Occurrence and Characteristics of Drug-Facilitated Sexual Assault
Media attention in the 1990s popularized the term “date-rape drugs.” Drugs, however, have been used to facilitate other crimes such as robbery or physical assault for centuries. “Micky Finns” (“knock-out drops”) were named after a Chicago bartender who mixed chloral hydrate into drinks he served his customers so he could rob them. , “Date-rape drugging” is more accurately referred to as drug-facilitated sexual assault (DFSA), defined as “… offenses in which victims are subjected to nonconsensual acts while they are incapacitated or unconscious due to the effects of alcohol and/or drugs, and are therefore prevented from resisting and/or are unable to consent. ”
A recent study found that 1.6% of teens ages 12 to 17 reported serious dating violence, with 0.9% reporting sexual assault. Just more than 10% of those sexual assaults were DFSA. The prevalence of DFSA is lower among younger adolescents. In a 2010 survey, almost 1% of 12-14 year-olds reported DFSA versus 4% of 15-17 year-olds. The Roofie Foundation was established in 1996 in the United Kingdom to serve as a helpline for victims of DFSA. As of October 2006, there had been 9887 reports to the helpline. Adolescents ages 14 to 18 years accounted for 7.3% of these cases. In an almost 10-year retrospective study of individuals seen for sexual assault in Canada, 15.4% of 1594 sexual assaults met criteria for DFSA, not including alcohol overuse and forcible injection of drugs. Adolescents had the highest baseline incidence rate, which rose from 15/100,000 in the first study period (1993 to 1998) to 59.3/100,000 in the second study period (1999 to 2000). Whether the increase in incidence is due to an increased in DFSA or improved recognition by law enforcement and clinicians is not known.
The true incidence of DFSA is difficult to determine since not all victims present for timely medical care or receive drug screening. Due to the nature of the assault, delayed reporting is common. Victims of drug-facilitated sexual assault often have limited memory of events occurring after drug ingestion (anterograde amnesia). Brief periods of awakening (“cameo appearances”) often occur in response to loud noises or pain. The victim might remember being unable to move or speak or might recall witnessing part of the assault. Once the victim sleeps off the drug, she is sometimes ambivalent about reporting the assault to law enforcement or accessing health care. In one study of DFSA, 24% of the victims had no recollection of events and 59% had unclear or “patchy” memories. Only 15% had “clear and concise” memories of the event. This worsens the crime, leaving victims unable to provide a history and powerless to fight back. Victims of DFSA are less likely than other sexual assault victims to report the crime to the police, are more likely to delay medical care, and are less likely to have genital and nongenital trauma. Cases with forensic evidence and victim injury are more likely to be prosecuted, so DFSA victims are less likely to see a just resolution of the crime. The ideal drug for surreptitious administration and facilitation of a crime should be colorless, odorless, tasteless, easily obtained, and have a rapid onset of action. The drug’s clinical effects should include sedation, disinhibition, relaxation of voluntary muscles, and anterograde amnesia. Anterograde amnesia involves impairment of acquisition, consolidation, and storage of memory, and can occur with little change in the victim’s outward behaviors. A list of drugs commonly reported as being used in DFSA is found in Table 15-1 .
| Category | Names of Drugs (Generic and Trade) |
|---|---|
| Alcohol | |
| Benzodiazepines |
|
| Cannabis | Marijuana |
| Stimulants and related substances |
|
| Non-benzodiazepine hypnotics |
|
| Barbiturates |
|
| GHB and related substances |
|
| Opiates and analgesics |
|
| Over-the-counter |
|
| Anti-cholinergics |
|
| Miscellaneous |
|
| Antidepressants |
|
Reports of “drink spiking” and “date rape” have focused largely on flunitrazepam (Rohypnol), gamma hydroxybutyrate (GHB), and ketamine (Ketanest, Ketaset, or Ketalar). Yet, flunitrazepam is rarely found in toxicological studies of DFSA, representing less than 1% of the drugs detected in these cases. Alcohol is much more common, and is found in 40% and 70% of cases, either alone or combined with other drugs.
