Party DRUGS - Australian Doctor

AD_ 0 2 9 _ _ _ SEPT 1 1 _ 0 9 . p d f
Pa ge
2 9
3 / 9 / 0 9 ,
3 : 3 8
PM
HowtoTreat
PULL-OUT SECTION
www.australiandoctor.com.au
COMPLETE HOW TO TREAT QUIZZES ONLINE (www.australiandoctor.com.au/cpd) to earn CPD or PDP points.
inside
Ecstasy (MDMA)
Cocaine and
methamphetamine
Gammahydroxybutyrate
Ketamine
The author
DR GLENYS DORE,
clinical director, senior staff
specialist psychiatrist, Northern
Sydney Drug & Alcohol Services,
St Leonards; and clinical
senior lecturer, University
of Sydney, NSW.
Party DRUGS
Background
THE term ‘party drugs’ (also sometimes called club drugs) refers to a
group of drugs used primarily by
young adults at entertainment
venues including clubs, parties, bars
and all-night dance parties called
‘raves’. While ecstasy is the most
commonly used party drug, other
substances commonly included
under this heading are methamphet-
amine, cocaine, GHB (gammahydroxybutyrate) and ketamine. The
term ERDs (ecstasy and related drugs)
is often used interchangeably with the
terms party drugs and club drugs.
Party drug users tend to be young,
relatively well educated, and either
employed or studying. Most are not
from socially deprived backgrounds
and have not been in trouble with
the police, and few have engaged in
crime or been involved in treatment
for a drug-related problem. Most
have begun ecstasy use in their late
teens, and most are poly-drug users.
Although the use of drugs such as
GHB, ketamine and methamphetamine has increased over time, there
are still relatively few dedicated
users compared with ecstasy users.
www.australiandoctor.com.au
The 2007 National Drug Strategy
Household Survey found that the
proportion of the general population
reporting they had ever used ecstasy
steadily increased from 3.1% in 1993
to 8.9% in 2007. Methamphetamine
had been tried by 6.3% of the population, GHB by 0.5%, ketamine by
1
1.1% and cocaine by 5.9%.
cont’d next page
11 September 2009 | Australian Doctor |
29
AD_ 0 3 0 _ _ _ SEPT 1 1 _ 0 9 . p d f
Pa ge
3 0
3 / 9 / 0 9 ,
3 : 3 9
PM
HOW TO TREAT Party drugs
Ecstasy (MDMA)
ECSTASY is the popular
name for 3,4-methylenedioxymethamphetamine or
MDMA. It is most commonly
found in tablets of various
sizes, shapes and colours with
distinctive markings on one
side, such as the Playboy
symbol, the Mitsubishi
symbol, a dove, E or yin/yang
symbol (figure 1). One tablet
costs around $30-$50. Ecstasy
is usually taken orally but can
be dissolved and injected, or
crushed and snorted. It may
also be sprinkled on cones and
smoked, or ‘shafted’ (inserted
into the rectum).
Common street names
include E, eckie, vitamin E,
love drug, hug drug, Adam,
XTC, X, essence and doves.
The potency of street samples is highly variable, with
tablets sold as ecstasy sometimes containing little or no
MDMA, but containing other
substances such as caffeine,
glucose, bicarbonate of soda,
methamphetamine, ephedrine,
ketamine, benzodiazepines
and paramethoxyamphetamine (PMA).
Given that up to 75% of
tablets sold as ecstasy are
cheap imitations and not
MDMA, the mental and
physical effects of the drug
taken are highly variable.
PMA (also called ‘death’) is
a particularly toxic derivative of amphetamine, and a
number of deaths have
occurred in young people
who took tablets they
believed were ecstasy but in
fact contained PMA. PMA
poisoning presents with clinical features similar to
ecstasy poisoning (hyperthermia, seizures, coma) but
these symptoms occur more
often and are more severe
with PMA.
Depression, low
mood, poor
concentration
and memory
problems are
relatively
common
midweek after
taking weekend
MDMA.
Effects of ecstasy
MDMA is classed as a hallucinogenic amphetamine. Its
psychedelic effects include
heightened insight, perception
and sensation, and its stimulant properties include mood
elevation and increased energy
levels. It has been called an
‘empathogen’ because it
heightens communication,
closeness and intimacy
between individuals.
While MDMA increases
levels of both dopamine and
noradrenaline in the brain,
its primary effect is through
increasing release and
inhibiting reuptake of serotonin.
The effects begin to show
between 30 and 60 minutes
after taking a dose; peak
effects occur at 60-90 minutes and may last for around
4-6 hours when taken orally.
The half-life of MDMA is
around seven hours.
Generally the effects of
MDMA can be described in
three main stages:
• Coming up. The drug
starts to take effect. This
stage can be experienced
30
| Australian Doctor | 11 September 2009
Figure 1: Different forms of ecstasy tablets.
example, Gowing et al.
reported 31 cases of psychiatric sequelae subsequent to
2
ecstasy use. Symptoms
included depression, anxiety,
panic disorders, flashbacks
and delusional beliefs. While
there are case reports of regular MDMA use resulting in
mild hallucinations, paranoia,
short-term and chronic psychosis, these case reports are
small in number.
Neurotoxicity and cognitive
deficits
as smooth or sudden and
bumpy, and the user may
feel a rush. During this
stage, the user may experience nausea or vomiting,
churning stomach, feeling
hot and sweating related
to an increase in body temperature, tachycardia,
increased blood pressure,
muscle tightening (particularly the jaw muscles
which may cause jaw
clenching and bruxism),
dilated pupils, feeling confused and panicky, and difficulty concentrating and
making sense of surroundings. This stage usually
lasts around 5-20 minutes
and the effects pass once
the plateau is reached.
