21st Century Street Drugs for the 21st Century Street Medic

21st Century Street Drugs for the 21st Century Street Medic
Street Drugs Part 2 21st Century Street Drugs for the 21st Century Street Medic

Ada County Paramedics Boise Idaho
Steve Cole Ada County Paramedics Boise Idaho

Overview We will review some common principles of caring for the “Pharmacologically gifted” We will discuss 6 of the new drugs that every paramedic should know. Strangely enough all of these “New Drugs” have been around for decades. We will discuss common signs of a RAVE. There is no way we can be all inclusive in an hour so bear with me.

Drugs we will cover MDDA (Ecstasy) PMA GHB analogs Rohypnol (roofies)
DXM Ketamine

The Rave Culture

What is a “Rave” “Countryside hideaways set the scene for psychedelic parties. The night adorned with luminescent tantric and alien banners, lit by black and colored lights, lasers and strobes; the day transforming into a ravers paradise, decorated with a colorful array of psychedelia and the wonders of mother nature. Here Electronic Music and its DJ's unite people in dance & freedom. Freedom to be who you want, wear what you want and to dance as if no one is watching” ----The internet

The Rave Culture Generally speaking, “Rave” applies not just to the parties but to an entire subculture It is a Multi-National culture, and is seen in multi-national cities (Seattle, New York, D.C., Miami, Frankfort (Ger.) etc). It has spread to some degree to every City in the US. Not just “Night time” Parties at clubs Can extend into multi-day events (Burning Man) Hallmarked by techno/new age music and Psychedelic visual displays.

The Rave Culture IN SIMPLISTIC TERMS: Think the Grateful Dead/Hippie ethics meet High energy electronic “Techno” Music, throw in a heavy dose of the larger “drug culture” and that gives you a start. As with any sub culture, this group has its slang, its distrust for outsiders (especially badge carrying authority figures), its Myths (“…don’t dial 911”). To be truly effective, the EMS provider must break down barriers, gain trust, to better treat the patient. An understanding of how these rave parties often work will give you a better insight into the patients medical condition. Gather as much information as possible from the scene. Frequently the patient is not in a position to admit to taking drugs due to loss of consciousness and the best source of information are friends. These friends are not likely to be as forthcoming as they might otherwise be if they fear the response of the accident and emergency staff. Confidentiality and an open and non judgmental attitude is not only the basis of an ethical approach to MDMA related problems, it is of vital clinical importance. The friends are your best source of information if the casualty is unconscious. They must feel confident in you. They must feel safe with you. The EMS provider must create a relationship of trust.

Anatomy of a Rave

Anatomy of a RAVE Day or Night
Tend to be “Sponsored” (A.K.A. “Promoters”), limits liability on both sides Sometimes marketed as “Drug Free Teen Dance Parties” If not at a formal club, they tend to be located in remote locations to limit outside interference. Often will have a DJ instead of a band. Some DJ’s are celebrities, called the “A-List”, traveling a “Circuit” ($ /hr)

Anatomy of a Rave Remember, the overall event doesn't have to be a rave to have a strong Raver presence….. Example: Boise High School drug free party

Anatomy of a Rave May have multiple Rooms, each with a Theme (“Jungle-Rave”) Usually has Multiple Water Venders ($$$) May or may not be BYOB Any where from 100 to 10,000 (“massives”) Some larger events hire an Private EMS agency to stand by, sometimes to limit police involvement. More respectable areas may even have a area for triage. All scenes are a potential volatile environment Jungle Rave: Drums and pipes, primative

Anatomy of a Rave- Clues
Light Sticks Water/Gatorade Bottles for sale H2O shut off in bathroom Crash Rooms/Candles/Etc. Have Dance Breaks/cool down periods

Anatomy of a Rave

Anatomy of a Rave-Common Medical concerns
Severe Dehydration and Hyperthermia Poly-Pharm involvement Date Rape Multiple Patients (approach with a plan) Volatile Crowds

Interacting with Ravers
Remember there is a cultural distrust Don’t be afraid to ask for interpretation of slang Generally not overtly violent singularly, but beware of crowds Our attitude and interaction may have a positive or negative impact on the crowd. Check for a “Trip Sitter” A trend is developing within night clubs that are intended to keep their customers safer. While this is controversial since it seems to smack of endorsement of drug abuse, the reality is that we're seeing night club owners and dance event organizers taking steps such as: The prevention of overcrowding. This is obviously of crucial importance in the control of the temperature but also the humidity of the night club or dance. The availability of drinking water or chilled soft drinks --particularly sports drinks which contain sodium. Air conditioning and ventilation to control temperature rises in the night clubs and prevent overheating. Provision of "chill out" areas where people can sit and cool down in a quieter and cooler environment. DJs giving dancers a rest periodically, by placing breaks in the music or by slowing the tempo down intermittently. The provision of first aid or paramedics, particularly at large or remote events. A controversial issue in New York City (April 2001) came to light when it was discovered that many clubs hired private ambulances for their clubs to treat customers and protect their confidentiality. This practice is under review since the big problem is that the 911 system is bypassed and Police are never notified of the overdoses and are essentially prevented from investigating illegal practices.

Questions?

The Drugs

MDMA (Ecstasy)-Introduction
methylenedioxy-n- methylamphetamine MDMA is *chemically* an amphetamine, but psychologically its what's known as an empathogen-entactogen Shares similarities to both mescaline (a hallucinogen) and amphetamines (A type of Stimulant) MDMA (also commonly known as Ecstacy, X, E, XTC, Adam, etc.) is a semi-synthetic chemical compound. In its pure form, it is a white crystalline powder. It usually seen in capsule form, in pressed pills, or as loose powder. Average cost ranges from $10-$30 (U.S.) a dose. Common routes of administration are swallowing or snorting, although it can be smoked or injected as well. Currently, MDMA is on the U.S. Schedule I of controlled substances, and is illegal to manufacture, possess, or sell in the United States. Most other countries have similar laws. According to Nicholas Saunders (1993), "MDMA was patented as long ago as 1913 by the German company Merck. [...] The patent doesn't mention uses.“ empathogen-entactogen: Entactogenesis ("touching within") This is a generalized feeling that all is right and good with the world. People on MDMA often describe feeling "at peace" or experiencing a generalized "happy" feeling. Empathogenesis Empathogenesis is a feeling of emotional closeness to others (and to one's self) coupled with a breakdown of personal communication barriers. People on MDMA report feeling much more at ease talking to others and that any hangups that one may have with regard to "opening up" to others may be reduced or even eliminated. This effect is partially responsible for MDMA's being known as a "hug drug" - the increased emotional closeness makes personal contact quite rewarding. Many people use MDMA primarily for this effect, reporting that it makes potentially awkward or uncomfortable social situations (singles bars, dance clubs, etc.) much more easily dealt with.

