Timothy B. Erickson, MD Professor: Department of Emergency Medicine University of Illinois @ Chicago - PowerPoint PPT Presentation

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Street Drugs of Abuse Timothy B. Erickson, MD Professor: Department of Emergency Medicine University of Illinois @ Chicago Case #1 History A 25 yr old male is found unresponsive by friends at an inner city night club called the “Passion Pit”. He is brought to your ER by paramedics.

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Timothy B. Erickson, MD Professor: Department of Emergency Medicine University of Illinois @ Chicago

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Street Drugs of Abuse

Timothy B. Erickson, MD

Professor: Department of Emergency Medicine

University of Illinois @ Chicago

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Case #1 History

  • A 25 yr old male is found unresponsive by friends at an inner city night club called the “Passion Pit”. He is brought to your ER by paramedics.

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Physical Exam

  • Gen: Disheveled appearance, shallow breathing, responds to painful stimuli

  • Vitals: P=56 RR=6 BP=110/70 T=95

  • Head: NC/AT

  • Eyes: Pinpoint pupils

  • Neck: Nontender no deformity

  • Lungs: Poor inspiratory effort, CTA

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Physical Exam

  • CV: Bradycardic RRR S1S2 no m’s

  • Abd: Soft with hypoactive BS

  • Rectal: Normal tone (-)Heme

  • G/U: Half-melted ice cubes placed on groin by friends at nightclub

  • Neuro: Moves all 4 ext, nonfocal

  • Skin: Cool, Arms with needle tracks

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Case Discussion

  • What are your priorities when managing this patient?

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Management Priorities

  • Airway

  • Breathing

  • Circulation

  • Assess for signs of trauma

  • Antidote administration

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Case Summary

  • Comatose patient

  • Pinpoint (miotic) pupils

  • Depressed respiratory drive

  • Bradycardia

  • Hypothermia

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Opioid Overdose

  • Heroin

  • Methadone

  • Codeine

  • Morphine

  • Fentanyl

  • Demeral

  • Propoxyphene

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  • Indicated in comatose patients with suspected drug overdose

  • Restrain patient prior to administration

  • Dose: 2-10mg IVP

  • Short half life (T1/2)

  • Naloxone drip may be required

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Clinical Course

  • After administration of 2mg of naloxone, the patient becomes more alert and begins to verbalize with spontaneous respiratory activity.

  • His vital signs are stable with NSR noted on the cardiac monitor.

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Clinical Course

  • Laboratory data including ECG and CXR are unremarkable.

  • The toxicology screen is positive for opiates.

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Clinical Course

  • The patient denies suicidal ideations and admits to frequent chronic IV heroin abuse claiming “I just had a bad cut tonight.”

  • He becomes more uncooperative and demands to be discharged….

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Case#2 History

  • The patient is a 28 yr old male who presents in police custody complaining of chest pain. He has no prior history of cardiac disease.

  • The patient was arrested at the local international airport for combative behavior while standing in line near the security area.

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Case Physical Exam

  • Gen: Patient is very agitated, clutching his chest

  • Vitals: P= 140 BP= 220/130 RR= 28 T=103.2 F

  • Eyes: Pupils equal: 7mm

  • Lungs: CTA

  • Ht: RRR S1S2 2/6 systolic murmur

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  • Abd: Distended with diffuse tenderness, hyperactive BS

  • Ext: Good pulse, no cyanosis, no needle tracks

  • Neuro: No focal defs

  • Skin: Diaphoretic

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“I’m having chest pain”

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Clinical Course

  • The patient now admits to swallowing several “condoms full of cocaine” before boarding the plane from Columbia to the U.S.

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Drug Smugglers

  • Describe the difference between a “Body Packer” and a “Body Stuffer”

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Packers and Stuffers

  • Body Packers: Drug smugglers who ingest large amounts of pure illegal contraband methodically wrapped in order to deliver “the goods” across international borders.

  • Body Stuffers: Individuals who “swallow the evidence” during drug raids (poorly wrapped but less pure).