• The plateau. During this
stage the desired effects of
the drug are experienced.
These include:
- Elevated mood with
euphoria, a sense of wellbeing and relaxation, lack
of inhibition, a sense of
communicating with an
‘inner self’ and a sense
that everyday life is temporarily transcended.
- Empathogenic effects:
feeling warm, open,
loving, understanding and
closely and uniquely connected to others (hence
the name ‘the love drug’).
- Stimulant effects including
increased alertness, confidence, talkativeness (logorrhoea) and increased
energy to dance.
- Mild hallucinogenic (psychedelic) effects where
mild changes in perception occur without frank
hallucinations.
This
involves heightening sensations such as sight,
touch and hearing,
making normal things
seem more interesting and
lasers and music seem
amazing. There may be a
sense of ‘seeing the world
for the first time’.
• Coming down. The effects
of the drug start to wear
off (‘what goes up must
come down’), as serotonin
levels become depleted.
During this stage the user
feels tired and often physically exhausted (especially
if dancing through the
night) with muscle aches
and pains, and difficulty
concentrating. Mood
changes include feeling flat
and depressed, and experiencing irritability, anxiety and sometimes paranoia. Symptoms generally
last one to two days but it
can take up to a week for
users to feel normal again
while serotonin levels are
being restored. Symptoms
are more intense in those
using high doses, injecting
the drug and using several
different drugs at the same
time.
Sexual effects
Sexual pleasure is heightened
during drug intoxication with
most ecstasy users describing
a sense of increased intimacy
due to increased communication and feelings of closeness.
www.australiandoctor.com.au
Inhibitions are significantly
lowered, with greater risktaking behaviour, and this
may lead to users having
unprotected sex with someone they would otherwise
find unattractive. At the same
time, arousal and the ability
to reach climax are often
inhibited, with men often
having difficulty attaining
and maintaining an erection.
Ecstasy is described as being
more ‘sensual’ than ‘sexual’.
Psychiatric sequelae of
MDMA use
MDMA is not frankly hallucinogenic when typical recreational doses are used. Higher
doses can result in perceptual
disturbances including depersonalisation, illusions and
visual hallucinations. These
symptoms may be accompanied by motor tics, restlessness, headaches, anxiety,
bruxism, nystagmus and trismus.
Depression, low mood,
poor concentration and
memory problems are relatively common midweek after
taking weekend MDMA (viz.
‘terrible Tuesday’).
The risk of significant psychiatric disturbances appears
to be greater with:
• More frequent heavy use.
• Longer-term use.
• Polysubstance use.
• Injecting and binge drug
use.
• A family or personal history
of psychiatric disorders.
The number of case reports
remains relatively low; for
Studies in rats and nonhuman primates have
demonstrated that MDMA
administration results in a
reduction in brain serotonin
caused by damage to brain
serotonin axons. This
damage occurs at oral doses
comparable to human recreational use and is more pronounced with higher doses
and more frequent use. Brain
regions rich in serotonin terminals, such as the cortex
and hippocampus, show the
most damage. Decreases in
the density of brain serotonin axons have been found
in squirrel monkeys more
than seven years after the
administration of MDMA,
suggesting the damage
induced is prolonged and
possibly permanent. Some
regrowth of axons occurred
but was incomplete and
abnormal in the neocortex
and hippocampus, which is
implicated in memory function.
CSF and neuroimaging
studies in humans suggest
the presence of degeneration
in the serotonin system of
recreational users, even with
moderate use. MDMA users
have lower concentrations of
serotonergic metabolites in
CSF than controls. Heavy
users have lower density of
serotonin transporter sites
compared with controls in
PET studies, indicating serotonin neuronal injury.
While these studies tend to
have small numbers and
many are confounded by
other drug use and unclear
histories of MDMA use,
they provide evidence of
likely neurotoxicity with
MDMA. A number of studies have also explored the
functional consequences of
the neurotoxic effects of
AD_ 0 3 1 _ _ _ SEPT 1 1 _ 0 9 . p d f
MDMA using psychological
and neurocognitive testing in
current and former MDMA
users and non-using controls.
Most human studies have
been confounded by a
number of variables, including not controlling for polydrug use (especially cannabis,
which has significant cognitive effects), for comorbid
depression and/or anxiety,
and for IQ. Studies generally
have widely varying cohorts,
use different assessment
measures, do not examine
the effects of long-term use
and have no capacity to
determine memory function
prior to drug use.
Despite these limitations,
the studies have consistently
found impairment in shortterm memory in ecstasy users
not explainable by the use of
other drugs, including
cannabis. While the neurotoxic effects of MDMA
appear established, it remains
unclear what the long-term
cognitive and mood effects of
the related serotonergic dysfunction are likely to be.
Acute adverse physical effects
related to MDMA use
Given the high prevalence of
Pa ge
3 1
3 / 9 / 0 9 ,
3 : 4 0
PM
Excessive water
consumption
during ecstasy
use may be a
deliberate
attempt to
manage adverse
effects of the
drug.
ecstasy use, the reported numbers of serious adverse effects
from the drug are relatively
low. However, the unpredictability of serious mortality
and morbidity from ecstasy
use in young people means
the health concerns are significant. Hyperthermia and
hyponatraemia are the most
significant acute adverse physical effects requiring rapid
intervention to avoid major
morbidity and mortality.
