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Toxicology – Moth Repellent Poisoning
Source
Moth repellents may contain naphthalene, paradichlorobenzene, or camphor. Their toxicity varies considerably: paradichlorobenzene is generally less toxic, while camphor can cause severe neurological effects, including seizures.
Typical Presentation
A young child accidentally puts mothballs in the mouth and later develops gastrointestinal symptoms, altered mental status, or seizures. The presentation depends on the specific chemical involved.
Clinical Features
- Camphor: Nausea, vomiting, abdominal pain, headache, dizziness, confusion, seizures, coma, and possible liver injury. Symptoms may begin rapidly.
- Naphthalene: GI irritation, headache, dizziness, fever, altered mental status, and occasionally seizures. It may also cause hemolytic anemia and methemoglobinemia, especially in patients with G6PD deficiency.
- Paradichlorobenzene: Usually causes milder GI symptoms and headache after acute exposure. Repeated or prolonged exposure may lead to ataxia and encephalopathy.
Mechanism of Action
The mechanism differs according to the chemical involved. Toxic effects may include direct gastrointestinal irritation, neurological toxicity, oxidative injury to red blood cells, and impaired oxygen transport.
Management
Treatment is mainly supportive:
- Remove the patient from further exposure.
- Provide airway, breathing, and circulatory support as needed.
- Treat seizures and other complications appropriately.
- Gastrointestinal decontamination may be considered in selected recent exposures under toxicology guidance.
Key Points
- Camphor poisoning tends to cause symptoms quickly and is particularly associated with seizures.
- Naphthalene toxicity may be delayed and can cause hemolysis or methemoglobinemia.
- Patients with G6PD deficiency are at greater risk of oxidative red-cell injury from naphthalene.
- Identifying the specific moth repellent ingredient helps predict the expected toxicity.
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Toxicology – Local Anesthetic Systemic Toxicity
Source
Local anesthetics associated with systemic toxicity include procaine, chloroprocaine, tetracaine, lidocaine, mepivacaine, and bupivacaine. Toxicity most often occurs after unintended entry of the drug into the bloodstream during a regional or local anesthetic procedure.
Typical Presentation
A patient receiving a nerve block or other local anesthetic injection develops early neurological symptoms such as ringing in the ears and numbness around the mouth, followed by altered consciousness, seizures, or cardiovascular instability.
Clinical Features
Symptoms often progress from neurological to cardiovascular toxicity:
- Perioral or tongue numbness
- Tinnitus
- Light-headedness
- Confusion
- Loss of consciousness
- Seizures
- Hypotension, arrhythmias, or cardiac collapse in severe cases
Mechanism of Action
Local anesthetics block voltage-gated sodium channels. At excessive systemic concentrations, this interferes with electrical conduction in the brain and heart, producing both neurotoxicity and cardiotoxicity.
Management
Treatment is primarily supportive and includes:
- Immediate airway and respiratory support
- Continuous cardiac monitoring
- Benzodiazepines for seizures
- IV lipid emulsion therapy for significant systemic toxicity, particularly severe cardiovascular toxicity
- Advanced resuscitation measures for cardiovascular collapse
Key Points
- Neurological symptoms commonly appear before cardiovascular toxicity.
- Bupivacaine is particularly associated with severe cardiotoxicity and may cause neurological and cardiac effects at the same time.
- Accidental intravascular administration is a classic cause of local anesthetic systemic toxicity.
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Toxicology – Benzocaine-Induced Methemoglobinemia
Source
Benzocaine is a topical local anesthetic found in some throat sprays, lozenges, oral pain products, and preparations used to numb the mouth or throat before procedures such as endoscopy.
Typical Presentation
Shortly after receiving topical benzocaine, a patient may suddenly develop shortness of breath and bluish discoloration of the skin or lips despite receiving oxygen. This should raise concern for methemoglobinemia.
Clinical Features
The main toxic effect is methemoglobinemia. Depending on severity, patients may develop:
- Cyanosis
- Shortness of breath
- Headache or dizziness
- Fatigue or weakness
- Tachycardia
- Confusion or other neurological symptoms in severe cases
Mechanism of Action
Benzocaine normally produces local anesthesia by blocking sodium channels. However, its metabolites can oxidize the iron in hemoglobin from Fe²⁺ (ferrous) to Fe³⁺ (ferric), forming methemoglobin. Methemoglobin cannot effectively carry oxygen, resulting in impaired tissue oxygen delivery.
Management
- Immediately discontinue benzocaine exposure.
- Provide supportive care and supplemental oxygen.
- Significant or symptomatic methemoglobinemia is treated with IV methylene blue under appropriate medical supervision.
- Patients who cannot safely receive methylene blue may require alternative specialist-directed treatment.
