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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 91 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 92 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 Hong Kong j. emerg. med. n Vol. 8(2) n Apr 2001 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 Yuen/The common drugs of abuse in HK 93 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 94 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) n Apr 2001 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. 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