While MDMA taken in
sufficient quantities can cause
hyperthermia in quiet surroundings, its toxicity
appears to be enhanced in
the setting of dance parties. It
appears to be a combination
of the direct effects of
MDMA on the hypothalamus (disrupting the normal
ability of the brain to regulate temperature), a hot envi-
www.australiandoctor.com.au
ronment, sustained physical
activity and inadequate fluid
replacement. Hyperthermia
is accompanied by a range of
clinical problems, including
disseminated intravascular
coagulation, rhabdomyolysis,
renal and liver impairment
and seizures.
Conversely, there are real
risks of hyponatraemia with
the drug. The death of 15year-old Anna Wood in 1995
from hyponatraemia and
cerebral oedema, after taking
ecstasy and drinking large
amounts of water at a dance
party, highlighted this risk.
Excessive water consumption
during ecstasy use may be a
deliberate attempt to manage
adverse effects of the drug,
and may be caused by
MDMA-induced repetitive
actions or thirst. In addition,
MDMA may result in the
inappropriate release of
antidiuretic hormone and this
in combination with hyperthermia would reduce the
body’s capacity to excrete
fluid consumed. While earlier
advice to drink large quantities of water to counteract the
hyperthermic effects of
MDMA is sound, the amount
of water consumed needs to
be limited to enable the body
to excrete it appropriately
and should be no more than
500mL per hour. Cases of
MDMA-related hyponatraemia have typically presented with confusion and
altered level of consciousness,
with or without seizures.
While most recover as
sodium levels normalise, rare
cases of fatal cerebral oedema
have occurred.
In addition, severe liver
damage with and without
hyperthermia has been
reported shortly after ecstasy
ingestion but also days or
weeks after single or multiple
episodes of ecstasy use. While
most cases resolve spontaneously, fatalities have
occurred.
Rare cases of cerebral haemorrhage or ischaemia have
been reported in patients with
pre-existing brain pathology
related to MDMA use without or without amphetamine
use. Seizures occurring with or
without hyperthermia or
hyponatraemia have been
reported but appear to have
been due to PMA or MDMA
in combination with other substances.
cont’d next page
11 September 2009 | Australian Doctor |
31
AD_ 0 3 2 _ _ SEPT 1 1 _ 0 9 . p d f
Pa ge
3 2
3 / 9 / 0 9 ,
3 : 4 1
PM
HOW TO TREAT Party drugs
Cocaine and methamphetamine
COCAINE and methamphetamine are potent
psychostimulants with
much higher rates of psychiatric and medical morbidity than MDMA.
Cocaine is inhaled
intranasally (known as
‘snorting’) or injected
(figure 2). The free base
(crack) may be smoked
from a heated device. It is
rapidly absorbed and delivered to the brain, resulting
in an intense but relatively
brief period of euphoria.
Cocaine is more addictive
than methamphetamine
because of the greater intensity of euphoria, the speed
of effect and the short duration of action. Because its
desired effects typically only
last around 30 minutes, it
is often used repeatedly in
a binge pattern of several
hours.
Methamphetamine is the
most widely available form
of amphetamine in Australia
since changes in legislation
in the early 1990s limited
access to the precursor
chemicals for amphetamine
manufacture. Methamphetamine is more potent and has
pseudoephedrine as its main
precursor.
The most readily available form of the drug in
Australia is methamphetamine powder (‘speed’).
However, since the late
1990s there has been
increased availability of
much more potent forms of
methamphetamine, namely
‘base’ methamphetamine
and crystalline methamphetamine (‘ice’). Base is a
sticky, waxy or oily form of
damp powder, paste or
crystal produced when
methamphetamine base is
incompletely converted to
methamphetamine crystal.
Ice is a high-purity crystalline form of methamphetamine that has the appearance of a coarse crystalline
powder or large translucent
to white crystals. It is also
known as crystal, crystal
meth, P, pure, shabu and
syabu. Crystal methamphetamine is usually smoked in
an ice pipe (figure 3) or
injected, with both methods
resulting in a rapid onset of
effects.
Since the emergence of
base and ice, there has been
an increase in psychotic
symptoms in methamphetamine users in Australia,
with associated violence,
fuelling media interest in
this drug.
Since the
emergence of
base and ice,
there has been an
increase in
psychotic
symptoms in
methamphetamine
users in Australia.
Pharmacological effects
of cocaine and
methamphetamine
Pharmacological effects of
cocaine and methamphetamine include:
• Central stimulant effects
such as euphoria, increased
energy and mental alertness, enhanced self-confi-
32
| Australian Doctor | 11 September 2009
Figure 2: Cocaine.
dence, insomnia, increased
libido, reduced appetite
and weight loss and
increased body temperature.
• Sympathetic
nervous
system effects including
tachycardia, raised blood
pressure, sweating, tremor,
dilated pupils and blurred
vision.
• Vasoconstrictor and local
anaesthetic actions for
cocaine, which led to its
use as a topical anaesthetic.
Adverse physical effects
can include hyperpyrexia,
muscle twitching, hypertension, tachycardia, cardiac
arrhythmias and sudden
death.
Cocaine use is associated
with myocardial ischaemia
and infarction because of
the marked coronary vasoconstriction, increased
myocardial oxygen demand, enhanced platelet
aggregation and thrombus
formation. High doses (particularly of cocaine) can
cause seizures, cerebral
haemorrhage and infarction.
Rhabdomyolysis causing
acute renal failure can
occur secondary to hyperthermia, seizures and vasoconstriction, or as a direct
effect of the drug.
The
vasoconstrictor
effects of cocaine can also
result in bowel ischaemia or
infarction, hepatic ischaemia
and necrosis, peripheral
ischaemia with gangrene,
arteritis and vasculitis.
Risky sexual behaviours
resulting from enhanced
libido and impaired judgment can increase the risk
of sexually transmitted
infections.
