Household Poisons

1. Ease of access
2. Climbing
3. Mouthing
4. Look like non-toxic items

o Product is known to have low toxicity in amount ingested
o Details of the exposure are known (ideally witnessed)
 Identification of active ingredients
 Time, amount and route of exposure
 Single substance only
o Patient is asymptomatic
o Examples of non-toxic or minimally toxic substances
 Air fresheners, cosmetics, crayon/markers
 Deodorant, glow sticks, lip balm
 Sidewalk chalk, silica gel, superglue

CAUSTICS
 Caustic = xenobiotic → both functional + histologic damage on contact with tissues
 Typically classified dichotomously (e.g. either acids or alkalis)
o Acids = proton donors (cause significant injury at pH <2)
o Alkalis = proton acceptors (cause significant injury at pH >12)

 Extent on injury is determined by several factors
o pH
o Concentration
o Volume
o Formulation (liquid vs. solid)
o Duration/extent of contact with tissues
o Penetration coefficient
o Gastric contents (oral exposures)
o Titratable acid/alkaline reserve

o Acids
 Hydrochloric (muriatic) acid: toilet bowl cleaners, mold/mildew removers
 Oxalic acid: furniture refinishers, metal polishes
 Phosphoric acid: toilet bowl cleaners, rust removers
 Sulfuric acid: automobile batteries, drain opener

o Alkalis
 Ammonium hydroxide: grease removers, glass cleaners, metal polishes/cleaners, hair dyes/tints, jewelry cleaners, wax removers, floor strippers
 Sodium hydroxide (lye): paint removers, drain cleaners/openers, oven cleaners, automatic dishwasher detergents, hair relaxer
 Sodium hypochlorite: bleach, swimming pool chlorinator

o Children
 1,000 children hospitalized each year for an average of 4 days
 Direct hospital costs: \$22 million

o Adolescents and adults
 Intent = deliberate self-harm attempts
 large volumes ingested
 Clinical manifestations typically more severe
• Hospitalization rates: children 39% vs. adults 48%
• Require treatment: children 8% vs. adults 81%

o Worldwide

 Public education campaigns
• Africa: sodium hydroxide stored in soda bottles
• Iran: 68.3% of unintentional exposure occurred in the kitchen
• Great Britain: direct ingestion of oven cleaning products/contaminated food
 Difference in regulation = differences in access
• US: Federal Hazardous Substances Act + Poison Prevention Packaging Act
• Acid ingestions more common in Asia vs. western countries
o Taiwan: 48% of cases involved industrial cleaners
o Iran: hydrochloric acid accounts for 70% of caustic ingestions in adults
 Suicide prevention resources
• China, India, Pakistan, Bangladesh, Sri Lanka: women commonly use caustics to commit suicide
• Tunisia: majority of caustic ingestions occurred in women 20-29 years old

o Alkalis: dissociated hydroxide ions (OH-) → liquefactive necrosis
 Protein dissolution, collagen destruction, fat saponification
 Cell membrane emulsification, transmural thrombosis, cell death
 continuous penetration until OH- neutralized by the tissues
o Acids: dissociated H+ ions → coagulative necrosis
 Edema, erythema, mucosal sloughing, ulceration and necrosis
 eschar formation = prevents deeper tissue penetration

o All routes of exposure: severe pain at site (lips, mouth, throat, abdomen, eyes, skin)
o Ocular: vision changes, redness, ulceration
o Dermal: local tissue damage, vesicle formation
o Pulmonary: dyspnea, respiratory compromise, pneumonitis, pulmonary edema
o Gastrointestinal
 Oropharyngeal: edema + burns, excessive salivation
 Esophageal: dysphagia, odynophagia
 Gastric: epigastric pain, hematemesis
 Complications: sepsis, perforation, stricture formation + narrowing of lumen

o Laboratory evaluation (limited clinical utility, can aid in planning)
 Basic metabolic panel
 Serum pH, lactic acid (metabolic acidosis ± anion gap – including alkali ingestions)
 CBC, coagulation panel, blood typing + cross-match
o Imaging
 Chest + abdominal radiographs (detect gross esophageal or gastric perforation + strictures)
 Endoscopy for all intentional ingestions or unintentional + stridor or >2 (pain, vomiting, drooling)
 Ideally should be performed within 12 hours of ingestion (no later than 24 hours)
 Should visualize esophagus, stomach + proximal duodenum
 If grade IIb or III esophageal burns prevent endoscopy → CT or surgical exploration