A program was established in the United States in the late 1990s to provide independent testing of urine samples in cases of suspected DFSA. Patient samples were submitted from 49 states. Of the 3303 urine samples tested, 73% were collected within 24 hours of drug ingestion and 98.8% by 72 hours. Samples were screened by immunoassay and confirmed by gas chromatography-mass spectrometry (GC-MS). Additional testing for benzodiazepines and GHB was performed. More than 60% of the samples were positive for one or more drugs, with an average of 1.6 drugs per sample. Alcohol was found in 67% of the positive samples. Alcohol and cannabis was the most frequent combination found, followed by alcohol and benzodiazepines. Benzodiazepines were found in 15.4% of the positive samples. GHB was not found in samples with detectable alcohol, but did occur in 4.9% of the positive samples. GHB might have been underestimated in this study due to its short half-life. Investigators found benzodiazepines alone in 98 samples (4.8%), but there was no medical or recreational drug history recorded in the study.
In an attempt to better answer the question of voluntary versus involuntary drug use, Hurley et al studied the drug screens of 76 cases of DFSA. Voluntary alcohol use was reported by 77% of subjects, with the consumption of at least four drinks in 71%. Prescription drug use was reported in 49%, and 26% reported recreational drug use. Unexpected drugs not knowingly consumed were found in 20% of the 76 subjects. While DFSA can occur through involuntary ingestion, voluntary ingestion, or a combination of both, the majority of cases of DFSA occur after the voluntary ingestion of recreational drugs and alcohol. It can be difficult to separate cases of surreptitious administration from voluntary ingestion. Regardless, incapacitation through drugs and alcohol eliminates the ability to consent. Careful history taking is essential to determine which drug might be contribing to the clinical symptoms. Table 15-2 lists the common historical and clinical features in DFSA.
| Common Clinical Effects | Common Clinical Patterns |
|---|---|
|
|
Substances Commonly Used in DFSA
Ethyl Alcohol
Ethyl alcohol is the most common drug detected in cases of alleged sexual assault, with a prevalence rate ranging from 40% to 70%. Among college students surveyed for rape and sexual assault, 1 in 20 women reported rape and in 72% of those cases, the rape occurred while the victim was intoxicated. Surveys of adolescents in grades 7 through 12 report that alcohol is involved in 12% to 20% of sexual assaults, with higher rates occurring in female adolescents 16 years of age or older. Alcohol-related assaults were more likely to occur at parties or at someone else’s home.
In a prospective study of patients presenting to emergency departments for suspected DFSA, 94% of the blood samples collected were positive for alcohol and 65% had blood alcohol concentrations greater than 160 mg/dL. In the study by Hurley et al, the average blood alcohol level in suspected DFSA victims was 0.11% (110 mg/dL). Based on the delay between the assault and the sampling, the authors estimated the average blood alcohol concentration at the time of the assault was from 0.22% to 0.33%. Performing back calculations of blood alcohol levels in victims of suspected DFSA can be helpful in understanding the degree of impairment at the time of the assault. Back calculations assume that no alcoholic beverages were consumed between the assault and the examination, and that the victim metabolizes alcohol with zero-order (linear) kinetics. Rates of alcohol metabolism can vary with gender, tolerance (social versus chronic drinkers), and phenotypic differences in alcohol dehydrogenase. , Alcohol has a half-life of approximately 4 hours and elimination rates can vary between 10 and 25 mg/dL/hr.
In one study of alleged DFSA, investigators recorded blood and urine alcohol concentrations and performed back calculations assuming an elimination rate of 18 mg/dL. Of the 391 samples obtained within 12 hours of assault, 81% were positive for alcohol. Sixty percent of those positive had back-calculated levels greater than 150 mg/dL (sufficient to cause drunkenness in a social drinker), 36% percent had levels greater than 200 mg/dL (“heavy drunkenness”), and 4% had levels greater than 300 mg/dL (“extreme drunkenness”).
