Newer psychoactive substances and club drugs were discussed. Synthetic cathinones like mephedrone and synthetic cannabinoids found in products like Spice/K2 were covered. Mephedrone is a stimulant that promotes monoamine release and inhibits reuptake. It was popular among clubgoers but can cause effects like sweating, hypertension, and psychosis. Spice contains synthetic cannabinoids that are full CB1 agonists and cause effects mimicking marijuana but can also cause seizures, psychosis, and withdrawal. Management focuses on supportive care and sedation for sympathomimetic toxicity and psychosis. MDMA was also discussed, working as a serotonin releaser/re

1. Newer Psychoactive
Substances &
Club Drugs
Dr (Maj) Ashutosh Ratnam

2. Newer Psychoactive Substances & Club Drugs
• Synthetic Cathinones – Meow Meow
• Synthetic Cannabinoids – Spice /K2
• Club Drugs
–MDMA
–GHB
–Ketamine
–Rohypnol

3. Drug Assessment
• History
• Clinical Pharmacology
• Appearance & Routes of Use
• Clinical Effects
–Desirable
–Undesirable
• Management Principles

4. Mephedrone
4-methylmethcathinone
• Meow Meow
• Bath Salts
• Miaow
• Drone
• Meph
• Bubbles
• Spice E
• Charge
• M-cat
• Rush
• Ronzio
• Fiskrens
• MMC Hammer
• Plant Food

5. Mephedrone – History
• Khat-extracted cathinones appeared in Israel in
early 2000s
– locally named as ‘Hagigat’
– Outlawed following several hospitalisations due to
exposure
• Due to the ban, chemists altered chemical structure
of cathinone to synthesize related unscheduled
compounds
• Availability for online purchase and related
popularity started in 2007 (Deluca et al. 2009)

7. Mephedrone – History
• Research led by the National Addiction Centre (London) on
2,295 readers of dance magazine ‘Mixmag’ disclosed that
41.7% of surveyed people had ever tried mephedrone and
33.2% had used during the last month
– making it the sixth most popular drug among clubbers, after
tobacco, alcohol, cannabis, ecstasy and cocaine
• 48.8% of users sourced mephedrone from street-level
dealers and 10.7% from Internet
• Mephedrone appearance on the UK market may have been
associated with an unprecedented decreasing purity of
both MDMA and cocaine (Hand and Rishiraj 2009; National Treatment
Agency 2010)
• Prior to its ban, many surveyed people thought 4-
methylmethcathinone not to be harmful because of its
appealing legal status (Daly 2010; Ramsey et al. 2010)

9. Mephedrone – Chemical Characteristics
• Semi-synthetic cathinone derivatives (or substituted
cathinones)
• Cathinone is a natural amphetamine-like alkaloid
– found in fresh leaves and stems of African shrub Catha
edulis
• Mephedrone differs from cathinone by methylation
of the amino group and the benzene ring

10. Mephedrone – Chemical Characteristics
• Mephedrone possesses a single chiral centre
thereby existing in two enantiomeric forms
– (S)- and (R)-mephedrone
– For cathinone, the S(−) form is more potent than the
R(−) enantiomer, this may be similar for mephedrone
• Relatively easy to produce mephedrone in
nonprofessional laboratories via
– Bromination of 4-methylpropiophenone followed by
reaction with methylamine or
– Oxidation of 4-methylephedrine (Archer 2009; Europol-EMCDDA 2010).

