Tag Archives: toxicology

Electronic Cigarettes and Liquid Nicotine Poisoning

By Jhonny E Ordonez*, Larissa Velez**, and Kurt C Kleinschmidt**
*Toxicology Fellow, UTSW
**Professor of Emergency Medicine / Toxicology, UTSW

Case

A 3 year-old boy is found by his parents with an open container of liquid nicotine, which his dad uses to refill his electronic cigarette. The toddler had just drunk some and the rest of the solution is spilled over his clothes and skin. The child soon becomes agitated and has vomiting, pallor, and tremor. He then has a generalized tonic clonic seizure. He is brought to the ED by ambulance.  What would you do?

What are e-cigarettes?

Electronic cigarettes, also known as e-cigarettes (e-cigs) or electronic nicotine delivery systems (ENDS) are battery-powered devices that heat a liquid solution of nicotine, or e-liquid. An e-cigarette contains a cartridge that is either disposable or refillable. This cartridge contains the liquid nicotine that is heated and vaporized, and inhaling this vapor is called “vaping.” E-cigarettes were first developed in China in 2003 and rapidly became very popular throughout Asia and Europe. They have become popular in the USA since first being marketed in 2007. E-cigs have become popular as reportedly safer alternatives to smoking. They do not expose smokers to some of the dangerous product of pyrolysis. There is no smoke produced; only vapor, which is more acceptable to those around the smoker. The use of these devices is often allowed in places where smoking is prohibited. In the past, e-cigs were also marketed as smoking cessation aids. Currently, there is no evidence that e-cigarettes are effective methods to quit smoking.20

There have been recent concerns about other chemicals in the e-liquid, besides nicotine. The vapor contents include cytotoxic substances; acrolein, acetaldehyde, and formaldehyde.7,8 Although found in small concentrations, the potential chronic effects of inhaling these is unknown. Propylene glycol and glycerin are also in e-cigs as moisturizers. There are reports of these agents causing slight irritation when inhaled.3,9

Nicotine poisoning

Nicotine is an agonist at the nicotinic acetylcholine receptors. Acute nicotine poisoning has a biphasic pattern. The early clinical phase is characterized by excessive stimulation, resulting in nausea, vomiting, pallor, abdominal pain, salivation, bronchorrhea, tachypnea, hypertension, tachycardia, miosis, ataxia, tremor, fasciculations, and seizures. The delayed phase consists of central nervous system and respiratory depression, dyspnea, bradycardia, hypotension, shock, mydriasis, weakness, muscle paralysis, and coma.13 There are few reports of fatal cases after exposure to nicotine-containing products and plants by several routes.11,15 To this date, there are no reports of deaths from accidental liquid nicotine exposure.

The management of acute nicotine poisoning is mainly supportive.  Decontamination by washing the skin and removing clothes is appropriate for dermal exposures. Benzodiazepines are used for seizures. Intubation might be needed for those with muscle weakness or ventilatory failure. Atropine can be used for symptomatic bradycardia.

Why are they dangerous?

Exposure to the nicotine solutions may be dangerous because they may be highly concentrated, with concentrations ranging from 6 to 100 mg/ml.18 The lethal dose of nicotine is uncertain but the oral LD50 is 6.5–13 mg/kg in dogs.12 Based on this LD50, the ingestion of only a few milliliters of some of the preparations could be toxic. In children, doses as low as 0.1 mg/kg can cause toxicity. For comparison, one cigarette has about 20-30 mg of nicotine, and historically, ingestion of one cigarette has caused clinical toxicity in a child. The volumes available for sale may be as large as 1 liter, compounding on the potential for significant morbidity.

The product packaging also yields potential problems. E-cigarettes are not subject to regulation by the FDA; therefore, there is no requirement for childproof packaging. Colorful packaging and attractive flavorings both make these solutions target for children. There is no current requirement to do any labeling regarding the dangers of these liquid solutions. Many people are not aware of the potential risk of toxicity if the liquid nicotine is ingested or absorbed through the skin, especially small children who can be exposed to these products at home. Many of these containers are left accessible and unattended, where small children can easily obtain them.