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Body Stuffer

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Body Packer

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  • Cocaine hydrochloride= usual street preparation

  • Freebase cocaine(cocaine alkaloid)= cocaine is extracted with alkaline (buffered ammonia) and solvent is added(acetone). Freebase pops or cracks when heated hence the term “crack”

  • Rock of crack= cocaine hydrochloride heated with baking soda until a rock is formed-these are smoked in paraphernalia

  • Speedball-heroin laced with cocaine-no narcan

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Cocaine Toxicity (Sympathomimetic)

  • Hypertension

  • Tachycarida

  • Hyperthermia

  • Diaphoresis

  • Anxiety

  • Seizures

  • CVA/Intracranial bleed

  • Myocardial infarction

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Gastric Decontamination

  • Activated charcaol

  • Polyethlene glycol solution (aka: Go-lytely)

  • Surgical removal

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Cocaine & Chest Pain

  • Oxygen

  • Benzodiazepines

  • Nitroglycerin

  • B-Blockers- contraindicated

  • Hypertension control

  • Thrombolytic Agents (TPA)

  • Cath Lab / Angioplasty

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Clinical Course

  • The patient’s chest pain and hypertension resolves with large doses of NTG and benzodiazepines

  • The patient is administered activated charcoal and PEG solution by the ER physician.

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Clinical Course

  • Because of the ST segment elevations on ECG, the cardiologist elects to give TPA.

  • Since thrombolytics were given, the general surgeon refuses to take the patient to the OR for an exploratory lap and removal of the cocaine packets.

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Clinical Course

  • The patient subsequently develops seizure activity, worsening hyperthermia, rhabdomyolysis, and intracranial hemorrhage.

  • He expires 48 hrs after admission

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Case #3 History

17 y/o CF presents to the community hospital emergency department at 2:00AM with “fever and strange behavior” as per her parents.

While waiting to be examined, the patient has a witnessed tonic-clonic seizure lasting 1 minute in duration.

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  • No PMH; No medications ; NKDA

  • Vitals: T=104.2F P=120 BP=100/90 RR=28

  • PE: Gen: restless, agitated, confused

    HEENT: pupils 6mm & reactive, MMM

    CV: RRR, no MRG Lungs: CTA

    Abd: Soft, (+)BS, mild tenderness

    Skin: warm, dry, no rashes

    Neuro: No focal defs

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  • CBC: WNL

  • Lytes: 120/3.9/87/21

  • Serum Osm=234, Urine Osm=261

  • Urine Na: 82

  • U/A: large blood (-)RBCs

  • CPK: 3,300

  • CT head: normal

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Earlier that night:

•Urine Tox Screen:

+ Amphetamines

+ Cannabis


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Ecstasy: The drug of a new generation.

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Ecstasy = MDMA

  • 3,4 methylenedioxymethamphetamine

  • X, E, M, XTC, Rolls, Adam, Bean, Hug Drug

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MDMA Properties and Mechanism of Action

  • Designer drug from the essential oil of the sassafras tree

  • Ring substituted amphetamine

  • Pharmacological effects are a blend of amphetamines and mescaline

  • Structure resembles natural neurotransmitters of Epi, DA

  • Biological actions and effects resemble those of Epi, DA, and serotonin

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  • Increases the net release of monoamine neurotransmitters (5-HT, NE, DA) from their axon terminals

  • MDMA binds to and blocks the serotonin reuptake transporter – flooding the terminals with 5-HT

  • Similar, weaker action on DA reuptake

  • Amphetamine like increase in NE

  • Increase in 5-HT and DA = mental effects

  • Increased NE=physical amphetamine effects

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MDMA analogues

  • MDA (3,4-methylenedioxyamphetamine) –

    “Love Drug” - similar in effect, more stimulating, twice as neurotoxic

  • MDE (N-ethyl-methylenedioxyamphetamine)

    “Eve” – more introspective experience

  • MMDA (3-methoxy-4,5-methylenedioxyamphetamine) – closed eye hallucinations, “brain movies”

  • MBDB (N-methyl-1-(1,3-benzodioxol-5-yl)-2-butanamine) – effects similar to MDA

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MDMA History

  • 1912 – first synthesized by Merck

  • 1914 – patented by Merck – manufactured as an appetite suppressant, never marketed

  • 1950’s- studied by US Army as potential agent in psychological warfare

  • 1970 – used in psychotherapy, “penicillin for the soul”

  • 1977 – class A illegal drug in UK

  • 1985 – Schedule I illegaldrug in U.S.