13. Mephedrone - Pharmacology
• Mephedrone is expected to act as a central nervous system
stimulant by
– promoting the release of monoamine neurotransmitters
– likely inhibiting their reuptake
• Given cathinone derivatives affiliation to beta-ketoamphetamines,
• In vitro studies on the effects of the cathinone derivatives
methcathinone and methylone confirm
– the main mechanism of action is very similar to that of
amphetamine
• characterized by a predominant action on plasma membrane catecholamine
transporters
– both amphetamines and cathinones bind to noradrenalin, dopamine
and serotonin transporters (Nagai et al. 2007)
– Presence of the ring substituent on the phenethylamine core modifies
the pharmacological properties & gives the compound some MDMA-like
effects
– Cathinones’ potencies are mostly lower than those of amphetamines

17. Mephedrone – Desired Effects
• Intense stimulation and alertness, euphoria
• Empathy/feelings of closeness, sociability and
talkativeness
• Intensification of sensory experiences
• Moderate sexual arousal
• Perceptual distortions (reported with higher dosages
only)
• According to Dargan et al. (2010), some 56% of those
who had used mephedrone may complain of at least
oneunwanted effect associated with its use

18. System Physical Findings
General •Hyperthermia and sweating (called mephedrone sweat,
characterized by a strong body odour)
•Painful nasal drip, nose and throat bleeds with burns and
ulcerations (following insufflation)
•Immunological toxicity (vasculitis, infections and ulcerations)
CNS •Tremors, tense jaws, trismus, bruxism, mild muscle clenching, stiff
neck/shoulders,
•Headache (very common), dizziness/lightheadedness, tinnitus,
seizures, nystagmus, pupil dilation, blurred vision,
•Numbness of tactile sensitivity (reported at higher dosages)
Psychiatric •Anxiety, agitation, confusion, dysphoria, irritability, aggression
•Depression, lack of motivation, anhedonia
•Time distortions, long-lasting hallucinations
•Paranoid delusions, short-term psychosis, short-term mania
•Insomnia and nightmares
•impaired short-term memory, poor concentration, mental fatigue
CVS Tachycardia, elevated blood pressure, respiratory difficulties, chest
pain, Peripheral vasoconstriction

19. Video 1 & 2

20. Spice/K2
Synthetic Cannabinoids
• Synthetic Cannabinoids were designed to
– pharmacologically evaluate the potential of
novel therapeutics
– probe specific mechanisms of action and
related health effects of marijuana and hashish
• JWH-018, JWH-073, JWH-122, JWH-210,
JWH-081
• CP-47,497 , (C8) CP-47,497
• AM-2201
• HU-210

21. Spice/K2 – History
• Around 2004, “street chemists” began producing
smokable herbal “K2” or “Spice” products
– legal alternatives to marijuana
• The manufacture, distribution and/or use of these
herbal products were neither controlled nor illegal
– even though they were laced with synthetic cannabinoids
characterized as full agonists with high affinity at human CB1
receptors
• Package labels clearly indicate “not for human
consumption”, “incense”, or “for aromatherapy use
only”
– Clinical toxicologists understand these products are
commonly used to obtain Δ9-THC-like psychological effects

23. Spice/K2 – Product Availability
• Spice/K2 = Synthetic Cannabinoid + Additives
• Changing Synthetic Cannabinoids
– JWH-018 and JWH-073
– CP-47,497 and its C8 homolog
– AM-2201
• Changes presumably in an attempt to continue to avoid
regulations
• Additives
– Fatty acids and their esters (linoleic acid, palmitic acid)
– Amide fatty acids (oleamide, palmitoylethanolamide)
– Plant-derived substances (eugenol, thymol, and flavors like acetyl
vanillin), preservatives (benzyl benzoate) and additives (alpha-
tocopherol)
– May contain high quantities of vitamin E
– Often contaminated with the ß2‐adrenergic agonist
clenbuterol (? basis for sympathomimetic-like effects)

24. Spice/K2 – Product availability
• Countless formulations available
• Package information typically lists vegetable
ingredients considered inert (white and blue water
lily, blue and pink lotus, etc)
– less frequently lists plants that naturally contain
potentially psychoactive alkaloids, like aporphines
(Dresen et al., 2010)
• However, due to lack of regulation, safety
information and a list of active pharmacological
agents are not typically provided

28. Spice/K2 – Pharmacology
• Unlike Δ9-THC metabolites, synthetic cannabinoid
metabolites retain varying amounts of biologic
activity
– can act as agonists, neutral antagonists, or inverse
agonists at CB1 receptors
• Some oxidized products of JWH-018 have affinity for CB1
receptors similar to the parent drug
• Other products have been found to exhibit affinity similar to
Δ9-THC

