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Toxicology – Crotalid Snake Envenomation
Source
Crotalid snakes (pit vipers) are the most common cause of venomous snakebites in the United States. These include rattlesnakes, copperheads, and cottonmouths (water moccasins). They are characterized by heat-sensing pits located near their eyes.
Typical Presentation
A patient presents after a snakebite, often involving provocation of the animal. Two puncture wounds (“fang marks”) are typically visible, followed by rapid onset of pain and swelling at the affected site.
Clinical Features
Initial symptoms include severe burning pain at the bite site, followed by redness, warmth, swelling, bruising, and blister formation. Edema may spread along the affected limb and can lead to compartment syndrome. Systemic manifestations may include nausea, vomiting, altered taste, tingling sensations, hypotension, coagulopathy (including disseminated intravascular coagulation), and cardiovascular collapse in severe cases.
Severity Classification
Mechanism of Action
Crotalid venom contains a mixture of cytotoxic, hemotoxic, and neurotoxic components that damage tissue, disrupt coagulation pathways, and may affect neuromuscular function.
Management
Initial evaluation includes laboratory studies such as complete blood count, coagulation profile (PT/PTT), fibrin levels, D-dimer, and creatine phosphokinase (CPK). Serial assessment of limb swelling is essential. Some bites may be “dry” (no venom injected) and require only supportive care.
For progressive local swelling or systemic toxicity, antivenom (CroFab) is indicated, typically starting with 4–6 vials. Patients require close monitoring, as repeat dosing may be necessary depending on clinical response.
Key Points
Source
Crotalid snakes (pit vipers) are the most common cause of venomous snakebites in the United States. These include rattlesnakes, copperheads, and cottonmouths (water moccasins). They are characterized by heat-sensing pits located near their eyes.
Typical Presentation
A patient presents after a snakebite, often involving provocation of the animal. Two puncture wounds (“fang marks”) are typically visible, followed by rapid onset of pain and swelling at the affected site.
Clinical Features
Initial symptoms include severe burning pain at the bite site, followed by redness, warmth, swelling, bruising, and blister formation. Edema may spread along the affected limb and can lead to compartment syndrome. Systemic manifestations may include nausea, vomiting, altered taste, tingling sensations, hypotension, coagulopathy (including disseminated intravascular coagulation), and cardiovascular collapse in severe cases.
Severity Classification
- Mild envenomation: Local pain and swelling without coagulation abnormalities
- Moderate envenomation: Local effects with evidence of coagulation disturbances
- Severe envenomation: Systemic toxicity such as shock, pulmonary edema, coagulopathy, and cardiovascular instability
Mechanism of Action
Crotalid venom contains a mixture of cytotoxic, hemotoxic, and neurotoxic components that damage tissue, disrupt coagulation pathways, and may affect neuromuscular function.
Management
Initial evaluation includes laboratory studies such as complete blood count, coagulation profile (PT/PTT), fibrin levels, D-dimer, and creatine phosphokinase (CPK). Serial assessment of limb swelling is essential. Some bites may be “dry” (no venom injected) and require only supportive care.
For progressive local swelling or systemic toxicity, antivenom (CroFab) is indicated, typically starting with 4–6 vials. Patients require close monitoring, as repeat dosing may be necessary depending on clinical response.
Key Points
- Not all snakebites result in envenomation; some are dry bites.
- Antivenom is the mainstay of treatment for significant envenomation.
- Surgical intervention such as fasciotomy is rarely required.
- Envenomation can evolve over time, so close observation is essential.
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Toxicology – Drug “Stuffers” and “Packers”
Overview
“Stuffers” and “packers” refer to individuals who conceal illicit drugs within their bodies, typically to evade law enforcement. These two groups differ significantly in the quantity of drugs involved, the method of concealment, and the associated risks.
Stuffers
Definition
Stuffers are individuals who rapidly swallow small amounts of drugs—commonly cocaine, crack, or heroin—when attempting to avoid detection. The packaging is often poorly secured, increasing the risk of leakage and absorption.
Detection
Diagnosis may rely on witness reports, patient disclosure, or clinical suspicion. Imaging studies such as plain abdominal X-rays may be used but are often unreliable in detecting small or poorly wrapped packets.
Toxicity
Symptoms can occur unpredictably depending on the substance and whether a packet ruptures. Sympathomimetic features (e.g., tachycardia, hypertension, agitation) are common with stimulant drugs, while other substances produce their respective toxidromes.