Another serious concern is the intentional use and abuse of e-cigs by older children and teenagers.  The CDC reports that the percentage of U.S middle and high school students who use e-cigs more than doubled from 2011 to 2012.  The percentage of high school students who reported ever using an e-cigarette rose from 4.7% in 2011 to 10% in 2012. Recently, a bill that prohibits advertisement, promotion, or marketing of electronic cigarettes to children under the age of 18 was approved.23 Although the sales of cigarettes have stayed relatively flat in the past years, the sales of e-cigarettes are growing.22

Little is known about the impact of exposure on overall public health. Poison Center calls have experienced a surge in the past year, averaging 200 calls per day in early 2014.21 Most of the exposures reported to US Poison Centers are unintentional, and about ½ of them are in the 0-5 years age group.21

Although no deaths have been reported after accidental exposures to liquid nicotine, the potential for significant morbidity and mortality exists.

So what happened to our patient?

The patient’s clothes had a strong odor of vanilla (the flavoring on the liquid nicotine), so they were removed and the skin was washed. He was admitted to the pediatrics service, where he remained sleepy for the next 4 hours. He did not have any other significant clinical findings of nicotine poisoning. There was no recurrence of the seizure. The parents were educated on the dangers of highly concentrated liquid nicotine solutions. The patient was discharged home 12 hours after the exposure.

References / Further Reading

  1. Bertholon J.F., Becquemin M.H., Annesi-Maesano I., & Dautzenberg B. (2013). Electronic Cigarettes: A Short Review. Respiration, 86, 433-438. doi: 10.1159/000353253
  2. Cantrell L. E. (2013). Cigarette exposures – nothing to get choked up about. Clinical Toxicology, 51, 684-685.
  3. Carmines EL, Gaworski CL. (2005). Toxicological evaluation of glycerin as a cigarette ingredient. Food Chem Toxicol 43(10):1521-39.
  4. Deyton L.R. (2013). Regulation of E-Cigarettes and Other Tobacco Products. FDA U.S. Food and Drug Administration.
  5. Etter J. F., & Bullen C. (2011). Electronic cigarette: users profile, utilization, satisfaction and perceived efficacy. Addiction, 106, 2017-2028. doi:10.1111/j.1360-0443.2011.03505.x
  6. Etter J.F., & Bullen C. (2013). A longitudinal study of electronic cigarette users. Addictive Behaviors, 39, 491-494.
  7. Goniewicz M.L., Knysak J., Gawron M., Knysak J., & Kosmider L. (2013). Levels of selected carcinogens and toxicants in vapour from electronic cigarettes. Tobacco Control, doi: 10.1136/tobaccocontrol-2012-050859:1–7
  8. Goniewicz M.L., Kuma T., Gawron M., Knysak J. & Kosmider L. (2013). Nicotine Levels in Electronic Cigarettes. Nicotine & Tobacco Research, 15, 158-166. doi:10.1093/ntr/nts103
  9. Gaworski C, Oldhama MJ, Cogginsb C. (2010). Toxicological considerations on the use of propylene glycol as a humectant in cigarettes. Toxicology 269, 54–66
  10. Jun Ho Cho J.H., Shin E., & Sang-Sik Moon (2011). Electronic-Cigarette Smoking Experience Among Adolescents. Journal of Adolescent Health, 49, 542–546. doi:10.1016/j.jadohealth.2011.08.001
  11. Lavoie F.W., & Harris .TM. (1991). Fatal nicotine ingestion. The Journal of Emergency Medicine, 9, 133-136.
  12. Mayer B. (2014). How much nicotine kills a human? Tracing back the generally accepted lethal dose to dubious self-experiments in the nineteenth century. Archives of Toxicology, 88, 5–7. doi: 10.1007/s00204-013-1127-0
  13. Metz C.N., Gregersen P.K., & Malhotra A.K. (2004). Metabolism and biochemical effects of nicotine for primary care providers. The Medical Clinics of North America, 88, 1399–1413. doi:10.1016/j.mcna.2004.06.004
  14. Pepper J.K., & Brewer N.T. (2013). Electronic nicotine delivery system (electronic cigarette) awareness, use, reactions and beliefs: a systematic review. Tobacco Control, 1-10. doi:10.1136/051122
  15. Solarino B., Rosenbaum F., Rießelmann B., Buschmann C.T. & Tsokos M. (2010). Death due to ingestion of nicotine-containing solution: case report and review of the literature. Forensic Science International, 195, 19-22. doi:10.1016/j.forsciint.2009.11.00
  16. Sutfin E.L., McCoyb T.P., Morrell H.E., Hoeppner B.B. & Wolfson M. (2013). Electronic cigarette use by college students. Drug and Alcohol Dependence, 131, 214–221.
  17. Thornton S., Oller L., & Sawyer T. (2013). Fatal intravenous injection of electronic cigarette “eLiquid” solution. Clinical Toxicology, 51, 683.
  18. Retrieved from www.myfreedomsmokes.com
  19. Valento M. (2013). Nicotine poisoning following ingestion of e-Liquid. Clinical Toxicology, 51,683-684.
  20. Bullen C, Howe C, Laugesen M, et al (2013). Electronic cigarettes for smoking cessation: a randomized controlled trial. Lancet, 382, 1629–37
  21. Chatham-Stephens K, MD1, Law R, Taylor E, et al (2014). Notes from the Field: Calls to Poison Centers for Exposures to Electronic Cigarettes — United States, September 2010–February 2014 Weekly. 63(13); 292-293. (Accessed on 05/06/2014)
  22. Herzog B,  Gerberi J, (2013). Equity Research. E-Cigs Revolutionizing The Tobacco Industry. Wells Fargo securities.(Accessed on 05/08/2014)
  23. Library of Congress. S.2047 – 113th Congress (2013-2014): Protecting Children from Electronic Cigarette Advertising Act of 2014. (Accessed on 05/13/2014)
Edited by Alex Koyfman