MDMA (Ecstasy)-STATS Average Tablet = 300mg Pure MDMA = 100mg
One Kilo MDMA = 10,000 Tablets Prices Per Dosage: $.50 to $2.00 at source (Netherlands/Belgium) (wholesale). $8.00 bulk quantity U.S. (wholesale). $20.00 to $30.00 U.S. (retail). (One Kilo MDMA Powder = $200,000 - $300,000

MDMA (Ecstasy)- How is it used?
Taken in Tabs Effects generally appear within minutes. Initial effects include a brief "rush" of energy, usually described as mild but euphoric. After this rush, the high levels off to a plateau which lasts 2-3 hours and is followed by a gradual "coming down" sensation, culminating in a feeling of fatigue. In about 4-6 hours MDMA exerts amphetamine-like effects These side effects are dose dependent. MDMA's enhancement of proprioception (deep body sense) makes movement notably pleasant, so Ravers on MDMA often dance for long periods of time (remember to drink water frequently!). The feeling of unity and shared ecstatic joy at a successful Rave can be overwhelmingly wonderful. Some ravers regard this as spiritual or religious practice. For more info on raves, subscribe to the newsgroup alt.rave or obtain the alt.rave FAQ from hyperreal.org.

MDMA (Ecstasy) How does it work?
It MDMA blocks the reuptake of serotonin (5-HT), Unlike those drugs MDMA appears to enter the neuron, and causes the release of 5-HT as well. Thus MDMA is primarily a seritonergic MDMA acts on 5-HT similarly to the way amphetamines act on dopamine. MDMA also agonist effects on 5HT2 muscarinic M1, alpha-2 adrenergic and histamine H1 receptors (Thus its stimulant effects) MDMA also causes some release of dopamine It blocks re-uptake of 5-HT similarly to SSRI (serotonin specific reuptake inhibiting) anti-depressants such as fluoxetine (Prozac), sertraline, and paroxetine. Agonist (stimulation rather than blocking) properties at the 5-HT2 receptor have been found to fairly universally be associated with "classical" psychedelic drugs such as LSD, psilocybin and mescaline. It is possible that some of MDMA's "psychedelic" effect occurs because of interactions with this receptor. The alpha-2 adrenergic receptor may be associated with some of the carciovascular effects of MDMA. MDMA also releases dopamine which may be central to both its psychological action and to its neurotoxicity in animal studies. Pre- treatment of an animal with a drug which blocks dopamine release will also block MDMA neurotoxicity. In summary, MDMA effects 5-HT similarly to the way that amphetamines effect dopamine, by inhibiting the reuptake and causing the release of 5-HT. This effect is somewhat similar to the effect that SSRI anti-depressant drugs have. It also effects the 5-HT2 (psychedelic) and alpha-2 adrenergic (cardiovascular) receptor sites. Also, its effects on dopamine appear, at this point, to be involved both with its neurotoxicity and psychological effects. Some people take SSRIs (selective serotonin reuptake inhibitors) several hours after taking MDMA. Thus is not to prolong or potentiate the MDMA trip but to prevent the possibility of a neurotoxin entering the 5-HT cell and damaging the cell's axons. This has been shown to happen in animals after relatively high or repeated doses. Chronic use of SSRIs, as is done in the treatment of depression, seems to reduce the effects of MDMA. That is, a higher dose of MDMA is required to achieve the entactogenic effect.

MDMA MDMA exerts a strong paradoxical effect of relaxation which may mask the stimulant side effects, followed by a gradual drop. Generally, the side effects of MDMA are similar to those of amphetamine. MDMA also appears to exert an adverse action on the immunological response of some individuals, particularly with heavy use. Long-term users often describe increasingly uncomfortable and prolonged "burn-out" periods, sometimes lasting two or more days Sore throats, flu like s/s, and other symptom are reported, its MOA is poorly understood MDMA exerts amphetamine-like effects which include dilated pupils, dry mouth and throat, tension in the lower jaw, grinding of the teeth, and overall stimulation. These side effects are dose dependent and will vary depending on the health of the individual user

MDMA (Ecstasy) Toxicity
MDMA is most often ingested orally, although inhalation and injection have been infrequently reported. The usual dose ranges from 100 to 150 mg. Toxicity may be seen at doses as little as 175 mg Ecstasy tablets are notoriously impure, often containing chemicals other than MDMA (such as PMA, PCP,or DXM) The Problem is that multiple drug combinations (especially stimulants)may lower the toxic threshold. MAO Inhibitors may lethally potentate this drug. Street doses of MDMA generally run from 50mg. to 150 mg. 100mg. or 1/10th of one gram is considered an average single dose. Monks have used lower doses (40-60 mg) to assist meditation, and therapists have sometimes taken similarly low doses to become more in tune with clients. A benchmark standard dose is often considered to be 2 mg of MDMA per kilogram of body weight (though response to the drug is not strictly proportional to body weight). Users will take 1/3-1/2 the original dose to maintain at approx 1 ½ hours after ward. Could it be possible to prolong its effect by new selective serotonin reuptake inhibitors?? Probably not. One of the ways (if not THE way) MDMA enters the 5-HT (serotonin) neuron is through the serotonin reuptake transporter. By blocking 5-HT reuptake, you also seem to significantly block MDMA's entry into the cell, thus probably reducing its effects. It is known that RATS do not respond to MDMA the way that humans do, do be careful w/ this data. Deaths have been reported of some MDMA users who were also taking Monoamine Oxidase Inhibitors (MAOIs are often prescribed as antidepressants). MDMA is *not* recommended to anyone taking any MAOI

