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Toxicology – Synthetic Drugs and “Research Chemicals”
Overview
Synthetic drugs emerged as a major public health concern around 2008, particularly in the United States and Europe. Many of these substances are manufactured abroad and imported in bulk as so-called “research chemicals,” often labeled “not for human consumption” to bypass regulatory scrutiny. Once distributed, they are repackaged and marketed based on their intended psychoactive effects.
How They Are Marketed
After importation, these compounds are disguised as legitimate products. Synthetic cannabinoids are sprayed onto plant material and sold as “herbal incense,” while stimulant-type drugs such as substituted cathinones are marketed as “bath salts,” “plant food,” or similar items. Their labeling and non-tablet form initially allowed them to evade regulation.
Common Categories and Examples
Synthetic Stimulants (“Bath Salts”)
These include substituted cathinones such as MDPV, mephedrone, and methylone, which produce effects similar to cocaine or amphetamines.
Synthetic Cannabinoids (“Spice,” “K2”)
These compounds act on cannabinoid receptors and include agents such as JWH-018, JWH-073, CP-47,497, HU-210, and AM-2201.
Hallucinogens
Compounds like Bromo-DragonFLY and 2C-I (“Smiles”) are potent serotonergic hallucinogens with effects similar to LSD.
Stimulant Analogs
Substances such as ethylphenidate (sometimes marketed as “glass cleaner”) resemble prescription stimulants like methylphenidate.
Sedative Analogs
Products sold as “herbal Xanax” may contain compounds like phenazepam, a long-acting benzodiazepine analog.
Opioid-Like and Mixed Products
Some substances, such as “Krypton,” combine kratom with opioid-like compounds (e.g., O-desmethyltramadol), increasing toxicity risk.
Other Street Names
Key Points
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Overview
Synthetic drugs emerged as a major public health concern around 2008, particularly in the United States and Europe. Many of these substances are manufactured abroad and imported in bulk as so-called “research chemicals,” often labeled “not for human consumption” to bypass regulatory scrutiny. Once distributed, they are repackaged and marketed based on their intended psychoactive effects.
How They Are Marketed
After importation, these compounds are disguised as legitimate products. Synthetic cannabinoids are sprayed onto plant material and sold as “herbal incense,” while stimulant-type drugs such as substituted cathinones are marketed as “bath salts,” “plant food,” or similar items. Their labeling and non-tablet form initially allowed them to evade regulation.
Common Categories and Examples
Synthetic Stimulants (“Bath Salts”)
These include substituted cathinones such as MDPV, mephedrone, and methylone, which produce effects similar to cocaine or amphetamines.
Synthetic Cannabinoids (“Spice,” “K2”)
These compounds act on cannabinoid receptors and include agents such as JWH-018, JWH-073, CP-47,497, HU-210, and AM-2201.
Hallucinogens
Compounds like Bromo-DragonFLY and 2C-I (“Smiles”) are potent serotonergic hallucinogens with effects similar to LSD.
Stimulant Analogs
Substances such as ethylphenidate (sometimes marketed as “glass cleaner”) resemble prescription stimulants like methylphenidate.
Sedative Analogs
Products sold as “herbal Xanax” may contain compounds like phenazepam, a long-acting benzodiazepine analog.
Opioid-Like and Mixed Products
Some substances, such as “Krypton,” combine kratom with opioid-like compounds (e.g., O-desmethyltramadol), increasing toxicity risk.
Other Street Names
- “Molly”: Marketed as pure MDMA but often contains synthetic cathinones
- “Meow-meow”: Another name for mephedrone
- “Plant food”: Often used to disguise stimulant cathinones
Key Points
- Synthetic drugs are chemically diverse and often unpredictable in potency and effects.
- They are frequently mislabeled, making identification and management challenging.
- Many are not detected on routine drug screening tests.
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Toxicology – Phencyclidine (PCP) Toxicity
Source
Phencyclidine (PCP) is a synthetically produced drug derived from cyclohexanone and piperidine. It is often applied to plant material such as marijuana, mint, or parsley and then smoked. It is known by various street names including “Sherm,” “Wet,” and “Fry.”