30. Spice/K2 – Pharmacology
• Some synthetic cannabinoids such as JWH-015 and JWH-133 show
affinity for the CB2 receptors also
– Highly expressed on the marginal zone of the spleen, tonsils and
immune cells
• (macrophages, B cells, natural killer cells, monocytes, T-lymphocytes,
polymorphonuclear neutrophils and astrocytes
– It can be anticipated that Spice drugs containing synthetic cannabinoids
with affinity for the CB2 receptor may also affect the immune system by
• modulating chemotaxis of T lymphocytes
• Inducing thymic atrophy and apoptosis
• Presence of CB2 receptors in neurons and glail cells in brain
– JWH-015 and JWH-133 might affect basic neural cell processes
like cell proliferation and survival
• Chronic exposure of mice to JWH-015 has been associated with increased
vulnerability to drug abuse and depression (Onaivi et al., 2008a,b)
• Intra-accumbens administration of JWH-133 has been found to dose-
dependently decrease the rewarding and locomotor stimulating effects of
cocaine in mice, likely by a dopamine-dependent mechanism

31. System Physical Findings
General • Nausea, Vomiting
•Appetite Changes
•Rhabdomyolysis
CNS •Seizures, Agitation, Anxiety, Irritability
•Pupil dilation, blurred vision
•Sedation, Confusion
Psychiatric •Anxiety, agitation, confusion, dysphoria, irritability,
aggression
•Psychosis
•Insomnia and nightmares
•Tolerence, withdrawal (nightmares, diaphoresis, headache,
tremors)
•Precipitation of Psychosis in vulnerable individuals
CVS Tachycardia, Tachyarrhythmia, Cardiotoxicity, Chest Pains

32. Video 3 & 4

33. Management of NPS
• Challenges to the laboratory detection of these substances
present in the urine, oral fluid, and serum samples of
people who have consumed Spice/Bath salt
– Contains synthetic cannabinoids/cathinones from different
chemical classes
– Contains minimal amount of these substances
– Composition that is constantly changing
• There are no commercially available laboratory
tests for the detection of synthetic cannabinoids /
cathinones
• Certain non-specific lab changes which have been
detected in Spice/Bath salt intoxication:

35. Red Flags: When to Suspect NPS toxicity?
Historical
Evidence
Recent intake of some unknown commercial herbal product
purchased online or definitive history of consumption of
Spice/Bath salts
Individual with history of regular intake of cannabis, stimulants
or other psychoactive substance
Demographic
Pointers
Young adults or adolescent males, with a homosexual
orientation brought from a night club
Evidence
from Physical
Findings
Conjunctival injection, odor of smoky chemical in the breath
Perforated/ulcerated nasal septum
Increased body temperature, palpitation, high blood pressure
Decreased urine output, bruxism, muscle tenderness
Suggestive
Clinical
Features
Seizure in an individual, who is a known cannabis user
Acute renal failure and rhabdomyolysis without any apparent
physical cause
Behavioural
indicators
acute onset agitation, hallucination, self mutilating behaviour
in an individual without any prior psychiatric history

36. Management Recommendations
• If a patient presents with sympathomimetic
toxidrome and presence of any red flag signs,
following investigations could be advised:
– Send a laboratory test for synthetic
cannabinoids/cathinones (SC) [if available]
– Urine drug screen for cannabinoids, amphetamines,
cocaine, heroin
– A positive test for SC- substantiate the diagnosis
– Negative test for SC- not rule out NPS toxicity
– Negative other drug screen- suggestive evidence

