Toxicology – Button Battery Ingestion

Sources

Button or coin batteries are commonly found in:

• Toys
• Watches
• Hearing aids
• Remote controls
• Small electronic devices

Young children are at greatest risk because the batteries are small, shiny, and easy to swallow.

Typical Presentation

A toddler may swallow a button battery and initially appear completely well.

The most dangerous situation is when the battery becomes lodged in the esophagus.

Clinical Features

Symptoms may include:

• Drooling
• Coughing
• Vomiting
• Dysphagia
• Chest discomfort
• Refusal to eat

However, some children with an esophageal battery may initially have few or no symptoms.

Serious complications include:

• Deep esophageal burns
• Perforation
• Tracheoesophageal fistula
• Injury to major blood vessels
• Mediastinitis

Batteries lodged in the nose or ear can also cause rapid local tissue injury.

Mechanism of Action

The main injury is caused by an electrical current that generates hydroxide ions at the battery surface.

This creates a strongly alkaline environment and causes liquefactive necrosis.

Severe tissue injury can begin within only a few hours.

Diagnosis

Plain radiographs are used to determine:

• Whether a battery is present
• Its location
• Whether it is still in the esophagus

Button batteries can usually be distinguished radiographically from coins by their characteristic layered appearance.

Management

An esophageal button battery is an emergency and requires prompt endoscopic removal.

Important principles include:

• Rapid localization with imaging
• Immediate specialty consultation
• Urgent removal if lodged in the esophagus
• Monitoring for delayed complications after significant esophageal injury

Batteries that have already passed into the stomach or intestine often pass spontaneously, but management depends on factors such as symptoms, battery size, age, location, and evidence of GI injury.

Key Points

• Esophageal impaction is the major emergency.
• Serious tissue injury can occur rapidly, sometimes within about 2 hours.
• A child may appear well despite significant internal injury.
• Large lithium coin cells are especially concerning.
• Batteries beyond the esophagus are often managed expectantly if the patient is asymptomatic and the battery continues to progress.
• Button batteries in the ear or nose also require prompt removal because they can cause rapid liquefactive tissue damage.

Toxicology – Caustic Ingestion: Acidic Agents

Sources

Common acidic caustic substances include:

• Battery acid
• Rust removers
• Toilet bowl cleaners
• Metal and brick cleaners
• Other strong industrial or household acids

Typical Presentation

A child or adult with an acid ingestion may develop:

• Burning mouth or throat pain
• Drooling
• Painful swallowing
• Vomiting
• Chest or abdominal pain

Severe cases may progress to airway compromise or gastrointestinal perforation.

Clinical Features

Possible findings include:

• Oral burns
• Drooling
• Nausea and vomiting
• Hematemesis
• Dysphagia
• Odynophagia
• Dyspnea
• Chest pain
• Abdominal pain

Serious systemic complications can include:

• Hemolysis
• Metabolic acidosis
• Acute kidney injury
• Shock

Endoscopy may show patchy or “skip” areas of injury, so visible damage may not be continuous.

Mechanism of Action

Acids cause coagulative necrosis.

This leads to protein denaturation and formation of an eschar, which may limit deeper penetration to some extent compared with strong alkalis, although severe injury can still occur.

Management

Treatment is mainly supportive:

• Assess and protect the airway
• Monitor cardiovascular status
• Evaluate for perforation and major GI injury
• Check relevant laboratory studies in significant exposures
• Use imaging when perforation or other complications are suspected

Endoscopy is often performed in selected symptomatic patients after stabilization to determine the extent of injury.

Avoid:

• Inducing vomiting
• Gastric lavage
• Activated charcoal
• Attempting to neutralize the acid with an alkali

Neutralization can generate heat and worsen tissue injury.

Routine dilution with milk or water is not generally recommended without poison-center or specialist guidance, particularly once symptoms are present.

