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Toxicology – Isopropyl Alcohol (Isopropanol) Toxicity
Source
Isopropyl alcohol is commonly found in products such as rubbing alcohol, disinfectants, cleaning solutions, deicers, solvents, and certain fuel additives.
Typical Presentation
Patients often present with signs of significant intoxication, sometimes mistaken for ethanol ingestion. A distinguishing clue may be a fruity or acetone-like odor on the breath.
Clinical Features
This produces a hypnosedative toxidrome, often more intense than ethanol. Symptoms include slurred speech, impaired coordination, unsteady gait, nystagmus, confusion, and disinhibition. Severe cases may progress to hypotension, hypothermia, coma, and respiratory arrest.
Gastrointestinal irritation is prominent, with abdominal pain and possible hemorrhagic gastritis or esophagitis. Laboratory findings may show:
Mechanism of Action
Isopropanol acts as a central nervous system depressant via GABA receptor activity. It is metabolized by alcohol dehydrogenase into acetone, which is less toxic and responsible for the characteristic fruity odor.
Management
Treatment is primarily supportive:
Hemodialysis may be considered in severe cases, particularly when there is persistent coma or refractory hypotension. Unlike other toxic alcohols, antidotes such as fomepizole are not used because the metabolite (acetone) is not highly toxic.
Key Points
Source
Isopropyl alcohol is commonly found in products such as rubbing alcohol, disinfectants, cleaning solutions, deicers, solvents, and certain fuel additives.
Typical Presentation
Patients often present with signs of significant intoxication, sometimes mistaken for ethanol ingestion. A distinguishing clue may be a fruity or acetone-like odor on the breath.
Clinical Features
This produces a hypnosedative toxidrome, often more intense than ethanol. Symptoms include slurred speech, impaired coordination, unsteady gait, nystagmus, confusion, and disinhibition. Severe cases may progress to hypotension, hypothermia, coma, and respiratory arrest.
Gastrointestinal irritation is prominent, with abdominal pain and possible hemorrhagic gastritis or esophagitis. Laboratory findings may show:
- Increased osmolal gap
- Presence of ketones (without significant acidosis)
- Nongap metabolic acidosis
- Falsely elevated creatinine
Mechanism of Action
Isopropanol acts as a central nervous system depressant via GABA receptor activity. It is metabolized by alcohol dehydrogenase into acetone, which is less toxic and responsible for the characteristic fruity odor.
Management
Treatment is primarily supportive:
- Airway protection and monitoring
- Intravenous fluids for hypotension
- Vasopressors if needed
Hemodialysis may be considered in severe cases, particularly when there is persistent coma or refractory hypotension. Unlike other toxic alcohols, antidotes such as fomepizole are not used because the metabolite (acetone) is not highly toxic.
Key Points
- More potent intoxicant than ethanol.
- Causes ketosis without significant anion gap acidosis.
- Fruity breath odor is due to acetone formation.
- Management is usually supportive, with dialysis reserved for severe toxicity.
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Toxicology – Ethanol (Alcohol) Intoxication
Source
Ethanol is commonly found in alcoholic beverages such as beer, wine, and spirits, but also in products like mouthwash, perfumes, cooking extracts, certain medications, and even hand sanitizers.
Typical Presentation
Patients usually present after excessive intake, ranging from mild intoxication to severe central nervous system depression. In extreme cases, individuals may be unconscious and require airway support.
Clinical Features
Ethanol produces a hypnosedative toxidrome. Common findings include slurred speech, impaired coordination, unsteady gait, nystagmus, and disinhibition. As toxicity worsens, patients may develop hypotension, low body temperature, nausea, vomiting, and memory impairment. Severe cases can progress to stupor, coma, respiratory depression, and death.
Metabolic disturbances may include hypoglycemia, lactic acidosis, ketoacidosis, electrolyte imbalances (low potassium, magnesium, calcium), and an increased osmolal gap.
Mechanism of Action
Ethanol acts as a central nervous system depressant by enhancing GABA activity. It is metabolized in the liver:
Treatment is mainly supportive:
Source
Ethanol is commonly found in alcoholic beverages such as beer, wine, and spirits, but also in products like mouthwash, perfumes, cooking extracts, certain medications, and even hand sanitizers.
Typical Presentation
Patients usually present after excessive intake, ranging from mild intoxication to severe central nervous system depression. In extreme cases, individuals may be unconscious and require airway support.