Typical Presentation
Patients may present with fluctuating levels of consciousness. A common pattern includes sudden awakening from an unresponsive state followed by extreme agitation, aggression, and attempts to escape or fight.
Clinical Features
Symptoms range from deep sedation or coma to severe agitation and psychosis. Individuals may exhibit unpredictable behavior, including violent outbursts and reduced sensitivity to pain. Physical findings often include nystagmus, hypertension, tachycardia, and seizures. Rapid shifts between sedation and agitation are characteristic.
Mechanism of Action
PCP is a lipophilic dissociative anesthetic that primarily blocks NMDA receptors in the brain. It also has mild effects on catecholamine reuptake, contributing to its stimulant and psychotropic effects.
Management
Treatment is supportive. Benzodiazepines are used to control agitation and anxiety. In cases of severe agitation or danger to others, physical or chemical restraints may be necessary.
Key Points
Source
Phencyclidine (PCP) is a synthetically produced drug derived from cyclohexanone and piperidine. It is often applied to plant material such as marijuana, mint, or parsley and then smoked. It is known by various street names including “Sherm,” “Wet,” and “Fry.”
Typical Presentation
Patients may present with fluctuating levels of consciousness. A common pattern includes sudden awakening from an unresponsive state followed by extreme agitation, aggression, and attempts to escape or fight.
Clinical Features
Symptoms range from deep sedation or coma to severe agitation and psychosis. Individuals may exhibit unpredictable behavior, including violent outbursts and reduced sensitivity to pain. Physical findings often include nystagmus, hypertension, tachycardia, and seizures. Rapid shifts between sedation and agitation are characteristic.
Mechanism of Action
PCP is a lipophilic dissociative anesthetic that primarily blocks NMDA receptors in the brain. It also has mild effects on catecholamine reuptake, contributing to its stimulant and psychotropic effects.
Management
Treatment is supportive. Benzodiazepines are used to control agitation and anxiety. In cases of severe agitation or danger to others, physical or chemical restraints may be necessary.
Key Points
- PCP intoxication often presents with alternating states of sedation and agitation.
- Patients may exhibit significant strength and decreased pain perception, making management challenging.
- A useful mnemonic for features includes “RED DANES”: rage, erythema, dilated pupils, delusions, amnesia, nystagmus, excitation, and skin dryness.
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Toxicology – Gamma-Hydroxybutyrate (GHB) Toxicity
Source
GHB is a synthetically produced compound available as a powder or dissolved liquid. Related substances such as gamma-butyrolactone (GBL) act as prodrugs and are converted into GHB in the body.
Typical Presentation
Exposure often occurs in social settings. Individuals may suddenly lose consciousness after ingestion, with rapid recovery hours later and little to no memory of events.
Clinical Features
At lower doses, GHB produces euphoria, disinhibition, and sedative effects. Higher doses can lead to central nervous system depression, amnesia, and coma. Additional findings may include bradycardia, hypotension, hypothermia, respiratory depression, seizures, and myoclonus. Coingestion with alcohol significantly increases the risk of severe toxicity and respiratory arrest. A characteristic feature is abrupt awakening after several hours due to a rebound effect.
Mechanism of Action
GHB is structurally related to GABA and readily crosses the blood–brain barrier. It acts on specific GHB receptors and, at higher concentrations, also stimulates GABA receptors. These effects increase dopamine release initially and then suppress neuronal activity, leading to sedation and coma. A rebound increase in dopamine may occur several hours after ingestion, explaining sudden recovery.
Management
Treatment is supportive, with early attention to airway protection and ventilation. There is no specific antidote. Agitated patients may require sedation, and benzodiazepines are used for seizure control.
Key Points
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Source
GHB is a synthetically produced compound available as a powder or dissolved liquid. Related substances such as gamma-butyrolactone (GBL) act as prodrugs and are converted into GHB in the body.