37. A. Management of sympathomimetic toxidrome
• Physical signs of most of the NPS intoxication (especially
Synthetic cathinones) are consistent with sympathomimetic
toxicity
– include hypertension, tachycardia, hyperthermia, dehydration,
and psychomotor agitation
– commonly reported adverse symptoms include palpitations,
headache, chest pain, trismus, bruxism, tremors, and insomnia
• Supportive care is the mainstay of therapy
• Aggressive sedation with benzodiazepines is indicated as
needed for agitation, seizure, tachycardia, or hypertension
• If hypertension persists, it is reasonable to treat with titratable
vasodilators (i.e., nitroglycerin or sodium nitroprusside)
• Beta blockade should be avoided due to potential exacerbation
of hypertension due to unopposed alpha-adrenergic
stimulation.
• Significant hyperthermia may require passive or active cooling if
not resolved with anxiolysis and sedation

38. B. Management of Psychiatric Symptoms
• Unprecedented hostility, violence, and suicidal behaviour may
manifest during Spice or Bath salt intoxication
• Patients need to be isolated in a safe and calm place with minimal
environmental stimulation
• Prescribe Benzodiazepines if violence cannot be managed
conservatively
– Dose and the choice of benzodiazepines remain speculative, evidence
suggests lorazepam in a slow intra-venous route with periodic monitoring
of vitals
• For psychopathological clinical features, benzodiazepines have been
used to treat anxiety, agitation, and seizures
• Antipsychotics are second-line agents for agitation, due to the lowered
seizure threshold with use of cathinone and phenethylamine designer
drugs
• If marked psychiatric symptoms persist longer than one or more weeks
after discontinuation, the patient should be evaluated carefully to
determine whether he or she has a co-occurring primary psychiatric
disorder
– treated with specific therapy

39. MDMA
3,4 Methylene Dioxy Meth Amphetamine
• Ecstasy
• X
• M
• E
• XTC
• Rolls
• Beans
• Clarity
• Adam
• Lover’s speed
• Hug drug

40. MDMA – History
• Developed in 1914 as an appetite suppressant
– animal tests were unimpressive, never tested in humans
• In the 1970s and 1980s, MDMA thought to be a useful
adjunct to psychotherapy
– Multidisciplinary Association for Psychedelic Studies (MAPS) is currently
supporting the progression of research to investigate the effectiveness
of MDMA as a therapeutic adjunct to psychotherapy
• Crime Survey for England and Wales (CSEW) shows that in
2013-14 it was the third most prevalent illicit drug after
cannabis and cocaine
– 1.6% of adults aged 16–59 and 3.9% of young adults(16–24 years)
having used it in the last year
• Factors predicting future Ecstacy use
– low risk perception
– high perceived behavioural control of obtaining Ecstasy (an estimated
Ecstasy procurement time less than 24h)
– current Ecstasy dependence

42. MDMA – Clinical Pharmacology
• Manner of use
– Tablet/Capsule
• ingested orally, can be crushed/snorted/dissolved/injected
• Onset of Action – 30 to 60 mins
• T ½ 5.8 ± 2.2hrs
• Manufacture
– Precursor 3,4-methylenedioxyphenyl-2-propanone (PMK)
• commercially available ketone
– Other common precursors include saffrol, isosaffrol, piperonal,
and safrole
• From sassafras oil
• MDMA being used in combination with ketamine and
selective serotonin reuptake inhibitors (SSRIs)
– produces a rush initially
– prolongs the pleasurable effect
– easier comedown following a high

43. MDMA – Neurobiology
• Principle effects are on the serotonin system
– Works as indirect serotonin agonist
1. MDMA inhibits tryptophan hydroxylase
– Decreases serotonin production
2. Induces the release of serotonin
3. Blocks serotonin re-uptake
• MDMA depletes serotonin stores in neurons
– subsequent doses produce diminished euphoria and
increase adverse effects such as depression and agitation
• MDMA also affects the noradrenergic, dopaminergic,
and cholinergic neurotransmitter systems

