2C9 Substrates. Lumacaftor may increase the serum concentration of CYP2C9 Substrates. Monitor therapy

Magnesium Sulfate: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Memantine: NMDA Receptor Antagonists may enhance the adverse/toxic effect of Memantine. Monitor therapy

Methotrimeprazine: CNS Depressants may enhance the CNS depressant effect of Methotrimeprazine. Methotrimeprazine may enhance the CNS depressant effect of CNS Depressants. Management: Reduce adult dose of CNS depressant agents by 50% with initiation of concomitant methotrimeprazine therapy. Further CNS depressant dosage adjustments should be initiated only after clinically effective methotrimeprazine dose is established. Consider therapy modification

MetyroSINE: CNS Depressants may enhance the sedative effect of MetyroSINE. Monitor therapy

MiFEPRIStone: May increase the serum concentration of CYP2C9 Substrates. Management: Use CYP2C9 substrates at the lowest recommended dose, and monitor closely for adverse effects, during and in the 2 weeks following mifepristone treatment. Consider therapy modification

MiFEPRIStone: May increase the serum concentration of CYP3A4 Substrates. Management: Minimize doses of CYP3A4 substrates, and monitor for increased concentrations/toxicity, during and 2 weeks following treatment with mifepristone. Avoid cyclosporine, dihydroergotamine, ergotamine, fentanyl, pimozide, quinidine, sirolimus, and tacrolimus. Consider therapy modification

Minocycline: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Mirtazapine: CNS Depressants may enhance the CNS depressant effect of Mirtazapine. Monitor therapy

Nabilone: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Netupitant: May increase the serum concentration of CYP3A4 Substrates. Monitor therapy

Orphenadrine: CNS Depressants may enhance the CNS depressant effect of Orphenadrine. Avoid combination

OxyCODONE: CNS Depressants may enhance the CNS depressant effect of OxyCODONE. Management: When oxycodone is combined with another CNS depressant, a dose reduction of one or both agents should be considered. The extended release oxycodone starting dose should be reduced 50% to 67% when initiated in patients already receiving CNS depressants. Consider therapy modification

Palbociclib: May increase the serum concentration of CYP3A4 Substrates. Monitor therapy

Paraldehyde: CNS Depressants may enhance the CNS depressant effect of Paraldehyde. Avoid combination

Perampanel: May enhance the CNS depressant effect of CNS Depressants. Management: Patients taking perampanel with any other drug that has CNS depressant activities should avoid complex and high-risk activities, particularly those such as driving that require alertness and coordination, until they have experience using the combination. Consider therapy modification

Piribedil [INT]: CNS Depressants may enhance the CNS depressant effect of Piribedil [INT]. Monitor therapy

Pramipexole: CNS Depressants may enhance the sedative effect of Pramipexole. Monitor therapy

ROPINIRole: CNS Depressants may enhance the sedative effect of ROPINIRole. Monitor therapy

Rotigotine: CNS Depressants may enhance the sedative effect of Rotigotine. Monitor therapy

Rufinamide: May enhance the adverse/toxic effect of CNS Depressants. Specifically, sleepiness and dizziness may be enhanced. Monitor therapy

Selective Serotonin Reuptake Inhibitors: CNS Depressants may enhance the adverse/toxic effect of Selective Serotonin Reuptake Inhibitors. Specifically, the risk of psychomotor impairment may be enhanced. Monitor therapy

Simeprevir: May increase the serum concentration of CYP3A4 Substrates. Monitor therapy

Sodium Oxybate: May enhance the CNS depressant effect of CNS Depressants. Management: Consider alternatives to combined use. When combined use is needed, consider minimizing doses of one or more drugs. Use of sodium oxybate with alcohol or sedative hypnotics is contraindicated. Consider therapy modification

Stiripentol: May increase the serum concentration of CYP3A4 Substrates. Management: Use of stiripentol with CYP3A4 substrates that are considered to have a narrow therapeutic index should be avoided due to the increased risk for adverse effects and toxicity. Any CYP3A4 substrate used with stiripentol requires closer monitoring. Consider therapy modification

Suvorexant: CNS Depressants may enhance the CNS depressant effect of Suvorexant. Management: Dose reduction of suvorexant and/or any other CNS depressant may be necessary. Use of suvorexant with alcohol is not recommended, and the use of suvorexant with any other drug to treat insomnia is not recommended. Consider therapy modification

Tapentadol: May enhance the CNS depressant effect of CNS Depressants. Management: Start tapentadol at a dose of one-third to one-half of the normal dose if being initiated in a patient who is taking another drug with CNS depressant effects. Monitor closely for evidence of excessive CNS depression. Consider therapy modification