Typical Presentation
Exposure often occurs in social settings. Individuals may suddenly lose consciousness after ingestion, with rapid recovery hours later and little to no memory of events.
Clinical Features
At lower doses, GHB produces euphoria, disinhibition, and sedative effects. Higher doses can lead to central nervous system depression, amnesia, and coma. Additional findings may include bradycardia, hypotension, hypothermia, respiratory depression, seizures, and myoclonus. Coingestion with alcohol significantly increases the risk of severe toxicity and respiratory arrest. A characteristic feature is abrupt awakening after several hours due to a rebound effect.
Mechanism of Action
GHB is structurally related to GABA and readily crosses the blood–brain barrier. It acts on specific GHB receptors and, at higher concentrations, also stimulates GABA receptors. These effects increase dopamine release initially and then suppress neuronal activity, leading to sedation and coma. A rebound increase in dopamine may occur several hours after ingestion, explaining sudden recovery.
Management
Treatment is supportive, with early attention to airway protection and ventilation. There is no specific antidote. Agitated patients may require sedation, and benzodiazepines are used for seizure control.
Key Points
- GHB has a characteristic salty taste when mixed in beverages.
- It is available medically in some settings for treatment of narcolepsy with cataplexy.
- Certain products have historically contained GHB or its precursors, leading to accidental poisonings.
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Toxicology – Synthetic Cannabinoids (“Spice,” “K2”)
Source
Synthetic cannabinoids are laboratory-made compounds sprayed onto plant material and sold as “herbal incense” or “smoking blends.” These products are often marketed in colorful packaging and labeled “not for human consumption,” despite being used recreationally.
Typical Presentation
Users may develop symptoms shortly after smoking these substances. A common presentation includes sudden onset of anxiety, paranoia, and altered perception, sometimes progressing to severe psychological distress.
Clinical Features
While some effects resemble natural cannabis, synthetic cannabinoids are more likely to cause severe neuropsychiatric symptoms such as intense anxiety, paranoia, hallucinations, delusions, and psychosis. Other findings may include tachycardia, agitation, and confusion. Serious complications such as seizures, myocardial infarction, acute kidney injury, and self-harm have been reported.
Mechanism of Action
These compounds act on cannabinoid receptors (CB1 and CB2), similar to THC. However, their potency, receptor affinity, and concentration vary widely, leading to unpredictable and often more severe effects compared to natural cannabis.
Management
Treatment is supportive. Benzodiazepines are commonly used to manage agitation, anxiety, tachycardia, and hallucinations.
Key Points
Source
Synthetic cannabinoids are laboratory-made compounds sprayed onto plant material and sold as “herbal incense” or “smoking blends.” These products are often marketed in colorful packaging and labeled “not for human consumption,” despite being used recreationally.
Typical Presentation
Users may develop symptoms shortly after smoking these substances. A common presentation includes sudden onset of anxiety, paranoia, and altered perception, sometimes progressing to severe psychological distress.
Clinical Features
While some effects resemble natural cannabis, synthetic cannabinoids are more likely to cause severe neuropsychiatric symptoms such as intense anxiety, paranoia, hallucinations, delusions, and psychosis. Other findings may include tachycardia, agitation, and confusion. Serious complications such as seizures, myocardial infarction, acute kidney injury, and self-harm have been reported.
Mechanism of Action
These compounds act on cannabinoid receptors (CB1 and CB2), similar to THC. However, their potency, receptor affinity, and concentration vary widely, leading to unpredictable and often more severe effects compared to natural cannabis.
Management
Treatment is supportive. Benzodiazepines are commonly used to manage agitation, anxiety, tachycardia, and hallucinations.
Key Points
- Synthetic cannabinoids are typically not detected on standard drug screening tests.
- Numerous compounds exist, including JWH-018, JWH-073, CP-47,497, HU-210, and cannabicyclohexanol, contributing to variable toxicity profiles.
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Toxicology – Synthetic Cathinones (“Bath Salts”)
Source
“Bath salts” refer to synthetic stimulant drugs derived from cathinones, compounds related to substances found in the khat plant (Catha edulis), native to East Africa and the Middle East. These products are often sold in retail settings under misleading names and packaging.