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Trends in Ecstasy Use

  • DEA seizures of Ecstasy Tablets:

  • 1996 – 13,342 tablets

  • 2000 – 949,257 tablets

  • 2001 - >4,000,000 tablets in 8 months

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Ecstasy Use by Students, 2000 (NIDA Studies)

Perceived availability by 12th graders 51.4% (40.1%)

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MDMA Production and Sales

  • Street value = $25 per pill

  • Wholesale price = $2-$8 per pill

  • Production cost = 2-5 cents per pill

  • Majority of production and distribution linked to well organized crime networks in Europe (Amsterdam, Germany, UK) and Israel

  • Smaller labs all over US and Europe

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Areas of Usage

  • Highest at raves, dance clubs (as high as 91% of clubbers in dance scene in Scotland)

  • Dramatic increase in college use, suburban teens, house parties

Millroy, CM, JRSM February 1999

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Physical CLUES

  • Glowsticks or lights

  • Lollipops

  • Pacifiers

  • Vick’s Vapor Rub and Nasal Inhaler

  • Fuzzy Mittens

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Most Predictive Factor of Drug Use = CLUB MUSIC!

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Methods of Administration

  • Mainly PO – stamped tablets, capsules

  • Intra-nasal – rapid absorption of crushed tablets or opened capsules

  • Intra-rectal – faster absorption than PO

  • Recreational usage varies from ½ pill to as much 15 pills in a 6 hour span

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Content and Purity

  • Numerous logos and names (Green Nike, Mitsubishi, Buddha, Smiley Face)

  • Pills tested and results posted on Internet sites such as dancesafe.org

  • Average MDMA content 90-100mg/pill

  • 60% MDMA, 20% MDEA, 10% MBDB, 10% no active ingredient or aspirin, 5% amphetamine, ephedrine, or caffeine

Millroy, CM, JRSM February 1999

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MDMA Adulterants

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  • Peak plasma concentration at ≈ 2 hrs 106ng/mL@50mg, 236ng/mL@125mg

  • Large tissue distribution

  • Metabolic breakdown by CYP2D6

  • Saturation kinetics

  • T1/2 ≈ 8 hours

  • Pharmacologically active first metabolite (MDA)

Kalant, H; Canadian Medical Association Journal, October, 2001

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Extreme euphoria

Increased energy

Feelings of belonging and closeness

Heightened sensations (touch, taste, smell, hearing)

Increased openness

Feelings of love and empathy

Bright, intense visual perceptions

Musical appreciation

Fear dissolution

“Profound” thought

Positive Effects

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Appetite loss

Vertical nystagmus (rolling)

Moderate increases in HR and BP

Mild visual hallucinations

Mind racing

Changes in thermoregulation

Restlessness, nervousness, shivering

Strong desire to take more drug during come down


Other Effects

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Mild to extreme trisma and bruxism

Short-memory loss


HA, vertigo, ataxia

Muscle tension

Nausea & vomiting

Concentration difficulties

“Crash” come down

Hangover lasting days to weeks

Depression and fatigue for up to a week

Psychological addiction

Panic attacks

Negative Side Effects

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Major Toxic Complications

  • Hyperthermia/Heat Stroke

  • Dehydration

  • Hyponatremia


  • Hepatitis/Liver Failure

  • Rhabdomyolysis/Renal Failure

  • Neurotoxic Effects

  • Acute Psychotic Break/Severe Depression

  • Death!