Synthetic Cannabinoids

Introduction

History

  • Synthetic cannabinoids were first designed after the structure of the primary psychoactive compound in marijuana, 9-tetrahydrocannabinol (9-THC), was figured out in the 1960s.
  • Synthetic cannabinoids have been used as a tool to study endocannabinoid biochemistry and also to design cannabinoid derivatives for medicinal use, for example in appetite stimulants and pain medications.
  • In the late 1990s, The John W. Huffman research group at Clemson University began to synthesize over 450 cannabinoids. JWH-018 was one such synthetic cannabinoid that his group created for research purposes but in 2004 it first appeared in Europe in recreational smoke blends under the marketed name “Spice” or “K2.”

k2

Synthetic Cannabinoid Types

  • There are many types of synthetic cannabinoids. More and more continue to be created to either produce a “better high” or evade detection in drug screens. Each has their own distinct binding affinity to the cannabinoid receptor subtypes (CB1 and CB2).
  • For example, HU210 is reported to bind to the CB1 and CB2 receptors with 100 times the affinity of 9-THC.
  • Blends of K2 contain JWH-018 (a full agonist at the CB1 and CB2 receptor), JWH-073 (somewhat selective for CB1), and JWH-250 (CB1 and CB2 agonist).
  • First generation synthetic cannabinoids are believed to be more benign than the newer generation cannabinoids, which are more likely to cause cardiotoxicity and neurotoxicity. One such newer generation synthetic cannabinoid is ADB-PINACA (N-[1-amino-3,3-dimethy-1-oxobutan-2-yl]-1-pentyl-1H-indazole-3-carboxamide), the compound identified in the recent Colorado outbreak known locally as Black Mamba.

aminoalkylindoles

Street Names

  • K2, Spice, Black Mamba, Blaze, Bliss, Bombay Blue, Fake Weed, Genie, Moon Rocks, Mr. Nice Guy, Skunk, Yucatan Fire and Zohai.