Clinical Features
Ethanol produces a hypnosedative toxidrome. Common findings include slurred speech, impaired coordination, unsteady gait, nystagmus, and disinhibition. As toxicity worsens, patients may develop hypotension, low body temperature, nausea, vomiting, and memory impairment. Severe cases can progress to stupor, coma, respiratory depression, and death.
Metabolic disturbances may include hypoglycemia, lactic acidosis, ketoacidosis, electrolyte imbalances (low potassium, magnesium, calcium), and an increased osmolal gap.
Mechanism of Action
Ethanol acts as a central nervous system depressant by enhancing GABA activity. It is metabolized in the liver:
- Alcohol dehydrogenase converts ethanol → acetaldehyde
- Aldehyde dehydrogenase converts acetaldehyde → acetate
Treatment is mainly supportive:
- Ensure airway protection and adequate breathing
- Provide IV fluids for dehydration
- Administer thiamine (vitamin B1) in chronic alcohol users, especially if mental status is altered, to prevent neurological complications
- Severe intoxication can lead to life-threatening respiratory depression.
- Children are at higher risk of dangerous hypoglycemia.
- Ethanol is primarily metabolized in the liver at a relatively constant rate.
- Non-beverage sources (e.g., mouthwash, sanitizers) can cause significant toxicity.
- Average metabolism rate is about 0.017% blood alcohol per hour.
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Toxicology – Methanol (Toxic Alcohol Exposure)
Source
Methanol is found in products such as antifreeze, windshield washer fluid, paint removers, fuels, cleaning agents, and improperly distilled alcohol (e.g., moonshine).
Typical Presentation
Patients often present hours after ingestion. Early symptoms may resemble simple intoxication, followed by a temporary symptom-free period before more severe toxicity develops—especially visual complaints.
Clinical Features
Methanol poisoning typically progresses through several stages:
Methanol itself is not highly toxic, but it is metabolized in the liver into formaldehyde and then formate. Formate is the primary toxic compound, causing mitochondrial dysfunction, metabolic acidosis, and selective damage to the optic nerve and brain.
Management
Treatment aims to block formation of toxic metabolites and remove methanol from the body:
Source
Methanol is found in products such as antifreeze, windshield washer fluid, paint removers, fuels, cleaning agents, and improperly distilled alcohol (e.g., moonshine).
Typical Presentation
Patients often present hours after ingestion. Early symptoms may resemble simple intoxication, followed by a temporary symptom-free period before more severe toxicity develops—especially visual complaints.
Clinical Features
Methanol poisoning typically progresses through several stages:
- Early (CNS) phase (30–120 minutes): Mild intoxication, poor coordination, drowsiness, slurred speech, and possible coma in severe cases.
- Latent phase (8–24 hours): Temporary improvement or absence of symptoms.
- Metabolic phase: Headache, nausea, vomiting, and development of a high anion gap metabolic acidosis with an increased osmolal gap.
- Ocular phase (12–48 hours): Visual disturbances such as blurred vision, light sensitivity, “snowfield” vision, and potential permanent blindness.
Methanol itself is not highly toxic, but it is metabolized in the liver into formaldehyde and then formate. Formate is the primary toxic compound, causing mitochondrial dysfunction, metabolic acidosis, and selective damage to the optic nerve and brain.
Management
Treatment aims to block formation of toxic metabolites and remove methanol from the body:
- Fomepizole is the preferred antidote; it inhibits alcohol dehydrogenase.
- Ethanol may be used as an alternative if fomepizole is unavailable.
- Hemodialysis is indicated in severe cases (e.g., high methanol levels, acidosis, or organ damage) to rapidly remove toxin and metabolites.
- Folic or folinic acid helps enhance metabolism of formate into non-toxic substances.
- Sodium bicarbonate is used to correct metabolic acidosis.
- Visual symptoms are a hallmark of methanol toxicity.
- Even small amounts can cause severe poisoning.
- Co-ingestion of ethanol may delay toxicity by competing for metabolism.
- Early treatment is critical to prevent permanent vision loss and death.
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Toxicology – Paralytic Shellfish Poisoning (PSP)
Source
PSP is caused by saxitoxin, a heat-stable toxin that accumulates in shellfish such as mussels, clams, oysters, and scallops. The toxin originates from dinoflagellates (marine algae), especially during algal blooms known as “red tides,” and becomes concentrated in shellfish consumed by humans
.