Key Points
- Benzocaine is a classic medication-associated cause of methemoglobinemia.
- Think of methemoglobinemia when cyanosis develops unexpectedly after topical anesthetic use.
- Oxygen saturation may remain abnormally low despite supplemental oxygen.
- Benzocaine is also present in several over-the-counter oral numbing products.
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Toxicology – Thyroid Hormone Toxicity
Source
Thyroid hormones such as T3 (triiodothyronine) and T4 (levothyroxine) are prescribed for hypothyroidism. Rarely, thyrotoxicosis can also occur after accidental ingestion of animal thyroid tissue in contaminated meat.
Typical Presentation
A patient may initially appear well after taking excess thyroid hormone, especially T4, and then develop symptoms hours to days later. Common complaints include palpitations, anxiety, nausea, vomiting, headache, and a rapid heart rate.
Clinical Features
Toxicity produces a hyperadrenergic picture resembling a sympathomimetic toxidrome. Possible findings include:
- Tachycardia and palpitations
- Hypertension
- Hyperthermia and sweating
- Rapid breathing
- Nausea, vomiting, and diarrhea
- Tremor, restlessness, and insomnia
- Headache and confusion
- Seizures in severe cases
ECG findings may include sinus tachycardia or supraventricular tachyarrhythmias.
T3 toxicity usually develops more rapidly, while T4 toxicity can be delayed because T4 must first be converted to active T3.
Mechanism of Action
Thyroid hormones increase basal metabolic activity and enhance sensitivity to catecholamines. T3 is the main biologically active form, while T4 acts largely as a precursor that is converted to T3 in peripheral tissues.
Management
Treatment is mainly supportive:
- Cardiac and temperature monitoring
- Beta-blockers, particularly propranolol, may help control tachycardia, tremor, palpitations, and anxiety
- Benzodiazepines may be used for severe agitation or seizures
- In significant T4 toxicity, medications that reduce peripheral conversion of T4 to T3 may be considered under specialist guidance
Because symptoms can be delayed, continued observation and appropriate follow-up may be necessary.
Key Points
- T4 overdose may have a delayed presentation.
- Thyroid hormone toxicity commonly resembles a sympathomimetic state.
- T3 acts faster because it is already biologically active.
- Most uncomplicated acute exposures improve with supportive treatment.
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Toxicology – Methotrexate (MTX) Toxicity
Source
Methotrexate is a folate-antagonist medication used in conditions such as rheumatoid arthritis, psoriasis, certain cancers, and ectopic pregnancy. Toxicity commonly occurs from dosing errors, particularly when a weekly regimen is accidentally taken every day.
Typical Presentation
A patient taking methotrexate develops painful mouth ulcers, nausea, vomiting, abdominal discomfort, and abnormal liver tests after receiving excessive or overly frequent doses.
Clinical Features
Oral methotrexate toxicity may cause:
- Nausea and vomiting
- Stomatitis and oral ulceration
- Bone marrow suppression
- Hepatitis and elevated liver enzymes
High-dose or intravenous exposure may additionally cause:
- Acute kidney injury
- Neurological dysfunction
Risk is increased in older adults, patients with impaired kidney function, those taking other nephrotoxic drugs, and patients with significant third-space fluid collections.
Mechanism of Action
Methotrexate inhibits dihydrofolate reductase (DHFR), reducing formation of biologically active folate. This interferes with DNA synthesis and particularly affects rapidly dividing tissues such as bone marrow and gastrointestinal mucosa.
Management
- Leucovorin (folinic acid rescue) should be started promptly when clinically significant toxicity is suspected.
- Supportive care includes fluids, monitoring of blood counts, kidney function, and liver function.
- Urinary alkalinization and hydration can improve methotrexate elimination in appropriate high-dose toxicity.
- Specialized therapy such as glucarpidase (carboxypeptidase G2) may be used in severe toxicity with delayed clearance, particularly when kidney function is impaired.
- Gastrointestinal decontamination may be considered in selected recent oral exposures.
Key Points
- Accidental daily administration of a medication intended to be taken weekly is a classic cause of methotrexate toxicity.
- Oral ulcers and bone marrow suppression are important warning signs.
- Reduced kidney function increases the risk of severe toxicity because methotrexate is primarily eliminated through the kidneys.
- Leucovorin is the main rescue therapy for significant methotrexate toxicity.
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Toxicology – Mushroom Poisoning
Source
Thousands of mushroom species exist, but only a relatively small number are known to be toxic. Most mushroom poisonings cause mild, self-limited gastrointestinal illness, although certain species can produce severe liver, kidney, neurological, or cholinergic toxicity.