MDMA (Ecstasy) Toxicity Mild s/s
Jaw clenching (Lower Jaw)/teeth grinding, and scratching (think Tweekers) Nystagmus, Dilated Pupils Tremors Tachycardia, increased B/P Sensation of chills (secondary to elevated temp) Auditory Hallucinations (non specific)/sensitivity Orthostatic s/s, syncope secondary to dehydration MDMA users may encounter problems similar to those experienced by amphetamine and cocaine users, including addiction MDMA use damages brain serotonin neurons. Serotonin is thought to play a role in regulating mood, memory, sleep, and appetite. Recent research indicates heavy MDMA use causes persistent memory problems in humans. Hyponatremia is defined as: a decrease in the plasma sodium concentration below 136 mEq/L caused by an excess of water relative to solute. Excessive perspiration, excessive urination and excessive thirst results in diluting sodium levels when the patient drinks too much water. If sodium is being lost, drinking plain water will not replace it. 'Isotonic' drinks, unlike pure water, will help replace some minerals like sodium and preserve the balance of fluids in circulation. Signs and symptoms of hyponatremia can be subtle and consist mainly of changes in mental status, including altered personality, lethargy, and confusion. When hyponatremia is accompanied by disturbances in total body sodium content, signs of volume depletion or overload are also present. As the plasma Na falls below 115 mEq/L, stupor, neuromuscular hyperexcitability, convulsions, prolonged coma, and death can result. Rarely, initial improvement in response to treatment may be followed by delayed neurologic symptoms culminating in coma, persistent vegetative state, or death. To treat this, infuse Normal Saline and titrate to support blood pressure and perfusion. In the Emergency Department hypertonic Saline can be administered. Low sodium levels cannot safely be corrected it the field.

MDMA (Ecstasy) Toxicity Major S/S
Severe Dehydration with Hyponatremia Malignant Hyperthermia (Think Heat Stroke, but worse) Disseminated Intravascular Coagulation (DIC) (may have rapid onset) Decreased LOC/Coma Stroke S/S, Seizures Severe Tachycardia, HTN, CHF Kidney Failure MDMA-related fatalities at raves have been reported. The stimulant effects of the drug, which enable the user to dance for extended periods, combined with the hot, crowded conditions usually found at raves can lead to dehydration, hyperthermia, and heart or kidney failure. Overheating, causing life threatening malignant hyperthermia and severe dehydration with sodium loss is a major complication associated with MDMA and many other abused drugs. MDMA causes the body's thermostat to malfunction. Very high core body temperatures have been reported. The overheating effect of ecstasy is exacerbated by the following factors: MDMA users are thought to dance well beyond the point of which a "normal" person would tire and sit down. DJ's play seamless sequences of records which keep dancers active, and therefore producing more heat, over long periods of time. The club atmosphere is hot and humid. The evaporation of sweat is an essential body defence mechanism to prevent overheating. Hyperthermia leads rapidly to Disseminated Intravascular Coagulation (DIC) and the victim bleeds to death (in the most severe cases). First excessive clotting occurs that depletes the body's clotting factors. The blood coagulation process uses the blood's clotting factors such as platelets, fibrinogen and other substances faster than they can be replaced. This leads to an absolute depletion in the quantity of these elements and is called Disseminated Intravascular Coagulation, or DIC. The result of the depletion of clotting elements is that the disorder causes significant internal bleeding. Bruising occurs, hemorrhage from body orifices, IV sites, gums and internally occurs. With MDMA the onset of DIC can occur very quickly. Gather as much information as possible from the scene. Frequently the patient is not in a position to admit to taking drugs due to loss of consciousness and the best source of information are friends. These friends are not likely to be as forthcoming as they might otherwise be if they fear the response of the accident and emergency staff. Confidentiality and an open and non judgmental attitude is not only the basis of an ethical approach to MDMA related problems, it is of vital clinical importance. The friends are your best source of information if the casualty is unconscious. They must feel confident in you. They must feel safe with you. The EMS provider must create a relationship of trust.

MDMA (Ecstasy) Toxicity Treatment
Calm low stimulus environment VOMIT, Fluid Resuscitation as needed Benzodiazepines Droperidol 2.5-5mg for sedation/chemical restraint IM/IV Haldol 5 mg IM/IV Consider short acting Beta Blockers for severe HTN/Tachycardia (Brevibloc 500 mcg) Active cooling if indicated The first step in treating an MDMA overdose is to secure your personal safety and the patient's safety. MDMA may cause agitation and violent behavior. Obtain assistance from Police as needed. A rapid tranquilization procedure can be used if your local protocols allow. If the patient is otherwise agitated and unmanageable you may administer IV/IM benzodiazepine agent like diazepam or lorazepam, or a sedative-hypnotic agent like Droperidol. Be careful when using physical restraint to prevent positional asphyxia. Gather as much information as possible from the scene. Frequently the patient is not in a position to admit to taking drugs due to loss of consciousness and the best source of information are friends. These friends are not likely to be as forthcoming as they might otherwise be if they fear the response of the accident and emergency staff. Confidentiality and an open and non judgmental attitude is not only the basis of an ethical approach to MDMA related problems, it is of vital clinical importance. The friends are your best source of information if the casualty is unconscious. They must feel confident in you. They must feel safe with you. The EMS provider must create a relationship of trust.

MDMA (Ecstasy) What does this mean to me?
Core Temp if unresponsive Fluid Resuscitation Watch for DIC, SZ P.U.H.A. IF GROSSLY SYMPTOMATIC.

PMA- Introduction Para-methoxyamphetamine, PMA, 4-METHOXYAMPHETAMINE
Chemically similar to MDMA, first created almost 25 years ago Since its cheaper to make, and uses non controlled substances, PMA is often misrepresented as MDMA. At doses considered “safe” for MDMA, PMA is highly toxic. PMA, Para-methoxyamphetamine, was originally documented as a drug in the early 70’s. PMA has remained mostly unseen for almost 25 years. However as early as 1994, it has begun a deadly return in the illicit drug market. Although still relatively rare, PMA is considered one of the most dangerous hallucinogens. Sold as a beige, white, or pink powder, or in tablets, PMA is often misrepresented as MDMA, methylene-dioxy-methamphetamine. However, at doses considered “safe” for MDMA, PMA is highly toxic. The hallucinogenic effects of PMA are similar to LSD. Several deaths have been reported in connection to its use, mainly in Australia, New Zealand, and North America.

PMA-How is it used? PMA is however more toxic than MDMA
It often appears identical to MDMA, sometimes simply thicker. Its onset of action is longer (almost 60 minutes) compared to MDMA at minutes Users will re-dose thinking its MDMA and push them selves into the toxic range Some people think they know their MDMA dose and apply this to PMA, thus going toxic Substances like Cocaine and Methamphetamine may exacerbate the toxic effects of either PMA or MDMA As much PMA and Ecstasy are alike, a major difference (aside from toxicity) is onset of action. PMA takes about an hour to have a noticeable effect while MDMA takes about minutes minutes. One possible reason that people overdose on PMA is because they think it's MDMA. After fifteen minutes with no results they take another "hit," thinking the first one was no good. In addition some people are believe they “know” their optimal Ecstasy dose, and apply this to what they think is MDMA, but is PMA instead. Still others mix their drugs. Substances like Cocaine and Methamphetamine may exacerbate the toxic effects of either PMA or MDMA.