Typical Presentation
Use typically occurs in social or party settings, where individuals may repeatedly take the substance. This can lead to escalating toxicity, including severe agitation and psychotic behavior, sometimes resulting in harm to self or others.
Clinical Features
These agents produce a sympathomimetic toxidrome characterized by agitation, hallucinations, paranoia, tremors, hyperreflexia, nausea, vomiting, tachycardia, hypertension, dilated pupils, and sweating. Severe complications may include violent behavior, rhabdomyolysis, acute kidney injury, myocardial infarction, and self-harm.
Mechanism of Action
Synthetic cathinones act similarly to amphetamines by increasing levels of serotonin, dopamine, and norepinephrine in the brain, leading to marked central nervous system stimulation.
Management
Treatment is supportive. Benzodiazepines are first-line therapy for agitation, anxiety, and tachycardia. In severe cases, physical or chemical restraints may be required to ensure safety.
Key Points
Source
“Bath salts” refer to synthetic stimulant drugs derived from cathinones, compounds related to substances found in the khat plant (Catha edulis), native to East Africa and the Middle East. These products are often sold in retail settings under misleading names and packaging.
Typical Presentation
Use typically occurs in social or party settings, where individuals may repeatedly take the substance. This can lead to escalating toxicity, including severe agitation and psychotic behavior, sometimes resulting in harm to self or others.
Clinical Features
These agents produce a sympathomimetic toxidrome characterized by agitation, hallucinations, paranoia, tremors, hyperreflexia, nausea, vomiting, tachycardia, hypertension, dilated pupils, and sweating. Severe complications may include violent behavior, rhabdomyolysis, acute kidney injury, myocardial infarction, and self-harm.
Mechanism of Action
Synthetic cathinones act similarly to amphetamines by increasing levels of serotonin, dopamine, and norepinephrine in the brain, leading to marked central nervous system stimulation.
Management
Treatment is supportive. Benzodiazepines are first-line therapy for agitation, anxiety, and tachycardia. In severe cases, physical or chemical restraints may be required to ensure safety.
Key Points
- These substances are often not detected on standard drug screening tests.
- Common compounds include MDPV, methylone, and mephedrone.
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Toxicology – Dextromethorphan (DXM) Toxicity
Source
Dextromethorphan is a synthetically produced compound found in many over-the-counter cough and cold medications, available in both liquid and tablet forms.
Typical Presentation
Misuse often involves ingestion of large quantities of cough syrup or tablets, particularly among adolescents. Patients may present with confusion, disorientation, or abnormal behavior following excessive intake.
Clinical Features
Effects are dose-dependent. At therapeutic levels, DXM acts as a cough suppressant. In higher doses, it can produce euphoria, agitation, hypertension, tachycardia, hyperthermia, sweating, hallucinations, and dissociative states. Severe toxicity may result in unresponsiveness and sensory detachment. When combined with serotonergic agents such as SSRIs or MAO inhibitors, serotonin syndrome may develop.
Mechanism of Action
DXM is metabolized into dextrorphan, its active metabolite. This compound acts on sigma opioid receptors to suppress cough. At higher doses, it blocks NMDA receptors and inhibits reuptake of monoamines, leading to dissociative and sympathomimetic effects. Unlike traditional opioids, it does not significantly affect μ or δ receptors, so classic opioid toxicity is not typically observed.
Management
Treatment is primarily supportive. Naloxone may provide partial benefit in some cases, although its effects are variable.
Key Points
Source
Dextromethorphan is a synthetically produced compound found in many over-the-counter cough and cold medications, available in both liquid and tablet forms.
Typical Presentation
Misuse often involves ingestion of large quantities of cough syrup or tablets, particularly among adolescents. Patients may present with confusion, disorientation, or abnormal behavior following excessive intake.