Injecting psychostimulants
increases the risk of exposure to infective disorders
including endocarditis, hepatitis B and C and HIV.
Symptoms of intoxication
with cocaine or methamphetamine can mimic a variety of psychiatric disorders.
These include the following.
Acute anxiety
Even with low to moderate
doses of stimulants, individ-
uals can experience anxiety,
restlessness, nervousness,
tachycardia, palpitations
and hyperventilation. Feelings of panic may occur,
and a sense of losing control or going mad. High
doses can produce an
obsessive-compulsive state,
for example, mechanically
pulling objects apart and
reassembling them, compulsive foraging for things
such as rubbish.
Figure 3: Ice pipe or crystal pipe.
Stimulant ‘crash’ and
withdrawal
Even when not dependent
on the drug, the individual
may experience ‘coming
down’ or a ‘crash’ after a
brief period of 1-2 days of
stimulant use. The crash
occurs as the effect of the
stimulant wears off, usually
8-36 hours after use and
lasts for several days. Acute
cocaine intoxication is followed by a shorter crash
period, lasting from hours
to days. Symptoms of the
crash include lethargy, irritability (which may result
in arguments or aggression), headache, anxiety
and depression of mood.
For those dependent on
stimulants, stimulant withdrawal may resemble atypical
depression
with
intensely depressed mood,
loss of all interest and
pleasure in life, anxiety, agitation and fatigue, in combination with overeating
and oversleeping. It is
important to do an assessment of suicide risk during
this phase.
These symptoms typically
have a delayed onset.
Amphetamine withdrawal
typically starts 2-4 days
after last use, peaking at 710 days and subsiding over
2-4 weeks. Withdrawal
symptoms start earlier with
cocaine because of its
shorter half-life, typically
starting 1-2 days after last
use, peaking at 4-7 days
and abating over 1-2
weeks. There may be a prolonged phase of up to 10
weeks after this when
mood, energy and sleep
levels fluctuate considerably
before normalising if absti-
www.australiandoctor.com.au
nence is maintained.
Treatment of withdrawal
may include short-term use
of benzodiazepines for agitation; antidepressants if
there is a pre-existing history of depression; hospitalisation if the patient is
severely depressed and suicidal; and relapse prevention to manage cravings
and triggers for relapse.
Mania and psychosis
Stimulant intoxication may
cause symptoms that mimic
mania, including euphoria,
increased energy levels, disinhibition, grandiosity,
impulsiveness, decreased
need for sleep, hypersexuality, decreased appetite,
impaired judgment, hypervigilance and marked agitation. This state may result
in illegal activities or
uncharacteristic sexual
behaviour or accidents.
While similar to mania, this
state subsides rapidly as the
action of the drug wears
off.
Stimulants can cause a
short-lived psychosis that
mimics paranoid schizophrenia but fully resolves
with abstinence. This usually occurs during a phase
of chronic high-dose use
but can be seen with one or
several large doses. The
predominant features are
delusional beliefs with or
without hallucinations,
with agitated and fearful
mood and lack of insight.
Hallucinations are commonly auditory, visual and
tactile (eg, the perception
that bugs are crawling
under the skin). Persecutory
delusions are common; the
individual might believe
they are being watched and
followed, and are at risk of
being attacked, possibly
murdered. As a result, the
user may become panicky,
frightened and agitated,
sometimes resorting to
‘defensive violence’ to protect themselves from their
would-be attackers. Stimulant psychosis is often associated with abnormal physical findings including
severe weight loss; skin
excoriations (from scratching at non-existent bugs);
elevated blood pressure,
heart rate and temperature;
and needle marks.
Once the stimulant use
stops, the psychosis usually
clears within several days
to a month. Management
of acute behavioural symptoms involves use of the
Mental Health Act, and
sedation with antipsychotic
medication and benzodiazepines in an acute care
setting.
Low levels of methamphetamine use may also
trigger psychotic symptoms
in someone with an underlying vulnerability to psychosis, such as patients
with schizophrenia.
AD_ 0 3 3 _ _ _ SEPT 1 1 _ 0 9 . p d f
Pa ge
3 3
3 / 9 / 0 9 ,
3 : 4 3
PM
Gamma-hydroxybutyrate
GHB, or sodium oxybate,
was developed as an anaesthetic, but withdrawn
because of its poor analgesic
effects and a range of
unwanted side effects. It
was marketed in the 1980s
as a fat burner and muscle
developer, and bodybuilders
have used it to increase the
production of growth hormone, as an alternative to
steroid use. It has also been
used for the treatment of
narcolepsy.
GHB is also a naturally
occurring chemical in the
human brain. Illicit GHB is
produced from commercially available industrial
solvents containing gammabutyrolactone (GBL) and
1,4 butanediol (1,4-BD).
The precursor substances of
GHB are rapidly converted
to GHB in the body and are
sometimes sold as GHB
substitutes. GBL is a thicker
liquid than GHB and more
like a clear hair serum or
gel. It tastes like petrol and
soap, can burn the tongue
and roof of the mouth and
is about twice as potent as
GHB, increasing the risk of
overdose if users are sold
GBL thinking it is GHB.
GHB is known by a variety of names by party drug
users including G, GBH,
grievous bodily harm, liquid
E, liquid ecstasy, liquid, X,
fantasy and Georgia home
boy. It is also known as a
date-rape drug because of
documented cases of rape
after drink spiking with
GHB.
It is commonly sold as a
clear odourless liquid, but
sometimes colourants are
used to distinguish it from
water. When bright blue
At moderate
doses the
individual
appears
inebriated with
blurred vision,
ataxia, dizziness,
drowsiness,
sedation,
agitation and
combativeness.
