T C DRUG AND LCOHOL FACILITATED SEXUAL ASSAULT

Marc A. LeBeau, PhD FABFTSenior Scientist

Scientific Analysis Section

FBI Laboratory

Quantico, Virginia

USA

[email protected]

THE CHALLENGES OF DRUG AND

ALCOHOL FACILITATED SEXUAL ASSAULT

INTRODUCTION

Increased reports of Drug-Facilitated Crimes (DFCs) in the media and the scientific literature

Belief that DFCs have increased Rise in commission?

Greater awareness?

Increased reporting?

True prevalence of DFCs will never be known Pharmacodynamic effects on reporting

Delayed reporting

Statistically capturing DFCs

OBJECTIVES

Describe media’s role in establishing myths about drug-facilitated crimes

List four major challenges encountered in alcohol and drug-facilitated sexual assault investigations

Categorize the most common drugs associated with drug-facilitated crimes and compare/contrast pharmacological effects

Recognize at least three “obscure” drugs associated with drug-facilitated crimes and reflect upon why they are used

Describe how to overcome some of the challenges of drug-facilitated crimes to improve the SART response

DEFINING DRUG-FACILITATED CRIMES

DRUG-FACILITATED CRIMES

Victim subjected to crime in which the pharmacological effects of a drug or drugs help the perpetrator carry out the crime

Usually strong, CNS depressants

Types:

Robbery

Human trafficking / kidnapping

Neglect by caregiver

Sexual Assault

SEXUAL ASSAULT

Incapacitated Sexual Assault

Voluntary ingestion of drug and/or alcohol

Strong CNS depression

Perpetrator takes advantage

Drug-Facilitated Sexual Assault

Perpetrator gives drug or alcohol to victim without their knowledge

Goal is to incapacitate the victim and commit the assault

COMMON SIGNS OF DFSA

Recalls having drink but cannot recall what happened for period of time afterwards

Suspects someone had sex with them but cannot remember the incident

Feels more intoxicated than their usual response to same quantity of alcohol

Wakes up hung over, experiences memory loss or cannot account for a period of time

MICKEY FINN

Bartender / Owner of the Lone Star Saloon and Palm Garden Restaurant

Located in the “Whiskey Row” section of Chicago’s State Street

Finn or one of his employees would slip chloral hydrate concoction into the drink of unsuspecting patrons.

In December of 1903, the bar was closed by Chicago authorities

CHALLENGES OF SURREPTITIOUS ADMINISTRATION

Most “drugs” will dissolve or disperse in beverages or food

Tablets / capsules contain insoluble fillers

Medications are bitter

CHALLENGES OF DFSA CASES

CHALLENGES SURROUNDING DFSA INVESTIGATIONS

Drugs

Reporting

Specimens

Labs


• Dosages

• Number of Candidates

• Pharmacokinetics

• Pharmacodynamics

Drugs

DRUGS REPORTEDLY USED TO COMMIT DFSA

Ethanol

Benzodiazepines

Flunitrazepam

Clonazepam

Lorazepam

Alprazolam

Triazolam

Chlordiazepoxide

Diazepam

Temazepam

Zolpidem

Barbiturates

GHB and analogs

Ketamine

Opiates

Antihistamines

Hallucinogens

Sedative Antidepressants

Chloral Hydrate

Muscle Relaxants

Scopolamine

Herbal Sedatives

Inhalants

• 1000 consecutive cases received from March 2015 to June 2016

• From 37 U.S. states and 1 territory (Puerto Rico)

• California (26%); Maryland (7.9%); Massachusetts (6.6%); Mississippi (5.4%)

• 78.4% were positive for one or more intoxicating substances

• Nearly 100 different intoxicating substances identified

PHARMACOKINETICS

Absorption

Distribution

Biotransformation(Metabolism)

Liberation

ExcretionAbsorption

Distribution


PHARMACOKINETICS

PROFILES IN BLOOD AND URINE

Time

Dru

g C

on

cen

trat

ion

BLOOD

URINE

PHARMACOKINETICS OF DFSA DRUGS

Variation in speed DFSA drugs are metabolized and eliminated

Wide window of time after ingestion drugs detected in samples

Presence may only be detectable 4 hours

For others, the drug is detectable for weeks

Not knowing drugs used makes it very difficult to interpret a negative toxicological finding

PHARMACODYNAMIC EFFECTS

Most DFSA drugs are strong, fast-acting CNS depressants

Effects mimic severe intoxication or general anesthetics

Includes amnesia and unconsciousness

DFSA cases less likely to be reported compared to forcible rape

Some victims are “unclear if a crime was committed” or didn’t think it was “serious enough” (Kilpatrick et al. 2009)


• Dosages

• Number of Candidates

• Pharmacokinetics

• Pharmacodynamics

Drugs


• Reported?