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Ecstasy Related Fatalities

87 cases reported in the literature caused by:

  • Hyperpyrexia – 30

  • Hepatic – 4

  • Cardiovascular/Cerebrovascular – 8

  • Cerebral, including Hyponatremia – 9

  • Drug Related Accidents or Suicide – 14

  • Unknown – 22

Kalant, H; Canadian Medical Association Journal, October, 2001

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Major Physical Toxicity - Hepatic

  • Mild viral hepatitis – jaundice, enlarged tender liver, elevated LFT’s/Coags – self limited, 2 wks-3 mo, related to glutathione decrease and oxidative cell destruction

  • Prolonged hepatitis – slow recovery with potential permanent fibrosis

  • Fulminant liver failure – fatal without liver transplant

Kalant, H; Canadian Medical Association Journal, October, 2001

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Major Physical Toxicity - Cardiovascular

  • NE responsible: HTN and tachycardia

  • Major intracranial hemorrhage

  • Petechial hemorrhages – brain and other organs

  • Retinal hemorrhage at autopsy

  • Intravascular thrombosis and CVA

  • Serious cardiac dysrhythmias

  • Pulmonary edema/heart failure

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Major Physical Toxicity- Cerebral

  • Hyponatremia- result of vigorous physical activity, profuse sweating, large Na+ loss, excessive water consumption

  • SIADH – less common mechanism of water retention, but can complicate picture

  • Cerebral edema w/hyponatremic seizures – therapy includes BZD’s and cautious replacement of Na with hypertonic saline

  • Brain stem and cerebellum compression

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Hyperpyrexic Pattern of Toxicity

  • Most dangerous form of ecstasy induced toxicity

  • Results from a combo of drug action, intense physical activity, and hot environment

  • Adulterants such as dextromorphan can inhibit sweating leading to further heat retention

  • Changes resemble those seen in severe heatstroke

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Features of Hyperpyrexia

  • Rhabdomyolysis – heat production and muscle necrosis

  • Myoglobinuria and renal failure – secondary to rhabdomyolysis

  • Hepatic necrosis

  • DIC

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Treatment of Hyperpyrexic Pattern of Toxicity

  • Mainly symptomatic – rehydration, monitor electrolytes, treat possible co-ingestions

  • Early rapid cooling measures: ice-water sponging, IV infusion of chilled saline, gastric and bladder lavage with cooled fluids, general supportive care

  • Dantrolene - 1mg/kg – good evidence for use as a potential life-saving measure

Kalant, H; Canadian Medical Association Journal, October, 2001

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Toxic Blood Levels

  • Poor correlation overall – shows importance of environmental factors

  • “Recreational” use: 100-250ng/mL

  • Most cases of serious toxicity or fatality w/ levels from 500ng/mL–10μg/mL – 40x higher than usual recreational range

  • Some cases of serious toxicity w/ levels as low as 111-255ng/mL

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  • Paramethoxyamphetamine

  • Pills contain 50mg of PMA, look like MDMA tablets

  • Longer duration to onset – toxic in doses of 60-80mg

  • Rapid rise in BP and temp leading to convulsions, coma, and death

  • Responsible for 10 deaths (3 in suburbs of Chicago)

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Case Revisited

  • Supportive care and rapid cooling measures

  • Volume replacement and Na+ correction with 3% NS

  • Labs corrected (Na=137 @ 30 hrs after admission

    • VSS, no further seizures, mental status improved throughout the day

  • Stable after 3 days in ICU

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    • The patient is a 23 yr old who suffered a witnessed seizure and is brought to the ED by concerned friends.

    • He has no prior seizure disorder and the friends deny history of drug use.

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    • Gen: Comatose, postictal

    • Vs: BP=150/90 P=60 RR=20 T=98.7

    • HEENT: NC/AT Pupils: 4mm (+)gag reflex

    • Lungs: CTA Ht: RRR S1S2

    • Abd: Benign Ext: (-)c/c/e good pulses

    • Neuro: Moves all 4 ext to pain, no focal defs

    • Skin: Cool diaphoretic

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    • CBC: WBC=14.5 H/H=13/38