Figure 4: Liquid GHB is sometimes sold in a soy sauce
container.
colourants are added it is
called ‘blue nitro’ or ‘liquid
nitro’. Less commonly it is
sold as a white or palecoloured crystal powder with
a soap-like texture, which can
be dissolved with water. It is
sold in small bottles or glass
vials and sometimes in fishshaped soy sauce containers
(figure 4).
It is generally swallowed
and is generally taken with
other drinks (such as isotonic sports drinks, eg,
Powerade) because of its
bitter, salty taste. Less commonly it is injected or
‘shelved’ (inserted into the
anus). It is sold at around
$7-$8 for each 1mL. The
usual dose taken is a 2mL
‘shot’ or ‘charge’ repeated
several times through a
night, but higher individual
doses may be taken (2.54mL), with increased risk of
overdose.
The onset of effects
occurs 10-20 minutes after
swallowing the drug, with
delayed onset if food is
taken. The primary effects
of the drug last 1-2 hours
and the after-effects 2-4
hours. The half-life is
around 20-50 minutes,
making it a drug that is
often undetectable in later
urinalysis.
The sought-after effects at
low doses are similar to
those of alcohol, inducing
euphoric effects, relaxation,
disinhibition, a sense of
wellbeing and increased
sociability. It also has
aphrodisiac effects, enhancing libido and sexual experience. Unlike alcohol, it has
no hangover effects, and
users who have overdosed
on it can awake feeling as
if they have had a really
good sleep. In addition, the
drug causes amnesia, with
no recall of any adverse
effects experienced during
intoxication. This can result
in users going straight back
to using it without any
appreciation of the consequences.
At moderate doses the
individual appears inebriated with blurred vision,
ataxia, dizziness, drowsiness, sedation, agitation and
combativeness. At higher
doses there is increased loss
of control, similar to alcohol intoxication. Signs
include somnolence, disorientation, severe ataxia,
short-term memory loss,
incoherent speech, nausea,
vomiting, sweating, nystagmus and loss of peripheral
vision.
As the level of overdose
severity increases, the individual may experience
muscle stiffness, myoclonic
jerks, uncontrolled shaking
or seizures as well as incontinence, bradycardia and
hypothermia. The clinical
state may progress to respiratory depression requiring
intubation, coma and death.
A GHB overdose is more
likely when the drug is combined with other CNS
depressants (particularly
alcohol and ketamine) and
when GBL is taken rather
than GHB.
Chronic use can result in
tolerance and both psychological and physiological
dependence. Withdrawal
symptoms occur 1-2 hours
after the last dose and may
last up to two weeks. Withdrawal symptoms include
anxiety, agitation, insomnia,
tremor,
tachycardia,
headache, dizziness, nausea,
vomiting, hypotension and
muscular cramps. Combativeness may occur, as may
confusion, agitated delirium
and psychotic symptoms
(paranoia and hallucinations of an auditory, tactile
and visual nature).
Acute withdrawal states
are treated with benzodiazepine loading to sedation,
with the use of antipsychotic medication as
required. The patient may
require scheduling under the
Mental Health Act in an
ICU or medical or psychiatric setting, depending on
the severity and nature of
symptoms.
Ketamine
KETAMINE is a short-acting general anaesthetic used in human
and veterinary medicine. It has
sedative-hypnotic, analgesic, sympathomimetic and hallucinogenic
properties and is commonly
described as a ‘dissociative anaesthetic’. This description refers to
its ability to induce a lack of
responsive awareness of the user’s
physical state and surrounding
environment as well as to pain,
without complete unconsciousness.
Ketamine’s use as a psychedelic
‘dance’ drug has become more
widespread with increasing use and
popularity since 2001. Ketamine is
known by a number of names
including Special K, K, vitamin K,
lady K, KitKat, cat valium, super
acid and bump. Ketamine is sometimes referred to as a horse tranquilliser, because of its use in veterinary medicine as an anaesthetic.
Ketamine for recreational use is
available as a white, crystalline
powder (similar to cocaine) or a
clear liquid but is sometimes passed
off in tablet form as ecstasy. The
drug can be injected, taken orally or
added to tobacco or marijuana cig-
Ketamine can be
injected, taken orally
or added to tobacco
or marijuana
cigarettes and
smoked.
arettes and smoked. It is commonly
snorted in small lines called ‘bumps’
(30-50mg) using a ‘bullet’ aerosol
dispenser.
The onset of effects is 15-20 minutes with oral use, 5-10 minutes
with snorting, 1-5 minutes with
injection and within seconds if
smoked. Effects usually last for 1-2
hours after oral use and 45-60 min-
utes with snorting. It is often readministered in a recreational setting
because of its short duration of
action. Users may feel the aftereffects for some hours or several
days.
The effects of ketamine are
mostly dose dependent. Lower
doses result in a mild dreamy feeling similar to that with nitrous
www.australiandoctor.com.au
oxide. Users report a floating feeling, as if the mind and body have
been separated.
Moderate doses usually result in
stimulation, with feelings of euphoria and energy, similar to those of
cocaine and ecstasy. This may promote dancing, particularly if the
drug is taken with stimulants. The
initial speedy effects are often followed by more sedative and hallucinatory effects which may include
slurred speech, impaired motor coordination, numbness, confusion,
amnesia, anxiety and agitation,
confusion, dizziness, tachycardia,
palpitations, nausea and vomiting.
Higher doses can result in intense
dissociative and hallucinogenic
effects. This overdose state is called
‘K-land’ or ‘a K-hole’ by users.
High-dose users describe six main
categories of mental effects:
• Out-of-body or near death experiences.