Typical Presentation
Symptoms usually begin quickly—within 10 to 30 minutes—after eating contaminated shellfish. Cases are often linked to harvesting shellfish during red tide events.
Clinical Features
Early signs include tingling or numbness around the mouth and in the extremities, often accompanied by a sensation of lightness or floating. As toxicity progresses, patients may develop nausea, vomiting, abdominal pain, dizziness, and poor coordination. Severe cases can lead to muscle weakness, paralysis, cranial nerve dysfunction, temporary vision loss, and respiratory failure requiring ventilatory support.
Mechanism of Action
Saxitoxin blocks voltage-gated sodium channels in nerve cells, preventing normal nerve conduction and leading to paralysis.
Management
There is no specific antidote. Treatment is supportive, with particular attention to airway protection and respiratory support if paralysis develops.
Key Points
Source
PSP is caused by saxitoxin, a heat-stable toxin that accumulates in shellfish such as mussels, clams, oysters, and scallops. The toxin originates from dinoflagellates (marine algae), especially during algal blooms known as “red tides,” and becomes concentrated in shellfish consumed by humans
.
Typical Presentation
Symptoms usually begin quickly—within 10 to 30 minutes—after eating contaminated shellfish. Cases are often linked to harvesting shellfish during red tide events.
Clinical Features
Early signs include tingling or numbness around the mouth and in the extremities, often accompanied by a sensation of lightness or floating. As toxicity progresses, patients may develop nausea, vomiting, abdominal pain, dizziness, and poor coordination. Severe cases can lead to muscle weakness, paralysis, cranial nerve dysfunction, temporary vision loss, and respiratory failure requiring ventilatory support.
Mechanism of Action
Saxitoxin blocks voltage-gated sodium channels in nerve cells, preventing normal nerve conduction and leading to paralysis.
Management
There is no specific antidote. Treatment is supportive, with particular attention to airway protection and respiratory support if paralysis develops.
Key Points
- Rapid onset of neurological symptoms after shellfish ingestion is characteristic.
- Cooking does not destroy the toxin.
- Red tide exposure can also cause symptoms through inhalation of aerosolized toxins.
- Part of a broader group of shellfish poisonings (PSP, ASP, DSP, NSP).
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Toxicology – Scombroid (Histamine Fish Poisoning)
Source
Scombroid poisoning results from eating fish that has been improperly stored, especially species from tropical or temperate waters such as tuna or mackerel. Poor refrigeration allows bacterial growth and toxin formation in the fish.
Typical Presentation
Symptoms develop rapidly—often within minutes—after consuming affected fish. Multiple individuals who shared the same meal are commonly affected, which helps distinguish it from true allergies.
Clinical Features
Patients typically experience flushing of the face and upper body, itching, and a tingling sensation around the mouth. This is followed by headache, dizziness, nausea, vomiting, diarrhea, difficulty swallowing, and palpitations. The fish may have an unusually sharp or “peppery” taste.
Mechanism of Action
Bacteria in improperly stored fish convert histidine (a natural amino acid) into histamine. This histamine is heat-stable and remains active even after cooking. Once ingested, it directly stimulates histamine receptors, producing symptoms similar to an allergic reaction.
Management
Treatment involves antihistamines. H1 blockers (such as diphenhydramine) relieve itching and flushing, while H2 blockers (such as ranitidine) can help reduce additional symptoms. Supportive care may be needed in more severe cases.
Key Points
- Caused by toxin formation, not a true seafood allergy.
- Often affects multiple people who ate the same meal.
- Cooking does not destroy the toxin.
- Usually self-limited with appropriate treatment.
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Toxicology – Tetrodotoxin (TTX) Poisoning
Source
Tetrodotoxin is found in certain marine animals, particularly pufferfish (fugu), as well as blue-ringed octopuses and some species of newts. The toxin is produced by symbiotic bacteria and accumulates in the tissues of these organisms.
Typical Presentation
Poisoning typically follows ingestion of contaminated seafood. Symptoms often begin rapidly, sometimes within minutes, and progress in a predictable neurological pattern.
Clinical Features
Early symptoms include headache, sweating, and numbness or tingling around the mouth and lips. This may progress to nausea, vomiting, muscle twitching, and weakness. As toxicity worsens, patients develop difficulty speaking and swallowing, followed by ascending paralysis. Severe cases can lead to respiratory failure and cardiovascular collapse.
Mechanism of Action
Tetrodotoxin blocks voltage-gated sodium channels, preventing nerve conduction and disrupting neuromuscular transmission. This leads to progressive paralysis without affecting consciousness in early stages.
