Transcript Ecstasy - University of Illinois at Chicago

Street Drugs of Abuse
Timothy B. Erickson, MD
Professor: Department of Emergency Medicine
University of Illinois @ Chicago
Case #1 History
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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.
Physical Exam
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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
Physical Exam
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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
Case Discussion
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What are your priorities when
managing this patient?
Management Priorities
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Airway
Breathing
Circulation
Assess for signs of trauma
Antidote administration
Case Summary
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Comatose patient
Pinpoint (miotic) pupils
Depressed respiratory drive
Bradycardia
Hypothermia
Opioid Overdose
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Heroin
Methadone
Codeine
Morphine
Fentanyl
Demeral
Propoxyphene
HEROIN
HEROIN
HEROIN
ANTIDOTE
NALOXONE
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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
Clinical Course
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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.
Clinical Course
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Laboratory data including ECG and
CXR are unremarkable.
The toxicology screen is positive for
opiates.
Clinical Course
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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….
Case#2 History
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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.
Case Physical Exam
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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
PHYSICAL EXAM
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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
“I’m having chest pain”
Clinical Course
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The patient now admits to swallowing
several “condoms full of cocaine”
before boarding the plane from
Columbia to the U.S.
Drug Smugglers
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Describe the difference between a
“Body Packer” and a “Body Stuffer”
Packers and Stuffers
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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).
Body Stuffer
Body Packer
Cocaine
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
Cocaine Toxicity
(Sympathomimetic)
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Hypertension
Tachycarida
Hyperthermia
Diaphoresis
Anxiety
Seizures
CVA/Intracranial bleed
Myocardial infarction
Gastric Decontamination
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Activated charcaol
Polyethlene glycol solution
(aka: Go-lytely)
Surgical removal
Cocaine & Chest Pain
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Oxygen
Benzodiazepines
Nitroglycerin
B-Blockers- contraindicated
Hypertension control
Thrombolytic Agents (TPA)
Cath Lab / Angioplasty
Clinical Course
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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.
Clinical Course
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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.
Clinical Course
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The patient subsequently develops
seizure activity, worsening
hyperthermia, rhabdomyolysis, and
intracranial hemorrhage.
He expires 48 hrs after admission
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
DIAGNOSTIC STUDIES
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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
Earlier that night:
•Urine Tox Screen:
+ Amphetamines
+ Cannabis
- EtOH, ASA, APAP
AMPHETAMINES
Ecstasy: The drug of a new
generation.
Ecstasy = MDMA
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3,4 methylenedioxymethamphetamine
X, E, M, XTC, Rolls, Adam, Bean, Hug Drug
MDMA
Properties and Mechanism of Action
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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
Pharmacodynamics
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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
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-4,5methylenedioxyamphetamine) – closed eye
hallucinations, “brain movies”
 MBDB (N-methyl-1-(1,3-benzodioxol-5-yl)-2butanamine) – effects similar to MDA
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MDMA History
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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 illegal drug in U.S.
Trends in Ecstasy Use
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DEA seizures of
Ecstasy Tablets:
1996 – 13,342
tablets
2000 – 949,257
tablets
2001 - >4,000,000
tablets in 8 months
Ecstasy Use by Students,
2000 (NIDA Studies)
8thGraders
10thGraders
12thGraders
Ever Used 4.3%
7.3%
11.0%
Used in
Past Year
(1999)
5.4%
(4.4%)
8.2%
(5.6%)
2.6%
3.6%
3.1%
(1.7%)
Past
1.4%
month use
Perceived availability by 12th graders 51.4% (40.1%)
MDMA
Production and Sales
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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
Areas of Usage
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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
Physical CLUES
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Glowsticks or lights
Lollipops
Pacifiers
Vick’s Vapor Rub
and Nasal Inhaler
Fuzzy Mittens
Most Predictive Factor of
Drug Use = CLUB MUSIC!
Methods of
Administration
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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
Content and Purity
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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
MDMA Adulterants
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MDEA
MBDB
MDA
PMA
Caffeine
Dextromorphan
Aspirin
Piracetam
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Methamphetamine
PCP
Ketamine
Heroin
Quinine
LSD
Marijuana
Ephedrine
MDMA
Onset
20-90
min
Rise up 5-20
min
Plateau 2-3
hours
Come
1-2
down
hours
After
3-24
Effects hrs
Pharmacokinetics
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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
Positive Effects
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Extreme euphoria
Increased energy
Feelings of
belonging and
closeness
Heightened
sensations (touch,
taste, smell,
hearing)
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Increased openness
Feelings of love and
empathy
Bright, intense
visual perceptions
Musical
appreciation
Fear dissolution
“Profound” thought
Other Effects
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Appetite loss
Vertical nystagmus
(rolling)
Moderate increases
in HR and BP
Mild visual
hallucinations
Mind racing
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Changes in
thermoregulation
Restlessness,
nervousness,
shivering
Strong desire to
take more drug
during come down
Mydriasis
Negative Side Effects
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Mild to extreme
trisma and bruxism
Short-memory loss
Confusion
HA, vertigo, ataxia
Muscle tension
Nausea & vomiting
Concentration
difficulties
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“Crash” come down
Hangover lasting
days to weeks
Depression and
fatigue for up to a
week
Psychological
addiction
Panic attacks
Major Toxic
Complications
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Hyperthermia/Heat Stroke
Dehydration
Hyponatremia
SIADH
Hepatitis/Liver Failure
Rhabdomyolysis/Renal Failure
Neurotoxic Effects
Acute Psychotic Break/Severe Depression
 Death!
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
Major Physical Toxicity Hepatic
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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
Major Physical Toxicity Cardiovascular
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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
Major Physical ToxicityCerebral
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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
Hyperpyrexic Pattern of
Toxicity
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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
Features of Hyperpyrexia
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Rhabdomyolysis – heat production
and muscle necrosis
Myoglobinuria and renal failure –
secondary to rhabdomyolysis
Hepatic necrosis
DIC
Treatment of Hyperpyrexic
Pattern of Toxicity
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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
Toxic Blood Levels
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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
PMA
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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)
Case Revisited
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Supportive care and rapid cooling
measures
Volume replacement and Na+
correction with 3% NS
Labs corrected (Na=137 @ 30 hrs
after admission
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VSS, no further seizures, mental status
improved throughout the day
Stable after 3 days in ICU
CASE #4 HISTORY
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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.
PHYSICAL EXAM
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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
DIAGNOSTIC STUDIES
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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
Clinical course
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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”
Gamma Hydroxybutyrate Acid
(GHB)
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Liquid ecstacy
Liquid G
Gamma Oh
Grievous bodily harm
Scoop
Samatomax
Bioski
Cow Growth Hormone
Georgia Home Boy
GHB
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
GHB
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
Gamma Hydroxybutyrate Acid
(GHB)
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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
GHB
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
GHB
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GHB - Toxicity
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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
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
GHB - Other forms
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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
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
GHB - Diagnosis
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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
GHB - Treatment
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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
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Enhanced Elimination
– no role
CASE #5 HISTORY
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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
PHYSICAL EXAM
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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
Ketamine
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Ketamine
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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
Ketamine - Toxicity
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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
Ketamine - Diagnosis
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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
Ketamine - Treatment
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Mainly supportive
No antidote
Pt should be placed in quiet room with
minimal stimulation
CASE #6 HISTORY
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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.
PHYSICAL EXAM
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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
LABORATORY
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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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Definitions
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VSAs: (Volatile Substances of Abuse)
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“
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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.
Inhalants--Street Names
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Air Blast
Bullet bolt
Disco-rama
Head Cleaner
Heart-On
High Ball
Hippie Crack
Honey Oil
Huff
Kick
Medusa
Moon Gas
Oz
Satan’s Secret
Sniff
Toilet Water
History