Key Points

• Acids classically cause coagulative necrosis with eschar formation.
• Severe injury can involve the esophagus, stomach, airway, and surrounding tissues.
• Do not induce emesis or attempt chemical neutralization.
• A relatively normal oral examination does not exclude serious internal injury.
• Airway compromise, perforation, acidosis, hemolysis, and renal injury are major complications.
• Corticosteroids are not routinely used solely to prevent strictures; their role depends on the specific clinical situation.

Toxicology – Caustic Ingestion: Alkaline Agents

Sources

Common alkaline caustic products include:

• Drain cleaners
• Lye
• Oven cleaners
• Ammonia-containing cleaners
• Some concentrated cleaning solutions
• Bleach, although household bleach is usually less corrosive than strong alkalis

Typical Presentation

A young child is found after getting into a household cleaner and develops:

• Coughing
• Sore throat
• Drooling
• Pain with swallowing

Severity depends on the concentration, amount, and duration of contact.

Clinical Features

Possible findings include:

• Oral or pharyngeal burns
• Drooling
• Nausea and vomiting
• Hematemesis
• Dysphagia
• Odynophagia
• Chest pain
• Abdominal pain
• Dyspnea or stridor

Serious complications include:

• Upper-airway edema
• Esophageal or gastric injury
• Perforation
• Mediastinitis or peritonitis
• Later esophageal stricture formation

Importantly, the absence of visible mouth burns does not exclude serious esophageal injury.

Mechanism of Action

Alkaline substances cause liquefactive necrosis and saponification of fats.

This allows deeper tissue penetration and can produce significant injury to the esophagus and surrounding structures.

Management

Initial priorities include:

• Airway assessment and protection
• Supportive care
• Evaluation for perforation or significant internal injury
• Early consultation with gastroenterology, surgery, and toxicology when severe exposure is suspected

Endoscopy is commonly used in selected symptomatic patients to assess the extent of injury, usually after stabilization and within an appropriate early time window.

Avoid:

• Inducing vomiting
• Gastric lavage
• Activated charcoal
• Attempting to neutralize the alkali with an acid

These measures can worsen tissue injury or increase aspiration risk.

Routine administration of milk or water after significant caustic ingestion is not generally recommended without poison-center or specialist guidance, especially once symptoms are present.

Key Points

• Alkalis cause liquefactive necrosis and can penetrate deeply.
• Drooling, dysphagia, odynophagia, chest pain, or respiratory symptoms suggest significant injury.
• A normal-looking mouth does not rule out esophageal burns.
• Do not induce emesis or attempt chemical neutralization.
• Airway compromise and GI perforation are the most dangerous early complications.
• Corticosteroids are not routinely recommended solely to prevent strictures; their use depends on the specific clinical situation.

Toxicology – Hydrocarbon Ingestion

Sources

Hydrocarbons are found in many fuels, solvents, and petroleum products. Examples include:

• Propane and butane
• Hexane and octane
• Gasoline
• Kerosene
• Motor oil

Typical Presentation

A person drinks a small amount of gasoline and immediately begins gagging and coughing. The main danger is often not absorption from the stomach, but aspiration into the lungs.

Clinical Features

Possible symptoms include:

• Coughing
• Gagging
• Vomiting
• Shortness of breath
• Hypoxia
• Altered mental status
• Syncope

Aspiration can cause:

• Chemical pneumonitis
• Pulmonary edema
• Respiratory distress

Inhalation of hydrocarbon vapors may also cause:

• CNS depression or intoxication
• Dizziness and impaired coordination
• Cardiac dysrhythmias

Repeated inhalational abuse can lead to chronic neurologic injury.

Mechanism of Action

Hydrocarbon toxicity depends greatly on the physical properties of the product.

Low-viscosity hydrocarbons spread easily and are more likely to enter the airway during swallowing or vomiting.

Once aspirated, they:

• Directly injure pulmonary tissue
• Disrupt surfactant
• Trigger inflammation and chemical pneumonitis

Some inhaled hydrocarbons can also sensitize the heart to catecholamines, increasing the risk of dangerous dysrhythmias.

Aspiration Risk

Aspiration risk is generally higher with low-viscosity hydrocarbons.