• The perception of contact with
aliens.
• Access into alternative realities.
• Personal and creative problemsolving.
cont’d next page
11 September 2009 | Australian Doctor |
33
AD_ 0 3 4 _ _ _ SEPT 1 1 _ 0 9 . p d f
Pa ge
3 4
3 / 9 / 0 9 ,
3 : 4 4
PM
HOW TO TREAT Party drugs
Minimising harm from party drug use
(from Ecstasy: Facts & Fiction. National
Drug &
3
Alcohol Research Centre)
• Avoid MDMA if taking medication for depression, weight loss
or hypertension; if there is a past history or family history of
cardiovascular, cardiac, renal or neurological disease, or any
psychiatric conditions; and if there has been a previous
adverse response to MDMA. These factors increase the risk
of an adverse event.
• Minimise the risk of developing blood-borne viruses by
swallowing or snorting the drug. If the drug is injected,
always use a new needle and pill filter and do not share
injecting equipment.
• Limit the number and amount of drugs used while dancing
and recovering.
• Avoid dehydration by taking regular breaks from dancing (15
minutes for every hour of dancing) and sipping water through
the night. Drink 250mL water or fruit juice hourly when not
dancing, and about 500mL when dancing. (This also reduces
the risk of water intoxication). Don’t drink isotonic sports
drinks such as Gatorade or Powerade as they can interact
with MDMA and dangerously elevate blood pressure. Don’t
drink alcohol as it can increase dehydration. Keep fluids and
food intake up once at home.
from previous page
• The perception of entry
into information networks.
• Tantra-like enhancement of
sexual activity.
Some users have become
convinced that their hallucinatory experiences were real and
that the drug has opened a
door into another world. On
some occasions overdose states
have led to development of a
paranoid psychosis.
Temporary paralysis, inability to move and to speak may
also occur, with most users
finding it very difficult to move
while in a K-hole, instead
needing to sit or lie down. Ketamine overdose can also cause
delirium, potentially fatal respiratory problems, convulsions
and loss of consciousness and
aspiration from vomiting
while unconscious, particularly
when combined with alcohol.
Risky sexual behaviour has
been noted with ketamine use,
particularly when combined
with other club drugs such as
ecstasy, GHB and methamphetamine. When on ketamine, users are less likely to
experience pain and could
suffer an injury without realising they have been hurt.
Visual disturbances or flashbacks can recur for days or
weeks after ketamine use, and
appear more frequent than
with other hallucinogenic
drugs. Possible long-term cognitive or neuropsychiatric
effects have not been sufficiently studied.
Long-term effects of the
drug include tolerance,
dependence and a physiological withdrawal syndrome with
chronic use. Chronic use has
been linked with serious urological effects (eg, pain, frequency, haematuria and incontinence).
Ketamine
overdose can be
fatal, particularly
when combined
with alcohol.
• Become familiar with the warning signs of overheating and
dehydration. If these symptoms occur stop dancing; get a
friend to stay with you until you feel better; slowly sip cold
water; cool yourself with cold water, a fan or a cool
environment; get help if symptoms persist.
• Always try to have at least one person around who is not
taking drugs; take turns if necessary. Avoid going home with
strangers and stay with familiar friends in a safe environment.
• Be familiar with first aid and CPR techniques, and get
medical assistance urgently if things are going wrong. Be
completely honest with medical personnel about what drugs
have been taken.
• Provide several days’ recovery time and try to get some
sleep.
• If agitated during the come-down period, focus on positive
strategies to feel better, such as relaxation techniques and
support from friends. Avoid people and places that increase
irritability.
• Don’t make important life decisions in the week after taking
drugs.
References
1. Australian Institute of
Health and Welfare. 2007
National Drug Strategy
Household Survey: First
Results. Drug Statistics
Series number 20. Cat. No.
PHE 98. Canberra: AIHW,
2008.
2. Gowing LR, et al. The
health effects of ecstasy: a
literature review. Drug and
Alcohol Review 2002;
21:53-63.
3. Topp L, et al. Ecstasy:
Facts & Fiction. Sydney,
National Drug & Alcohol
Research Centre.
Online resources
Two very useful sites for
doctors, patients and
families are:
• National Drug & Alcohol
Research Centre:
www.ndarc.med.unsw.edu.
au
• DrugInfo Clearinghouse
(a program of the
Australian Drug
Foundation):
www.druginfo.adf.org.au
An addtional useful site for
young people is:
• Celebrate Safely:
www.celebratesafely.com.au
cont’d page 36
PBS information: KARVEA: General Benefit. Hypertension.
KARVEZIDE: Restricted Benefit. Hypertension in patients who are not adequately
controlled with either hydrochlorothiazide or irbesartan monotherapy.