Legal Status

  • In July 2012, the Synthetic Drug Abuse Prevention Act of 2012 was signed into law, which banned 26 substances commonly found in synthetic marijuana, placing them under Schedule I of the Controlled Substances Act.
  • Despite legislation banning its use, synthetic cannabinoid use is becoming increasingly popular and is still readily available. Synthetic cannabinoids have been found in smoke shops, gas stations, and can be found for sale on the internet. They can be found in legal retail stores and packaged as incense or potpourri and may be labeled “not for human consumption.”

Growing Popularity and Media Attention

  • In 2010, the DEA reported that 30–35% of specimens submitted by juvenile probation departments tested positive for synthetic cannabinoids.
  • According to the 2011 National Institutes of Drug Abuse (NIDA)-sponsored Monitoring the Future survey, 11% of high school seniors reported smoking synthetic marijuana, making it one of the most commonly abused drugs in this population — second only to marijuana.
  • 4.5% of urine specimens collected from 5,956 U.S. athletes tested positive for synthetic cannabinoids, the highest of all drug classes detected.
  • A recent NEJM letter to the editor described an outbreak in Colorado where a total of 263 cases of possible synthetic cannabinoid exposure were identified during August 21-September 19 2013, however only 15 of these cases were reported to the state poison control center. Of the 263 cases, 76 sought medical attention in emergency departments and 7 were admitted to intensive care units. Colorado health officials identified a novel synthetic cannabinoid, ADB-PINACA, which was associated with neurotoxicity and cardiotoxicity.

Clinical Highlights

Route of Ingestion

  • Synthetic cannabinoids can be smoked, insufflated, or orally ingested.

Symptoms

  • The psychoactive effects are similar to 9-THC and include altered time perception, anxiety, changes in mood, confusion, hallucinations, and psychomotor agitation. There have been case reports of induced psychoses, unmasking of underlying psychiatric disease, and suicidal attempts especially in individuals with a personal or family history of psychiatric conditions. Additional undesirable effects include dry mouth, nausea, vomiting, tachycardia, palpitations.
  • Life-threatening neurotoxic effects, like seizures or ischemic stroke, and cardiotoxic effects, like arrhythmia or acute coronary syndrome / myocardial infarction, rarely occur with synthetic cannabinoid intoxication and likely occur more often with the newer synthetic cannabinoids presumably due increased potency to the cannabinoid receptors.

Treatment

  • Similar to marijuana intoxication, patients typically do not need measures other than symptomatic or supportive treatment. No antidote exists for synthetic cannabinoid poisoning. Seizure control and agitation can be treated with benzodiazepines. Gastrointestinal decontamination typically has no role in patients using synthetic cannabinoids, but it may be considered in large-quantity ingestions.
  • For severe intoxication, especially with the newer generation synthetic cannabinoids, intensive care monitoring and management for seizures, ischemic stroke, and possible cardiotoxicity may be required. Death due to neurotoxicity or cardiotoxicity as well as suicidality has been reported with synthetic cannabinoid use.

Detection

  • Synthetic cannabinoids do not show up in the standard urine drug screens available in most hospitals, which test for Tetrahydrocannabinol. The best methods for detecting synthetic cannabinoids are liquid chromatography / tandem mass spectrometry (LC-MS/MS) and gas chromatography / mass spectrometry (GC/MS) and are only available in select laboratories.
  • The inability to detect synthetic cannabinoids using standard urine drug screens adds to its growing popularity.

Bottom Line

  • Suspect synthetic cannabinoids in your patients who present with marijuana-like symptoms but screen negative for cannabis using standard urine drug screens. Most patients require symptomatic support as you would normally do for your patient presenting with marijuana intoxication.
  • However, there have been a growing number of cases associated with life-threatening neurotoxic effects (seizures, strokes) and cardiotoxic effects (arrhythmia, acute coronary syndrome / myocardial infarction), presumably due to increased potency to the cannabinoid receptors in the newer synthetic cannabinoids.