Management
Treatment is entirely supportive, with a strong focus on airway protection and respiratory support. Mechanical ventilation may be required until the toxin is cleared.
Key Points
Source
Tetrodotoxin is found in certain marine animals, particularly pufferfish (fugu), as well as blue-ringed octopuses and some species of newts. The toxin is produced by symbiotic bacteria and accumulates in the tissues of these organisms.
Typical Presentation
Poisoning typically follows ingestion of contaminated seafood. Symptoms often begin rapidly, sometimes within minutes, and progress in a predictable neurological pattern.
Clinical Features
Early symptoms include headache, sweating, and numbness or tingling around the mouth and lips. This may progress to nausea, vomiting, muscle twitching, and weakness. As toxicity worsens, patients develop difficulty speaking and swallowing, followed by ascending paralysis. Severe cases can lead to respiratory failure and cardiovascular collapse.
Mechanism of Action
Tetrodotoxin blocks voltage-gated sodium channels, preventing nerve conduction and disrupting neuromuscular transmission. This leads to progressive paralysis without affecting consciousness in early stages.
Management
Treatment is entirely supportive, with a strong focus on airway protection and respiratory support. Mechanical ventilation may be required until the toxin is cleared.
Key Points
- Rapid onset of neurological symptoms after ingestion is characteristic.
- The toxin is heat-stable and not destroyed by cooking.
- Highest concentrations are found in organs such as the liver and ovaries of affected animals.
- Early respiratory support is critical for survival.
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Toxicology – Ciguatera (Ciguatoxin) Poisoning
Source
Ciguatera poisoning occurs after eating large reef fish from warm tropical waters, such as barracuda, grouper, or snapper. These fish accumulate toxin produced by marine microorganisms (dinoflagellates) that enter the food chain and become concentrated in larger predators.
Typical Presentation
Symptoms usually begin within a day after consuming contaminated fish. Patients initially develop gastrointestinal complaints, followed by distinctive neurological symptoms that may persist.
Clinical Features
Early symptoms include headache, sweating, dizziness, nausea, vomiting, abdominal pain, and diarrhea. Neurological manifestations are characteristic and may include tingling sensations, muscle aches, imbalance, vertigo, metallic taste, and unusual sensory disturbances such as reversal of hot and cold perception. Some patients describe a sensation of loose teeth. In certain cases, neurological symptoms can last for weeks or become chronic.
Mechanism of Action
Ciguatoxin is a heat-stable compound that accumulates through the marine food chain. It acts by keeping voltage-gated sodium channels open, leading to abnormal nerve signaling and the characteristic neurological symptoms. Cooking does not destroy the toxin.
Management
Treatment is supportive, focusing on symptom control and hydration. Some reports suggest that intravenous mannitol may help reduce neurological symptoms, although evidence is limited.
Key Points
Source
Ciguatera poisoning occurs after eating large reef fish from warm tropical waters, such as barracuda, grouper, or snapper. These fish accumulate toxin produced by marine microorganisms (dinoflagellates) that enter the food chain and become concentrated in larger predators.
Typical Presentation
Symptoms usually begin within a day after consuming contaminated fish. Patients initially develop gastrointestinal complaints, followed by distinctive neurological symptoms that may persist.
Clinical Features
Early symptoms include headache, sweating, dizziness, nausea, vomiting, abdominal pain, and diarrhea. Neurological manifestations are characteristic and may include tingling sensations, muscle aches, imbalance, vertigo, metallic taste, and unusual sensory disturbances such as reversal of hot and cold perception. Some patients describe a sensation of loose teeth. In certain cases, neurological symptoms can last for weeks or become chronic.
Mechanism of Action
Ciguatoxin is a heat-stable compound that accumulates through the marine food chain. It acts by keeping voltage-gated sodium channels open, leading to abnormal nerve signaling and the characteristic neurological symptoms. Cooking does not destroy the toxin.
Management
Treatment is supportive, focusing on symptom control and hydration. Some reports suggest that intravenous mannitol may help reduce neurological symptoms, although evidence is limited.
Key Points
- Larger reef fish carry higher toxin levels due to bioaccumulation.
- Cooking does not inactivate the toxin.
- Reversal of hot and cold sensation is a hallmark feature.
- Neurological symptoms may persist long after initial illness.
