Download The common drugs of abuse in Hong Kong

Hong Kong Journal of Emergency Medicine
The common drugs of abuse in Hong Kong
ECP Yuen
Drug abuse has been a problem with every society and across every generation. In this review, the
recent trends of drug abuse and the clinical features of the new drug of abuse in Hong Kong, namely
Ecstasy, Ketamine and Gamma Hydroxybutyrate (GHB) are discussed. The data are collected from
the Hong Kong Government Central Registry of drug abuse. It showed a rise in the total number of
drug abusers in 2000. More alarmingly, we saw a dramatic rise (42.1%) in the under 21 years old age
group. The drugs of abuse are also changing. Ecstasy was the most abused drug (51.5%) for the under
21 years old and overall it has become the second most common drug of abuse. The use of ketamine is
also on the increase. The treatment and rehabilitation options available in Hong Kong are also discussed.
(Hong Kong j.emerg.med. 2001;8:90-95)
Keywords: Ecstasy, Gamma Hydroxybutyrate, Ketamine, MDMA, trend
Introduction
Drug abuse has caused much alarm amongst the
public recently. With the introduction of ''Rave''
party, drugs of abuse are easily available. The
situation is worst in the younger age group. The
number of total drug abuse is on the rise, especially
for the under 21. In this review, the current trend
of drug abuse is examined, with disucssion on the
common drugs of abuse.
The scope of problem
younger. We saw a steep rise of 42.1% in the under
21 age group in the year 2000. Most of whom were
between 16 to 18 years old.
Man or woman?
More women are becoming of drug abusers. There
was an increase of 19.1% in the total number of
female drug abuser. The overall male was 84.7%
and 15.3% for female, with a mean age of 33 years
old. For the under 21 group, female constituted
30.5% of the cases. More young girls are now using
drugs.
Drug abuse has been a problem in every society
across every generation. It can ruin a society and
result in a country going to war. An example was
the notorious ''Opium war'' in the "Ching'' dynasty.
According to the data from the ''Central Registry
of Drug Abuse'' of Hong Kong,1 the incidence of
reported drug abuse has decreased since 1995, but
rose again in 2000, peaking at 10219 that year. The
more alarming fact is that the abusers are now
Which drug?
Heroin is still the most common drug of abuse
in the over 21. Heroin is taken by 78.9% while
10.9% took Ecstasy and 5% took Cannabis. It was
also found that 14.2% of them abused more than
one drug. The situation is different for the under
21. Eastasy is the most commonly abused drug,
accounting for 51.5% while only 26.1% took
Heroin, and 10.4% took Ketamine, whereas 32.2%
of them took more than one drug.
Correspondence to:
Yuen Cheuk Pun, Eddie, MEChB, FRCS(Edin)
Prince of Wales Hospital, Accident and Emergency
Department, Shatin, N.T., Hong Kong
Email: [email protected]
Why?
Survey by the ''Central Registry of Drug Abuse''
of Hong Kong had looked into the causes of drug
abuse and the demographic data of the abusers. It
was found that 45.2% abuse drugs because of
Yuen/The common drugs of abuse in HK
addiction, 41.3% claimed that they were under peer
pressure. 22.3% said they were curious and 21.5%
claimed they wanted to be ''High''.
For the under 21, 65.9% claimed that they were
under peer pressure. 46.3% wanted to feel
''High''. Up to 36.2% were curious and 27.7% were
bored!
How much?
They spent an average of $236 a day on drugs. The
over 21 spent more, with an average spending of
$248/day, while an average of $138/day was spent
by the under 21.
Who?
Up to 52.6% of abusers were unemployed and
only 0.8% of them received tertiary education. A
astonishing 78% of them had previous criminal records.
Where?
Kwun Tong housed the most abusers in the
territories, with 10.5% in that area, Shamshuipo
came close at 9.3% and Tuen Mun was third on the
list with 8.5%.
Single or married?
Singles made up 63.7% of abusers. It was also found
that 44.1% of the partners of female abusers were
abusing drug as well.