Typical Presentation
A patient develops nausea, vomiting, abdominal discomfort, or other symptoms after eating wild-picked mushrooms. The timing of symptom onset is important: symptoms beginning within about 6 hours are generally associated with less dangerous exposures, whereas delayed symptoms may indicate potentially serious toxins such as amatoxins.
Clinical Features
Presentation varies according to the toxin involved:
- Allenic norleucine: Early GI illness followed by possible acute kidney failure.
- Amatoxins: Delayed gastrointestinal symptoms followed by severe liver injury and potentially fatal multiorgan failure.
- Coprine: Produces a disulfiram-like reaction when alcohol is consumed.
- GI irritants: Most common form; causes rapidly developing nausea, vomiting, abdominal cramps, and diarrhea.
- Gyromitrin: Delayed GI and neurological effects; seizures and liver or kidney injury may occur.
- Isoxazoles (muscimol/ibotenic acid): May cause agitation, unusual behavior, somnolence, or transient coma.
- Muscarine: Produces a cholinergic toxidrome with excessive secretions and other parasympathetic effects.
- Orellanine: Delayed gastrointestinal illness followed by kidney failure.
- Polyporic acid: Delayed neurological symptoms, weakness, and possible liver and kidney dysfunction.
- Psilocybin: Produces hallucinations and altered perception, usually with relatively rapid onset.
Mechanism of Action
There is no single mechanism because mushroom species contain different toxins. Effects may involve inhibition of cellular protein synthesis, cholinergic stimulation, neurotoxicity, or direct damage to the liver and kidneys.
Management
Treatment depends on the suspected toxin and is primarily supportive:
- Airway, circulation, fluid, and electrolyte management
- Activated charcoal may be considered after appropriate recent exposures
- Pyridoxine (vitamin B6) may be used for gyromitrin-associated seizures
- Atropine may be used for severe muscarinic/cholinergic symptoms
- N-acetylcysteine (NAC) and specialist-directed therapies such as silibinin may be considered in suspected amatoxin poisoning
- Severe liver or kidney failure may require advanced supportive care or transplantation evaluation
Key Points
- Most mushroom ingestions cause gastrointestinal symptoms only.
- Delayed onset of symptoms is more concerning than rapid onset.
- Amatoxin poisoning causes the majority of fatal mushroom poisonings.
- Amatoxins, orellanine, and allenic norleucine are particularly associated with delayed toxicity.
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Toxicology – Levodopa/Carbidopa Toxicity
Source
Levodopa and carbidopa are commonly prescribed together for Parkinson disease. Levodopa is a precursor of dopamine that can cross the blood–brain barrier, while carbidopa reduces its conversion to dopamine outside the central nervous system.
Typical Presentation
Patients with overdose may appear markedly agitated or confused and can develop hallucinations or bizarre behavior. The presentation may resemble a sympathomimetic or anticholinergic toxidrome, particularly in older adults.
Clinical Features
Acute toxicity commonly causes tachycardia, hypertension, dilated pupils, psychomotor agitation, delusions, and hallucinations. Nausea, vomiting, urinary retention, and involuntary choreoathetoid movements may also occur. Blood pressure can fluctuate, with early hypertension followed by hypotension or orthostatic hypotension. Sustained-release formulations may produce delayed or recurrent symptoms for up to 48 hours.
Mechanism of Action
Levodopa crosses into the brain and is converted into dopamine. Carbidopa inhibits peripheral dopamine formation, allowing more levodopa to reach the CNS. In overdose, excessive dopamine and catecholamine activity produces both neurological and cardiovascular stimulation.
Management
Treatment is mainly supportive, with cardiac and blood pressure monitoring. Activated charcoal may be considered after a recent significant ingestion. Patients who ingest large amounts of sustained-release formulations may require prolonged observation because symptoms can recur after an initial period of improvement.
Key Points
- Mydriasis, agitation, and hallucinations in a patient taking dopaminergic medications should raise concern for overdose.
- Hypertension may later transition to hypotension, so antihypertensive treatment should be used cautiously.
- Sustained-release products can cause delayed recurrent toxicity.
- Abrupt reduction or withdrawal of levodopa/carbidopa during therapeutic use can precipitate a neuroleptic malignant syndrome–like reaction.
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Source
Isoniazid (INH) is a first-line antitubercular medication used to treat both latent and active tuberculosis. It is structurally related to pyridoxine (vitamin B6).
Typical Presentation
Acute overdose classically presents with severe, refractory seizures and metabolic acidosis. Children are particularly vulnerable, and toxicity may occur rapidly after ingestion. Chronic use is associated with liver injury and neurological complications.