PMA- How does it work? PMA is over 20 times as potent as MDMA as an inhibitor of 5-HT. (in rat studies) Like MDMA, PMA blocks the reuptake of serotonin (5-HT), Also PMA appears to enter the neuron, and causes the release of 5-HT as well. PMA acts on 5-HT similarly to the way amphetamines act on dopamine. PMA also agonist effects on 5HT2 muscarinic M1, alpha-2 adrenergic and histamine H1 receptors (Thus its stimulant effects) A major metabolites of amphetamine is 4-hydroxyamphetamine, from oxidation at the 4-position. It has been long known that with chronic amphetamine usage there is the generation of tolerance, which encourages ever-increasing doses to be used. When the daily load gets up around one or two hundred milligrams, the subject can become quite psychotic. The question was asked: might the chronic amphetamine user be methylating his endogenously produced 4-hydroxyamphet-amine to produce 4-methoxyamphetamine (4-MA), and maybe this is the agent that promotes the psychosis? To address this question, several studies were done with normal subjects, about 20 years ago, to see if 4-MA might produce a psychotic state (it didn't at the highest levels tried, 75 milligrams) and to see if it was excreted to some extent unchanged in the urines of these normal subjects (it was seen even at the lowest dosage tried, 10 milligrams). It produced excitation and other central effects, it produced adrenergic pressor effects, and it consistently produced measur-able quantities of 4-MA in the urine, but it produced no amphetamine-like crazies. And since the administration of up to 600 milligrams of amphetamine produced no detectable 4-MA in the urine, this theory of psychotomimesis is not valid. It blocks re-uptake of 5-HT similarly to SSRI (serotonin specific reuptake inhibiting) anti-depressants such as fluoxetine (Prozac), sertraline, and paroxetine. Agonist (stimulation rather than blocking) properties at the 5-HT2 receptor have been found to fairly universally be associated with "classical" psychedelic drugs such as LSD, psilocybin and mescaline. It is possible that some of MDMA's "psychedelic" effect occurs because of interactions with this receptor. The alpha-2 adrenergic receptor may be associated with some of the carciovascular effects of MDMA. MDMA also releases dopamine which may be central to both its psychological action and to its neurotoxicity in animal studies. Pre- treatment of an animal with a drug which blocks dopamine release will also block MDMA neurotoxicity. In summary, MDMA effects 5-HT similarly to the way that amphetamines effect dopamine, by inhibiting the reuptake and causing the release of 5-HT. This effect is somewhat similar to the effect that SSRI anti-depressant drugs have. It also effects the 5-HT2 (psychedelic) and alpha-2 adrenergic (cardiovascular) receptor sites. Also, its effects on dopamine appear, at this point, to be involved both with its neurotoxicity and psychological effects. Some people take SSRIs (selective serotonin reuptake inhibitors) several hours after taking MDMA. Thus is not to prolong or potentiate the MDMA trip but to prevent the possibility of a neurotoxin entering the 5-HT cell and damaging the cell's axons. This has been shown to happen in animals after relatively high or repeated doses. Chronic use of SSRIs, as is done in the treatment of depression, seems to reduce the effects of MDMA. That is, a higher dose of MDMA is required to achieve the entactogenic effect.

PMA- Toxicity Street doses of MDMA generally run from 50mg. to 150 mg. 100mg. or 1/10th of one gram is considered an average single dose. However the street dose for PMA usually less than about 50 mg, with toxic effects seen at even slightly higher doses (making toxicity likely) When mixed with other drugs (including alcohol) or more tablets are taken, the toxic effects become more apparent.

PMA-Toxicity With PMA one should not thing about mild vs. severe toxicity. Think about How much time before the patient develops severe toxicity. Deaths have been seen with as few as 2-3 tablets of PMA.

PMA -Toxicity Hypertension Tachycardia and Cardiac arrhythmias,
Tachypnea Severe hyperthermia (as high as 108 degrees F) Dehydration (may be severe) Renal Failure Hallucinations, Behavioral disturbances (similar to Ecstasy or LSD) Nausea, vomiting Erratic eye motion Seizures DIC CHF Coma Typically any MDMA s/s Severe S/S may follow w/in the hour Muscle spasms, muscle cramps. Coma, Coagulopathy problems Severe S/S may follow with in the hour.

PMA- Treatment Calm low stimulus environment
VOMIT, Fluid Resuscitation as needed Benzodiazepines Droperidol 2.5-5mg for sedation/chemical restraint IM/IV Haldol 5 mg IM/IV Consider short acting Beta Blockers for severe HTN/Tachycardia (Brevibloc 500 mcg) Active cooling if indicated Treatment is similar as for MDMA, generally focused at reducing body temperature and response to presenting symptoms. Transport should be rapid, as once symptoms present, progression to life threatening problems may be rapid. A recent series of post mortem toxicology screens found other types of methamphetamine in 5 of 6 PMA related deaths Treatment is generally focused at reducing body temperature and response to presenting symptoms. Transport should be rapid, as once symptoms present, progression to life threatening problems may be rapid. Prehospital providers are cautioned to be aware of possible poly-pharmaceutical involvement. A recent series of post mortem toxicology screens found other methamphetamine in 5 of 6 PMA related deaths. However Prehospital providers should note that any drug sold as Ecstasy may be PMA instead. As such, any otherwise “stable patient” should be strongly considered for ALS evaluation and transport, complete with EKG and IV access, as it may be difficult to assess when the substance they ingested may reach “peak effects”.

PMA-What does this mean to me?
1st you identify a probable MDMA/PMA user. Then you get a good subjective Hx , By gauging the time of onset of s/s, you can have a suspicion for PMA and potential toxicity. This combined with the knowledge of PMA’s Toxicity risk, should help insure the pt. gets transported to a medical facility regardless of stable presentation. Core Temp if unresponsive ‘Fluid Resuscitation Watch for DIC, SZ P.U.H.A. IF GROSSLY SYMPTOMATIC However Prehospital providers should note that any drug sold as Ecstasy may be PMA instead. As such, any otherwise “stable patient” should be strongly considered for ALS evaluation and transport, complete with EKG and IV access, as it may be difficult to assess when the substance they ingested may reach “peak effects”. PMA is a potentially deadly substance being sold to unsuspecting 'partyers' as Ecstasy (MDMA). As with any illicit drug, one can never be sure of the exact composition or dose ingested. PMA’s effects are more toxic at lower levels than MDMA, and this seems to be the predominate cause for the deaths associated with it. Prehospital providers may come to care for these patients for any number of reasons relating to either life style mishap, and find an altogether unsuspected complication resultant. This just shows that prehospital providers must be ever vigilant not just in cardiology, trauma, and pediatrics, but toxicology as well.