Treatment and rehabilitation in Hong
Kong
Various modalities of rehabilitation services are
available in Hong Kong. This can be broadly divided
into compulsory and voluntary rehabilitation.2
The Correction Service Department (CSD) operates
two compulsory treatment centres. The Hei Ling
Chau Addiction Treatment Centre for men and Chi
Ma Wan Drug Addiction Treatment Centre for
women. Drug abusers sentenced to imprisonment
for any offence may be ordered by court to undergo
compulsory treatment instead. Detention period
ranges from 2 to 12 months depending on the
inmate's progress. There is compulsory aftercare
supervision. If illicit drug use is detected before the
end of the supervision period, the abuser will be
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recalled to the centre for further treatment.
Eleven voluntary treatment centres are available for
the abusers. Most of these are operated by nongovernment organisation. The Department of
Health provides 21 Methadone Clinics for
maintenance and detoxification on outpatient basis.
Six substance abuse clinics are available under the
umbrella of Hospital Authority for medical and
psychiatric treatment. They are in Kowloon
Hospital, Pamela Youde Nethersole Easter n
Hospital, Prince of Wales Hospital, Queen Mary
Hospital, South Kwai Chung Polyclinic and Castle
Peak Hospital. Counselling services are also offered
by various other organisations.
New era of drug abuse
From the data, it is clear Ecstasy and Ketamine are
becoming the favourite drug for the under 21 years
old. Liquid ecstasy (GHB) is creating a new scare
for the ladies. We will examine these new drugs in
this section, including their origin, mode of action,
clinical features.
Ecstasy
The proper chemical name is 3,4-methylenedioxymethamphetamine (MDMA). It was originally
synthesized in Germany as an appetite suppressant
in 1914.3 It became popular for psychotherapy in
the 1970s and was used as street drug in 1980s.4 It
was widely used by ''Raver'' in United Kingdom
and United States.5 It can be mixed with other drugs
like Ketamine and ephedrine. MDMA is not
difficult to make and books on how to synthesize
it are widely available on the Internet.
MDMA is metabolised by N-demethylation to
3,4-methylenedioxyamphetamine (MDA). 6 The
effect lasts for 5 hours and 65% of the MDMA is
excreted in the urine. 5 It increases the release of
serotonin, dopamine and noradrenaline from
presynaptic neurons. It inhibits the reuptake of these
neurotransmitters and prevents destr uction
by inhibiting monoamine oxidase. An excess
amount of serotonin, dopamine and noradrenaline
are found in the synapse and this accounts for its
clinical manifestation. MDMA also has some
amphetamine-like activity and can act as a central
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stimulant through an increase in catecholamines.
Serotonin is primarily responsible for the
hyperthermia and locomotive hyperactivity (''fling
head''). MDMA is addictive. It increases the extracellular dopamine in neuron accumbens which
accounts for its reward properties. 7 It has been
shown that it can cause long-term neurotoxicity in
non-human primates through destruction of
serotonin and dopamine neurones in the brain.
Recent studies show long-term serotonin neurones
injury in MDMA users and it is believed that
neuropsychiartric presentation is due to this neurone
damage.8 The effects of MDMA start at about 30
minutes, peaking at 90 minutes and persist for 8
hours. 5
Clinical features of MDMA poisoning
1. Cardiovascular systems
Hypertension, tachycardia, arrhythmia, palpitation,
atrioventricular block, cardiogenic shock with
pulmonary edema, asystole are seen.6 Death results
from the arrhythmia, or exacerbation of underlying
cardiac disease. Diffuse vascular spasm could cause
mesenteric ischaemia.9
2. Musculoskeletal system
It can cause muscle spasm and aches, rigidity,
trismus, motor tics, rhabdomyolysis with acute
renal failure.10 Hyperthermia, end-organ damages
with acute hepatic and renal failure are also seen.