• Time elapsed?

• Honesty?

Reporting


• Right one(s)?

• Enough?

• Preservation?

Specimens


• Many tests

• Sensitivity

• Right lab?

Labs


Drugs

Reporting

Specimens

Labs

VICTIM REENGAGEMENTVictims reengage with offendersAttempt to reclaim lost dignity

Denial that the rape actually happened

Foggy memoriesVeronique N. Valliere, Psy.D.

Understanding the Non-Stranger Rapist

2007

Marsalis exploited their confusion Acted gentlemanly afterwards

Asked to see them again

Pennsylvania law prevented expert testimony to explain the behavior of rape victims

ETHANOL

ETHANOL AND DFSA

Easy to obtain

Can be administered in a social environment without suspicion

Victims commonly consume voluntarily

Drug most commonly associated with rape

Can cause decreased inhibitions, impaired perceptions, loss of consciousness and amnesia

Prosecution more challenging than with others

Excretion

PHARMACOKINETICS

Absorption

Distribution


ALCOHOL -ABSORPTION

Numerous variables affect how intoxicated one becomes after consuming alcohol

Some variables are easy to control

Others are not

4-6%

12 oz

12-15%

4-5 oz

40-50%

1-1.5 oz

Each contain about 0.6 oz (14 g) of pure ethanolEach contain about 0.6 oz (14 g) of pure ethanol

STANDARD ALCOHOLIC DRINKS

ALCOHOLIC DRINKS

Remember to ask

What they drank

How many they drank

Size of the drinks

ALCOHOL UNITS(UK VERSION)

Simple way of expressing quantity of pure ethanol in drinks

1 Unit = 10mL (8g) of pure ethanol

Approximate amount of alcohol the average adult can process in an hour

Number of units in a drink dependent on size and alcohol strength

5%

12 oz

12%

5 oz

40%

1.5 oz

Each contain about 10 ml (8 g) of pure ethanol = “Unit”Each contain about 10 ml (8 g) of pure ethanol = “Unit”

UNITS OF ALCOHOL (UK VERSION)

1.8 units 1.8 units 1.8 units

ALCOHOL UNITS(UK VERSION)

Simple way of expressing quantity of pure ethanol in drinks

1 Unit = 10mL (8g) of pure ethanol

Approximate amount of alcohol the average adult can process in an hour

Number of units in a drink dependent on size and alcohol strength

Drink Type # of Units

Small shot (25mL, 40%) 1

Large shot (35mL, 40%) 1.4

Small wine (125mL, 12%) 1.5

Bottle of beer (330mL, 5%) 1.7

Pint of low alcohol beer or cider

(568mL, 3.6%)2

Standard wine (175mL, 12%) 2.1

Pint of high alcohol beer or cider

(568mL, 12%)3

Large wine (250mL, 12%) 3

PHARMACOKINETICS OF ETHANOL

Mainly by ingestion, but also by dermal contact, inhalation, or injection

Rapidly absorbed into the blood

Faster drinking enhances

Carbonated beverages enhances

Fatty/oily beverages slows

Ethanol concentration effects absorption

Higher altitude promotes

Dehydration enhances

Food delays

Widely distributed in body water and CNS

Elimination averages about 0.015 g% / hour

CNS DEPRESSION OF ETHANOL

Impairs judgment

Depresses learned social and cultural inhibitions

Impairs self-evaluation

Euphoria

Memory loss

Shortened attention span

Sedation

Blurred vision

Nystagmus

Altered distance perception

Impaired hearing

Reduced muscle coordination

Increased reaction time

Light fixation

STAGES OF ALCOHOL INTOXICATION

0.00% 0.10% 0.20% 0.30% 0.40% 0.50%

Subclinical 0.01 to 0.05% Behavior nearly normal

Euphoria Diminished attention, judgement, and control;0.03 to 0.12% decreased inhibitions; loss of efficiency; talkativeness