    • Na=140 K=4.2 Cl=105 HCO3=19

    • Glucose: 180 BUN/Cr= 10/0.9

    • ABG: pH=7.35 PO2=110 PCO2=35

    • Tox screen: Neg ETOH= 57

    • ECG: NSR no ectopy, no ischemia

    • CT Head: No bleed, no mass

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    Clinical course

    • No initial response to D50 or naloxone

    • 4 hours after ED presentation, the patient becomes more alert and oriented

    • He admits to taking 1 tbs of “growth hormone powder” mixed with H2O 45 min prior to presentation purchased at a local health food store

    • The powder had been advertised as a “muscle builder”

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    Gamma Hydroxybutyrate Acid (GHB)

    • Liquid ecstacy

    • Liquid G

    • Gamma Oh

    • Grievous bodily harm

    • Scoop

    • Samatomax

    • Bioski

    • Cow Growth Hormone

    • Georgia Home Boy

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    • Analogue of inhibitory neurotransmitter gamma-aminobutyirc acid- CNS depressant

    • Synthesized in 1960 and used in 1970’s for sleep disorders because it induces REM sleep

    • Used in Europe as anesthetic agent until found that it caused seizures

    • 1977, study claimed it stimulated effects of Growth Hormone

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    • Unapproved drug in US, but legally obtainable under FDA investigational New Drug exemption for treatment of narcolepsy

      • 20 states have controlled its use with penalties similar to marijuana possession


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    Gamma Hydroxybutyrate Acid (GHB)

    • Readily available in drug market and inexpensive and relatively easy to make

      • recipes are obtainable on the internet

    • Obtainable as clear and odorless liquid, gel, or powder which have a salty taste

      • however, taste is masked by ETOH which increases its clinical effects

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    • Used in date rape because:

      • quick onset of effect

      • easily obtainable

      • small quantities are needed

      • causes hallucinations and amnesia making the patient an unreliable witness

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    GHB - Toxicity

    • Acts as neurotransmitter affecting GHB and GABA- B receptors causing CNS depression

      • takes effects in 15-30 minutes causing drowsiness, dizziness, and disorientation

      • duration of action up to 3 hours

      • half life of 20 min to 1 hour

      • hallmark is marked agitation upon stimulation despite apnea and hypoxia

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    • 10mg/kg causes vomiting, rapid onset of coma and amnesia

    • 20-30mg/kg cause rapid cycles of REM and non-REM sleep

    • 50mg/kg can cause resp depression, bradycardia, clonic muscle contractions, and decreased cardiac output

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    GHB - Other forms

    • Gamma butyrolactone (GBL) - can be purchased from chemical supply stores or catalogues and converted to GHB with NaOH

      • GBL is rapidly converted to GHB by peripheral lactonases within minutes

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    • 1,4-Butanediol - can be purchased in similar manner as GBL

      • converted to gamma hydroxybutyaldehyde by alcohol dehydrogenase

      • then, converted to GHB by aldehyde dehydrogenase

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    GHB - Diagnosis

    • High clinical suspicion based on history and clinical presentation

      • abrupt on set of coma with recovery within a few hours

    • Lab tests for GHB not readily available

      • few national reference labs

    • Duration of detection of GHB in blood and urine are 6 and 12 hours, respectively

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    GHB - Treatment

    • Mainly supportive

    • Antidotes for GHB: Physostigmine?

    • Decontamination

      • charcoal has doubtful benefits since small amounts used are absorbed rapidly and may increase risk of pulmonary aspiration

    • Enhanced Elimination

      • no role

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    • The patient is an 18 yr old transferred from the H.S. health center to the ED after he was caught wondering the hallways by the art department demonstrating “bizzare behavior”

    • The patient is normally healthy

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    • Gen: Sleepy, blank catatonic stare when awakened, good airway

    • Vs: P=90 BP=110/70 RR=16 T=99

    • HEENT: NC/AT Eyes: Pupils 3mm Rotary nystagmus noted; moist mm’s (+)drooling

    • Lungs: CTA CV: RRR S1S2

    • Abd: Benign Ext: Good pulses

    • Neuro: Motor sensory grossly intact no focal defs

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    • AKA: Special K, Super Acid, Super C