Examples:

• Gasoline and kerosene: relatively high aspiration risk
• Motor oil: lower aspiration risk because of higher viscosity

Management

Treatment is mainly supportive:

• Remove the patient from further exposure
• Support airway and breathing
• Provide supplemental oxygen if needed
• Monitor for respiratory deterioration

There is no specific antidote for hydrocarbon aspiration.

Inducing vomiting is avoided because it can increase the risk of aspiration. Activated charcoal is generally not useful for uncomplicated aliphatic hydrocarbon ingestion.

Key Points

• The major danger after ingestion is often aspiration, not systemic absorption.
• Low viscosity = higher aspiration risk.
• Chemical pneumonitis may develop after coughing or choking during ingestion.
• High-viscosity products such as motor oil usually pose less aspiration risk.
• Treatment is primarily supportive, with attention to respiratory symptoms and cardiac rhythm abnormalities.

Toxicology – Hydrofluoric Acid (HF) Exposure

Sources

Hydrofluoric acid is used in several industrial and commercial processes, including:

• Glass etching
• Semiconductor and computer-chip manufacturing
• Oil refining
• Chemical production
• Metallurgy
• Some rust removers and wheel-cleaning products

Typical Presentation

A worker exposed to HF develops severe, deep pain several hours after skin contact, despite relatively minor-looking surface burns.

Pain that seems out of proportion to the visible injury is an important clue.

Clinical Features

Skin exposure may cause:

• Severe burning or throbbing pain
• Tissue destruction that can extend deeply beneath the skin
• Delayed symptoms, particularly with more dilute solutions

Significant exposure can produce systemic electrolyte abnormalities, especially:

• Hypocalcemia
• Hypomagnesemia

These may cause:

• Muscle cramps or spasms
• Tetany
• Chvostek or Trousseau signs
• QT prolongation
• Ventricular dysrhythmias
• Cardiovascular collapse in severe poisoning

Inhalational exposure can also cause significant respiratory tract and pulmonary injury.

Mechanism of Action

HF toxicity is unusual because both components contribute to injury.

The hydrogen ion produces local corrosive damage, while absorbed fluoride ions penetrate deeply and bind calcium and magnesium.

This sequestration can cause profound electrolyte disturbances and disrupt cardiac electrical activity.

Management

HF exposure is a medical emergency. Initial treatment includes:

• Immediate removal from the source
• Prompt removal of contaminated clothing
• Copious water irrigation of exposed skin
• Early cardiac monitoring for significant exposures
• Serial monitoring of calcium, magnesium, potassium, and ECG findings

After initial decontamination, calcium gluconate is used to bind fluoride and limit ongoing tissue injury. The route of calcium treatment depends on the location and severity of exposure and should be directed by experienced clinicians or a poison center.

Severe exposures may require intensive treatment of electrolyte abnormalities, dysrhythmias, and respiratory complications.

Key Points

• Severe pain out of proportion to the visible burn is characteristic of HF exposure.
• HF can penetrate deeply even when the surface injury initially appears mild.
• Fluoride binds calcium and magnesium, potentially causing life-threatening electrolyte disturbances.
• Significant exposure can produce QT prolongation and dangerous ventricular dysrhythmias.
• Rapid decontamination and calcium-based treatment are central to management.
• Because deterioration can be delayed, significant HF exposure requires urgent medical evaluation and toxicology guidance.

Toxicology – Magnesium Toxicity

Sources

Hypermagnesemia may result from excessive exposure to magnesium-containing products such as:

• Magnesium sulfate
• Magnesium citrate
• Milk of magnesia
• Other magnesium-containing antacids or laxatives

Risk is increased in patients with renal impairment, because magnesium is primarily eliminated by the kidneys.

Typical Presentation

A patient receiving magnesium therapy, such as during treatment of preeclampsia, develops:

• Weakness
• Nausea
• Flushing
• Diminished reflexes
• Hypotension
• Bradycardia

Severe toxicity may progress to respiratory depression and cardiac conduction abnormalities.