Disseminated Intravascular Coagulation (DIC) and
Adult Respiratory distress Syndrome are seen in
severe cases.9
3. Metabolic effect
Metabolic acidosis, hyperkalemia, hyponatremia
are seen. SIADH has been reported.11
4. Neurological system
Diaphoresis and mydriasis result from sympathetic
stimulation. Psychedelic effect like sensor y
enhancement, illusion, hallucination (visual &
tactile) from serotonergic stimulation. Hyperreflexia, nystagmus and ataxia are also seen. 9
It also causes empathy, feeling of closeness, mood
alteration with sensual and emotional overtones,
euphoria, increase self-esteem, paranoia. Chronic
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usage is associated with panic attack, Obsessive
Compulsive disorder, fatigue, poor concentration,
depression, insomnia, restlessness and paranoid
psychosis which can be indistinguishable from
schizophrenia. 9
In severe case, it causes seizure, cerebral infarct &
haemorrhage, coma and respiratory failure.9
Investigation
Continuous cardiac monitoring is needed, together
with regular measurement of blood pressure, urine
output and core temperature. Blood should be
checked for renal and liver function and creatinine
phosphatase kinase (CPK). CT brain is needed to
rule out intracranial haemorrhage or other causes
of hyperthermia. Some laboratories provide liquid
chromatography for detecting MDMA.12
Treatment
As in any poisoning cases, we need to secure airway,
breathing and circulation (ABC). There is no
antidote for MDMA. Tachycardia and hypertension
will usually subside with benzodiazepine. The use
of pure b-blocker should be avoided as this can cause
an unopposed a-stimulation. Nitroprusside is an
alternative drug to use in hypertension.9
Hyperthermia should be treated aggressively as it
afffects the prognosis. The temperature can be
reduced by tepid-water mist, large fan, sedation with
benzodiazepine. Paralytic agents can be used in
severe cases to reduce heat generation and shivering.
The cooling should be stopped at 38 oC to prevent
iatrogenic hypothermia.13 Some authors advocates
the use of Dantrolene at 1 mg/kg intravenously,
when the temperature exceed 39 oC. This can be
repeated up to a maximum dose of 10 mg/kg in
24 hours.
Rehydration is frequently needed, but we should
look out for hypernatremia or hyponatremia which
may result from the process, and causing cerebral
oedema.11
For patient at risk of rhabdomyolsis, mannitol
can be added to ensure adequate urine output,
likewise, bicarbonate can be used for alkalinization
of urine.4
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Death can occur early from arrhythmia, hyperthermia, seizure or intracerebral haemorrhage.
Hyperthermia is known to cause DIC and multiple
organ failure. Outcome is directly related to the
degree of hyperthermia and the effectiveness of
cooling. 14
illusion. Some reported subjective experiences of
being out of the body, floating sensation and states
similar to near-death experience.15 The dissociation
can cause the user to experience a separation from
reality and difficulty in movement of limbs.
Impaired memory and learning ability have been
reported with chronic usage.17
Ketamine
2. Cardiovascular system
The effects are due to sympathetic stimulation.
These include palpitation, tachycardia, hypertension, increase systemic vascular resistance and
cardiac output. 15
Ketamine is a Phencyclidine Hydrochloride (PCP)
derivative. It was originally used as a dissociate
anaesthetic in the 1960s. It can be used with MDMA
or on its own. It causes a disruption in the flow of
information from the conscious to unconscious
state. 15 It has a relatively high bioavailability. 16
It can be administered orally, intranasally,
intravenously or smoked.17 There are abusers who
inhale it with glass fragment nasally, as the glass
will break the nasal mucosa and increases
absorption of the drug!
Ketamine acts mainly on the PCP receptor within
the N-methyl-D-aspartate (NMDA) channel. It also
interacts with the nicotinic and muscarinic
cholinergic receptors. It inhibits the glutamate
channel noncompetitively and also stimulates the
synthesis of nitric oxide and inhibits the neuronal
reuptake of noradrenaline, dopamine and serotonin.
It is metabolised to Norketamine, which is more
active and less potent then ketamine. It undergoes
e xtensive first pass mechanism by he patic
cytochrome P450 isoenzyme. It is then hydroxylated, conjugated and then excreted in the urine.
The half-life is about 2 hours. 16 The effect of the
drug starts abruptly and lasts for 30-45 minutes.17
Clinical features of Ketamine poisoning
1. Neurological system
It causes movement disorder like bizarre facial and
limb movement, loss of coordination, dystonic
reaction, rigidity, and persistent repetitive acts,
wo rd s o r s h o u t i n g. 18 T h e s e m ay r e s u l t i n
rhabdomyolysis. Nystagmus and mydriasis are also
seen. The speech will be slurred. 17
Positive and negative symptoms of schizophrenia
are also seen. 19 There will be psychological
dissociation, with hallucination, vivid dreams and
3. Respiratory system
The increase in catecholamine causes bronchodilatation.16 Respiratory depression, apnoea and
massive pulmonary oedema are also seen in severe
cases.20
Management
The ketamine level is not helpful,21 and the initial
assessment should focus on ABC. There is no
antidote and the mainstay of treatment is
supportive. Blood should be checked for renal
function and CPK. Disturbed patients may require
sedation with midazolam. 16 The prognosis is
generally good and death is rare.