    • used as an anesthetic in EM and veterinary medicine

    • Ketamine is a controlled substance in 18 states as schedule III drug

    • Used in date rape because:

      • rapid onset

      • dissociative hallucinogenic

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    Ketamine - Toxicity

    • Chemically related to PCP

    • takes effect 15-20 minutes, producing analgesia

    • Higher doses produces dissociative hallucinations, delirium, resp depresion, Sz, arrythmias and cardiac arrest

    • Effects last 20-45min

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    Ketamine - Diagnosis

    • High index of suspicion based on history and presentation

    • Urine tox screens may mistakenly ID as PCP since structurally related to PCP

    • Specific test for ketamine not widely available

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    Ketamine - Treatment

    • Mainly supportive

    • No antidote

    • Pt should be placed in quiet room with minimal stimulation

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    • The patient is a 16 yr old male who presents to the ED complaining of facial swelling, drooling, and blisters on his fingers from “doing a little painting”

    • He also claims that the top of a freon propellant can “fell off” while he was sleeping next to it.

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    • Gen: Alert, oriented, mild resp distress

    • Vs: P=120 RR=28 BP=110/60 T=96

    • HEENT: Extensive edema, scattered blisters and bullae of the lips, oral mucosal/tongue with obvious facial deformity

    • Lungs: CTA CV: Tachy RRR S1S2

    • Ext: Blisters of distal phalanges

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    • CBC: WBC: 22K Hgb: 11.5

    • Lytes: Na=140 K=2.9 Cl=117 HCO3=18

    • BUN/Cr: 29/2.1 Glucose=140

    • Tox screen: (+)cannabinoids

    • ETOH: 20

    • ECG: Sinus tach 120/min, no ischemia

    • CXR: No infiltrates or pulm edema

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    • VSAs: (Volatile Substances of Abuse)

    • “Sniffing”: inhaling raw vapors.

    • “Huffing”: inhaling vapors from a soaked cloth held next to mouth or nose.

    • “Bagging”: inhaling vapors from a bag, balloon, or other vessel which is then held over mouth or nose.

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    Inhalants--Street Names

    • Air Blast

    • Bullet bolt

    • Disco-rama

    • Head Cleaner

    • Heart-On

    • High Ball

    • Hippie Crack

    • Honey Oil




    Moon Gas


    Satan’s Secret


    Toilet Water

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    • Ancient Greece: the Pythia sat above a cleft in the rocks and inhaled cold vapors emanating from inside the earth, which induced an ecstatic alteration of mind

    • Proverbs (27:9) “ointment and perfume rejoice the heart.”

    • Ether “frolics” and N2O “sniffing parties” starting in 1700s (25 cent admission).

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    • N2O discovered in 1776 by Sir Humphrey Davy/Joseph Priestly, used by Winston Churchill, Samuel Taylor Coleridge.

    • Ether was first used for surgery and then sold in the late 1800s as a 'medicinal' for women.

    • WW II: Ether used as EtOH substitute.

    • Current abuse trend first noticed in 1950s in California.

      (Bass, et al, JAMA June 1970)

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    Robert Hinkley, 1893

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    Scope of the Problem

    • Total reported PCC cases: 2,271,188

    • Inhalation: 138,647 (6.1%)

    • Reported PCC fatalities: 1,001

    • Inhalation fatalities: 85 (8.5%)

      2000 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System

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    Scope of the Problem

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    Scope of the Problem

    • Brazil: Glue sniffing is used as a replacement for food.

    • Egypt, India, Romania,Guatemala, Native Canadians: A coping mechanism. Children use VSAs to stay awake for work, to alert toward possible violence, to sleep, or to dull physical or emotional pain.

    • VSAs also used in many cultures and countries as social outcries against government and society.

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    General Types/Classification

    • Volatile Hydrocarbons/Solvents

    • Volatile Nitrites

    • Gases

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    Volatile Hydrocarbons/Solvents

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    Substances Involved in Inhalant Abuse Cases


    Total: 165 cases

    Spiller HA, Krenzelok EP. (1997) Kentucky RPC, Pittsburgh PC.