Clinical Features

As magnesium levels rise, findings may include:

• Nausea and vomiting
• Flushing
• Thirst
• Generalized weakness
• Lethargy
• Decreased or absent deep tendon reflexes
• Hypotension
• Bradycardia
• Respiratory depression
• Prolonged cardiac conduction
• Wide QRS complexes
• Complete heart block
• Cardiac arrest in extreme cases

Loss of deep tendon reflexes is an important early bedside clue during magnesium therapy.

Mechanism of Action

Excess magnesium depresses neuromuscular and cardiac function.

It:

• Reduces acetylcholine release at the neuromuscular junction
• Interferes with calcium-dependent processes
• Alters sodium and potassium channel activity
• Slows cardiac conduction
• Produces peripheral vasodilation

Management

Treatment includes:

• Immediately stopping the magnesium source
• Airway and respiratory support when needed
• IV fluids and cardiovascular support
• Continuous ECG monitoring in significant toxicity

IV calcium, usually calcium gluconate, can temporarily antagonize the cardiac and neuromuscular effects of magnesium.

Patients with adequate renal function may eliminate excess magnesium with supportive care. Hemodialysis is particularly useful in severe toxicity or when renal failure prevents magnesium excretion.

Key Points

• Think of weakness + diminished reflexes + hypotension/bradycardia in a patient receiving magnesium.
• Renal failure greatly increases the risk of magnesium accumulation.
• Calcium antagonizes the physiologic effects of magnesium and is used for significant toxicity.
• Severe hypermagnesemia can cause respiratory failure and heart block.
• Magnesium-containing laxatives should be used cautiously in patients with impaired renal function.

 Toxicology – Thallium Poisoning

Sources

Thallium exposure may occur from:

• Certain industrial processes
• Some older rodenticides
• Fireworks or pyrotechnic materials
• Contaminated products
• Intentional poisoning

Historical medical uses are largely obsolete.

Typical Presentation

Thallium poisoning often begins with gastrointestinal symptoms, followed days later by characteristic neurologic and skin findings.

A classic clue is the combination of:

• Abdominal pain
• Painful peripheral neuropathy
• Hair loss

Clinical Features

Early findings

• Nausea
• Vomiting
• Abdominal pain
• Diarrhea
• Occasionally GI bleeding
• Tachycardia
• Hypertension
• Chest discomfort

Neurologic findings

• Painful paresthesias
• Peripheral neuropathy
• Headache
• Ataxia
• Visual disturbances
• Altered mental status
• Seizures in severe cases

Delayed skin and hair findings

• Alopecia, often developing days to weeks after exposure
• Scaling or abnormalities of the palms and soles
• Acneiform or pustular skin eruptions
• Abnormal nail growth

Mechanism of Action

Thallium behaves similarly to potassium and can enter cells through potassium transport pathways.

It interferes with:

• Potassium-dependent cellular processes
• Mitochondrial energy production
• Sulfhydryl-containing enzymes
• Protein and keratin synthesis

These effects help explain its prominent neurologic toxicity and characteristic abnormalities of the hair, skin, and nails.

Management

Treatment includes:

• Immediate removal from the exposure source
• Supportive care
• Management of seizures, cardiovascular instability, and electrolyte abnormalities
• Gastrointestinal decontamination in selected recent exposures

Prussian blue is the specific antidotal therapy. It binds thallium in the gastrointestinal tract and interrupts enterohepatic and enteric recycling, increasing fecal elimination.

Repeated-dose activated charcoal may also be considered in selected cases under toxicology guidance.

Extracorporeal removal may be considered in severe poisoning, particularly early in the course.

Key Points

• Think of GI symptoms + painful neuropathy + delayed alopecia.
• Thallium mimics potassium and disrupts mitochondrial and enzymatic function.
• Prussian blue is the key specific antidote.
• Hair loss is often delayed and may become a major diagnostic clue.
• Conventional chelators are generally not useful for thallium poisoning.

Toxicology – Arsenic Poisoning

Sources

Arsenic exposure may occur from:

• Contaminated groundwater or food
• Certain traditional or nonstandard medicines
• Some pesticides and industrial products
• Pigments and manufacturing processes
• Contaminated occupational environments

Inorganic arsenic is generally responsible for the most significant systemic toxicity.