Management
Treatment often includes activated charcoal, particularly for substances like cocaine that bind well to it. Whole bowel irrigation (WBI) with polyethylene glycol solution may be considered depending on the situation.
Packers (“Body Packers”)
Definition
Packers, often referred to as “drug mules,” intentionally ingest large quantities of drugs—typically well-packaged—for transport across borders. The total amount can be substantial, often reaching hundreds of grams or more.
Detection
Imaging is more reliable in these cases. Plain abdominal X-rays may reveal multiple uniform radiopaque packets. If inconclusive, computed tomography (CT) with contrast is more sensitive.
Toxicity
If a packet ruptures, massive drug release can occur, often resulting in severe toxicity and a high risk of death, particularly with stimulants like cocaine.
Management
Patients with signs of obstruction or suspected packet rupture require urgent surgical evaluation. In stable, asymptomatic individuals, whole bowel irrigation is commonly used to facilitate passage of packets. Adjunctive medications such as antiemetics or prokinetics may be used. Activated charcoal may be considered selectively.
Key Points
Overview
“Stuffers” and “packers” refer to individuals who conceal illicit drugs within their bodies, typically to evade law enforcement. These two groups differ significantly in the quantity of drugs involved, the method of concealment, and the associated risks.
Stuffers
Definition
Stuffers are individuals who rapidly swallow small amounts of drugs—commonly cocaine, crack, or heroin—when attempting to avoid detection. The packaging is often poorly secured, increasing the risk of leakage and absorption.
Detection
Diagnosis may rely on witness reports, patient disclosure, or clinical suspicion. Imaging studies such as plain abdominal X-rays may be used but are often unreliable in detecting small or poorly wrapped packets.
Toxicity
Symptoms can occur unpredictably depending on the substance and whether a packet ruptures. Sympathomimetic features (e.g., tachycardia, hypertension, agitation) are common with stimulant drugs, while other substances produce their respective toxidromes.
Management
Treatment often includes activated charcoal, particularly for substances like cocaine that bind well to it. Whole bowel irrigation (WBI) with polyethylene glycol solution may be considered depending on the situation.
Packers (“Body Packers”)
Definition
Packers, often referred to as “drug mules,” intentionally ingest large quantities of drugs—typically well-packaged—for transport across borders. The total amount can be substantial, often reaching hundreds of grams or more.
Detection
Imaging is more reliable in these cases. Plain abdominal X-rays may reveal multiple uniform radiopaque packets. If inconclusive, computed tomography (CT) with contrast is more sensitive.
Toxicity
If a packet ruptures, massive drug release can occur, often resulting in severe toxicity and a high risk of death, particularly with stimulants like cocaine.
Management
Patients with signs of obstruction or suspected packet rupture require urgent surgical evaluation. In stable, asymptomatic individuals, whole bowel irrigation is commonly used to facilitate passage of packets. Adjunctive medications such as antiemetics or prokinetics may be used. Activated charcoal may be considered selectively.
Key Points
- Stuffers involve smaller amounts with higher risk of leakage due to poor packaging.
- Packers carry larger quantities with potentially fatal consequences if rupture occurs.
- Imaging plays a crucial role in diagnosis, especially in packers.
- Management ranges from supportive care to urgent surgical intervention depending on clinical status.
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Toxicology – Methylenedioxymethamphetamine (MDMA, “Ecstasy”)
Source
MDMA is a synthetic recreational drug commonly sold as colorful tablets or capsules, often branded with logos. Due to its illicit production, purity is highly variable, and tablets are frequently mixed with other substances such as amphetamines, dextromethorphan, synthetic cathinones, or opioids. It is also known as ecstasy, E, X, or XTC.
Typical Presentation
Users often present after recreational use in party or club settings, describing heightened sensory experiences and emotional changes. Physical findings may include increased heart rate, elevated blood pressure, and mild sweating.
Clinical Features
Effects typically begin within 30–45 minutes and last several hours. Stimulant effects include tachycardia, hypertension, increased energy, rapid breathing, and dilated pupils. Psychologically, users may experience enhanced empathy, emotional openness, and altered perception. Adverse effects include agitation, hyperthermia, hyponatremia, and risk of serotonin syndrome. After the drug wears off, users often report fatigue and low mood. Chronic use has been associated with depressive symptoms.