The symptoms seen in alcohol intoxication can progress from nausea and vomiting to respiratory depression and loss of consciousness, depending on blood levels and on an individual’s tolerance level ( Table 15-3 ). Alcohol is hydrophilic and absorbed through the gastrointestinal system with simple diffusion. Absorption rates and peak blood alcohol concentrations (BAC) vary depending on the alcohol content of the beverage and whether food was ingested simultaneously. Calculators are available online to estimate BAC based on gender, weight, number of standard drinks, and length of time over which the drinks were consumed ( http://www.ou.edu/oupd/bac.htm ).
| Blood Alcohol Content (%) | Clinical Effects | Psychomotor Impairment |
|---|---|---|
| 0.02 | Relaxation, lightheaded | No loss coordination |
| 0.05 | Lowered inhibitions, euphoria, feelings of well-being, warmth |
|
| 0.08 |
|
|
| 0.10 |
|
|
| 0.15 |
| Severe impairment of motor (staggering), speech (slurred), vision (blurring), judgment |
| 0.20 |
|
|
| 0.25 |
|
|
| 0.30 |
|
|
| 0.35 | Difficult to arouse |
|
| 0.40 or greater |
|
|
Benzodiazepines and Flunitrazepam
Benzodiazepines are central nervous system (CNS) depressants that cause dizziness, disorientation, lack of coordination, slurred speech, loss of consciousness, flaccid muscle tone, nystagmus, and anterograde amnesia due to their effects on specific neurotransmitter receptor sites for gamma-aminobutyric acid (GABA). Twenty-six different classes of benzodiazepines have different affinities for the receptor. Flunitrazepam, a member of the 7-nitrobenzodiazepine class, has a high affinity for the receptor. ,
Benzodiazepines are ideal agents for drug-facilitated sexual assault. In combination with alcohol, smaller doses are needed and the effects are synergistic. As a single drug, benzodiazepines are found less frequently in DFSA patients than alcohol, marijuana, or cocaine, but in one large study, 58% of the victims with more than one substance detected were positive for benzodiapezines. Used in combination with alcohol, benzodiazepines were second only to marijuana. Flunitrazepam was seen in very few samples (7 out of 2003). Oxazepam, diazepam, lorazepam, and clonazepam represented the majority of benzodiazepines detected.
Sexually active females between the ages of 14 to 26 years were surveyed at family planning clinics about voluntary use of flunitrazepam; 5.9% reported using the drug at some time. First use occurred on average at 17 years, with some using the drug at as young as 11 years of age. Seventy-four percent reported taking the drug with alcohol; 10% of users reported physical or sexual assaults after voluntary use.
In the United States importation of flunitrazepam was banned 1996, but it is still available and popular in Europe and Latin America. It is tasteless, odorless, and colorless, and dissolves easily in alcohol. The manufacturer has recently reformulated the drug to give a blue color when dissolved in clear drinks and to cause haziness in colored beverages.
“Roached out” is slang for being under the influence of flunitrazepam. Other street names of the drug include roofies, rophies, roopies, rib, rope, pappas, peanuts, pastas, forget pills, row-shays, roaches, Mexican valium, circles, rubies, and roche 2. , The hypnotic effects of flunitrazepam predominate over the sedative and anxiolytic effects. It has been used as a sleep-inducing drug at the 2 mg dose with little psychomotor impairment (hangover effects) in the morning. It has a high-affinity for the GABA receptor, with 10 times the potency of diazepam and longer amnesia. More than 80% of the drug is absorbed from the gastrointestinal tract. Clinical effects occur in 20 minutes and can persist up to 24 hours. Flunitrazepam metabolizes to 7-aminoflunitrazepam and norflunitrazepam. It is detectable up to 2 days in blood and 4 days in urine, but is not captured by traditional immunoassay urine drug screening. Other testing such as GC-ECD (electron capture detection) and GC-MS are quite sensitive in detecting its metabolites.
The prevalence of flunitrazepam use has diminished as the use of clonazepam (Klonopin) has risen. Clonazepam also is sold under the street name of “roofies” with clinical effects quite similar to flunitrazepam. It has been found twice as often as flunitrazepam in suspected DFSA victims. Dowd et al compared the behavioral and cognitive effects of flunitrazepam and clonazepam in two groups of volunteers. Cognitive testing was performed at baseline and repeated after drug exposure. Subjects appeared disinhibited to the investigators. The groups reported “patchy amnesia” for what occurred after drug ingestion. Six of 10 subjects exposed to clonazepam had no memory of a second set of evaluations. Clonazepam had a longer half-life than flunitrazepam and a longer period of impairment. Effects are experienced 30 to 60 minutes after ingestion and last up to 12 hours. It is metabolized by the liver to 7-aminoclonazepam. Clonazepam has been detected up to 14 to 21 days in urine with targeted testing.