Clinical Features
Effects are dose-dependent. At therapeutic levels, DXM acts as a cough suppressant. In higher doses, it can produce euphoria, agitation, hypertension, tachycardia, hyperthermia, sweating, hallucinations, and dissociative states. Severe toxicity may result in unresponsiveness and sensory detachment. When combined with serotonergic agents such as SSRIs or MAO inhibitors, serotonin syndrome may develop.
Mechanism of Action
DXM is metabolized into dextrorphan, its active metabolite. This compound acts on sigma opioid receptors to suppress cough. At higher doses, it blocks NMDA receptors and inhibits reuptake of monoamines, leading to dissociative and sympathomimetic effects. Unlike traditional opioids, it does not significantly affect μ or δ receptors, so classic opioid toxicity is not typically observed.
Management
Treatment is primarily supportive. Naloxone may provide partial benefit in some cases, although its effects are variable.
Key Points
- Many DXM-containing products also include acetaminophen, so levels should be checked in suspected overdose.
- DXM is sometimes misused as a recreational substance and marketed as an alternative to other psychoactive drugs.
- Certain formulations (e.g., combination cold medications) are commonly abused for their DXM content.
- Chronic use may lead to bromide toxicity, particularly with tablet formulations.
- DXM can cause false-positive results for PCP on urine drug screens.
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Toxicology – Inhalant Abuse (“Huffing”)
Source
Inhalant abuse involves breathing in vapors from volatile substances such as gasoline (hydrocarbons), aerosol sprays and computer dusters (halogenated hydrocarbons), nail polish remover (ketones), lighter fluid (butane), spray paints (toluene), nitrites (“poppers”), and nitrous oxide from whipped cream canisters.
Typical Presentation
Patients are often adolescents found with evidence of inhalant use, such as chemical-soaked materials. They may present with altered consciousness or unresponsiveness after exposure.
Clinical Features
Symptoms vary depending on the substance but may include skin flushing, irritation of the eyes and airways, poor coordination, slurred speech, hallucinations, lethargy, vomiting, seizures, respiratory depression, coma, or sudden death. Examination may reveal chemical odors, cardiac arrhythmias, QT prolongation, hypoxia, metabolic acidosis, anemia, or muscle breakdown. Chronic use can lead to cardiomyopathy, nerve damage, and brain dysfunction.
Mechanism of Action
The effects of inhalants are diverse and not fully understood. Many act as central nervous system depressants, possibly through NMDA receptor inhibition or GABA enhancement. They can also displace oxygen in the lungs, leading to hypoxia. A dangerous phenomenon known as “sudden sniffing death” can occur when a surge of catecholamines triggers fatal arrhythmias in a sensitized heart.
Management
Treatment is supportive, focusing on airway protection, oxygenation, and management of complications such as arrhythmias or seizures.
Key Points
Source
Inhalant abuse involves breathing in vapors from volatile substances such as gasoline (hydrocarbons), aerosol sprays and computer dusters (halogenated hydrocarbons), nail polish remover (ketones), lighter fluid (butane), spray paints (toluene), nitrites (“poppers”), and nitrous oxide from whipped cream canisters.
Typical Presentation
Patients are often adolescents found with evidence of inhalant use, such as chemical-soaked materials. They may present with altered consciousness or unresponsiveness after exposure.
Clinical Features
Symptoms vary depending on the substance but may include skin flushing, irritation of the eyes and airways, poor coordination, slurred speech, hallucinations, lethargy, vomiting, seizures, respiratory depression, coma, or sudden death. Examination may reveal chemical odors, cardiac arrhythmias, QT prolongation, hypoxia, metabolic acidosis, anemia, or muscle breakdown. Chronic use can lead to cardiomyopathy, nerve damage, and brain dysfunction.
Mechanism of Action
The effects of inhalants are diverse and not fully understood. Many act as central nervous system depressants, possibly through NMDA receptor inhibition or GABA enhancement. They can also displace oxygen in the lungs, leading to hypoxia. A dangerous phenomenon known as “sudden sniffing death” can occur when a surge of catecholamines triggers fatal arrhythmias in a sensitized heart.