o Decontamination (oral and dermal exposures)
 Remove clothing, jewelry, etc. + copious irrigation with water
 Blisters should be popped
 No role for gastric decontamination (activated charcoal, induction of emesis, etc.)
 Dilutional therapy (e.g. drinking water): avoid unless asymptomatic + within first few first few minutes of ingestion

o Symptomatic and supportive care
 Basic resuscitative principles: airway inspection and intubation
 Airway inflammation: dexamethasone
 Hypotension (third spacing or perforation): IV fluid repletion
 Surgical intervention as necessary
 No role for empiric antibiotics (only if source of infection is identified)

o Remove contact lenses, false eye lashes, etc.
o Immediate + copious irrigation
 Hold eyes open for continuous irrigation for at least 15 minutes
 Use room temperature (tepid) water or 0.9% sodium chloride
• Tilt head to the side and pour water over bridge of nose
• “Burrito method” in children: place arms at their sides and wrap in towel
o Some situations warrant hospital evaluation/care
 Refer if: strong or concentrated caustic or pain, swelling, lacrimation, or photophobia despite irrigation
 At healthcare facility
• Test pH of fluid in conjunctival sac (litmus paper) – goal pH 7
• Specially designated lenses placed below the eyelids that enable direct flushing (+ local anesthetic)

Liberation of F- ions leads to toxicity (not H+)

 Unintentional (dermal, ocular)
• Dermal: blanching, coagulative necrosis (>20%)
• Ocular: stromal corneal edema, conjunctival ischemia, sloughing, long term dry eye
• Pulmonary: throat burning, shortness of breath, ulceration, pulmonary edema
 Intentional (oral)
• Almost invariably fatal
• Precipitous deterioration
• Gastrointestinal: significant gastritis, vomiting, abdominal pain
• Cardiac: hypocalcemia + hypomagnesemia + hyperkalemia → ventricular dysrhythmias

 Decontamination (water or saline)
 Airway management
• Especially if: inhalation or ingestions, vomiting or respiratory distress, altered mental status
• Avoid succinylcholine (hyperkalemia)
 Pain control
• Topical calcium gluconate gels (commercially available or compounded)
• Avoid sedating analgesics (sedation is marker of systemic toxicity)
• Nebulized calcium for pulmonary exposures (4 mL 2.5% or 5% calcium gluconate solution)
 Electrolyte repletion: calcium + magnesium
• Administer orally ASAP to prevent penetration (milk, calcium carbonate)
• Immediate IV repletion for severe toxicity: gluconate > chloride?

 Hypochlorite: aqueous solution formed by reaction of chlorine gas + water
 Household bleach (3-5% sodium hypochlorite)
o Mechanism of toxicity: local irritant
o Clinical manifestations: mild-moderate irritation with no further injury expected (GI tract, eyes)
o Management: dilute with water (copious irrigation with tepid water in ocular exposures)
 Industrial strength cleaners/swimming pool disinfectants (up to 20% hypochlorite)
o Mechanism of toxicity: corrosive
o Clinical manifestations: serious corrosive injury, dysphagia, severe pain, hematemesis, perforation
o Diagnosis: flexible endoscopy, chest and abdominal x-ray
o Management: symptomatic and supportive care

o Hypochlorite + acid = chlorine gas
o Hypochlorite + ammonia = chloramine gas
o Chlorine and chloramine are both irritant gases
 Chlorine dissolution → hydrochloric acid + hypochlorous acid
 Chloramine dissolution → hypochlorous acid + ammonia + oxygen radicals
o Affect moist mucus membranes (eyes, lungs, throat)
o Higher water solubility = faster time to symptoms onset: chlorine > chloramine
 Dyspnea, wheezing, bronchospasm
 Pulmonary edema

o Management: fresh air (supplemental oxygen/bronchodilators as needed)

 3 major types: nonionic, anionic + cationic
 Typically made up of 3 major components
o Soluble alkali salt: removes dirt + grease
o Surfactant: disperse grease into water
o Enzymatic agent: degrades stains and soils

o Anionic and nonionic detergents: local tissue irritants
o Cationic detergents: precipitate and denature proteins
 Quaternary ammonium compounds: keratolytic and corrosive effects
o Enzyme-containing detergents: release bradykinin + histamine → bronchospasm

o Vary based on active ingredients + concentration
o Serious morbidity and mortality are rare (cationic + dishwasher detergents = more dangerous)
o Gastrointestinal: vomiting, diarrhea, hematemesis, corrosive injuries (upper GI tract)
o Ocular exposures: mild to serious corrosive injury