Further Reading

Edited by Alex Koyfman, MD

Alternative “Legal” Highs: Kratom, Salvia Divinorum, Methoxetamine

General Info / Intro

Kratom
  • Mitragyna speciosa Korth; leafy tree indigenous to SE Asia / Thailand
  • Alternative medicine for diarrhea, cough, opioid addiction, HTN, MSK pain, fatigue
  • Distributed in smart-shops and on Internet; growing interest in Western countries
Salvia
  • Hallucinogenic herb (Diviner’s Sage, La Pastora, Yerba Maria); small region of Mexico
  • Used for spiritual healing and divination
  • Alternative to LSD and marijuana; distributed as above
Methoxetamine
  • “Legal and bladder-friendly ketamine” (MXE, Mexxy, m-ket, Special M)
  • First detected in UK in 2010 and banned in 2012

Clinical Highlights

Kratom
  • Ingested or inhaled usually
  • Active ingredients = mitragynine, 7-hydroxymitragynine
  • Stimulant (dopamine, serotonin) / opioid-like effects (mu / kappa receptors) => used for chronic pain management and opioid withdrawal
  • Supportive Tx
Salvia
  • Smoked or chewed usually
  • Active ingredient: salvinorin A
  • Binds kappa opioid receptor
  • Tachycardia (CV), euphoria / AMS / hallucinations / memory impairment (Neuro), n/v (GI)
  • Supportive Tx
Methoxetamine
  • Oral or intranasal usually; slower onset and longer duration than ketamine
  • Dissociative anesthetic / NMDA antagonist / dopamine agonist
  • Tachy / htn / agitation / hyperthermia (sympathomimetic), hallucinations / derealization / depersonalization (dissociative), truncal ataxia / dysarthria (cerebellar), mood disturbance / suicide attempt (behavioral health issues)
  • Supportive Tx

Bottom Line

Think about the aforementioned substances in a patient with either an opioid, sympathomimetic, or hallucinogenic toxidrome.

kratom
Kratom

 

Salvia
Salvia Divinorum

 

Methoxetamine
Methoxetamine

Images from Journal of Forensic Sciences, January 2013

Further Reading

Discussion Questions/Future Exploration

  • “Legal highs” come and go; which will stay / what are the most dangerous to our pts
  • How does the market adapt to state / federal bans

Bath Salts

Introduction

Classification: Cathinone

Background

  • Sharp increase in reported exposures in 2011.
  • Considered “legal highs” available in small packages and billed as “not for consumption” to avoid regulation.
  • Added to Schedule I agents list by DEA in October 2011.
  • More common cathinones officially banned by President Obama in July 2012, along with other designer chemicals.
  • Serious medical effects or death observed in approximately 16% of cases.

Chemical Classification

  • Amphetamine analogs
  • Naturally occurring beta-ketone amphetamine found in leaves of Catha edulis plant, or khat

Chemical Names

butylone, dimethylcathinone, ethcathinone, ethylone, fluoromethcathinone, mephedrone, methedrone, methylone, pyrovalerone, methylenedioxypyrovalerone (MDPV)

Street Names

  • Categories of items sold: Bath salts, plant food, jewelry cleaner, phone screen cleaner, ladybug attractant.
  • Product names: Ivory Wave, Blizzard, Vanilla Sky, Bloom, Scarface, White Lightning/Rush, Bliss, Cloud 9, Red Dove, Zoom, Night Lights.

Pharmacology and Physiologic Effects

  • Studies limited regarding mechanism, but thought to be similar to other amphetamines.
  • Alpha, beta adrenergic stimulation – HTN, hyperacuity, tachycardia, mydriasis, diaphoresis
  • Dopamine, serotonin, norepinephrine release and reuptake inhibition – psychotic, hallucinogenic properties
  • Lipophilic – easily crosses blood-brain barrier
  • Effects peak approximately 1 hour after ingestion
  • Half-life varies 3-24 hours

Methods of Ingestion

  • Ingestion of pill/tablet/capsule
  • Insufflation
  • “Bombing” – powder wrapped in cigarette paper and swallowed
  • “Keying” – dipping key into powder and insufflating, 5-8 keys per gram
  • Less commonly, rectal, gingival, inhalation, IM, IV
  • Khat leaves are often chewed in Africa