Typical Presentation

A patient with substantial arsenic exposure may develop severe gastrointestinal illness followed by cardiovascular and neurologic toxicity. Chronic exposure can produce characteristic skin changes and a painful stocking-glove peripheral neuropathy.

A garlic-like odor on the breath has traditionally been described but is neither sensitive nor specific.

Clinical Features

Acute poisoning may cause:

• Severe nausea and vomiting
• Profuse watery diarrhea
• Abdominal pain
• Dehydration
• Tachycardia
• Hypotension and shock
• Altered mental status
• Seizures
• Peripheral neuropathy, sometimes developing after the initial illness
• Cardiac dysrhythmias and QT prolongation
• Cardiovascular collapse in severe cases

Chronic poisoning may cause:

• Hyperkeratosis, especially of the palms and soles
• Abnormal skin pigmentation
• Peripheral neuropathy
• Metabolic abnormalities, including increased risk of diabetes
• Cardiovascular disease
• Increased risk of several cancers, particularly skin, lung, and bladder cancers

Mechanism of Action

Arsenic disrupts cellular energy production. Inorganic arsenic can inhibit enzymes such as pyruvate dehydrogenase, interfering with formation of acetyl-CoA and ATP.

It can also impair:

• Oxidative phosphorylation
• Glucose metabolism
• Other essential enzyme systems

The result is widespread cellular dysfunction affecting the gastrointestinal, cardiovascular, neurologic, and other organ systems.

Management

Treatment includes:

• Immediate removal from the exposure source
• Aggressive supportive care
• IV fluids and cardiovascular stabilization
• Correction of electrolyte abnormalities
• ECG monitoring in significant acute poisoning

Chelation may be required for clinically important poisoning. Agents include:

• Dimercaprol (BAL) in selected severe acute cases
• Succimer (DMSA)
• DMPS, where available

Chelation decisions should be made with a medical toxicologist or poison center because the preferred agent depends on the type and severity of exposure.

Key Points

• Acute arsenic poisoning often begins with severe GI symptoms and can progress to shock, dysrhythmias, and neurologic injury.
• Painful stocking-glove neuropathy is an important clue.
• Chronic exposure can cause hyperkeratosis and characteristic pigmentation changes.
• Arsenic interferes with cellular energy production.
• Chronic inorganic arsenic exposure is associated with increased cancer risk.
• Groundwater contamination remains an important source of arsenic exposure worldwide.

Toxicology – Mercury Poisoning

Sources

Mercury exists in several forms, and toxicity depends strongly on the form and route of exposure.

• Elemental mercury: thermometers, some older thermostats, dental amalgam, industrial processes, and gold extraction
• Inorganic mercury salts: some industrial chemicals, older disinfectants, pigments, and manufacturing processes
• Organic mercury compounds: especially methylmercury, which can accumulate in large predatory fish

Typical Presentation

A person with chronic occupational mercury exposure may develop:

• Tremor
• Irritability or personality change
• Memory problems
• Excessive sweating
• Gingivitis or inflammation of the mouth

Clinical Features

Elemental mercury vapor inhalation

• Cough
• Dyspnea
• Chemical pneumonitis
• Noncardiogenic pulmonary edema in severe exposure

Chronic vapor exposure can produce the classic combination of:

• Neuropsychiatric changes
• Tremor
• Gingivostomatitis

Neuropsychiatric symptoms may include irritability, insomnia, poor concentration, memory impairment, and emotional instability.

Inorganic mercury salts

Ingestion can cause:

• Severe nausea and vomiting
• Abdominal pain
• Hemorrhagic gastroenteritis
• Acute tubular injury
• Acute kidney failure

Chronic exposure can also produce neurologic abnormalities.

Organic mercury

Methylmercury primarily damages the nervous system and may cause:

• Paresthesias
• Ataxia
• Tremor or other movement abnormalities
• Visual impairment
• Hearing impairment
• Hyperreflexia
• Cognitive dysfunction

Developing fetuses and young children are particularly vulnerable to the neurologic effects of methylmercury.