o Endoscopy if suspect corrosive injuries to GI tract
o CXR for pulmonary symptoms

o Decontamination: dilute with water or milk (water or saline only for ocular exposures)
o Symptomatic and supportive care

o Highly concentrated detergents surrounded by polyvinyl alcohol film
 Usually contain: nonionic + anionic surfactants, fatty acids, ethanol, propylene glycol

o Mechanism of toxicity
 Concentrated surfactants → irritant + corrosive
 Propylene glycol, ethanol → CNS depression (especially in children)

o Clinical manifestations
 Gastrointestinal: vomiting, diarrhea, esophageal/stomach burning + ulceration
 Pulmonary: aspiration, pneumonitis, pulmonary edema, respiratory depression/failure, ARDS
 CNS: CNS depression ranging from drowsiness → coma, seizures
 Ocular: pain/irritation, conjunctivitis, corneal abrasions, ocular burns
 Metabolic: metabolic acidosis, hyperlactatemia

 Oxidizer with weak antiseptic properties
o Household uses: mouth gargles, local wound care, hair bleaching
o Industrial uses: produce washing, bleaching textiles/wool, foam rubber/rocket fuel production
 Generally available in 2 strengths
o Commercial/household (3-9%)
o Industrial use (27.5-70%)
o 35% solutions available from health food stores (“hyperoxygenation”)

o Extent of injury/gas formation is determined by concentration of H2O2
o Local tissue injury
 Low concentrations: irritant
 High concentrations: corrosive
o Gas formation
 H2O2 interacts with tissue catalase → O2 + H2O liberation
 1 mL of 3% H2O2 → 10 mL O2 vs. 1 mL 35% H2O2 → >100 mL O2

o Focused on detection of local tissue damage and gas embolism
o Local tissue damage (only if symptoms warrant)
 Investigate if presentation consistent with esophageal, gastric or intestinal injury
 Endoscopy
o Gas embolism
 CXR (for gas on cardiac chambers, mediastinum + pleural space)
 Abdominal x-ray (for gas in GI tract or portal system, also defines extent of bowel distention)
 MRI or head CT (for brain and/or spinal cord lesions) – for any neurologic symptoms

o Low concentrations can usually be managed at home
 Dilute with water (oral and ocular exposures)
 Remove contaminated clothing + jewelry
o High concentrations require immediate evaluation
 Decontamination
• Oral exposures: No role for gastric decontamination
• Ocular exposures: copious irrigation with tepid water
 Monitor airway and intubate as needed
 Trendelenburg position if evidence of gas in the heart
 Consider gastric suctioning in setting of abdominal distention
 Life threatening gas emboli: hyperbaric oxygen

 Found in a variety of household products
o Mouthwash (up to 75%)
o Hand sanitizer, rubbing alcohol (60-95%)
o Colognes, perfumes, aftershaves (40-60%)
o Food flavoring extracts (e.g. vanilla, almond, lemon) (~35%)

o Enhanced GABA effects + NMDA receptor blockade
o Oxidation of ethanol → ↑ acetyl-CoA + change in redox potential → hypoglycemia
 More common in children and malnourished patients

o CNS depressant at low doses, general depressant at high doses (e.g. respiratory depressant)
o Hypoglycemia, vomiting

o Majority of cases require observation only
o Changes in mental status → hospital evaluation
 Serum ethanol
 Complete metabolic panel (including blood glucose)
 Head CT if altered mental status is inconsistent with measured serum ethanol

o Symptomatic and supportive
 CNS/respiratory depression: intubate as needed
 Chronic EtOH abuse: thiamine, folic acid, fluid repletion, dextrose
o Hypoglycemia: dextrose supplementation as needed (sugary beverages)

 Nail polish
o Ingredients: Butyl acetate, ethyl acetate
o Generally considered non-toxic in small amounts
 Nail polish remover
o Ingredients: acetone, isopropanol
o CNS depression ± hypoglycemia → sugary beverage
 Artificial nail remover
o Ingredient: acetonitrile (endogenously converted to cyanide)
o Automatic 24-hour hospital observation (symptoms can be delayed 8-14 hours)
 Mild: nausea, vomiting, headache
 Severe: weakness, respiratory depression, seizures, acidosis, shock, coma