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Toxicology – Riot Control Agents (Tear Gas & Pepper Spray)
Source
Riot control agents are chemical irritants designed for law enforcement and personal defense. Common examples include pepper spray (oleoresin capsicum, derived from chili peppers), tear gases such as CS and CR, and older agents like CN (commonly known as mace). These substances are intended to be nonlethal but cause intense irritation.
Typical Presentation
Exposure usually occurs during confrontations or accidental discharge of self-defense sprays. Patients often present with acute eye and skin irritation shortly after exposure.
Clinical Features
Symptoms include intense eye pain, excessive tearing, redness, and involuntary eyelid closure, which can result in temporary visual impairment. Skin exposure causes burning and redness. Inhalation may lead to coughing, bronchospasm, and airway irritation. Symptoms typically improve within an hour, with full recovery expected within a day in most cases.
Mechanism of Action
Pepper spray works by activating pain receptors, triggering release of inflammatory mediators that cause burning and swelling. Tear gases act as chemical irritants, leading to inflammation of the eyes, skin, and respiratory tract. These effects result in vasodilation, redness, and increased secretions.
Management
Treatment involves immediate removal from the contaminated environment and thorough irrigation of exposed areas, especially the eyes and skin, with water. Supportive care is usually sufficient.
Key Points
Source
Riot control agents are chemical irritants designed for law enforcement and personal defense. Common examples include pepper spray (oleoresin capsicum, derived from chili peppers), tear gases such as CS and CR, and older agents like CN (commonly known as mace). These substances are intended to be nonlethal but cause intense irritation.
Typical Presentation
Exposure usually occurs during confrontations or accidental discharge of self-defense sprays. Patients often present with acute eye and skin irritation shortly after exposure.
Clinical Features
Symptoms include intense eye pain, excessive tearing, redness, and involuntary eyelid closure, which can result in temporary visual impairment. Skin exposure causes burning and redness. Inhalation may lead to coughing, bronchospasm, and airway irritation. Symptoms typically improve within an hour, with full recovery expected within a day in most cases.
Mechanism of Action
Pepper spray works by activating pain receptors, triggering release of inflammatory mediators that cause burning and swelling. Tear gases act as chemical irritants, leading to inflammation of the eyes, skin, and respiratory tract. These effects result in vasodilation, redness, and increased secretions.
Management
Treatment involves immediate removal from the contaminated environment and thorough irrigation of exposed areas, especially the eyes and skin, with water. Supportive care is usually sufficient.
Key Points
- Effects are rapid but generally short-lived.
- Eye exposure leads to temporary visual impairment due to intense irritation.
- Inhalation may worsen symptoms in individuals with respiratory conditions.
- Most exposures resolve completely with simple decontamination.
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Toxicology – LSD and Psilocybin (Hallucinogen Toxicity)
Source
Lysergic acid diethylamide (LSD) is a synthetic hallucinogen derived from ergot and is typically administered on blotter paper, sugar cubes, gelatin, or as liquid placed on the tongue. Psilocybin is a naturally occurring psychedelic compound found in certain mushrooms, commonly referred to as “magic mushrooms.”
Typical Presentation
Individuals often present after recreational use with altered perception. A common scenario involves a person experiencing a “bad trip” characterized by fear, anxiety, or distress following ingestion.
Clinical Features
Neuropsychiatric effects predominate, including visual and auditory hallucinations, synesthesia (blending of senses), and distorted perception of time. In adverse reactions, patients may experience intense fear, panic, depression, or psychosis. Physical findings may include dilated pupils, increased heart rate, elevated blood pressure, hyperthermia, and agitation. These substances can also worsen or reveal underlying psychiatric conditions.
Mechanism of Action
Both LSD and psilocybin act primarily on serotonin receptors, particularly the 5-HT2A subtype, producing their hallucinogenic effects. After oral ingestion, onset typically occurs within 1 to 2 hours, with effects lasting up to 12 hours depending on dose. Tolerance develops quickly but also resolves rapidly after discontinuation.
Management
Treatment is supportive. A calm environment and reassurance are essential. Benzodiazepines may be used to manage anxiety, agitation, and autonomic symptoms such as tachycardia.
Key Points
Source
Lysergic acid diethylamide (LSD) is a synthetic hallucinogen derived from ergot and is typically administered on blotter paper, sugar cubes, gelatin, or as liquid placed on the tongue. Psilocybin is a naturally occurring psychedelic compound found in certain mushrooms, commonly referred to as “magic mushrooms.”