Mechanism of Action

Mercury binds strongly to sulfhydryl groups in proteins.

This interferes with:

• Enzyme activity
• Cellular metabolism
• Membrane function
• Antioxidant defenses

The nervous system and kidneys are major targets of toxicity.

Management

Treatment includes:

• Immediate removal from the exposure source
• Supportive care
• Respiratory support for severe inhalational injury
• Renal monitoring after significant inorganic mercury exposure

Chelation may be considered in clinically significant poisoning, commonly with agents such as:

• Succimer (DMSA)
• DMPS

Choice of therapy depends on the mercury compound, exposure severity, symptoms, and specialist guidance.

Key Points

• Mercury toxicity differs markedly between elemental, inorganic, and organic forms.
• Swallowed liquid elemental mercury is poorly absorbed from an intact GI tract, whereas inhaled mercury vapor can be highly toxic.
• Chronic elemental mercury exposure classically causes tremor + neuropsychiatric changes + gingivostomatitis.
• Inorganic mercury mainly causes severe GI and renal toxicity.
• Methylmercury predominantly causes neurologic toxicity.
• Significant suspected mercury poisoning should be discussed with a medical toxicologist or poison center.

Toxicology – Lead Poisoning

Sources

Common sources of lead exposure include:

• Older lead-based paint and contaminated household dust
• Batteries
• Ceramics and pottery glazes
• Plumbing and contaminated water
• Certain toys, jewelry, figurines, and imported products
• Some traditional or nonstandard medicines
• Occupational or industrial exposure

Typical Presentation

A child living in an older home may present with:

• Developmental delay
• Learning difficulties
• Behavioral problems
• Fatigue
• Vague abdominal complaints

Chronic exposure is often subtle and may be discovered only after screening.

Clinical Features

Acute lead toxicity may cause:

• Nausea and vomiting
• Abdominal pain
• Diarrhea
• Hemolysis
• Acute kidney injury
• Severe neurologic toxicity in major exposures

Chronic lead toxicity may cause:

• Recurrent abdominal pain
• Constipation
• Fatigue
• Headache
• Cognitive and learning impairment
• Behavioral changes
• Anemia
• Peripheral neuropathy
• Motor weakness, including wrist drop

Children are particularly vulnerable to the neurodevelopmental effects of lead.

Mechanism of Action

Lead disrupts multiple cellular processes and can damage several organ systems, especially:

• Central and peripheral nervous systems
• Kidneys
• Bone and bone marrow
• Gastrointestinal tract
• Cardiovascular system

It also interferes with enzymes involved in heme synthesis, contributing to anemia.

Laboratory Findings

Diagnosis is based primarily on an elevated blood lead level.

Other possible findings include:

• Microcytic or normocytic anemia
• Basophilic stippling on peripheral blood smear
• Increased erythrocyte protoporphyrin in significant chronic exposure

These findings support the diagnosis but are not as specific as the blood lead concentration.

Characteristic Findings

Classic but less commonly seen findings include:

• Burton lines: blue-gray discoloration along the gingival margin
• Lead lines: dense metaphyseal bands seen on radiographs of growing bones in chronically exposed children

Management

The most important intervention is to identify and eliminate the source of exposure.

Chelation may be required for significant poisoning. Agents used include:

• Succimer (DMSA)
• Calcium disodium EDTA
• Dimercaprol in selected severe cases

The choice of chelator depends on the blood lead level, symptoms, and severity of toxicity. Severe neurologic toxicity requires urgent specialist management.

Key Points

• Children are especially susceptible to lead-related cognitive and developmental injury.
• Chronic poisoning may present with abdominal pain, constipation, anemia, and behavioral or learning problems.
• Basophilic stippling is a classic clue but is not diagnostic by itself.
• Treatment begins with removal of the exposure source.
• Chelation is reserved for sufficiently elevated blood lead levels or clinically significant poisoning.