Tetrahydrocannabinol: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Thalidomide: CNS Depressants may enhance the CNS depressant effect of Thalidomide. Avoid combination

Thiopental: Ketamine may enhance the adverse/toxic effect of Thiopental. Monitor therapy

Thiotepa: May increase the serum concentration of CYP2B6 Substrates. Monitor therapy

Trimeprazine: May enhance the CNS depressant effect of CNS Depressants. Monitor therapy

Zolpidem: CNS Depressants may enhance the CNS depressant effect of Zolpidem. Management: Reduce the Intermezzo brand sublingual zolpidem adult dose to 1.75 mg for men who are also receiving other CNS depressants. No such dose change is recommended for women. Avoid use with other CNS depressants at bedtime; avoid use with alcohol. Consider therapy modification

Test Interactions

May interfere with urine detection of phencyclidine (false-positive).

Adverse Reactions

Frequency not always defined.

Cardiovascular: Bradycardia, cardiac arrhythmia, hypotension, increased blood pressure, increased pulse

Central nervous system: Prolonged emergence from anesthesia (~12%; includes confusion, delirium, dreamlike state, excitement, hallucinations, irrational behavior, vivid imagery), drug dependence, hypertonia (tonic-clonic movements sometimes resembling seizures), increased cerebrospinal fluid pressure

Dermatologic: Erythema (transient), morbilliform rash (transient), rash at injection site

Endocrine & metabolic: Central diabetes insipidus (Hatab 2014)

Gastrointestinal: Anorexia, nausea, sialorrhea (Hatab 2014), vomiting

Genitourinary (adverse reactions can be severe in patients with a history of chronic ketamine use/abuse): Cystitis, irritable bladder, urethritis, urinary tract irritation

Hypersensitivity: Anaphylaxis

Local: Pain at injection site

Neuromuscular & skeletal: Laryngospasm

Ophthalmic: Diplopia, increased intraocular pressure, nystagmus

Respiratory: Airway obstruction, apnea, respiratory depression

Warnings/Precautions

Concerns related to adverse effects:

• Airway complications: When used for procedural sedation for major procedures involving the posterior pharynx (eg, endoscopy) or when used for patients with an active pulmonary infection or disease (including upper respiratory disease or asthma), the use of ketamine increases the risk of laryngospasm. Patients with a history of airway instability, tracheal surgery, or tracheal stenosis may be at a higher risk of airway complications. The American College of Emergency Physicians considers these situations relative contraindications for the use of ketamine (ACEP [Green 2011]). The manufacturer recommends against the use of ketamine alone in surgery or diagnostic procedures of the pharynx, larynx, or bronchial tree; mechanical stimulation of the pharynx should be avoided, whenever possible, if ketamine is used alone.

• CNS depression: May cause CNS depression, which may impair physical or mental abilities; patients must be cautioned about performing tasks which require mental alertness (eg, operating machinery or driving). When used for outpatient surgery, the patient should be accompanied by a responsible adult. Driving, operating hazardous machinery or engaging in hazardous activities should not be undertaken for ≥24 hours after anesthesia according to the manufacturer.

• Dependence: May cause dependence (withdrawal symptoms on discontinuation) and tolerance with prolonged use. A withdrawal syndrome with psychotic features has been described following discontinuation of long-term use.

• Emergence reactions: Postanesthetic emergence reactions which can manifest as vivid dreams, hallucinations, and/or frank delirium occur; these reactions are less common in patients <16 years of age and >65 years and when given intramuscularly (White 1982). Emergence reactions, confusion, or irrational behavior may occur up to 24 hours postoperatively and may be reduced by pretreatment with a benzodiazepine, use of ketamine at the lower end of the dosing range, and minimizing verbal and tactile stimulation of the patient during the recovery period. Avoid use in patients with schizophrenia; may exacerbate psychotic symptoms (Lahti 1995; Malhotra 1997). The American College of Emergency Physicians considers the use of ketamine in patients with known or suspected schizophrenia (even if currently stable or controlled with medications) an absolute contraindication (ACEP [Green 2011]).

• Increased intracranial pressure: The American College of Emergency Physicians considers the use of ketamine in patients with CNS masses, CNS abnormalities, or hydrocephalus a relative contraindication due to increased intracranial pressure produced by ketamine (ACEP [Green 2011]).