DXM- Introduction Yes, Its in cough Syrup
Dextromethorphan acts as a cough suppressant via its agonist (activating) activity at mu-opioid receptors. In Canada: Contac CoughCaps (30 mg DXM) Related in effects to Ketamine and PCP antitussive analog of morphine Several years ago, JW Olney discovered that dizocilpine (MK-801), a chemical being tested to prevent brain damage from strokes, actually caused damage to specific areas of the brain in rats. Since this time, numerous other drugs in the same class (the dissociatives) have been tested, and they all share this problem. As some of you might know, I have spent a great deal of time trying to make sure that the Internet community, and the larger world, has detailed information about this complex, difficult-to-use, and often dangerous class of drugs.

DXM- How is it used? “Robo-ing” (Old Term from early 90’s)
DXM is available over-the-counter in tablet form in several countries as a cough med. Robitussin Maximum Strength Cough (not Robitussin DM) syrup Users often refer to DXM in “plateaus” Dose of Robitussin Maximum Strength Cough syrup is two to five full "shots" using the shot glass that comes with the bottle. Additionally, prolonged use of DXM can and has led to psychosis similar to PCP-induced psychosis. Individual differences in NMDA receptors may be at work here, but you're still potentially at risk. Effects at low dosage can be similar to alcohol producing carefree clumsiness with a touch of psychedelic and speedy effect. Intense and rhythmic music induces a state of euphoria and dancing becomes fun. On a higher dose imagination can become vividly experienced (not always pleasant), feelings of dissociation from the body can occur and on very high doses profound alterations in consciousness. Doses greater than 1000 mg are generally regarded as foolhardy 1st plateau ( mg/kg): 2nd plateau ( mg/kg): 3rd plateau ( mg/kg): 4th plateau (15mg/kg-): 5th plateau (usually reported above 30 mg/kg): Overdose

DXM- How does it work? DXM is in the same class as ketamine, PCP, MK-801, and several other NMDA open channel blockers Dose ranges from mg. Fatal may be in excess of 1500 mg, but may be lowered by other drugs. Duration is about 2-4 hours, but some effects may linger for weeks It is classified (generally) as a Dissociative Anesthetic Some times “educated” users take a barbiturate or benzodiazepine to prevent brain damage while taking this drug (Olney's Lesions) NMDA open channel blockers / sigma opioid The sigma opioid receptor's function is unknown but it may be implicated in schizophrenia. Sigma opioid agonists produce both the positive and the negative symptoms of schizophrenia, unlike dopaminergics which produce only the positive symptoms. The term "dissociative" derives from "dissociative anaesthetic", a class of anaesthetics which produce unresponsiveness to stimuli by dissociating various elements of the mind (in simple terms, they knock you out by putting you 'out of your body'). Consciousness, memory, perception, and motor activity are all dissociatied from each other. The dissociative anaesthetics all block the N-methyl-D-aspartate (NMDA) neuroreceptor, though many act on other receptors like sigma. I prefer "dissociative" to "dissociative anaesthetic" when discussing these drugs, for two reasons: first, most recreational use occurs below the anaesthetic level; second, some drugs in this category are not, and probably never will be, marketed as anaesthetics.

DXM- How does it work In simple terms, they knock you out by putting you 'out of your body‘ Effects at low dosage can be similar to alcohol producing carefree clumsiness with a touch of psychedelic and speedy effect. Intense and rhythmic music induces a state of euphoria and dancing becomes fun. (thus its rave use) On a higher dose imagination can become vividly experienced (not always pleasant), feelings of dissociation from the body can occur and on very high doses profound alterations in consciousness, violent outburst, SZ. The psychedelic effects of the dissociatives are difficult to explain. They are nothing whatsoever like LSD or related drugs (mescaline, DMT, mushrooms, etc.) but they are clearly psychedelic Dissociatives are not frequently used as anaesthetics in humans because of what are known as "emergence effects", various odd effects that can happen when people come out of anesthesia. All anesthetics can produce these effects, but with the dissociatives it is much more common and much more severe. Dissociative anesthetics (Ketamine and tiletamine) are used in veterinary practice, since animals don't often complain about out-of-body experiences.

DXM- Toxicity (Acute) Dissociative anesthesia/coma/CNS depression
mild hallucinations, Violent Outbursts/behavior control (may last beyond the period of “intoxication”) Seizures (lowers the SZ threshold) Enhanced auditory perceptions, Tactile sensations (crawling skin), Visual disturbances with motion. Nausea/vertigo can occur DXM has some stimulant effects GHB may act synergistically w/ DXM to lower the SZ threshold In terms of effects on humans, described effects include dissociative anaesthesia, mild hallucinations, enhanced response to music (including highly pleasurable responses), and disturbances in motion. Nausea can occur. DXM has some stimulant effects. Dissociatives definitely cause brain damage if used heavily. One sub-anaesthetic "line dose" of ketamine, an equivalent dose of PCP, or a third plateau DXM dose, is probably at least as damaging to your brain as a few day "bender" on hard liquor, and possibly more so because it affects specific areas of the brain. The risk of brain damage is worse the longer you stay high at any given time; constant moderate-dose use is probably just as damaging as a brief, high-dose use. Reaching the anaesthetic level is exceedingly hard on your brain. Ketamine is probably the least harmful, PCP the most, and DXM somewhere in the middle, but this is a rough guesstimate. In addition to brain damage, these drugs can also trigger psychosis, limbic seizures, temporal lability, depression, and other neurological and psychological diseases much more frequently than other types of drugs. The dissociatives can be highly addictive to a minority of users. In comparison, the marijuana and the serotonergic psychedelics (LSD, psilocybin mushrooms, peyote, DMT) are many times safer.