Excitement Loss of judgement; impaired balance, perception, 0.09 to 0.25% and memory; loss of vision; drowsiness

Confusion Disorientation; emotional; slurred speech;0.18 to 0.30% blurred vision; staggering; pain tolerance

Stupor Unable to stand or walk; vomiting;0.25 to 0.40% no response to stimuli

Coma0.35 to 0.50% Unconscious

0.45+ Death

Adapted from K.M. Dubowski “Stages of Acute Alcoholic Influence/Intoxication”

ESTIMATIONS OF ETHANOL CONCENTRATIONS

Widmark Formula:A = (WRC / 0.8)

A = Amount of ethanol (mL)

W = Body Weight (grams)

R = Distribution ratio

(0.68 males / 0.55 females)

0.8 = Specific gravity of ethanol

Useful exercise to evaluate the role that ethanol may have played

in contributing to the symptoms that the DFC victim described

Useful exercise to evaluate the role that ethanol may have played

in contributing to the symptoms that the DFC victim described

0.00% 0.10% 0.20% 0.30% 0.40% 0.50%

Subclinical 0.01 to 0.05% Behavior nearly normal

Euphoria Diminished attention, judgement, and control;0.03 to 0.12% decreased inhibitions; loss of efficiency; talkativeness

Excitement Loss of judgement; impaired balance, perception, 0.09 to 0.25% and memory; loss of vision; drowsiness

Confusion Disorientation; emotional; slurred speech;0.18 to 0.30% blurred vision; staggering; pain tolerance

Stupor Unable to stand or walk; vomiting;0.25 to 0.40% no response to stimuli

Coma0.35 to 0.50% Unconscious

0.45+ Death

?

STAGES OF ALCOHOL INTOXICATION

ALCOHOL-INDUCED

BLACKOUTS

Memory loss (anterograde amnesia) that occurs during any part of a drinking episode without loss of consciousness

Not the same as “passing out”

May be awake and conscious, engaged in activity or conversation, and may appear to be oriented

Memory loss may be significant, but may be reversible

Information may be recalled later, sometimes spontaneously

Women seem to be more susceptible to blackouts and undergo a slower recovery from cognitive impairment than men

MEMORY

AMNESIA

Retrograde

Loss of earlier memories

Usually from cerebral injuries or disease states

Far more common

Anterograde

Impaired information acquisition, consolidation, and storage

Alcohol and some CNS depressants cause

Likely due to impact on GABA-receptor complex

Less clear when these end because people tend to fall asleep before they are over

Goodwin, D.R. et al. Am J of Psychiatry 66 (1975)

ALCOHOL-INDUCED BLACKOUTS

Two types of alcohol blackoutsComplete (en bloc) Begins and ends at definitive points

Full permanent amnesia

Loss of time

Requires high BACs to disrupt memories from encoding

Fragmentary (gray outs) Memories often recalled when prompted

Occur more often

Experienced over wider range of BACs

ALCOHOL-INDUCED BLACKOUTS

Two mechanisms Encoding deficit

Alcohol temporarily inhibits biochemical processes in brain needed to form new memories

Retrieval deficit

Information stored as a memory while intoxicated is inaccessible when the individual is sober

Ingestion of large amounts of alcohol may have more significant effect on input, acquisition, or processing of new memories

Research suggests alcohol-induced blackouts disrupt transfer of information from short-term to long-term storage

PROBLEMS WITH BLACKOUT STUDIES

Most have involved white, male alcoholics as subjects

Many have relied upon subject’s ability to recall previous episodes of blackout months or years before“remember not remembering”

Number of drinks consumed over what period of time?