44. MDMA – Clinical Effects
• Desired
– Increased energy and psychomotor drive, self-confidence, well-being
– Positive mood, heightened sensory awareness (intensified
perceptions), derealization, depersonalization
– Increase responsiveness to emotions and sense of closeness to
others
– Increased sexual arousal & sensuality of sexual experiences
• reports where MDMA was specifically used to increase the sexual vigor
• Negative effects
– while under the influence of the drug and during the comedown period
– anxiety and thought disorder
– jaw clenching (bruxism)
– lack of appetite, difficulty concentrating
– disturbance of balance
– increase in blood pressure

45. Video 5 & 6

46. MDMA – Fatalities
• Death usually related to severe dehydration,
strokes, hyperthermia, and hyponatremia
– seizures, tachyarrhythmias, hypertension, diaphoresis,
and pupillary dilation
• Body Temperatures range from 104-110F
– Rhabdomyolysis, DIC
• MDMA ingestion directly causes a rise in
antidiuretic hormone
• Excessive water intake and severe hyponatremia
– Heat from the exertion of dancing in a crowded room
– MDMA-induced hyperthermia

47. MDMA – Management
• MDMA is excreted as
– unchanged drug
– 3,4-methylene dioxy amphetamine (MDA)
– free and glucuronidated/sulfated 4-hydroxy-3-
methoxymethamphetamine (HMMA)
– 4-hydroxy-3-methoxyamphetamine (HMA)
• Gas chromatography-mass spectroscopy (GC-MS)

48. MDMA – Management of Toxicity
• Interventions required are clinical monitoring, observation and
reassurance, and symptomatic treatment, including fluids
– average duration of hospital stay reported by the Australian study was
three hours
• Intravenous fluids were administered to 31% of patients in a UK
study,130 and to 71% of cases in a Swiss study
• Important to note that symptoms following ecstasy use range from
severe dehydration to severe hyponatraemia
• Hyponatremia patients require fluid restriction
– it is dangerous to give hypotonic fluids or normal saline to patients prior
to proper assessment
• No evidence to support gastric decontamination with activated
charcoal
– may be appropriate for cases presenting within 1 hour of ingestion
• Patients presenting with body temperatures above 39̊ C need
aggressive cooling measures
– Ice-baths or internal cooling
– benzodiazepine sedation

49. Gamma-Hydroxy Butyrate (GHB)
• “Date Rape Drug”
• “Get-her-to-Bed”
• “Great Hormones at
Bedtime”
• “G”
• “Liquid Ecstasy”
• “Easy Lay”
• “Grievous Bodily Harm,”
• “Liquid X”
• Heaven
• “Soap”
• “Blue Nitro”
• “EZ Lay”
• “Fantasy”
• “Grievous Bodily Harm”
• “Liquid E”
• “Liquid Ectasy”
• “Liquid G”
• “Liquid X”

50. GHB – History
• In the 1960s suggested for medical use in anesthesia,
obstetrics, and psychiatry (including possible use for alcohol
and narcotic withdrawal symptoms, fibromyalgia &
narcolepsy)
• In 1990s, marketed for illicit use in weight control
management
– Purported anabolic properties and associated muscle growth
made it a popular drug with body builders
• GHB implicated for use in sexual assault as victims have
difficulty resisting the assault due to the level of intoxication
produced
• Date Rape Drug
– Associated memory problems
– Clears from the body quickly (within 12 h) make detection difficult
and increase the complexity of attempts to prosecute

51. GHB – Clinical Pharmacology
• GHB is a short-chain fatty acid
– Occurs naturally in mammals
• GHB can form salts (e.g. sodium and potassium
salts) which are soluble in water and alcohol
– Colourless and easily mix in aqueous solutions
• GHB precursors
– GBL (gamma butyrolactone)
– 1,4-BD (1,4-butanediol)
• Obtained over the Internet
• Marketed as solvents such as ink jet printer fluid or as GHB
alternatives in health food stores, gyms, raves, and nightclubs.
• GHB and GBL are subject to interconversion in aqueous media

53. GHB – Clinical Pharmacology
• GHB metabolism via TCA cycle produces carbon
dioxide and water
• Half-life is short after small doses
– High doses cause slow & prolonged absorption; longer
half life
• At low doses, GHB is eliminated through the
respiratory system, higher doses via renal clearance
• Less than 2% is eliminated unchanged through
urine