Before prescribing please review full Product Information – available from sanofi-aventis. Karvea® (irbesartan)/ Karvezide® (irbesartan/hydrochlorothiazide) Indication: Karvea/
Karvezide: Hypertension. Treatment not to be initiated with the fixed dose combination. Karvea only: Delaying progression of renal disease in hypertensive type II diabetics with persistent micro-albuminuria ( 30 mg
per 24 hours) or urinary protein in excess of 900 mg per 24 hours. Dosage: Karvea: Hypertension: 150 mg once daily increase to 300 mg once daily if insufficient BP response. Hypertension and type II diabetic renal
disease: 300 mg once daily preferred maintenance dose. Start at 75 mg in patients with volume and/or salt depletion, or undergoing haemodialysis. Karvezide: Replacement Therapy: combination may be substituted
for the titrated components. Dose Titration by Clinical Effect: in patients whose BP is insufficiently controlled by hydrochlorothiazide or 150 mg irbesartan, give Karvezide 150/12.5 once daily; in patients whose BP is
insufficiently controlled by 300 mg irbesartan or by Karvezide 150/12.5, give Karvezide 300/12.5 once daily; in patients whose BP is insufficiently controlled by Karvezide 300/12.5, give Karvezide 300/25. Doses
higher than 300 mg irbesartan/25 mg hydrochlorothiazide once daily not recommended. When necessary, Karvezide may be administered with another antihypertensive drug. Recommended daily dose 150/12.5 in
elderly or patients with mild to moderate renal impairment. Contraindications: Karvea/Karvezide: hypersensitivity to irbesartan, or any component of formulation; pregnancy. Karvezide only: Sulphonamide-derived
drugs e.g. thiazides; anuria. Precautions: Karvea/Karvezide: hypotension – sodium and/or volume-depleted patients; renal function changes & impairment (moderate to severe); renal artery stenosis; hyperkalaemia;
CHF; cardiac arrhythmia; ventricular dysfunction; ventricular dysfunction; cardiac arrhythmias; pregnancy; lactation; elderly; children; driving or operating machinery. Karvezide only: primary aldosteronism;
postsympathectomy; impaired hepatic function; metabolic and endocrine effects; systemic lupus erythematosus. Drug Interactions: Karvea/Karvezide: Potassium sparing diuretics; potassium supplements; potassium
containing salt substitutes; lithium; combination use of ACE inhibitors or angiotensin receptor antagonists, anti-inflammatory drugs, diuretics (including thiazides); Karvezide only: alcohol; barbiturates; narcotics;
antidiabetic drugs; insulin; antigout medications; cardiac glycosides; antiarrhythmic drugs; calcium salts; cholestyramine resin; cholestipol HCl; antihypertensives; drugs used during surgery; pressor amines;
corticosteroids; ACTH; beta blockers; diazoxide; anticholinergic agents; amantadine; cytoxic drugs; other diuretics; NSAIDs, see full PI. Adverse Reactions: Karvea: musculoskeletal trauma; dizziness; orthostatic
dizziness; orthostatic hypotension; hyperkalaemia; others. Karvezide: fatigue; nausea/vomiting; sexual dysfunction; increases in blood urea nitrogen & serum creatinine; others. For more details and other ADEs,
see full PI. PBS Dispensed Prices: Karvea® 75 mg: $20.68, 150 mg: $24.72, 300 mg: $28.91. Karvezide® 150 mg/12.5 mg: $26.94, 300 mg/12.5 mg: $32.03, 300 mg/25 mg: $34.26.
sanofi-aventis australia pty ltd, ABN 31 008 558 807, 12-24 Talavera Road, Macquarie Park, NSW 2113. ®Registered Trademark. AU.IRB.08.08.07. 08/09 SSK0275 PUBLICIS LIFE BRANDS
34
| Australian Doctor | 11 September 2009
www.australiandoctor.com.au
AD_ 0 3 6 _ _ _ SEPT 1 1 _ 0 9 . p d f
Pa ge
3 6
3 / 9 / 0 9 ,
3 : 4 4
PM
HOW TO TREAT Party drugs
Author’s case study
A 28-YEAR-old single Australian hairdresser presented
for inpatient treatment of
methamphetamine dependence. She reported using
GHB and ice at rave parties
every weekend for the past
12 months. She would use
a 2mL shot of GHB every
two hours, consuming a
total of 10mL during an
evening. On one previous
occasion she became unconscious and was hospitalised
when she used alcohol in
combination with GHB.
Since then she avoided alcohol use in combination with
GHB. She always took the
drug with girlfriends
around, aware of the risk of
having her drink spiked
with this relatively tasteless,
odourless and colourless
drug.
She also used ice every
weekend to allow her to
stay up dancing until the
early hours of the morning.
It made her feel very confident, excitable and sociable.
She found the effects of
smoking an ice pipe were
very rapid in onset and
highly reinforcing. She
Practice points
• Psychiatric complications can occur with MDMA use but are
much less frequent than with methamphetamine use.
• MDMA use in humans appears to be associated with shortterm memory dysfunction, attention problems, and problems
with executive functioning. The basis of this dysfunction is
impaired serotonergic function, with the long-term effects on
memory and mood as yet unestablished.
• While rare, deaths from MDMA use have occurred related to
hyperthermia, water intoxication with hyponatraemia, and
liver failure.
• Symptoms of intoxication with cocaine or methamphetamine
can mimic a variety of psychiatric disorders, particularly
anxiety attacks, withdrawal depression, mania and a druginduced psychosis that appears like paranoid schizophrenia.
• GHB in low to moderate doses induces euphoric and
aphrodisiac effects and mimics the effects of alcohol. GHB
has a narrow therapeutic window, and small increases in
dose can result in unconsciousness and respiratory
difficulties. A GHB overdose is more likely when the drug is
combined with other CNS depressants (particularly alcohol
and ketamine) and when GBL is taken rather than GHB.
began using ice during
weekdays to enhance her
mood, and found that she
became dependent on the
drug. She was smoking
around 0.25g daily. Once
she stopped using it she
would sleep most of the day
for two days, then wake
feeling irritable, depressed
and fatigued with strong
drug cravings for many days
How to Treat Quiz
afterwards. She rapidly
relapsed to reduce the cravings and withdrawal symptoms. After 10 days in the
inpatient unit, her mood
and sleep were more stable.
She was taught relapse-prevention techniques to help
her manage the cravings,
which had become less
intense by the time of discharge.