Modern Internal Review Boards would not likely approve of normal subjects “binge” drinking to increase BACs to levels consistent with blackouts

RISK FACTORS FOR ALCOHOL-INDUCED BLACKOUTSPrior or current history of alcoholism

Family history of alcoholism

Age of drinking onset

Prior history of blackouts

Family history of blackouts

Capacity/tolerance for high quantities of alcohol

Ingests high quantity of alcohol such that they often exceed 0.2%

Rapid drinking – gulping or binging

Head trauma

Loss of control

Failure to eat properly Pressman, MR and Caudill, DS; J Forensic Sci; Vol 25, 4, 2013

GHB

GHB AND DFSA

Easy to obtain

Fast acting, sedative properties

Mimics ethanol

Amnesiac

Rapidly eliminated from the body

Many labs don’t have assays for GHB

Naturally occurring

Requires careful interpretation of results

BACKGROUND AND OVERVIEW

-Hydroxybutyrate (GHB) and its metabolic precursors are among the most favored for DFSA

Hard to prove because of strong sedative, amnesiac effects and rapid elimination

Naturally occurring metabolite of GABA

Human urine and other biological specimens contain measurable amounts

Popular recreational drugs of abuse

HISTORY

Three groups use GHB:

Bodybuilders/Dieters

Recreational abusers

Rapists / Robbers

Nearly always abused orally

Disguised in aqueous matrix

Consumed by capful or teaspoon

Street names include “Easy Lay”, “Georgia Home Boy”, “Liquid Ecstasy”, “G”, “Liquid X”, “Fantasy”

Club drug

GHB AND ANALOGS PHARMACOKINETICS

Rapidly absorbed after ingestion

GBL and 1,4-BD quickly metabolize to GHB

If co-ingestion of 1,4-BD and alcohol, effects may be more severe and detection times may be longer

Less than 5% of the original dose of GHB is excreted unchanged into the urine

GHBCLINICAL EFFECTSUsers pass from full consciousness to unconsciousness within 10-15 minutes

Strong CNS depressantOften confused with effects of alcohol

Symptoms:drowsiness, confusion, dizziness, vomiting, respiratory depression, bradycardia, amnesia

Alert patients may show tachycardia, combativeness, hypertension, agitation, psychotic symptoms (paranoia and hallucinations)

GHB-assisted sleep generally only lasts about 3-4 hrs People exposed to GHB usually wake up without a so-called “hangover” effect

Forensic Science Review 14: 101-121; 2002

BENZODIAZEPINES

BENZODIAZEPINES AND DFSA

One of the world’s most widely prescribed drug class

Anxiolytics, muscle relaxants, sedative/hypnotics, anesthetic adjuncts, anticonvulsants, panic disorders, obsessive-compulsive disorders

Symptoms: slurred speech

irritability

agitation

loss of inhibition

sedation

sleepiness

memory impairment

anterograde amnesia

Forensic Science Review 14: 1-14; 2002

PHARMACOKINETICS OF BENZODIAZEPINES

Most benzodiazepines are administered orally in DFSA cases, but injections have also occurred

Peak blood levels within 30 min to 6 hrs. after ingestion

When pre-dissolved into a liquid, absorption is much faster

The duration of action of benzodiazepines is based largely on their pharmacokinetic half-lives

Short-acting benzodiazepines (e.g., midazolam, triazolam) will be detected for much shorter periods than long-acting benzodiazepines (e.g., diazepam, clonazepam)

Long-acting benzodiazepines tend to exhibit a longer and more severe “hangover”

CATEGORIES OF BENZODIAZEPINES

FDA Approved

Alprazolam (Xanax®)

Chlordiazepoxide (Librium®)

Clonazepam (Klonopin®)

Diazepam (Valium®)

Flurazepam (Dalmane®)

Lorazepam (Ativan®)

Temazepam (Restoril®)

Triazolam (Halcion®)

Non-FDA Approved

Approved in Other Countries:

• Etizolam

• Flunitrazepam (Rohypnol®)

• Phenazepam

Designer:

• Clonazolam

• Cloniprazepam

• Flualprazolam

• Flubromazelam

• Flubromazepam

• Ketazolam

FLUNITRAZEPAM (ROHYPNOL®)

MORE potent than diazepam (Valium)

Onset 15-30 minutes, duration 2-12 hours

Passivity, disinhibition, lack of resistance, muscle relaxation, slurred speech, confusion, ataxia

Anterograde amnesia

Soluble in alcohol, colorless, odorless, tasteless

Requires sensitive methods of analysis

In 1990s, Rohypnol became popular drug to use in DFSA

Very potent drug

Typically used as an adjunct to general anesthetics

Not available for use in U.S.