54. GHB – Neurobiology
• GHB is both a metabolite and a precursor of the
inhibitory neurotransmitter GABA
– Acts as a neuromodulator in the GABA system
• GHB acts on GABA-B receptors
– Highest density of these receptors in
• hippocampus, cortex, and dopaminergic areas (striatum,
olfactory tracts, and substantia nigra)
• GHB increases central dopamine levels by
– Inhibiting dopamine release
– Activating tyrosine hydroxylase
• Increase in central dopamine likely to be associated with the
reinforcing effects of GHB

55. CNS CNS depression usually persists for 1-3 hours with patients making a complete
recovery typically within 4-8 hours
•ataxia, incoordination
•disorientation, dizziness, confusion, amnesia
•hallucinations, euphoria
•somnolence, slurred speech, dysarthria, headache,
•hypotonia, hyporeflexia, tremor, and myoclonus
•Miosis is common while mydriasis and horizontal and vertical gaze
nystagmus may also occur. Pupils may also be sluggish or nonreactive
•Rare
•bruxism, vertigo, increased sexual arousal, delusions, extrapyramidal
side effects, dystonias, and athetoid posturing
Psych •agitation, bizarre behaviour, and combativeness
•either at presentation to the treatment facility
•or upon wakening
Metab
•Hyperglycaemia, hypokalaemia, and potentially hypernatremia if large
doses of the sodium salt are ingested
•Elevated creatine kinase activity/rhabdomyolysis may also occur
CVS Bradycardia & Hypotension
Resp Dose-related respiratory depression, bradypnoea, periodic (Cheyne-Stokes)
respirations, and apnoea and respiratory failure

56. Video

57. GHB Toxicity Management
• As symptoms are non-specific, it is difficult to
differentiate GHB poisoning from other sedative
hypnotic intoxications
• GHB is detected by routine urine screens in the western
countries which are not available in India now
– GHB has a half-life of 27 min and it is virtually undetected in
the urine 12 h after ingestion
• Decontamination unlikely to be beneficial in the
majority of cases
– drug’s rapid absorption, particularly when consumed in a
liquid form
– Activated charcoal (50-100 g) should only be considered in
patients who are alert, stable, and cooperative, or have a
protected airway

58. GHB Toxicity Management
• Supportive care is the mainstay of management
– emphasis on respiratory and cardiovascular support
• Initial treatment
– Securing intravenous access and continuous cardiac and blood
pressure monitoring
– pulse oximetry and arterial blood gas monitoring
– Airway protection including rapid sequence induction with
endotracheal intubation and/or assisted ventilation is indicated
(IV)
– Atropine may be needed for patients with haemodynamically
unstable hypotension which is treated with crystalloids (IV)
– Myoclonic movements typically do not require any specific
treatment
• benzodiazepine administration may be useful (IV).
– Seizures may be treated with lorazepam or diazepam

59. GHB Withdrawal
• Withdrawal syndrome consistent with other hypnotic/
sedative withdrawal syndromes
• Commonly reported symptoms
– auditory and visual hallucinations, tremors, tachycardia,
hypertension, sweating, agitation, anxiety, paranoia, insomnia,
disorientation, confusion, and aggression/combativeness
– Miosis, nystagmus, cardiac palpitations, dyspnea, tachypnoea,
nausea and vomiting, diarrhoea, and abdominal pain, though this
is less common.
• Withdrawal can occur rapidly following the last dose taken by
the user
– in one case series, it developed within 1-12 hours
– duration of these clinical effects may continue for three to twenty-
one days
• In severe cases, delirium, psychosis, rhabdomyolysis, and
seizures, are observed which may become life-threatening.