GHB (Liquid Ecstasy)
Gamma Hydroxybutyrate (GHB) was originally
synthesized in 1960 as an anesthetic agent.22 It was
not widely used because of its poor analgesic
properties and seizure-like EEG pattern.23 It became
popular with the bodybuilder in the 1980s for its
ability to improve sleep and induce euphoria. Some
claimed it can improve muscle development and
burn fat. 22 The prodrug gamma-butyrolactone
(GHL) and 1,4-butanediol are easily available.
Conversion from GHL to GHB is not difficult. 24
GHB is colourless, tasteless and water-soluble! It
can be absorbed rapidly from the gastrointestinal
tract. It readily crosses the blood-brain barrier and
the placenta. It is metabolised to g ammaaminobutyric (GABA). It has a half-life of only 27
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minutes and is excreted in the urine in the first few
hours of ingestion.22
GHB is found endogenously in substania nigra,
hypothalamus and thalamus. It mediates sleep
cycles, temperature regulation, cerebral glucose
metabolism and blood flow. It affects memory
and emotional control. It is believed to be
neuroprotective. The exact mechanism of action is
not known. Some suggested that dopaminergic
pathway modulation through GHB receptor is
accountable for its effect. 22 Tolerance and
withdrawal syndrome have been reported. 25
It has synergistic effect with ethanol and produce
respiratory and central nervous system (CNS)
depression.24 The effect is dose dependent. An oral
dose of 10 mg/kg can induce sleep. Higher dose of
30 mg/kg can induce memory loss. At 50 mg/kg,
it causes general anaesthesia.26
Clinical features of GHB intoxication
1. CNS effect
It can cause CNS depression, drowsiness, confusion,
amnesia and coma. Nystagmus, tunnel vision,
incontinence, ataxia, twitching, tremors and
random clonic movement face and limbs are seen.
Seizures are also seen.22
2. Cardiovascular system and others
It causes bradycardia, which can be followed by
tachycardia as the patient recovers.24 Respiratory
depression and apnoea are also seen.22 It can cause
nausea and vomiting. Hypother mia has been
reported.24
All symptoms resolve within 2-7 hours. Withdrawal
syndromes have been reported with chronic usage.23
Management
GHB is not detected by conventional urine testing.27
The mainstay of treatment is supportive and there
is no antidote. Priorities are given to supporting
ABC. Rapid sequence intubation is needed if the
airway or ventilation is not adequate. The airway
should be protected until the effects of toxicity
Hong Kong j. emerg. med. n Vol. 8(2)
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resolve. Atropine can be used for bradycardia.22 The
prognosis is generally good, but the addition of
other agents may prolong CNS depression. Death
is a possibility but rare.22
Conclusion
The trend of drug abuse in Hong Kong has changed
More young people taking these new drugs as they
are easily accessible in disco and rave parties. Ecstasy
and ketamine are their favourite these days. As
emergency physicians who provide frontline care,
we ought to be familiar with the clinical presentation
and management of these drug abusers.
References
1. Central Registry of Drug Abuse. Report No 46.
1991-2000:3-7.
2. H o n g Ko n g n a rc o t i c s re p o r t 2 0 0 0 . A c t i o n
Committee Against Narcotics, 2000:73-83.
3. Rattray M. Ecstasy: towards an understanding of the
biochemical basis of the actions of MDMA. Essays
Biochem 1991;26:77-87.
4. Kolecki P, T homas R. Designer dr ugs and
hallucinogens. Top Emerg Med 1997;19:53-63.
5. Schwartz RH, Miller NS. MDMA (''Ecstasy'') and
the rave. A review. Paediatrics 1997;100:705-8.
6. Green AR, Cross AJ, Goodwin GM. Review of the
pharmacology and clinical pharmacology of 3,4methylenedioxymethamphetamine (MDMA or
''Ecstasy''). Psychopharmacology (Berl) 1995;119(3):
247-60.