Management
Treatment is supportive, focusing on airway protection, oxygenation, and management of complications such as arrhythmias or seizures.
Key Points
- Inhalants are often among the first substances misused by adolescents due to accessibility and low cost.
- Sudden death may occur unexpectedly, particularly during stress or sudden fright.
- Methods of use include “sniffing” (direct inhalation), “huffing” (using a soaked cloth), and “bagging” (inhaling from a container or bag).
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Toxicology – Nitrous Oxide
Source
Nitrous oxide is a dissociative anesthetic available from medical gas supplies, automotive sources, and small canisters (“chargers”) used in whipped cream dispensers. It is often inhaled directly from these sources or via balloons at social events.
Typical Presentation
A college student presents with numbness and tingling in the hands and feet along with difficulty walking. On further questioning, he admits to frequent recreational use of nitrous oxide at parties, often inhaling it from balloons over several months.
Clinical Features
Acute effects include euphoria, analgesia, depersonalization, derealization, impaired coordination, reduced anxiety, and altered auditory perception. With chronic use, vitamin B12 deficiency may develop, leading to neurological symptoms such as paresthesia, ataxia, and hematologic abnormalities including megaloblastic anemia.
Mechanism of Action
Nitrous oxide acts as a weak dissociative anesthetic, likely through NMDA receptor antagonism and GABA receptor activation.
Management
Treatment involves discontinuation of exposure and supportive care. Vitamin B12 supplementation is indicated in patients with deficiency and neurological complications.
Key Points
Source
Nitrous oxide is a dissociative anesthetic available from medical gas supplies, automotive sources, and small canisters (“chargers”) used in whipped cream dispensers. It is often inhaled directly from these sources or via balloons at social events.
Typical Presentation
A college student presents with numbness and tingling in the hands and feet along with difficulty walking. On further questioning, he admits to frequent recreational use of nitrous oxide at parties, often inhaling it from balloons over several months.
Clinical Features
Acute effects include euphoria, analgesia, depersonalization, derealization, impaired coordination, reduced anxiety, and altered auditory perception. With chronic use, vitamin B12 deficiency may develop, leading to neurological symptoms such as paresthesia, ataxia, and hematologic abnormalities including megaloblastic anemia.
Mechanism of Action
Nitrous oxide acts as a weak dissociative anesthetic, likely through NMDA receptor antagonism and GABA receptor activation.
Management
Treatment involves discontinuation of exposure and supportive care. Vitamin B12 supplementation is indicated in patients with deficiency and neurological complications.
Key Points
- Recreational use often involves specialized devices (“crackers”) to release gas from small canisters.
- Nitrous oxide is widely accessible and commonly misused in social settings.
- Chronic exposure can lead to significant neurological and hematologic complications due to vitamin B12 depletion.
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Toxicology – Nitrates and Nitrites
Source
Nitrates such as nitroglycerin and isosorbide dinitrate are commonly used in the treatment of coronary artery disease due to their vasodilatory effects. Nitrites, including amyl, butyl, and isobutyl nitrite, are often misused recreationally as inhalants and may be marketed under misleading labels such as “poppers,” cleaners, or deodorizers.
Typical Presentation
Individuals may present after inhaling these substances recreationally, often experiencing rapid onset of flushing, headache, and palpitations shortly after exposure.
Clinical Features
Common findings include headache, facial flushing, tachycardia, and hypotension due to vasodilation. In some cases, especially with nitrite exposure, methemoglobinemia may develop, leading to reduced oxygen delivery, cyanosis, and symptoms of hypoxia.
Mechanism of Action
Both nitrates and nitrites act as potent vasodilators, causing relaxation of vascular smooth muscle and resulting in decreased blood pressure with compensatory increase in heart rate. They can also oxidize hemoglobin to methemoglobin, impairing oxygen transport—this effect is more pronounced with nitrites.
Management
Treatment includes removal from exposure and supportive care. Intravenous fluids may be used for hypotension. In cases of methemoglobinemia, methylene blue (1–2 mg/kg IV) is the treatment of choice.