DXM- Toxicity (Acute) Hyperthermia Histamine Release Hypertension
Tachycardia

DXM- Toxicity (Long Term)
Olney's Lesions: vacuoles (essentially, tiny holes) in their brains. Specifically, the vacuoles showed up in the posterior cingulate cortex and retrosplenial cortex People who have used dissociatives heavily have shown clear evidence of brain damage ranging from impaired memory to a schizophrenia-like syndrome. Many of the impairments correspond exactly to the areas of the brain damaged in lab animals. When NMDA antagonists were first studied they seemed like a dream come true: here were drugs which could block from part to all of the damage from strokes, head injury, hypoxia, polio, and a variety of other conditions. However, it seems that nature never gives something for nothing, and here too there was another side to the coin. The dream ended when Olney et al. demonstrated that animals given high doses of dizocilpine (MK-801), a new dissociative used in research, showed curious vacuoles (essentially, tiny holes) in their brains. Specifically, the vacuoles showed up in the posterior cingulate cortex and retrosplenial cortex (see I.1 for an explanation of what these parts of the brain do). Further research showed that other indicators of damage were present, such as proliferation of microglia, secretion of a protein called HSP70 (Heat-Shock Protein 70), and expression of certain genes. Since then, Onley's lesions, also known as NMDA Antagonist Neurotoxicity or NAN, have been discovered with ketamine, PCP, and dextrorphan (the metabolite of DXM), as well as a bunch of dissociative drugs you won't find outside of a research lab. PCP causes additional damage to the cerebellum and other areas, by the way. For a long time, nobody knew whether Olney's lesions applied to human beings or not, or at what dosage they applied. However, there have been reports from many hundreds of users of DXM, some of whom have used it heavily and been clearly harmed. Second, more recent studies have shown that damage occurs to lab animals' brains even at lower doses (including ordinary anaesthetic doses of ketamine and dizocilpine!). Third, reports of ketamine-related brain damage have started to show up. Finally, the type of impairment people are reporting coincides exactly with the areas of the brain damaged in lab animals. This may be transient as some people have reported that their "brain damage" cleared up after a few months. IMPORTANT NOTE: Olney's lesions are WORSE in female animals than males, probably because females have different limbic connections. This may apply to humans. To sum up: these are the skills which damage to these areas might impair: Memory, especially language-related (e.g., finding words) Understanding metaphors Evaluating, and possibly controlling, your own behaviour Multi-sensory thinking Learning in new situations Certain aspects of visual perception Autobiographical memory Declarative memory (as opposed to remembering skills) Place-memory (learning and remembering your way around) Coupling of emotions to experience

DXM- Coricidin Toxicity
Coricidin Cough and Cold Caps, 30 mg DXM and 4 mgs of Chlorphineramine maleate Non Specific reports of “Respiratory Failure” at high doses.

DXM- Treatment VOMIT Symptomatic TX.
Be alert for and (Cautiously) treat hypertension or hypotension, and rarely, cardiovascular problems Restraints (?) Avoid Chemical Restraint (Haldol, Droperidol), and use Benzodiazepines with caution (Be prepared to manage the airway) Benadryl may be given for Dystonic reactions, and for s/s of histamine release. Anticholinergic deliriants (atropine, scopolamine, and anti-nausea drugs) may increase damage to the hippocampus Major tranquilizers (antipsychotics) may specifically increase damage to certain areas

DXM- What does this mean to me?
Be Careful, take the same precautions you would with a PCP patient. ALS eval is a must ( HTN, Hyperthermia, Respiratory Depression, and self harm) DXM differs from other drugs. Its presentation of s/s extend well beyond simple CNS depression and hallucinations but into basic cognitive functions as well. Understanding that DXM effects last well beyond the 4 hours of intoxication , and that side effects may include “Psychotic Breaks” will help determine deposition of patients. Mental health referral is a necessary step for all DXM overdoses for both substance abuse screening and education as well as for neuropsychological evaluation for long-term side effects (Olney's Lesions)

Ketamine- Introduction
Another Disassociative Amnesiac “Special K, Vitamin K, new Ecstasy, psychedelic heroin, Cat Valium, Ketalar, Ketaject, Super-K, breakfast cereal, date rape drug. Slang” "Special K" or "K" (Ketamine) is an anesthetic. Use of a small amount of ketamine results in loss of attention span, learning ability, and memory. At higher doses, ketamine can cause delirium, amnesia, high blood pressure, depression, and severe breathing problems. Slang and street names include: Special K, Vitamin K, new Ecstasy, psychedelic heroin, Cat Valiums, Ketalar, Ketaject, Super-K, breakfast cereal, date rape drug. Slang Liquid Ketamine was developed in the early 1960s as an anesthetic for surgeries, and was used on the battlefields of Vietnam as an anesthetic. Powdered Ketamine emerged as a recreational drug in the 1970s, and was known as "Vitamin K" in the 1980s. It resurfaced in the 1990s rave scene as "Special K." Ketamine is most often injected intramuscularly, but can also be taken orally or nasally. Common recreational doses are between 25mg. and 300mg. depending on body size and the method of administration. Ketamine is a produced into a white powder, similar to cocaine. Normally found in injectable form, it is converted into a powder and re-packaged in small ziplock bags or capsules. Ketamine is generally snorted but is sometimes sprinkled on tobacco or marijuana and smoked. Special K is frequently used in combination with other drugs, such as Ecstasy, heroin and cocaine. What are its short-term effects? Users sometimes call the high caused by Special K "K hole" and describe profound hallucinations that include visual distortions and a lost sense of time, sense and identity. Other effects can include delirium, impaired motor function, potentially fatal respiratory problems, convulsions, and vomiting when mixed with alcohol and out of body experiences. Overdose Treatment A suspected ketamine overdose needs routine ALS care: high flow O2, cardiac monitoring, vital signs and intravenous access. The emergency treatment of a typical ketamine overdose is generally supportive in nature. Depending on how severe the signs and symptoms are. The worst problems associated with ketamine are seizures, arrhythmias, respiratory arrest, dystonic reactions, coma and cardiac arrest. The psychotropic affects are usually what we are faced with. The psych effects are similar to LSD, mushrooms or Angel Dust (PCP). IV medications that can be used include Droperidol (Inapsine) and benzodiazepines. These drugs can be administered to reduce sensory stimuli and get the patient under control. Benzodiazepines have been shown to markedly reduce the incidence of dreams, hallucinations and illusions after ketamine overdose and their administration has been recommended on a routine basis. Assume that ketamine was NOT the only drug ingested. Do NOT sedate patient's routinely, only when it is safer to manage the patient and prevent excessive physical restraint that can lead to positional asphyxia. Follow your local protocols and always contact medical control. Acute dystonic reactions, can be managed with diphenhydramine. Seizures occur are managed with diazepam (Adults: 5-10 mg IV initially repeated every minutes as needed. Children: mg/kg initially, repeat every 5 minutes as needed) or lorazepam (Adults: 4-8 mg IV and Children: mg/kg IV). Follow your local protocols for dosing. Monitor for respiratory depression and hypotension. If IV access is not available diazepam can be administered rectally. Once in the ED, urine toxicology screening should be performed on a routine basis. Plasma ketamine levels are not clinically useful in the treatment of overdoses. Mental health referral is a necessary step for all ketamine overdoses for both substance abuse screening and education as well as for neuropsychological evaluation for long-term side effects. Prompt identification and treatment of ketamine overdoses generally result in full recovery of most patients.