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    Volatile Substances of Abuse Commonly Found in Commercial Products

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    Volatile Nitrites (poppers)

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    “Offer good until November 30th”

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    Total: 165 cases

    Spiller HA, Krenzelok EP. (1997) Kentucky RPC, Pittsburgh PC.

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    Acute Organ System Effects: Cardiovascular

    • Myocardial sensitization to catecholamines

      First mentioned by Bass, et al JAMA 1970

      • Mostly with Solvents/HCs

      •  incidence of epinephrine-induced dysrhythmia in rats exposed to VSAs

      • Direct VSA-induced  in endogenous catecholamines

      • Arrhythmia ;decreased contractility

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    Acute Organ System Effects: Pulmonary

    • Asphyxia: VSA displaces O2

      • HYPOXEMIA (esp N2O)

    • Direct irritation  chemical PNEUMONITIS, wheezing, rales

    • Direct CNS effect  RESPIRATORY DEPRESSION or arrest

    •  airway reflexes +  N/V ASPIRATION

    • VASOVAGAL effect- Direct spraying of propellant into mouth

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    Cortical Atrophy

    Normal brain

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    Long-Term Effects

    • Mostly neurologic (rare):

      • impaired neuro-cognitive function

    • Can also severely affect liver, kidneys, heart, lungs, bone marrow

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    Special Situations

    • Typewriter correction fluid

      • May contain halogenated HCs: TCE, Cl3-ethylene, perchloroethylene

      • Cause dysrhythmia, seizure, CNS depression

      • Massive hepatic necrosis

      • Mustard oil recently added as irritant to  deliberate inhalation

      • Gasoline- historically, lead level helpful, but now there is  use of leaded gas

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    Some Specific Toxicities

    Pediatric Annals, January 1996.

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    Special Situations

    • Alkyl Nitrites

      • Can get HYPOTENSION: caution use with VIAGRA, other Nitrates (NTG)

      • Methemoglobinemia

    • Methylene Chloride

      • CO is a metabolite

    • N2O

      • Hypoxemia

    • Ether: FLAMMABLE

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    Sudden Sniffing Death

    • Mechanism of Death

      • Induce V-fib.

        • Most frequently with toluene and halogenated HCs:

      • VSA-induced/catechol sensitized myocardium

        • Clinical and animal studies corroborate Bass’ suggestion

      • Hypokalemia: additional cause of arrhythmia

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    Detection/Identification: Demographic

    • Males > Females

    • Onset: ~6-8 yo

    • Peak age: 14-15 yo

    • Lower socioeconomic status

    • Poor school performance

    • Family dysfunction

    • Hispanic, Latin American, Native Americans

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    Detection/Identification: Historical

    • Rags, bags, empty containers

    • N/V, loss of appetite

    • Irritability/behavior change

    • Depression

    • Blindness, Deafness: Toluene

    • Numbness: Nitrous Oxide

      Hexane (peripheral neuropathy)


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    Detection/Identification: Clinical

    • Chemical odor on breath or clothing

    • Paint stained clothing and/or skin

    • “Glue-sniffer’s rash”

    • Disoriented

    • Slurred speech

    • Ataxia

    • Peripheral neuropathy

    • Hypotension

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    Detection/Identification: Lab

    • Methylene Chloride

      • CO-Hb level with monitoring for ~12-24h

    • Alkyl Nitrite

      • Methemglobinemia

    • CCl4, Chloroform, Xylene

      • Watch LFTs closely (acute hepatic necrosis)

    • Lead level

      • Gasoline?

    • Nitrous Oxide

      • Megaloblastic anemia (B12 def.)

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    Detection/Identification: Lab

    • Routine Testing:

      • CBC, Electrolytes, BUN/CR, ABG, UA, LFTs, PT/PTT/INR

      • Tox screen (UDS, serum drug screen)

      • ECG if symptomatic

      • CT for non-improving AMS

      • CXR with pulmonary symptoms

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    • ABCs/ACLS

    • Remove exposure-

    • Decontaminate skin/eyes

    • Oxygen

      • Hyperventilation:  pulmonary excretion

    • IV: 0.9 NS initially.