Old tablets vs New Tablets Blue dye in core is released when dissolved

Not incorporated into generic versions

Relatively few proven cases of this drug’s use in DFSA

Other benzodiazepines more likely to be used

FLUNITRAZEPAM (ROHYPNOL®)

KETAMINE

KETAMINE

Dissociative anesthetic with analgesic properties

Also used as veterinarian tranquilizer

Structurally similar to PCP

Club drug

Smoked, injected, snorted, or taken orally

Popular hallucinogen

Users deem effects superior to PCP or LSD

Less connected with a sense of self and reality around them

“K-hole” – when large amounts ingested and no idea what is going on around them

KETAMINE

May not remember the experience after regaining consciousness – similar to how one may forget a dream

Emerging from under the influence is slow

User gradually becomes aware of surroundings

At first they may not remember their name

Movement may be extremely difficult

Ketamine is quickly metabolized to norketamine and dehydronorketamine

May be excreted in the urine for at least 72 hours after ingestion

RESERVE, NM

Wildlife researchers were studying behavior of black bears in rural NM

Woman was hospitalized in 1997

Investigators found 6 hours of video tape showing the man drugging and raping victim

Ketamine found in hair of victim

Sentenced to 33 years

CANNABINOIDS

CANNABINOIDS AND DFSA

Sedative properties

Hallucinogenic properties

Impairs memory

Impairs cognition

Popular recreational drugs

Very easy to obtain

Additive effects when mixed with ethanol

OPIOIDS

OPIOIDS AND DFSA

Very sedating

Analgesic effect

Readily available

May be voluntarily ingested

OPIOIDS

Buprenorphine

Codeine

Fentanyl

Heroin

Hydrocodone

Hydromorphone

Meperidine

Methadone

Morphine

Oxycodone

Oxymorphone

Pentazocine

Propoxyphene

Tramadol

PHARMACODYNAMICS OF OPIOIDS

Analgesics (“Pain Killers”) that also produce euphoria and a sense of well-being

Strong CNS depression

When morphine is combined with alcohol, the depressant effects of alcohol are enhanced; the elimination of morphine is slowed, and potent metabolites are produced at a faster rate

Opioids act by binding to opioid specific receptors

Side effects may include nausea/vomiting and constipation

M.A. LeBeau and A. Mozayani. (2001) Drug-Facilitated Sexual Assault A Forensic Handbook. San Diego, CA: Academic Press

ANTIHISTAMINES

ANTIHISTAMINES

Recent increase abuse of first-generation antihistamines

Oldest and cheapest of the antihistamines on the market

Widespread availability

Effects include sedation, euphoria, dizziness, blurred vision, ringing in the ears (tinnitus), incoordination, hallucinations, and psychosis

Additive depressant effect when combined with alcohol

May experience paradoxical effect

Readily absorbed after oral administration

Onset of action generally occurring within 1 hr

Detectable for hours to days


TRICYCLIC ANTIDEPRESSANTS


First used in 1950s

Common TCAs:

amitriptyline (Elavil)

clomipramine (Anafranil)

desipramine (Norpramin)

doxepin (Adapin)

imipramine (Tofranil)

nortriptyline (Pamelor)

protriptyline (Vivactil)

trimipramine (Surmontil)


Causes heavy sedationMay be prescribed as anti-anxiety medication

Additive effects when combined with ethanol and other CNS depressants

Additional side-effects:Sleepiness

Lightheadedness

Slight drop in BP

Unsteadiness

Amnesia

R.C.Baselt. (2004) Disposition of Toxic Drugs and Chemicals in Man. Foster City, CA: Biomedical Publications

M.A. LeBeau and A. Mozayani. (2001) Drug-Facilitated Sexual Assault A Forensic Handbook. San Diego, CA:

Academic Press

TRUTH OR CONSEQUENCES, NEW MEXICO

March 1999 –woman reports kidnapping and sexual torture in Elephant Butte, NM

Find Ray’s “Toy Box”

Investigation suggests hundreds of victimsAt least 14 victims were dismembered and discarded

DAVID PARKER RAY

Evidence suggests Ray used alcohol combined with amitriptyline to keep women sedated and under control

April – May 2001: Ray convicted and sentenced to 224 years

May 2002: Ray died of heart attack in prison

“Z” DRUGS

THE “Z” DRUGS

Zolpidem (Ambien, Stilnox), Zopiclone (Imovane, Zimovane, Lunesta), and Zaleplon (Sonata, Starnoc)