Although they are rapid and inexpensive, immunoassay urine drug screening tests using competitive binding between an antibody and a drug antigen are limited in their ability to detect benzodiazepines. The antibody is most specific and sensitive to the drug used to generate the antibody. For benzodiazepines, oxazepam is commonly used as the antigen. Benzodiazepines that do not metabolize to oxazepam (e.g., clonazepam, lorazepam, alprazolam, and triazolam) will not be detected. In addition, a small amount of drug might not produce sufficient metabolites to yield a positive screen. False-negative urine screens for benzodiazepines often occur. , If a patient’s clinical symptoms are concerning for DFSA, urine drug confirmation for benzodiazepines is necessary even if the screen is negative.
Cannabis
Marijuana is perhaps the most common illicit drug found in urine samples analyzed for suspected DFSA, and is found in 18% to 26% of samples analyzed. It is found as a solitary agent in 7% to 11% of cases. Clinical effects include relaxation, an altered sense of time, euphoria, drowsiness, and impairment of short-term memory. Unique cannabinoid receptors are present in the brain, the peripheral nervous system, and the immune system. Onset of action can occur within 15 to 30 minutes when smoked and the effects can last 4 to 6 hours. It is extremely lipid soluble and has a half-life of several days, which may contribute to its high prevalence in samples. In one study of 260 samples positive for cannabinoids, 63 subjects (24%) admitted to voluntary use. Cannabinoids are detected by routine immunoassay urine drug screening, and is present in urine for several days after acute ingestion and for weeks in chronic users. Its persistence can make it difficult to determine its role in an acute assault.
Cocaine
Cocaine is a CNS stimulant producing generalized nervous system activation and reuptake inhibition of multiple neurotransmitters including dopamine, norepinephrine, and serotonin. In addition to tachycardia, hyperactivity, and restlessness, clinical effects include euphoria, increased energy, appetite suppression, and increased self-confidence and libido. Cocaine can be inhaled, smoked, and injected. “Speed-balling” is the street term for the intravenous injection of heroine and cocaine. A “liquid lady” refers to the combination of alcohol and cocaine. It is frequently found in combination with alcohol and other drugs, perhaps to attenuate the abrupt onset and cessation of clinical effects. In toxicological studies of DFSA, the most common illicit drug found in combination with cocaine is cannabis. , The prevalence of cocaine in samples submitted for analysis for DFSA ranges from 8% to 11%. As the sole drug, it is present in just less than 2% of cases.
Cocaine and its primary metabolite, benzoylecgonine is routinely detected on immunoassay urine drug screens. Metabolism of cocaine to benzoylecgonine occurs through hepatic carboxylesterase enzymes, which are inhibited if alcohol ingestion precedes cocaine use. Depending on dosing, metabolites of cocaine can be detected for 2 to 3 days in urine and up to a week at higher doses. There is little cross-reactivity with other substances and few false positives. False negatives occur with very low drug levels. Despite the high positive predictive value of the urine drug screen for cocaine, drug confirmation is still recommended for legal purposes.
Amphetamines/Methamphetamines
Amphetamine and methamphetamine is found in 4% to 7% of samples from DFSA cases. They are often found in combination with other drugs such as alcohol, cocaine, benzodiazepines, and marijuana. They are found as the solitary drug in DFSA in less than 2% of cases. This class of drugs is often used at “raves” (drug-fueled dance parties), and is called crystal meth, speed, crys, jip, and meth. Methamphetamines come in powder form and are easily taken orally, smoked, or inhaled. Clinical effects include tachycardia, hypertension, hyperthermia, and sweating. Amphetamines and methamphetamines are detected by routine drug screening, but drug screens have cut-off thresholds for positive tests that are quite high. Another rave favorite, ecstasy (3,4-methylenedioxymethamphetamine or MDMA), has both stimulant and hallucinogenic effects with a toxicity similar to amphetamines and cocaine. Ecstasy is often used in combination with alcohol, cocaine, GHB, cannabis, and amphetamines. Clinical symptoms of intoxication are largely related to sympathetic activation including palpitations, dizziness, weakness, and anxiety. When ecstasy is used in combination with other drugs, clinical symptom patterns can change dramatically. For example, when ecstasy is combined with GHB ingestion, coma and hypothermia can be seen. Severe medical complications of ecstasy, especially when combined with other drugs, include cardiac arrest, hyperthermia, rhabdomyolysis, disseminated intravascular coagulation, renal insufficiency, and liver failure. The use of ecstasy in DFSA has been rarely studied, as most investigators group amphetamines and methamphetamines as a class. In one study screening for ecstasy in 1014 DFSA cases, it was detected in 5%. Ecstasy in high doses can be detected on routine urine drug screening as amphetamines, but in low doses it is undetectable. Ecstasy is notorious for being impure, which affects toxicological analyses.