      • Glucose may exacerbate hypokalemia

    • Electrolyte replacement as needed (K, Ca, P, Mg)

    • Admit: Psych, if intentional. (Addiction treatment)

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    • Catecholamine surge/sensitzation

      • Sympathomimetic amines and pressors should be used CAUTIOUSLY 2 to sensitized myocardium.

      • Bronchospasm: Inhaled 2-agonists useful, but may be pro-arrhythmic.

      • Treat seizures/agitation with BENZOS first to avoid excess catecholamine stimulation.

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    -blockers shown in some cases (limited data/evidence) to be helpful to arrhythmias.

    Amiodarone may be more helpful for V-fib/arrhythmias (limited data/evidence).

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    • Specific Therapies

      • Amyl Nitrite

        • Methylene Blue for Methemoglobinemia

      • Hepatic/Renal Toxicity (Chlorofrom, TCE, TC-Ethylene)

        • N-Acetylcysteine

      • Methylene Chloride

        • 100% O2 HBO

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    Special thanks to:

    • Ryan Snitowsky- Ecstacy

    • Joe Garcia- Inhalants

    • Javier Rangel- GHB

    References l.jpg


    • 1991; 9: Holden R, Jackson MA. Near-fatal hyponatremic coma due to vasopressin over-secretion after “ecstasy” (3,4-MDMA). The Lancet 1996;347:1052.

    • Kalant H. The pharmacology and toxicity of “ecstasy” (MDMA) and related drugs. CMAJ 2001;165(7):917-928.

    • Milroy CM. Ten years of ecstasy. JRSM 1999;92(2):68-72.

    • Schwartz RH, Miller NS. MDMA (Ecstasy) and the rave: A review. Pediatrics 1997;100(4): 705-708.

    • www.erowid.orgwww.dancesafe.org

    • Centers for Disease Control and Prevention: GHB use 1995-1996 JAMA 1997; 277;1511.

    • Dyer JE: GHB: A health-food product producing coma and seizures. Am J Emerg Med 321-324.

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    • Gussow, Leon “Inhalants of Abuse” in Clinical Toxicology, ed. Ford, Delaney, Ling, Erickson (Philadelphia, PA: WB Saunders, 2001) pp. 651-656.

    • Bass, Millard, “Sudden Sniffing Death.” JAMA 1970 June 22; 212(12): 2075-79.

    • Committee on Substance Abuse and Committee on Native American Child Health, “Inhalant abuse.” Pediatrics 1996 Mar;97(3):420-3.

    • Henretig, Fred. “Inhalant abuse in children and adolescents.” Pediatric Annals 1996 Jan;25(1):47-52.

    • 2001 Research Report "Inhalant Abuse.”

    • Steffee CH, Davis GJ, Nicol KK. “A whiff of death: fatal volatile solvent inhalation abuse.” South Med J 1996 Sep;89(9):879-84.

    • (www.drugabuse.gov/ResearchReports/Inhalants/RRInhalants.pdf)

    • MICROMEDEX, Inc., Greenwood Village, Colorado (Edition expires 12/2001).

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    • 2001 NIDA Infofax: “Inhalants” (www.drugabuse.gov/Infofax/inhalants.html)

    • Brecher, Edward M., et al “The Consumers Union Report on Licit and Illicit Drugs.” www.druglibrary.org/schaffer/Library/studies/cu/CU43.htm

    • ONDCP Drug Policy Information Clearinghouse Fact Sheet, June, 2001. (www.whitehousedrugpolicy.gov/publications/pdf/inhalants_factsheet.pdf)

    • Broussard LA, “The role of the laboratory in detecting inhalant abuse.” Clin Lab Sci 2000 Fall;13(4):205-9

    • Spiller HA, Krenzelok EP. “Epidemiology of inhalant abuse reported to two regional poison centers.” J Toxicol Clin Toxicol 1997;35(2):167-73.

    • Litovitz TL, “2000 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System.” Am J Emerg Med - 01-Sep-2001; 19(5): 337-95.

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