7. White SR, Obradovic T, Imel KM, et al. The effects
of methylenedioxymethamphetamine (MDMA,
Ecstasy) on monoaminergic neurotransmission in
the central nervous system. Prog Neurobiol 1996;
49(5):455-79.
8. McCann UD, Szabo Z, Scheffel U, et al. Positron
emission tomographic evidence of toxic effect of
MDMA (''Ecstasy'') on brain serotonin neurons in
human beings. Lancet 1998;352(9138):1433-7.
9. Buchanan JF, Brown CR. Designer drugs. A
problem in clinical toxicology. Med Toxicol Adverse
Drug Exp 1988;3(1):1-17.
10. Steele TD, McCann UD, Ricaur te GA. 3,4m e t hy l e n e d i ox y m e t h a m p h e t a m i n e ( M D M A ,
''Ecstasy''). Pharmacology and toxicology in animals
and humans. Addiction 1994;89(5):539-51.
11. H o l m e s S B, B a n e r j e e A D, A l e x a n d e r W D.
Hyponatraemia and seizures after ecstasy use.
Postgrad Med J 1999;75(879):32-3.
12. M o e l l e r M R , S t e i n m e y e r S, K r a e m e r T.
Yuen/The common drugs of abuse in HK
13.
14.
15.
16.
17.
18.
19.
20.
21.
Deter mination of drugs of abuse in blood. J
Chromatogr B Biomed Sci Appl 1998;713(1):91-109.
Chan TC, Evans SD, Clark RF. Drug-induced
hyperthermia. Clin Crit Care 1997;13(4):785-808.
McCann UD, Slate SO, Ricaurte GA. Adverse
reactions with 3,4-methylenedioxymethamphetamine (MDMA; ''Ecstasy''). Drug Saf
1996;15(2):107-17.
Kohrs R, Durieux ME. Ketamine: teaching an old
drug new tricks. Anesth Analg 1998;87(5):1186-93.
Reich DL, Silvay G. Ketamine. An update on the
first twenty-five years of clinical experience. Can J
Anaesth 1989;36(2):186-97.
Jansen KL. Nonmedical use of ketamine. BMJ 1993;
306(6878):601-2.
Marai W. Gammahydroxybutyrate. An endogenous
regulator of energy metabolism. Neurosci Biobehav
Rev 1997;13:187-98.
K r y s t a l J H , K a r p e r L P, S e i b y l J P, e t a l .
Subanaesthetic effects of the noncompetitive NMDA
antagonist, ketamine, in humans. Psychotomimetic,
perceptual, cognitive, and neuroendocrine response.
Arch Gen Psychiatry 1994;51(3):199-214.
Licata M, Pierini G, Popoli G. A fatal ketamine
poisoning. J Forensic Sci 1994;39(5):1314-20.
Zacny JP, Galinkin JL. Psychotropic drugs used in
95
22.
23.
24.
25.
26.
27.
anesthesia practice abuse liability and epidemiology
of abuse. Anesthesiology 1999;90(1):269-88.
Li J, Stokes SA, Woeckener A. A tale of novel
intoxication. A review of the effects of gammahydroxybutyric acid with recommendations for
management. Ann Emerg Med 1998;31(6):729-36.
Tu n n i c l i f f G. S i t e s o f a c t i o n o f g a m m a hydroxybutyrate (GHB) – a neuroactive drug with
abuse potential. J Toxicol Clin Toxicol 1997;35(6):
581-90.
CDC. Adverse events associated with ingestion of
gamma-butyrolactone – Minnesota, New Mexico,
and Texas, 1998-1999. Morb Mortal Wkly Rep 1999;
48(7):137-40.
Addolarato G, Caputo F, Capristo E. A case of gammahydroxybutyric acid withdrawal syndrome during
alcohol addiction treatment: utility of diazepam
administration. Clin Neuropharmacol 1999;22(1):60-2.
Gibson KM, Hoffmann GF, Hodson AK, et al. 4hydroxybutyric acid and the clinical phenotype of
succinic semialdehyde dehydrogenase deficiency, an
inborn error of GABA metabolism. Neuropediatrics
1998;29(1):14-22.
Badcock NR, Zotti R. Rapid screening test for
gamma-hydroxybutyric acid (GHB, Fantasy) in
urine. Ther Drug Monit 1999;21(3):376.