 Toothpaste
o Ingredient of concern: fluoride
o Requires enormous ingestion to cause toxicity (1 mg fluoride per gram of toothpaste)
o Limited to GI effects: nausea, vomiting, diarrhea
o Give milk (calcium will bind fluoride)
 Denture cleaning tablets
o Ingredients: citric acid, sodium bicarbonate, borates
o Single, acute ingestion usually benign: nausea, vomiting, diarrhea (greenish-blue color)
o Chronic or large ingestions: dehydration, hypotension, lethargy, seizures, renal failure
 Mouthwash
o Ethanol – previously covered

 Traditional lithium batteries = not a problem
o Treat like a foreign body: screen stool for passage of battery
 button batteries (watches, hearing aids, cameras, etc.) = serious problem
o Contain caustic metal salts (mercuric chloride)  leak
o Local discharge of electrical current
 Obtain x-ray to localize
o Esophagus: emergent removal by endoscopy
o Stomach of intestine: only remove if signs of obstruction or perforation

 Single magnet = not a problem
o Manage as a foreign body ingestion at home
o Screen stool for passive of magnet
 2 magnets or 1 magnet + metallic object= referral to healthcare facility
o Neodymium magnets are 10x stronger than other household magnets
o Attraction of adjacent magnets through different bowel loops  obstruction or
 Radio-opaque nature slows for easy detection
o X-ray: may need multiple views to determine if >1 magnet is ingested
 Removal of the foreign bodies
o Endoscopic removal
o Surgery

o Sniffing: inhalation directly from container
o Huffing: pour substance onto fabric and place over mouth/nose
o Bagging: instill solvent into plastic or paper bag and rebreathe from the bag

o Reports began in the 1960s of sudden cardiac arrest in young, otherwise healthy patients
o Common factor: inhalant use + sudden physical activity → death
o No other anatomical explanation for deaths

o CNS
 enhance GABAA receptor effects
 Inhibit NMDA mediated current (dose dependent)
o Cardiac
 Increased sensitivity or myocardium to epinephrine
 Slow repolarization/conduction (Na, Ca, K channels)
o Pulmonary
 Aspiration → direct pulmonary necrosis/inflammation
 Ventilation/perfusion mismatch → hypoxia + bronchospasm
o Renal
 metabolite → metabolic acidosis (hippuric acid)
 Oxidative stress → proximal tubule dysfunction

o CNS
 Stage 1: euphoria → excitability, disinhibition + impulsive behavior
 Stage 2: CNS depression (slurred speech, confusion, weakness) + hallucinations, tremors
 Stage 3: seizures, coma, death
o Pulmonary: respiratory depression
o Cardiac: arrhythmias, brady-asystolic arrest
o Renal: renal dysfunction
o Dermal: irritation -> frostbite, perioral eczema
o Chronic abuse: muscle weakness, tremor, spasticity, peripheral neuropathy, mood changes, loos of coordination, gait disturbances, dementia, learning impairments

o Gastrointestinal decontamination: no role (risk of aspiration > benefits)
o Airway management
 Observe for symptom development for 6 hours
 Symptoms usually = admission (unpredictable progression of symptoms)
 No need for routine use of antibiotics or steroids
o Arrhythmias
 Potential role for short-acting beta blockade
 Avoid exogenous catecholamines in acute exposures (can precipitate arrhythmias)
o Electrolyte replacement
o Benzodiazepines for seizures/agitation

 Contain one of 3 main ingredients
o Paradichlorobenzene (most common in United States)
o Naphthalene (traditional mothballs – e.g. Enoz)
o Camphor (use restricted to Japan)
 Difficult to distinguish based on appearance, odor, texture or size

 Paradichlorobenzene
o Ingestions are usually innocuous + managed at home (exception: massive ingestions)
o Clinical manifestations: nausea, vomiting, headache
o Management: dilute with water (no milk – will enhance absorption), antiemetics if needed

 Naphthalene
o Ingestion of >1 mothball must be referred to healthcare facility
o Mechanism of toxicity: oxidant stress  hemolysis + methemoglobinemia
o Clinical manifestations: nausea, vomiting, lethargy, seizures, methemoglobinemia, hemolysis
 Hemolysis + methemoglobinemia become clinically evident 24-72 hours post-ingestion → anemia (3-5 days)
 Methemoglobinemia + hemolysis: tachycardia, tachypnea, cyanosis, jaundice, weakness, altered mental status
o Management: consider transfusion (packed red blood cells), methylene blue (1-2 mg/kg IV)

 Camphor
o Ingestions >30 mg/kg must be referred to healthcare facility
o Mechanism of toxicity: unknown
o Clinical manifestations: nausea, vomiting, confusion, tremors, seizures
o Management: symptomatic + supportive, benzos → propofol, barbiturates