• Increased ocular pressure: Use with caution in patients with increased intraocular pressure and avoid use in patients with an open eye injury or other ophthalmologic disorder where an increase in intraocular pressure would prove to be detrimental; ketamine may further increase intraocular pressure (Cunningham 1986; Miller 2010; Nagdeve 2006). The American College of Emergency Physicians considers the use of ketamine in patients with glaucoma or acute globe injury a relative contraindication (ACEP [Green 2011]).

• Porphyria: The American College of Emergency Physicians considers the use of ketamine in patients with porphyria a relative contraindication due to enhanced sympathomimetic effect produced by ketamine (ACEP [Green 2011]).

• Respiratory depression: Rapid IV administration or overdose may cause respiratory depression or apnea. Resuscitative equipment should be available during use.

• Thyroid disorders: The American College of Emergency Physicians considers the use of ketamine in patients with a thyroid disorder or receiving a thyroid medication a relative contraindication due to enhanced sympathomimetic effect produced by ketamine (ACEP [Green 2011]).

Disease-related concerns:

• Cardiovascular disease: Use with caution in patients with coronary artery disease, catecholamine depletion, hypertension, and tachycardia. Cardiac function should be continuously monitored in patients with increased blood pressure or cardiac decompensation. Ketamine increases blood pressure, heart rate, and cardiac output thereby increasing myocardial oxygen demand. The mechanism by which ketamine causes a sympathetic surge to stimulate the cardiovascular system has yet to be elucidated. The use of concurrent benzodiazepine, inhaled anesthetics, and propofol or administration of ketamine as a continuous infusion may reduce these cardiovascular effects (Miller 2010). The American College of Emergency Physicians recommends avoidance in patients who are already hypertensive and in older adults with risk factors for coronary artery disease (ACEP [Green 2011]).

• Cerebrospinal fluid (CSF) pressure elevation: Use with caution in patients with CSF pressure elevation; an increase in CSF pressure may be associated with use.

• Ethanol use: Use with caution in the chronic alcoholic or acutely alcohol-intoxicated.

Concurrent drug therapy issues:

• Drug-drug interactions: Potentially significant interactions may exist, requiring dose or frequency adjustment, additional monitoring, and/or selection of alternative therapy. Consult drug interactions database for more detailed information.

Other warnings/precautions:

• Experienced personnel: Use requires careful patient monitoring, should only be used by experienced personnel who are not actively engaged in the procedure or surgery. If used in a nonintubated and/or nonmechanically-ventilated patient, qualified personnel and appropriate equipment for rapid institution of respiratory and/or cardiovascular support must be immediately available. Use to induce moderate (conscious) sedation in patients warrants monitoring equivalent to that seen with deep anesthesia. Consult local regulations and individual institutional policies and procedures.

Monitoring Parameters

Heart rate, blood pressure, respiratory rate, transcutaneous O2 saturation, emergence reactions; cardiac function should be continuously monitored in patients with increased blood pressure or cardiac decompensation

Pregnancy Considerations

Adverse events have not been observed in animal reproduction studies. Ketamine crosses the placenta and can be detected in fetal tissue. Ketamine produces dose dependent increases in uterine contractions; effects may vary by trimester. The plasma clearance of ketamine is reduced during pregnancy. Dose related neonatal depression and decreased APGAR scores have been reported with large doses administered at delivery (Ghoneim 1977; Little 1972; White 1982). Although ketamine has been used during vaginal delivery and cesarean section, use in pregnancy, including obstetrics (either vaginal or abdominal delivery) is not recommended by the manufacturer (Akamatsu 1974; Little 1972; Mercier 1998).

Patient Education

• Discuss specific use of drug and side effects with patient as it relates to treatment. (HCAHPS: During this hospital stay, were you given any medicine that you had not taken before? Before giving you any new medicine, how often did hospital staff tell you what the medicine was for? How often did hospital staff describe possible side effects in a way you could understand?)

• Patient may experience fatigue, lack of appetite, vomiting, or nausea. Have patient report immediately to prescriber severe dizziness, passing out, difficulty breathing, slow breathing, shallow breathing, tachycardia, bradycardia, arrhythmia, severe headache, confusion, hallucinations, behavioral changes, muscle rigidity, seizures, vision changes, involuntary eye movements, painful urination, or severe injection site irritation (HCAHPS).

• Educate patient about signs of a significant reaction (eg, wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat). Note: This is not a comprehensive list of all side effects. Patient should consult prescriber for additional questions.

Intended Use and Disclaimer: Should not be printed and given to patients. This information is intended to serve as a concise initial reference for healthcare professionals to use when discussing medications with a patient. You must ultimately rely on your own discretion, experience and judgment in diagnosing, treating and advising patients.

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