Not benzodiazepines but act on the same receptor in the brain

Effects include euphoria, drowsiness, muscle relaxation, feeling of drunkenness, hallucinations, amnesia, and strong sedation

Very low-dose medications

Most laboratories will not be able to detect parent drugs at therapeutic levels

Numerous cases in last decade


CHLORAL HYDRATE

CHLORAL HYDRATE

Oldest Sedative/Hypnotic still used today

Liquid-filled gel-cap or syrup

Very rapidly metabolized; must look for metabolite (TCE)

Very strong sedative effect usually for the treatment of insomnia or presurgical sedative


B. Levine. (2003) Principles of Forensic Toxicology. Washington, DC: AACC Press

CHEMICAL SOLVENTS

VOLATILE ORGANIC

COMPOUNDS (VOCS) AND

DFSA

Easy to obtain

Generally overt and forced

Difficult to detect in biological specimens

CHEMICAL SOLVENTS

Chloroform

Ether

Nitrous oxide

Cyclopropane

Propane

Butane

Toluene

Xylene

May be voluntary exposure through “huffing” or “sniffing”

Rag placed over mouth and nose

OVERCOMING SOME OF THE CHALLENGES


Drugs

Reporting

Specimens

Labs

SOFT DFSA COMMITTEE

1998:

Group of forensic toxicologists met to discuss the problems and challenges we face in DFSA cases

1999:

Published recommendations for investigators, medical professionals, and toxicologists for DFSA cases

2000:

Formation of SOFT DFSA Committee

RECOMMENDATIONS

Get first urine sample from victim

At least 100 mL within first 5 days

# of times urinated prior to collection

Blood supplements urine

At least 10 mL in grey-top tube within first 24 hours

Info about ethanol, recreational, and prescription drug use

Other evidence

Choose your lab carefully

Understand what lab results really mean

WHY WERE NO DRUGS DETECTED?

141

Limit of Detection

Detection Time in Urine

Time

Dru

g C

on

cen

trat

ion URINE

BLOOD

Detection Time in Blood

142

Limit of Detection

Detection Time in Urine

Time

Dru

g C

on

cen

trat

ion URINE

BLOOD

Detection Time in Blood

WHY WERE NO DRUGS DETECTED?

SOFT DFC COMMITTEE

MAXIMUM RECOMMENDED

DETECTION LIMITS FOR

URINE

Contains

most prevalent drugs that have been associated with DFCs (not a complete list of all drugs that may be used)

most significant metabolites

suggested “maximum” detection limits

drugs known to potentiate the effects of DFC drugs

Based upon published methods and/or an estimated concentration from use of single dose

Should be achievable using standard instrumentation

“Maximum” detection limits

Test at even lower limits than these recommendations, if possible, with advanced technology that may be available

STANDARD FOR THE ANALYTICAL SCOPE AND SENSITIVITY OF FORENSIC TOXICOLOGY URINE TESTING IN DRUG-FACILITATED CRIME INVESTIGATIONS

• Delineates the minimum requirements for target analytes and analytical sensitivity for the toxicological testing of urine specimens collected from alleged victims of drug-facilitated crimes (DFC)

• This document does not cover the analysis of blood and other evidence that may be collected in DFC cases

REQUIREMENTS FOR FORENSIC TOXICOLOGICAL TESTING OF URINE SPECIMENS IN INVESTIGATIONS OF DRUG-FACILITATED CRIME

Urine specimen collected from an alleged victim of DFC within 120 hours (5 days) of the incident shall be tested

Case-specific circumstances may warrant testing of specimens collected past 5 days

Toxicological testing of urine specimens collected from alleged victims of DFCs shall include, at a minimum, the compounds listed in Table 1.

Analytical sensitivity shall meet or exceed (be lower than) the concentrations listed in Table 1.

The table reflects total concentrations, which may be achieved via hydrolysis or direct analysis of conjugated compounds.