Clinical Features
Acute Toxicity
Symptoms may begin within 30 minutes of ingestion and include:
- Refractory seizures
- Altered mental status or coma
- Vomiting
- Slurred speech
- Hyperreflexia or hyporeflexia
- Tachycardia
- Oliguria
- High anion gap metabolic acidosis
- Elevated lactate levels
Long-term exposure may cause:
- Elevated liver enzymes and hepatitis
- Hepatocellular necrosis
- Peripheral neuropathy
- Optic neuritis
- Vitamin B6 deficiency
- Autoimmune manifestations (e.g., anemia, arthritis, eosinophilia)
INH interferes with pyridoxine (vitamin B6) metabolism, impairing pyridoxine-dependent enzymatic pathways. This leads to depletion of GABA and excess glutamate activity, predisposing patients to seizures.
Management
Treatment focuses on seizure control, airway stabilization, and reversal of vitamin B6 depletion:
- Benzodiazepines, propofol, or barbiturates for seizures
- Sodium bicarbonate for severe acidosis
- Supportive airway and hemodynamic management
- Ideally given gram-for-gram equal to the amount of INH ingested
- If the dose is unknown, an initial 5 g IV dose is recommended and may be repeated if seizures continue
Key Points
- Consider INH poisoning in patients with seizures unresponsive to standard anticonvulsants.
- Refractory seizures plus metabolic acidosis is highly suggestive.
- Pyridoxine is the definitive antidote.
- Chronic therapy may cause neuropathy and hepatotoxicity.
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Source
Colchicine is a medication commonly prescribed for gout, pericarditis, and familial Mediterranean fever. It is derived from the autumn crocus plant (Colchicum autumnale) and has a narrow therapeutic index.
Typical Presentation
Patients usually present after an overdose with severe gastrointestinal symptoms that may initially resemble infectious gastroenteritis. Toxicity can rapidly progress to multiorgan failure over the following days.
Clinical Features
Colchicine poisoning classically progresses through three stages:
- Phase 1 (within hours): Severe nausea, vomiting, diarrhea, abdominal pain, dehydration, tachycardia, hypotension, and early kidney injury.
- Phase 2 (days later): Multisystem toxicity develops, including bone marrow suppression, low white blood cell counts, kidney and liver failure, rhabdomyolysis, pulmonary edema, ARDS, cardiovascular collapse, and pancytopenia.
- Phase 3 (recovery phase): Survivors may later develop hair loss (alopecia) and ascending peripheral neuropathy.
Colchicine disrupts microtubule formation and inhibits mitosis, impairing rapidly dividing cells such as those in the gastrointestinal tract and bone marrow.
Management
Treatment is primarily supportive and includes:
- Aggressive IV fluid resuscitation
- Airway and hemodynamic support
- Antiemetics for severe GI symptoms
- Activated charcoal to reduce enterohepatic recirculation
Key Points
- Early symptoms may mimic viral gastroenteritis.
- Toxicity can progress rapidly to fatal multiorgan failure.
- Bone marrow suppression is a major complication.
- Dialysis is not useful in colchicine overdose.
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Source
Radiation exposure can occur in medical settings (e.g., imaging and cancer therapy), research environments, industrial operations, and nuclear incidents. Radioactive materials are also used in energy production and, in rare cases, weaponized forms.
Typical Presentation
Exposure may be accidental, occupational, or intentional. Large-scale incidents (such as nuclear accidents) or isolated exposures (such as ingestion of radioactive substances) can both lead to radiation sickness. Symptoms may not appear immediately and often depend on the dose received.
Clinical Features
The severity and timing of symptoms are dose-dependent. Acute radiation syndrome generally presents in three major patterns:
- Hematopoietic syndrome: Characterized by bone marrow suppression, leading to reduced blood cell production, anemia, and increased infection risk.
- Gastrointestinal syndrome: Includes nausea, vomiting, diarrhea, and abdominal pain due to damage to the intestinal lining.
- Neurovascular syndrome: Occurs with very high doses and presents with headache, dizziness, confusion, and rapid neurological decline.
Mechanism of Action
Radiation damages cells by directly disrupting DNA or indirectly generating free radicals that injure cellular structures. Different types of radiation vary in penetration: alpha particles have low penetration and are mainly harmful if ingested or inhaled, while gamma rays and X-rays penetrate deeply into tissues.
Management
Treatment is largely supportive. Immediate steps include removal from the radiation source and decontamination if necessary. Supportive care may involve intravenous fluids, antiemetics, and management of infections. In cases of bone marrow suppression, growth factors may be used to stimulate blood cell production.
Key Points
- Clinical severity depends on radiation dose and duration of exposure.
- Early decline in lymphocyte count can help estimate severity and prognosis.
- Alpha radiation is dangerous mainly when internalized, while gamma radiation penetrates deeply.
- Long-term risks include malignancy and organ damage.