60. Ketamine
• Special K
• Vitamin K
• K
• kit-kat
• keets
• super acid
• super K
• cat valiums
• jet

62. Ketamine
• Phencyclidine derivative, NMDA receptor antagonist
• Dissociative anaesthesia
– Prevents ‘wind-up’, i.e. neurons in the spinal cord becoming
sensitized to painful stimuli
– low doses of ketamine given before, during and after surgery
improves post-operative pain relief
• In humans low doses (0.1–0.5 mg/kg/hour) can be used as local
anaesthetics and co-analgesics
• particularly effective for neuropathic pain
• Low-dose ketamine is also effective in treating complex regional pain
syndrome
– Intravenous Ketamine also has short lasting effect on suicidal
cognition of depressed patients
– Ketamine is an immune modulator and behaves as an
immunosuppressive drug
• Anaesthesia doses are 2-10 mg/kg while recreational doses
can range between 50–100 mg

65. Neurobiology
• Blockade in calcium flow through these NMDA
receptor channels
– associated with altered perception, memory, and
cognition
– NMDA blockade is associated with increased dopamine
release in prefrontal cortex and midbrain
– Suggested that ketamine, through its binding to the
NMDA receptor, can inhibit the reuptake of serotonin,
dopamine, and norepinephrine,
• mechanism underlying this action is not clear

66. Domain Symptoms
CVS & Resp Tachycardia, Hypertension
Respiratory Depression
Psychiatric Dissociation, Recurrent Flashbacks
Delirium
Amnesia, Schizophrenia symptoms
Unintentional self-injury due to anesthesia
Sexually assaultive behaviour (dissociation)
Immobility
Chronic Use Cognitive difficulties
B/L white matter frontotemporal changes
Dose
Dependent
K-Land = Relaxation
K-Hole = Oneroid state, Hallucinations, visual
distortions, Sensation of near-death
experiences

67. Ketamine – Acute Toxicity Mgt
• Ketamine use should be considered when people (especially
young people) present with agitation, tachycardia and either
visual hallucinations or nystagmus
– the absence of the latter two findings does not rule out the
possibility of ketamine misuse
• No antidote exists for ketamine overdose
• Patients best managed with standard supportive care
– special attention to cardiac and respiratory functions, as the
effects of the drug are usually short-lived (IV).
• Benzodiazepines can be used for agitated patients (IV)
• Patient should be kept in a quiet environment
– minimal external stimuli which prevents excessive agitation
• Profoundly obtunded patients may require airway support
• Titrated benzodiazepine therapy patient is agitated,
hyperthermic or showing overt sympathomimetic signs

68. In conclusion…..
• Serious public health problem as
– These are often perceived to be safe or benign compared to
the “hard drugs” such as heroin, cocaine
– Some of these drugs (e.g., GHB, Rohypnol) are notorious as
“rape drugs” and their use is associated with crimes like
date-rape, party rape
– Some of these (e.g., MDMA) are directly neurotoxic in short
and long term use
– Contrary to their popular perception, all these drugs can
have substantial toxic effects on several systems of the body
and can be potentially lethal
– These are difficult to detect through routine toxicological
screening
– Management needs to be started early and can be difficult

69. References
• Seely K.A., et al., Spice drugs are more than harmless herbal blends:
A review of the pharmacology and toxicology of synthetic
cannabinoids, Prog Neuro-Psychopharmacol Biol Psychiatry (2012)
• Gc Britt And Ef Mccance-katz A Brief Overview of the Clinical
Pharmacology of “Club Drugs” Substance Use & Misuse, 40:1189–
1201 (2005)
• K Chakraborty, RNeogi & D Basu, Club drugs: review of the ‘rave’ with
a note of concern for the Indian scenario, Indian J Med Res 133, June
2011, pp 594-604
• Draft Clinical Practice Guidelines on NEWER AND EMERGING
ADDICTIONS IN INDIA, Indian Psychiatric Society Specialty Section
on Substance Use Disorders 2016
• K Smith, Ll Larive, And F Romanelli Club drugs:
methylenedioxymethamphetamine, flunitrazepam, ketamine
hydrochloride,
and γ-hydroxybutyrate Am J Health-Syst Pharm—Vol 59 Jun 1, 2002

70. Thank You