• Moderate doses of ketamine usually result in stimulation with
feelings of euphoria and energy, similar to the effects of
cocaine and ecstasy. Higher doses can result in intense
dissociative and hallucinogenic effects. Ketamine overdose
can be fatal, particularly when combined with alcohol.
INSTRUCTIONS
Complete this quiz online and fill in the GP evaluation form to earn 2 CPD or PDP points. We no longer accept quizzes
by post or fax.
The mark required to obtain points is 80%. Please note that some questions have more than one correct answer.
Party drugs — 11 September 2009
1. Which TWO statements about the
epidemiology of party drug use in Australia
are correct?
a) Most party drug users are from socially
deprived backgrounds and have often been in
trouble with the police
b) Most party drug users are poly-drug users
c) The 2007 National Drug Strategy Household
Survey found that the proportion of the
population who had ever used ecstasy largely
remained the same between 1993 and 2007
d) There are relatively few dedicated users of
ketamine and gamma-hydroxybutyrate (GHB)
compared with ecstasy
2. Which TWO statements about ecstasy (3,4methylenedioxymethamphetamine [MDMA])
are correct?
a) MDMA is classed as a hallucinogenic
amphetamine
b) Ecstasy can only be taken orally
c) The potency of street samples of ecstasy sold
in Australia is generally fairly consistent
d) The mental and physical effects of tablets
sold as ecstasy are highly variable
3. Which TWO statements about the effects
of MDMA are correct?
a) The primary effect of ecstasy is through
increasing levels of dopamine and
noradrenaline in the brain
b) Initial effects of MDMA may include
nausea/vomiting, increased temperature,
heart rate and blood pressure, muscle
tightening and confusion
c) Sexual effects of MDMA in men may include
erectile dysfunction
d) Symptoms experienced as the effects of
MDMA wear off, such as tiredness, aches and
low mood, only last up to 24 hours
4. Which TWO statements about adverse
effects of MDMA use are correct?
a) Psychiatric complications can occur with
MDMA use, but are much less frequent than
with methamphetamine use
b) MDMA use in humans has been found to be
associated with effects on long-term memory
c) Deaths from MDMA use have occurred,
related to hyperthermia and water intoxication
with hyponatraemia
d) Liver damage has been reported after ecstasy
ingestion but in all cases has resolved
spontaneously without major adverse effects
5. Which TWO statements about cocaine and
methamphetamine are correct?
a) Cocaine can only be taken intranasally
b) The free base of cocaine (crack) may be
smoked from a heated device
c) The most readily available form of
methamphetamine in Australia is
ONLINE ONLY
www.australiandoctor.com.au/cpd/ for immediate feedback
‘base’ methamphetamine
d) Crystal methamphetamine (‘ice’) may be
smoked in an ice pipe or injected
6. Which TWO statements about the
pharmacological effects of cocaine and
methamphetamine are correct?
a) Low doses of stimulants do not cause
symptoms of anxiety
b) Stimulants can cause a short-lived psychosis
that mimics paranoid schizophrenia
c) A crash may occur after the effect of the
stimulant wears off, but this only occurs in
those who are dependent on the drug
d) For those dependent on stimulants, stimulant
withdrawal may resemble atypical depression
7. Which TWO statements about GHB are
correct?
a) GHB is only available for sale in liquid form
b) GHB is generally swallowed or, less
commonly, injected or inserted into the anus
c) Because of the short half-life of GHB it is
often undetectable in later urinalysis
d) Gamma-butyrolactone (GBL) is a precursor
substance of GHB and is about half as potent
as GHB
8. Which TWO statements about GHB are
correct?
a) In low to moderate doses GHB mimics the
effects of alcohol, in particular causing
marked hangover effects the next day
b) Small increases in dose of GHB can result in
unconsciousness and respiratory difficulties
c) A GHB overdose is more likely when the drug
is combined with other CNS depressants
d) Chronic GHB use does not result in
dependence
9. Which TWO statements about ketamine
are correct?
a) Ketamine is available as a white crystalline
powder or a clear liquid
b) Ketamine cannot be inhaled
c) Moderate doses of ketamine usually result in
stimulation, with feelings of euphoria and
energy
d) Ketamine does not produce hallucinogenic
effects
10. Which TWO statements about ketamine
are correct?
a) On some occasions overdose states with
ketamine have led to development of a
paranoid psychosis
b) Ketamine overdose can be fatal, particularly
when combined with alcohol
c) Chronic ketamine use does not result in
tolerance
d) Long-term cognitive and neuropsychiatric
effects of ketamine are well established
CPD QUIZ UPDATE
The RACGP now requires that a brief GP evaluation form be completed with every quiz to obtain category 2 CPD or PDP points for the 2008-10 triennium. You
can complete this online along with the quiz at www.australiandoctor.com.au. Because this is a requirement, we are no longer able to accept the quiz by post
or fax. However, we have included the quiz questions here for those who like to prepare the answers before completing the quiz online.
HOW TO TREAT Editor: Dr Wendy Morgan
Co-ordinator: Julian McAllan
Quiz: Dr Wendy Morgan
NEXT WEEK Coronary artery disease remains Australia’s number one killer despite advances in primary prevention and reduced rates of smoking. Angina is not only a source of significant morbidity but also
an important marker of risk for future atherosclerotic events. The next How to Treat focuses on stable angina pectoris. The authors are Dr Jens Kilian, director of cardiology, Bankstown Hospital, Bankstown,
NSW, and conjoint senior lecturer, University of New South Wales; and Dr James Otton, advanced trainee cardiology registrar, St Vincent’s Hospital, Darlinghurst, NSW.
36
| Australian Doctor | 11 September 2009
www.australiandoctor.com.au