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).
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)
Robert Hinkley, 1893
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
Scope of the Problem

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.
General Types/Classification

Volatile Hydrocarbons/Solvents

Volatile Nitrites

Gases
Volatile Hydrocarbons/Solvents
Aliphatic HC Methane, ethane
acetylene, propane,
butane, gasoline,
kerosene, hexane
Liquid fuel, lighter fluid, fuels,
paint thinner, solvents
Aromatic HC Benzene, xylene,
toluene
Glues/rubber cement,
solvents, paints, varnishes,
shoe polish, correction fluid
Alkyl Halides Methylene chloride,
trichloroethane,
trichloroethylene,
CFCs/freons, CCl4
Paint stripper, dry cleaner,
spot cleaner, correction
fluid, aerosol propellants,
fire extinguishers
refrigerants
Ketones
Glues, adhesives, dyes, nail
polish remover
Acetone, methylethyl
ketone, methyl
isobutyl ketone
Substances Involved in Inhalant Abuse Cases
~2/3
Total:
165 cases
Spiller HA, Krenzelok EP. (1997) Kentucky RPC, Pittsburgh PC.
Volatile Substances of Abuse
Commonly Found in Commercial
Products
Volatile Nitrites (poppers)
“Offer good until November 30th”

Gases/Aerosols
Effects
Total: 165 cases
Spiller HA, Krenzelok EP. (1997)
Kentucky RPC, Pittsburgh PC.
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
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-
Cortical Atrophy
Normal brain
Long-Term Effects

Mostly neurologic (rare):
– impaired neuro-cognitive function

Can also severely affect liver, kidneys,
heart, lungs, bone marrow
Special Situations

Typewriter correction fluid
– May contain halogenated HCs: TCE, Cl3ethylene, 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
Some
Specific
Toxicities
Pediatric Annals, January
1996.
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
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
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
Detection/Identification:
Historical






Rags, bags, empty containers
N/V, loss of appetite
Irritability/behavior change
Depression
Blindness, Deafness: Toluene
Numbness: Nitrous Oxide
Hexane
Xylene
(peripheral neuropathy)
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
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.)
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
Management
– 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)
Management

Catecholamine surge/sensitzation
– Sympathomimetic amines and
pressors should be used
CAUTIOUSLY 2 to sensitized
myocardium.
– Bronchospasm: Inhaled 2agonists useful, but may be proarrhythmic.
– Treat seizures/agitation with
BENZOS first to avoid excess
catecholamine stimulation.
CARDIAC
–-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).
Management

Specific Therapies
– Amyl Nitrite

Methylene Blue for Methemoglobinemia
– Hepatic/Renal Toxicity (Chlorofrom,
TCE, TC-Ethylene)

N-Acetylcysteine
– Methylene Chloride

100% O2 HBO
Special thanks to:



Ryan Snitowsky- Ecstacy
Joe Garcia- Inhalants
Javier Rangel- GHB
References
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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):6872.
Schwartz RH, Miller NS. MDMA (Ecstasy) and the rave:
A review. Pediatrics 1997;100(4): 705-708.
www.erowid.org www.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/RRInhalant
s.pdf)
MICROMEDEX, Inc., Greenwood Village, Colorado (Edition expires 12/2001).
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_facts
heet.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.