Ketamine-How is it used
Used legally as a Veterinary anesthetic Illegally used as a Date Rape Drug Liquid Ketamine was developed in the early 1960s as an anesthetic for surgeries, and was used in Vietnam as an anesthetic. Powdered Ketamine emerged as a recreational drug in the 1970s, and was known as "Vitamin K" in the 1980s. It resurfaced in the 1990s rave scene as "Special K.“ Ketamine is most often injected intramuscularly, but can also be taken orally or nasally. What is it and what does it look like?

Ketamine-What does it do?
central nervous system depressant rapid-acting general anesthetic sedative-hypnotic, analgesic, and hallucinogenic properties Works similar to DXM. Ketamine hydrochloride is a central nervous system depressant and a rapid-acting general anesthetic. It has sedative-hypnotic, analgesic, and hallucinogenic properties. It is marketed in the US and a number of foreign countries for use as a general anesthetic in both human and veterinary medical practice. Veterinarians use ketamine to tranquilize animals. Perhaps the most important property of ketamine is that, despite the induction of both anesthesia and dissociation, the cough and gag reflexes *USUALLY* are not affected. Ketamine HCl, available as 100mg/ml injectable under the trade name Vetalar (Parke-Davis) and Ketaset (Bristol) is used in veterinary work as a general anesthetic. The dosage used produces analgesia but with normal pharyngeal and laryngeal reflexes. It only causes mild respiratory depression. The advantage of this anesthetic is that you don't need to support respiration while performing any procedures.

Ketamine-Toxicity Common recreational doses are between 25mg. and 500mg. depending on body size and the method of administration Effects can include delirium, impaired motor function, potentially fatal respiratory problems, convulsions, and vomiting and out of body experiences. (Think DXM) The worst problems associated with Ketamine are seizures, arrhythmias, respiratory arrest, dystonic reactions, coma and cardiac arrest. Dosages are discussed in the PDR, but are generally in the range of mg. Conventional useage is intravenous or intramuscular, but "recreational" use is apparently more often through insufflation (snorting) or solution ingestion The insert states that the recommended dosage for anesthesia (5 to 10 minute duration) is 2mg/kg. Of course it is the coming OFF not the going ON that is where all the wierd stuff occurs. Medically these are called emergence reactions, but I call them hallucinations! :) If being awake and paralyzed doesn't scare you, the hallucination is cool. If it frightens you, or if you become frightened, you will snowball into a very bad trip.

Ketamine-Toxicity The psych effects are similar to LSD, mushrooms or Angel Dust (PCP). Seizures Arrhythmias, cardiac arrest Respiratory arrest Dystonic reactions coma

Ketamine-Treatment supportive in nature.
Benadryl for dystonic reactions Benzodiazepines are the preferred drug for sedation and restraint. Use Inapsine and Haldol w/ caution Mental health referral is a necessary step for all Ketamine overdoses for both substance abuse screening and education as well as for neuropsychological evaluation for long-term side effects (Olney's Lesions) Think DXM

Ketamine- What does this mean to me?
When trying to remember what drug does what, remember that PCP, DXM, and Katamine are all related neuro-chemically Prompt identification and treatment of Ketamine overdoses generally result in full recovery of most patients. Katamine differs from other drugs. Its presentation of s/s extend well beyond simple CNS depression and hallucinations but into basic cognitive functions as well When considering destination of these patients, consider the Psychiatric capability as well. ALS eval is a must ( HTN, Hyperthermia, Respiratory Depression, and self harm) Monitor for respiratory depression and hypotension. If IV access is not available diazepam can be administered rectally. Once in the ED, urine toxicology screening should be performed on a routine basis. Plasma ketamine levels are not clinically useful in the treatment of overdoses. Mental health referral is a necessary step for all ketamine overdoses for both substance abuse screening and education as well as for neuropsychological evaluation for long-term side effects. Prompt identification and treatment of ketamine overdoses generally result in full recovery of most patients.

GHB Analogs- Introduction
Gamma-hydroxybutyrate (GHB) may be made in homes by using recipes with common ingredients. "Liquid Ecstasy," "Georgia Home Boy," "Grievous Bodily Harm, "liquid ecstasy," do not confuse w/ MDMA GBL, GBH, One 4 B Very easy to make, no cooking is required. Since no longer commercially available, its potency in variable. GBL, GBH One 4 B

GHB analogs How is it used?
GHB can be produced in clear liquid, or a white powder, tablet, and capsule forms, and it is often used in combination with alcohol, making it even more dangerous It is often carried in an eye dropper, or in water/Gatorade bottles and passed around. Typically measured out in capfuls. Occasionally blue food coloring is used to identify it at some raves. It is occasionally used as a body building aid GHB is usually abused either for its intoxicating, sedative, and euphoriant properties. GHB's intoxicating and depressant effects on the CNS begin 10 to 20 minutes after the drug is taken orally. The effects typically last up to 4 hours, depending on the dosage. At lower doses, GHB can relieve anxiety and produce relaxation; however, as the dose increases, the sedative effects may result in sleep and eventual coma or death. The line between achieving euphoric effects and toxicity resulting in life threatening side effects is very narrow. GHB is often used with alcohol potentate its effects and increasing the likelihood of side effects and toxicity. Dose Effect 10 mg/kg Amnesia, hypotonia 20 mg/kg Drowsiness, somnolence, dizziness, euphoria 50 mg/kg Vomiting, bradycardia, Cheyne-Stokes respirations, seizures, coma and death.

GHB analogs- what does it do
At lower doses, GHB has sedative effects, but, as the dose increases, GHB effects may result in sleep ,eventual coma, respiratory arrest, or death. It is these effects that make it both a prime drug at Raves, and for Date Rape Coma and seizures can occur following abuse of GHB and, when combined with methamphetamine, there appears to be an increased risk of seizure. Combining use with other drugs such as alcohol can result in nausea and difficulty breathing. GHB may also produce withdrawal effects, including insomnia, anxiety, tremors, and sweating. Because of concern about Rohypnol, GHB, and other similarly abused sedative-hypnotics, Congress passed the "Drug-Induced Rape Prevention and Punishment Act of 1996" in October This legislation increased Federal penalties for use of any controlled substance to aid in sexual assault. GHB is cleared from the body relatively quickly, so it is sometimes difficult to detect in emergency rooms and other treatment facilities. In fact, only about 2-5% of GHB is excreted renally. In those cases where it has been renally excreted, GHB can be found in urine samples that test specifically for the substance within 4-7 hours after ingestion. GHB is not part of routine urine toxicological testing.