Key Points
Source
Nitrates such as nitroglycerin and isosorbide dinitrate are commonly used in the treatment of coronary artery disease due to their vasodilatory effects. Nitrites, including amyl, butyl, and isobutyl nitrite, are often misused recreationally as inhalants and may be marketed under misleading labels such as “poppers,” cleaners, or deodorizers.
Typical Presentation
Individuals may present after inhaling these substances recreationally, often experiencing rapid onset of flushing, headache, and palpitations shortly after exposure.
Clinical Features
Common findings include headache, facial flushing, tachycardia, and hypotension due to vasodilation. In some cases, especially with nitrite exposure, methemoglobinemia may develop, leading to reduced oxygen delivery, cyanosis, and symptoms of hypoxia.
Mechanism of Action
Both nitrates and nitrites act as potent vasodilators, causing relaxation of vascular smooth muscle and resulting in decreased blood pressure with compensatory increase in heart rate. They can also oxidize hemoglobin to methemoglobin, impairing oxygen transport—this effect is more pronounced with nitrites.
Management
Treatment includes removal from exposure and supportive care. Intravenous fluids may be used for hypotension. In cases of methemoglobinemia, methylene blue (1–2 mg/kg IV) is the treatment of choice.
Key Points
- Nitrites are more likely than nitrates to cause methemoglobinemia.
- These substances are sometimes misused for their short-lived vasodilatory and sensory effects
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Toxicology – Salvia (Salvia divinorum)
Source
Salvia divinorum is a plant from the mint family native to Oaxaca, Mexico. Its leaves or concentrated extracts are commonly sold online or in specialty shops and are typically smoked to produce psychoactive effects.
Typical Presentation
Users often experience a rapid onset of intense but short-lived hallucinations after smoking. During intoxication, individuals may appear disconnected from reality, mumbling, or reacting to internal stimuli. Upon recovery, they may describe vivid, unusual experiences or feelings of entering alternate realities.
Clinical Features
Effects are brief, usually lasting only a few minutes. Common features include visual and tactile hallucinations, dissociation, inappropriate laughter, altered perception of reality, and unusual sensations such as merging with objects or changes in body form. Some individuals experience distress or fear during recovery, similar to an emergence reaction seen with dissociative anesthetics.
Mechanism of Action
The active compound, salvinorin A, is a potent and selective kappa-opioid receptor agonist. Unlike traditional opioids, it does not significantly depress respiration.
Management
Treatment is supportive. Because symptoms are short-lived, most cases resolve without medical intervention. Reassurance is usually sufficient for individuals experiencing anxiety or a “bad trip.”
Key Points
Source
Salvia divinorum is a plant from the mint family native to Oaxaca, Mexico. Its leaves or concentrated extracts are commonly sold online or in specialty shops and are typically smoked to produce psychoactive effects.
Typical Presentation
Users often experience a rapid onset of intense but short-lived hallucinations after smoking. During intoxication, individuals may appear disconnected from reality, mumbling, or reacting to internal stimuli. Upon recovery, they may describe vivid, unusual experiences or feelings of entering alternate realities.
Clinical Features
Effects are brief, usually lasting only a few minutes. Common features include visual and tactile hallucinations, dissociation, inappropriate laughter, altered perception of reality, and unusual sensations such as merging with objects or changes in body form. Some individuals experience distress or fear during recovery, similar to an emergence reaction seen with dissociative anesthetics.
Mechanism of Action
The active compound, salvinorin A, is a potent and selective kappa-opioid receptor agonist. Unlike traditional opioids, it does not significantly depress respiration.
Management
Treatment is supportive. Because symptoms are short-lived, most cases resolve without medical intervention. Reassurance is usually sufficient for individuals experiencing anxiety or a “bad trip.”
Key Points
- Effects are rapid in onset and short in duration compared to many other hallucinogens.
- The substance is often smoked using specialized equipment due to its high vaporization temperature.
- Oral ingestion is generally ineffective because the active compound is inactivated in the gastrointestinal tract.
- Many users report the experience as unpleasant and do not continue use.