High-Dose Sedatives

Ethanol (alcohol)2 0.01 g/dL

Gamma hydroxybutyrate

(GHB)3

10 µg/mL

Antidepressants

Amitriptyline 10 ng/mL

Nortriptyline 10 ng/mL

Imipramine 10 ng/mL

Desipramine 10 ng/mL

Chlorophenylpiperazine

(Trazodone metabolite)

10 ng/mL

Antihistamines

Brompheniramine 10 ng/mL

Chlorpheniramine 10 ng/mL

Diphenhydramine 10 ng/mL

Doxylamine 10 ng/mL

Norchlorcyclizine 10 ng/mL

Barbiturates

Butalbital 100 ng/mL

Phenobarbital 100 ng/mL

Benzodiazepines

α-hydroxyalprazolam 5 ng/mL

7-aminoclonazepam 5 ng/mL

Lorazepam 5 ng/mL

Nordiazepam 10 ng/mL

Oxazepam 10 ng/mL

Temazepam 10 ng/mL

Cannabinoids

Carboxy-tetrahydrocannabinol

(THC-COOH)

10 ng/mL

CNS Stimulants

Methylenedioxyamphetamine

(MDA)

25 ng/mL

Methylenedioxymethampheta

mine (MDMA)

25 ng/mL

Amphetamine 25 ng/mL

Methamphetamine 25 ng/mL

Benzoylecgonine 50 ng/mL

Miscellaneous

Cyclobenzaprine 10 ng/mL

Methorphan 10 ng/mL

Norketamine 10 ng/mL

Zolpidem carboxylic acid 10 ng/mL

Zopiclone 10 ng/mL

Carisoprodol 100 ng/mL

Meprobamate 100 ng/mL

Opioids

Fentanyl 1 ng/mL

Norfentanyl 1 ng/mL

Codeine 10 ng/mL

Morphine 10 ng/mL

Hydromorphone 10 ng/mL

Hydrocodone 10 ng/mL

Oxymorphone 10 ng/mL

Oxycodone 10 ng/mL

Tramadol 10 ng/mL

SOME WORDS ABOUT HAIR IN DFSA CASESDrugs can be trapped in hair from: Blood

Sebum

Sweat

Environment

Useful when reporting is delayed weeks or longer

Some drugs can remain in hair for months or years

Hair grows about 0.5 inch per month

It takes about 2 weeks for drugs deposited at hair root to emerge above the scalp

Typically head hair is used

SOME WORDS ABOUT HAIR IN DFSA CASESBest to wait 2 months or longer before collection

Collect about 200 strands in a bundle, cut close to the scalp Width of a #2 pencil

Difficulties with hair: Assuming 1x exposure, it may be

difficult to detect Negative results may be misleading Doesn’t always prove “ingestion” Can’t readily screen hair for multiple

drugs Should be done by laboratory with

newer technology and experience with hair

1. Beware of “Fake News”

A lot of misinformation about how crime is committed, drugs used, and prevalence of occurrence

2. “Drugs are Bad”

It’s more than just Roofies and GHB…check the medicine cabinet

3. “Responsible Drinking” doesn’t mean “Don’t spill your drink”

Too many variables in absorption to predict exactly how intoxicated one may become

“1 unit per hour” rule will keep you safe

4. If I were to give a Sermon, it would be About Getting Urine

In most cases, urine improves the chance of finding drugs

5. “Double Negatives” are a “No-No”

A negative toxicology finding does not mean “no drugs were involved”

DRUG-FACILITATED SEXUAL ASSAULT: A FORENSIC HANDBOOK

The Victim - Abarbanel

The Perpetrators and Their Modus Operandi - Welner

Ethanol - Garriott and Mozayani

Rohypnol and Other Benzodiazepines - Robertson and Raymon

Gamma-Hydroxybutyrate (GHB) and Related Products - Ferrara, Frison, Tedeschi and LeBeau

Hallucinogens - Raymon and Robertson

Opioids - Jufer and Jenkins

Miscellaneous Prescription and Over-the-Counter Medications - Jones and Singer

Collection of Evidence from DFSA - LeBeau and Mozayani

Analysis of Biological Evidence from DFSA Cases -LeBeau and Noziglia

Sexual Assault Nurse Examiners - Ledray

Investigating DFSA Cases - Archambault, Porrata and Sturman

Prosecution of DFSA - Kerlin, Riveira and Paterson

CONCLUSIONS

DFSA cases are not new

Today the numbers of DFSA cases are increasing, but the true prevalence will never be known

Many different drugs are being used –and each year new ones will be used

Many of the challenges of DFSA can be overcome Education is key

A thorough investigation is a must

Teamwork is vital

Documents

T C DRUG AND LCOHOL FACILITATED SEXUAL ASSAULT