Clinical Features

  • What is it like to get high with bath salts?
    • Similar to cocaine, but prolonged effect and more satisfying
    • Approximately 20% have adverse reaction
    • >80% will have co-ingestion or co-abuse with other recreational drugs, so DO NOT ASSUME PATIENT IS ONLY TAKING BATH SALTS
  • Most common symptom of overdose is agitation, can range from mild aggression to psychosis
  • Vitals – hypertension, hyperthermia, and tachycardia
  • Cardio – not directly proarrhythmic, often causes chest pain
  • CNS – agitation, hallucinations, paranoia, self-inflicted injuries, violence against others, seizures
  • Musculoskeletal – similar to other methamphetamines – myoclonus, tremors – risk of rhabdomyolysis
  • Renal, electrolyte – case reports of ATN, hyponatremia (thought to be similar to ecstasy)
  • Heme – Case reports of death due to DIC in those ingesting bath salts

Differential Diagnosis

  • CO-INGESTION, as noted above. Be on the lookout for signs of other intoxication.
  • Other causes of sympathomimetic intoxication, in particular
    • Cocaine, amphetamines, pseudoephedrine, phenlpropanolamine, theophylline, caffeine
    • Bath salts are unique in class of sympathomimetics in that the DURATION IS LONGER and is associated with PSYCHOSIS that can last for days to weeks.
  • Hallucinogen intoxication
    • Hallucinogens do not typically cause hypertension and tachycardia like cathinones and amphetamines.
  • Anticholinergic intoxication
    • Similar features to cathinone intoxication include agitation, tachycardia, and HTN.
    • Anticholinergics tend not to have diaphoresis.
  • Cessation/withdrawal from other drugs of abuse can be similar to cathinone intoxication.
  • Medical problems: thyroid, pheochromocytoma, heat stroke, psychiatric conditions

Diagnosis

  • No testing available to specifically diagnose intoxication with bath salts. Cathinone intoxication is a CLINICAL DIAGNOSIS.
  • Workup is similar to other tox workup
  • Labs: Accucheck, APAP, ASA, CMP (metabolized by liver, also evaluate hyponatremia)
    • Consider CK if there is concern for rhabdo
    • Consider coags to assess for DIC
  • EKG

Management

  • Focused on controlling agitation and keeping staff and patient safe.
  • Management is very similar to other sympathomimetics.
  • Consider avoiding ketamine for RSI due to dissociative effects.
  • Only consider gastric decontamination if recent ingestion of large amount of drug, such as a body-stuffer.
  • Controlling agitation
    • Large doses of benzos may be needed.
    • Haloperidol and antipsychotics may lower seizure threshold and prolong QT, therefore are not recommended.
    • As with other sympathomimetic intoxications, beta blockers are not recommended due to risk of unopposed alpha stimulation.
      • Nitroprusside and phentolamine are appropriate for addressing HTN.
  • Be aggressive with control of hyperthermia, sedate and paralyze if necessary.
  • Dispo – admission for persistent psychosis, electrolyte abnormalities, or rhabdo
  • Withdrawal – self-reported in 0.7-22% of users
  • Older individuals tend to be at higher risk for medical complications.

Recap Basics, Pearls

  • Cathinone intoxication = sympathomimetic intoxication + psychomotor agitation + hallucinations.
  • Be aware that patients are likely abusing multiple recreational drugs when cathinones are involved.
  • Diagnosis is clinical. No test is available currently. Workup is standard tox workup.
  • Treatment is geared towards control of agitation and management of medical complications such as HTN, rhabdomyolysis, and hyponatremia.

What’s New

  • Three key cathinones have been outlawed, however, new formulations can be found that avoid regulation.
  • More investigation needed regarding designer drugs such as cathinones and synthetic marijuanas.