Mechanism of Action
MDMA increases the release of serotonin, norepinephrine, and dopamine from presynaptic neurons, leading to both stimulant and empathogenic effects.
Management
Treatment is supportive. Benzodiazepines are used to control agitation, anxiety, and autonomic symptoms such as tachycardia. Careful monitoring for complications such as hyperthermia and electrolyte disturbances is important.
Key Points
Source
MDMA is a synthetic recreational drug commonly sold as colorful tablets or capsules, often branded with logos. Due to its illicit production, purity is highly variable, and tablets are frequently mixed with other substances such as amphetamines, dextromethorphan, synthetic cathinones, or opioids. It is also known as ecstasy, E, X, or XTC.
Typical Presentation
Users often present after recreational use in party or club settings, describing heightened sensory experiences and emotional changes. Physical findings may include increased heart rate, elevated blood pressure, and mild sweating.
Clinical Features
Effects typically begin within 30–45 minutes and last several hours. Stimulant effects include tachycardia, hypertension, increased energy, rapid breathing, and dilated pupils. Psychologically, users may experience enhanced empathy, emotional openness, and altered perception. Adverse effects include agitation, hyperthermia, hyponatremia, and risk of serotonin syndrome. After the drug wears off, users often report fatigue and low mood. Chronic use has been associated with depressive symptoms.
Mechanism of Action
MDMA increases the release of serotonin, norepinephrine, and dopamine from presynaptic neurons, leading to both stimulant and empathogenic effects.
Management
Treatment is supportive. Benzodiazepines are used to control agitation, anxiety, and autonomic symptoms such as tachycardia. Careful monitoring for complications such as hyperthermia and electrolyte disturbances is important.
Key Points
- Effects are unpredictable due to frequent adulteration.
- Hyponatremia and hyperthermia are important complications to monitor.
- Combining MDMA with other psychoactive substances increases risk of toxicity.
- Products marketed as “Molly” may not contain pure MDMA and can include other synthetic compounds.
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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 – 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 – 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.
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Toxicology – Kratom Toxicity
Source
Kratom is derived from the leaves of the Mitragyna speciosa tree native to Southeast Asia. It is commonly sold as a powdered product in shops and online, often used in teas or capsules.
Typical Presentation
Use may produce stimulant-like effects at lower doses and opioid-like effects at higher doses. Users may report increased energy initially, followed by more sedative effects with larger amounts.
Clinical Features
At low doses, kratom can cause mild stimulation and euphoria. At higher doses, effects resemble opioids and include pinpoint pupils (miosis), nausea, vomiting, decreased appetite, headache, and mild respiratory depression. Chronic use may lead to dependence, and withdrawal symptoms can occur after cessation.
Mechanism of Action
Kratom contains active alkaloids, primarily mitragynine and 7-hydroxymitragynine, which act on opioid receptors. Mitragynine also has some activity at alpha-adrenergic receptors, contributing to stimulant effects at lower doses. Compared to traditional opioids, its respiratory depressant effects are generally less pronounced.
Management
Treatment is supportive. In cases of significant opioid-like toxicity, naloxone may be considered, although its effectiveness may vary.
Key Points
Source
Kratom is derived from the leaves of the Mitragyna speciosa tree native to Southeast Asia. It is commonly sold as a powdered product in shops and online, often used in teas or capsules.
Typical Presentation
Use may produce stimulant-like effects at lower doses and opioid-like effects at higher doses. Users may report increased energy initially, followed by more sedative effects with larger amounts.
Clinical Features
At low doses, kratom can cause mild stimulation and euphoria. At higher doses, effects resemble opioids and include pinpoint pupils (miosis), nausea, vomiting, decreased appetite, headache, and mild respiratory depression. Chronic use may lead to dependence, and withdrawal symptoms can occur after cessation.
Mechanism of Action
Kratom contains active alkaloids, primarily mitragynine and 7-hydroxymitragynine, which act on opioid receptors. Mitragynine also has some activity at alpha-adrenergic receptors, contributing to stimulant effects at lower doses. Compared to traditional opioids, its respiratory depressant effects are generally less pronounced.
Management
Treatment is supportive. In cases of significant opioid-like toxicity, naloxone may be considered, although its effectiveness may vary.
Key Points
- Kratom has both stimulant and opioid-like properties depending on dose.
- It is sometimes used by individuals attempting to reduce opioid dependence.
- Severe toxicity and fatalities are uncommon and often involve coingestants or adulterants.
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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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