GHB (Gamma-Hydroxybutyric Acid), GBL (Gamma-Butyrolactone), and 1,4 BD (1,4-Butanediol)
Grievous bodily harm, Georgia home boy, liquid ecstasy, liquid X, liquid E, GBH, soap, scoop, easy lay, salty water, g-riffick, cherry meth, organic quaalude, natural sleep-500, and somatomax are just a few of the street names for gamma-hydroxybutyric acid (GHB). , Over the years GHB has been marketed as a sleep aid, weight aid, performance enhancer, and sex enhancer, and it has been used for the treatment of depression, anxiety, and alcohol and opiate withdrawal. In 2000, GHB was declared a Schedule I controlled substance by the U.S. Food and Drug Administration. GHB in the form of sodium oxybutyrate (Xyrem) is still available by prescription as a Schedule III orphan drug for use in the treatment of narcolepsy and cataplexy.
GHB is a naturally occurring metabolite of gamma-aminobutyric acid (GABA). It is present in both the peripheral and central nervous systems at concentrations less than 1.0 µg/ml. It is reversibly metabolized to GABA in the central nervous system. GABA is metabolized to succinic semialdehyde (SSA) and enters the Krebs cycle. A small portion of SSA is then metabolized back to GHB. GBL and 1,4-BD enter the process as precursors for GHB. Recipes for the home-based manufacture of GHB from GBL and sodium hydroxide are easily located on the Internet. GBL is available as an industrial solvent. Both GBL (called renew trient, blue nitro, or revivarant) and 1,4-BD (with street names of weight belt cleaner, soma, inner G) can be ingested without laboratory conversion to GHB. , GBL has a greater bioavailability and is rapidly converted to GHB by enzymes in the blood and liver. , All three drugs come in a white powder or tablet form and dissolve easily in water. GHB is a sodium salt, hence the terminology “salty water.”
GHB crosses the blood-brain barrier, affects the endogenous opioid system, and increases dopamine levels. GHB has an affinity for both the GHB-specific receptor and the GABA type B receptor. Ingestion of GHB causes CNS depression, sedation, nausea, drowsiness, dizziness, decreased inhibitions, euphoria, and increased sensuality. Effects are easily confused with those of alcohol ingestion and are synergistic with alcohol. Dose dependent effects occur within 15 to 30 minutes, , and range from amnesia and hypotonia at 10 mg/kg, rapid eye movement (REM) and non-REM sleep at 20 to 30 mg/kg, anesthesia at 50 mg/kg, and severe respiratory depression and coma at doses exceeding 50 mg/kg. A recreational dose of 1 g can produce amnesia and hypotonia, 2 g deep sleep, and 4 g coma. Effects can last several hours. Patients with GHB intoxication and overdose have clinical effects lasting from 20 minutes to as long as 10 hours. Coma in nonintubated patients rarely lasts longer than 4 hours. Victims often recover spontaneously in as little as 1 to 2 hours. , Coingestion of alcohol and other drugs can alter the symptom pattern and increase the depth and length of a coma.
Routine immunoassay urine drug screening does not include GHB. GHB is an endogenous substance and is excreted in urine. A forensic threshold of 10 µg/mL has been suggested as the lower limit for a positive test. Urine GHB levels ranged from 0.9 to 3.5 µg/mL in volunteers not taking the drug.
The prevalence of GHB in suspected DFSA is approximately 3% to 4%. Reported prevalence rates of GHB are quite likely underestimated as the metabolism and clearance is so rapid.
Table 15-4 summarizes other drugs that are uncommonly reported to be associated with DFSA.