GHB analogs toxicity- mild
Lethargy, easily aroused with repeated stimulation Drowsiness, somnolence, dizziness, euphoria Confusion (dazed and confused) Amnesia, Susceptible to suggestion There were some homicide cases linked to GHB, it is believed that the subject used GHB in a date rape type of scenario, and when the victim did not respond quickly enough, that more GHB was added to her drink, becoming toxic.

GHB analogs Toxicity- Severe
66% with GCS <9, ½ of these may have GCS at 3! Frequent Vomiting, bradycardia, Respiratory depression or arrest Seizures Sudden onset of coma . patients often demonstrate extreme SUDDEN combativeness and agitation despite such profound CNS and respiratory depression Death (usually secondary to respiratory failure or aspiration) Dose Effect 10 mg/kg Amnesia, hypotonia 20 mg/kg Drowsiness, somnolence, dizziness, euphoria 50 mg/kg Vomiting, bradycardia, Cheyne-Stokes respirations, seizures, coma and death. Use with alcohol and stimulants (Meth, MDMA) are known to potentiate its effects. Seizures, Sudden onset of coma: Most often the cause of EMS notification

GHB analogs Toxicity It is worth noting that alcohol severely exacerbates GHB’s effects. GHB analog Butanediol and Ethanol are metabolized through the same pathways, making concombant use of ETOH very dangerous.

GHB analogs-Treatment
Primary Supportive Beware of positional Asphyxia, But soft restraints are a good Idea Due to the risk of sudden airway failure, aspiration, and respiratory collapse, these patients need aggressive airway monitoring by ALS providers As with other CNS depressants the emergency management is geared towards supporting a patient airway, supporting ventilation, oxygenation and adequate perfusion. There are no specific antidotes or completely safe reversal agents that can be administered. Although Physostigmine, a cholinergic drug, has been shown to reverse sedation, it is widely believed that the risks of bradycardia, seizures, AV block, cholinergic crisis, or asystole outweigh the potential benefits of reversal. Provide a patent airway. Suction sections as needed. Anticipate vomiting. Consider and assess for associated trauma or sexual assault that may have occurred. Position the patient for airway protection and to optimize perfusion. Oxygenate and ventilate if hypoventilation occurs. Reassess often for changes. Assess for concomitant problems such as hypoglycemia, opiate overdose, alcohol ingestion, other drugs. Monitor the cardiac rhythm. Bradycardia accompanies approximately 36% of ingestions. If bradycardia is present Atropine may be administered to hemodynamically unstable patients. Documented cardiac rhythms include first-degree heart block, atrial fibrillation, right-bundle branch block, and ventricular ectopy. Hypotension accompanies about 10% of GHB ingestions. This usually is associated with co-ingestion of GHB and alcohol or another drug and usually is mild. If hypotension is not resolved readily by stimulation or atropine administration, another ingestion or co-ingestion must be considered. When co-ingestion of another substance is suspected gastric decontamination by lavage with Activated charcoal with sorbitol is indicated. because GHB is rapidly absorbed from the GI system, lavage with an isolated GHB ingestion is probably not useful. Keep the patient warm. Mild hypothermia has been reported in about 70% of cases.

GHB analogs-Treatment
Protect your self VOMIT Be cautious using respiratory depressants Making the decision to tube/not tube is tough, these patients do frequently vomit. ETT placement is uncommon, but post ETT sedation/paralysis and restraint should be mandatory in the field A recent study noted that two thirds of patients present with a GCS of less than 9, and a full third present with a GCS of 3. According to physician reports one peculiar characteristic of GHB toxicity is that patients often demonstrate extreme combativeness and agitation despite such profound CNS and respiratory depression. Several physicians have been surprised when the individual suddenly awakens during an intubation attempt. The coma usually lasts from 3 to 6 hours and spontaneously resolves. Those patients intubated for respiratory depression typically have a longer time to recovery, but extubation within 8-10 hours is common; extubation in the ED has been described. The resolution is characteristically rapid and usually accompanied by seizure-like movements, myoclonic jerks and agitation. (Cameron, e-medicine.com, 2001)

GHB analogs- What does this mean to me?
GHB analogs are unpredictable in clinical course, other than duration. GHB analogs cause a rapid change in mental and respiratory status that makes it difficult to plan treatment and care GHB’s presentation often mimics ETOH abuse and is often co-imbibed.

Rohypnol Introduction
Roofies is a common drug used overseas It has seen rising use in the US in the Date Rape scene. It should be noted that similar drugs may be sold under this name as well. (“Roche”)

Rohypnol- How is it used
Frequently used as a date rape drug Generally placed illicitly in alcoholic drinks. Is odorless/tasteless, and dissolves easily into carbonated drinks. Clonazepam (A similar US marketed drug) are often used as Roofies. “Roche”

Rohypnol- What does it do
Benzodiazepine, Sedative-hypnotic Respiratory depressant Antitrade amnesia (Like Versed)

Rohypnol-Toxicity 1 MG of Rohypnol can impair the pt for up to 8 hours
3 mg of Clonazepam causes significant CNS depression and somnolence in 50% of adults on one study(with no other drug use) (Comes in .5, 1 and 3 mg tablets) like those produced by other CNS depressants, include somnolence, confusion, coma and diminished reflexes

Rohypnol-Treatment Flumazenil is not indicated in patients with epilepsy who have been treated with benzodiazepines. Antagonism of the benzodiazepine effect in such patients may provoke seizures. It is also Contraindicated in Poly-Pharm cases. Otherwise care is supportive and based on Respiratory status.

Rohypnol- What does this mean to me?
Treat these calls and the patients as potential criminal cases Flumazinil is generally contraindicated in the field Airway and respiratory concerns are the predominate medical problem Do not r/o other drug involvement.

Summery “..Due to the poly-pharmacy drugs that are being sold to ravers, all of these patients deserve ALS evaluation…” MDMA and other abused drugs can have serious consequences that are often unpredictable. EMS providers need to understand the unique problems associated with MDMA, realize the likelihood of a multiple drug and alcohol ingestion and be prepared for any of the medical complications that can occur. The drugs continue to gain popularity and the data indicate this is not a passing trend.

21st Century Street Drugs for the 21st Century Street Medic

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