Further Reading

Discussion Questions/Future Exploration

  • Are designer cathinones not on Schedule I list still available for purchase?
  • Has cathinone use remained popular, given extensive media coverage of strange cases reportedly involving bath salts?
  • How often do cathinone ingestion diagnoses get missed, given lack of specific testing and high rates of co-ingestion?
  • Do patients who tend to abuse cathinones tend to abuse other designer drugs, or tend to abuse more traditional recreational drugs?
Edited by Alex Koyfman

Krokodil (Desomorphine) Update

Background & Introduction

  • Krokodil is a mixture of several substances with the main ingredient being desomorphine – an opioid analog.
  • Media reports of krokodil use began surfacing in 2003 in Russia; the drug has been gaining popularity in the US since 2010.
  • In 2011, anecdotal reports from Russia suggest that 10 tablets of over-the-counter codeine with acetaminophen could be purchased for 120 Russian Rubles or $3.71 USD. This quantity was said to produce enough desomorphine to substitute for 500 Rubles or $15.46 USD worth of heroin.  There is no available data on price in the United States.
  • Originally synthesized with the intention to create an alternative to morphine with improved side effect profile, but it failed- and has showed an increased dependence on morphine – likely due to the quicker onset of action and shorter half-life.
  • Can be synthesized at home with codeine, iodine and red phosphorous: 5-10 codeine tablets are boiled with a diluting agent (paint thinner) and lighter fluid, hydrochloric acid, iodine and red phosphorous (scraped from striking pads of matchboxes), in this process desomorphine is generated from codeine via 2 intermediate steps.

Mechanism of action

  • The core ingredient is desomorphine (4,5-α-Epoxy-17-methymorphinan-3-ol) an opioid analog.
  • Mechanism of action: potent mu receptor agonist
  • 8-10 times higher analgesic potency compared to morphine and has a faster onset of action and shorter elimination half life
  • Effects are similar to other opioids. Positive effects often include euphoria, sedation, and analgesia. Common negative effects include constipation, nausea and vomiting, itching, urinary retention, decreased libido, and respiratory depression. Serious medical complications can include respiratory failure, allergic reactions, seizures, and physical and psychological dependency. When impure or acidic desomorphine is injected, it can cause pain, skin discoloration, and additional serious medical problems.

Dangers

  • Iodine used in the synthesis process can cause thyroid and muscle damage.
  • Phosphorus, also a contaminant, is known to damage cartilage.
  • The damaged tissue is susceptible to infection, which may lead to abscesses and thrombophlebitis; the constellation of related tissue damage has led to many media reports to refer to desomorphine as a “flesh eating” or “flesh rotting” drug.
  • Desomorphine itself does not have any innate corrosive effects, rather it is the contaminants it is mixed with that can cause damage and infection.
  • The use of a psychoactive substance with a high dependence potential accompanied by toxic byproducts leads to a mean survival time of 2 years after the first krokodil use according to reports from the media, but no scientific studies have been conducted that support this.

Bottom Line/Pearls & Pitfalls

  • Krokodil is desomorphine accompanied by various toxic agents that emerge during the self-production process.
  • The pharmacodynamics and pharmacokinetic properties of a shorter half-life and faster onset of action as well as the easy home manufacture from codeine (which is relatively cheap) make the drug highly addictive.
  • IV application of krokodil with contaminants is associated with high risk of local and systemic tissue damage regularly leading to death within the first few years of use.

Further Reading

  • Gahr M, Freudenmann RW, Hiemke C, Gunst IM, Connemann BJ, Schönfeldt-Lecuona C. “Krokodil” – Revival of an Old Drug with New Problems. Substance Use & Misuse. 2012; 47 (7): 861-863.
  • Eddy NB et al; Synthetic Substances with Morphine-like Effect: Clinical Experience: Potency, Side-Effects, Addiction Liability (Monographs on Individual Drugs: Desomorphine); Bull World Health Organization 17: 569-863 (1957)]
  • Gahr, M et al. Desomorphine goes “crocodile”. Journal of Addictive Disease, 31:4,407-412, PMID: 22468632
  • Grund JC, Latypov A, Harris M. “Breaking worse: The emergence of krokodil and excessive injuries among people who inject drugs in Eurasia.” International Journal of Drug Policy. 2013;24:265-274.
Edited by Adaira Landry