Typical Presentation
Individuals often present after recreational use with altered perception. A common scenario involves a person experiencing a “bad trip” characterized by fear, anxiety, or distress following ingestion.
Clinical Features
Neuropsychiatric effects predominate, including visual and auditory hallucinations, synesthesia (blending of senses), and distorted perception of time. In adverse reactions, patients may experience intense fear, panic, depression, or psychosis. Physical findings may include dilated pupils, increased heart rate, elevated blood pressure, hyperthermia, and agitation. These substances can also worsen or reveal underlying psychiatric conditions.
Mechanism of Action
Both LSD and psilocybin act primarily on serotonin receptors, particularly the 5-HT2A subtype, producing their hallucinogenic effects. After oral ingestion, onset typically occurs within 1 to 2 hours, with effects lasting up to 12 hours depending on dose. Tolerance develops quickly but also resolves rapidly after discontinuation.
Management
Treatment is supportive. A calm environment and reassurance are essential. Benzodiazepines may be used to manage anxiety, agitation, and autonomic symptoms such as tachycardia.
Key Points
- The user’s mindset (“set”) and environment (“setting”) strongly influence the experience.
- Hallucinogen effects can vary widely depending on dose and individual susceptibility.
- These substances can precipitate or exacerbate psychiatric disorders in vulnerable individuals.
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Toxicology – Cocaine and Crack Toxicity
Source
Cocaine is derived from the leaves of the coca plant. It is commonly used as a powder for nasal insufflation, while crack cocaine is a solid form that is typically smoked using a pipe or glass tube.
Typical Presentation
Use often produces an immediate sense of intense euphoria, energy, and confidence. These effects are short-lived, leading to repeated dosing. As toxicity develops, individuals may experience anxiety, paranoia, palpitations, and chest pain.
Clinical Features
Cocaine toxicity presents as a classic sympathomimetic toxidrome, including tachycardia, hypertension, vasoconstriction (both peripheral and coronary), dilated pupils, sweating, hyperthermia, and agitation. Severe complications may include seizures, rhabdomyolysis, cardiac arrhythmias, and coma.
Mechanism of Action
Cocaine exerts its effects by blocking the reuptake of serotonin, dopamine, and norepinephrine, resulting in increased sympathetic activity. It also blocks sodium channels, giving it local anesthetic properties and contributing to cardiac conduction abnormalities and arrhythmias.
Management
Treatment is primarily supportive. Benzodiazepines are first-line therapy for agitation, anxiety, and chest pain. Aspirin and nitroglycerin are safe and effective in managing cocaine-associated chest pain. Beta-blockers should be avoided due to the risk of unopposed alpha-adrenergic stimulation; calcium channel blockers are a safer alternative if needed.
Key Points
Source
Cocaine is derived from the leaves of the coca plant. It is commonly used as a powder for nasal insufflation, while crack cocaine is a solid form that is typically smoked using a pipe or glass tube.
Typical Presentation
Use often produces an immediate sense of intense euphoria, energy, and confidence. These effects are short-lived, leading to repeated dosing. As toxicity develops, individuals may experience anxiety, paranoia, palpitations, and chest pain.
Clinical Features
Cocaine toxicity presents as a classic sympathomimetic toxidrome, including tachycardia, hypertension, vasoconstriction (both peripheral and coronary), dilated pupils, sweating, hyperthermia, and agitation. Severe complications may include seizures, rhabdomyolysis, cardiac arrhythmias, and coma.
Mechanism of Action
Cocaine exerts its effects by blocking the reuptake of serotonin, dopamine, and norepinephrine, resulting in increased sympathetic activity. It also blocks sodium channels, giving it local anesthetic properties and contributing to cardiac conduction abnormalities and arrhythmias.
Management
Treatment is primarily supportive. Benzodiazepines are first-line therapy for agitation, anxiety, and chest pain. Aspirin and nitroglycerin are safe and effective in managing cocaine-associated chest pain. Beta-blockers should be avoided due to the risk of unopposed alpha-adrenergic stimulation; calcium channel blockers are a safer alternative if needed.
Key Points
- Beta-blockers can worsen coronary vasoconstriction in cocaine toxicity and should be avoided.
- Cocaine is often adulterated with substances such as levamisole, which can cause serious complications including agranulocytosis and vasculitis.
- Crack cocaine is a highly addictive, smokable form known for rapid onset and intense effects.
- Some users combine cocaine with opioids (“speedballing”), increasing the risk of severe toxicity and overdose.
