• Transfer and storage of substances to unlabeled or mislabeled food containers is a common occurrence and poses a significant poisoning hazard
• Plastic drink bottles (soda, water, milk, sports) are the most common secondary containers in exposures 
• Food imitating products (brightly colored, sweet smelling or tasting, similarity in color or consistency to known food products) are particularly hazardous
• Cleaning products and hydrocarbons are the most cited transferred products
• Serious toxicity is reported from herbicides (paraquat), corrosive chemicals, nicotine products, rodenticides, hydrocarbons, and glycols (antifreeze and brake fluids)
• Identification of substances in unlabeled containers can be difficult.  In the case of an ingestion of an unknown substance medical observation is recommended
• Prevention is key… Never reuse food containers for storage of substances.  Always keep substances in their original containers with manufacturer labels intact. Never store chemicals in the same cabinet, shelf, or area as food.

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Water beads are a colorful, fun, popular, and widely available product found in children’s toys, stress squeeze balls, arts and crafts supplies, plant hydration products, air fresheners, and first aid ice packs.  

These jelly-like small super-absorbent polymer balls are similar to the material found in diapers and absorb water expanding 100-800 percent of original size.

Pediatric ingestion is by far the most common poisoning exposure route but insertion into ears and nose and aspiration can occur and has led to serious adverse effects. More than 8000  water bead-related ingestion injuries have been treated in U.S. Emergency Departments.

Over the past 10 years, U.S. Poison Centers reported 19,660 exposures with 55% occurring in 2023 alone. In the majority of cases, no clinical effects (~88%) were seen, however in >11% of cases mild to moderate effects (abdominal discomfort, nausea, and vomiting) were reported and severe effects including complete bowel obstruction, necrosis, and surgical intervention in 0.11%.  The Consumer Product Safety Commission reported at least one death of a 10-month-old girl in 2023 due to water bead ingestion.

Ingested water beads quickly pass into the small intestines where they continue to expand over the next few days and can become large enough (especially in children less than 2 year of age) to be unable to pass through the ileocecal valve causing small bowel obstruction requiring surgical intervention.   

There is little data to guide management after ingestion.  The majority of cases have no clinical effects and home observation is appropriate for asymptomatic for patients greater than 2 years. Recommendations from a report of case series and literature review , in patients less than 2 years of age with evidence of ingestion and symptomatic patients include hospitalization, imaging with US or CT, and close monitoring.   CT, ultrasound, and endoscopy are not 100% reliable and often do not visualize these intraluminal foreign bodies.

 In December 2025, the CPSC approved new federal safety standards for water beads toys setting limits on maximum expansion size of beads and amount of allowable acrylamide.

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• Nitrous oxide (N2O) aka “laughing gas”, used clinically for its psychotropic properties as an inhalational anesthetic, is one of the most abused inhalants for decades due to its unregulated wide availability and public perception that it is a safe high. Social media trends have popularized use by teens and young adults.
• Easily purchased online, in groceries stores, gas stations,  smoke and vape shops it is used as a food processing  propellant in steel aerosol containers like whipped cream and available in small canisters marketed as whipped cream chargers called “whippets”.
• Between January 1, 2014 - Dec 31, 2023, nitrous oxide nearly doubled in exposure rate with a total of 2,322 exposures reported to U.S Poison Centers.  From 2010-2023,  1240 US deaths were reported between the ages of 15-74 attributable to nitrous oxide poisoning.
• Similar to Ketamine and phencyclidine, nitrous oxide causes antagonism at the NMDA receptor resulting in short lived reversible euphoria and sedation and analgesic effects through the K-opioid receptor.
• Nitrous oxide fatalities occur primarily due to asphyxiation and oxygen deprivation causing neurologic sequela, hypotension, arrythmias, and death. N2O depresses the sensation of shortness of breath so users may not seek fresh air.
•  Chronic recreational N2O exposure impedes vitamin B12 function and causes a distinct neurological syndrome manifested by numbness, gait disturbances, loss of coordination, changes in mentation, and loss of bowel and bladder control, and hematologic abnormalities.
• On June 6, 2025, the FDA issued a public advisory warning consumers not to inhale nitrous oxide products due to potential for severe adverse events if used for recreational nonfood purposes.

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Cyanide is one of the deadliest known poisons causing immediate toxic effects and lethality within seconds to minutes. Exposures are rare, most commonly by inhalational route (HCN gas) from structural fires due to combustion of synthetic materials or from ingestion of cyanide salts. Cyanide toxicity can also occur from dermal or parental (sodium nitroprusside) exposure. 

• Cyanide is a mitochondrial poison act by binding the heme portion of cytochrome oxidase a3 in the electron transport chain halting ATP production from oxygen shifting cellular respiration from aerobic to anaerobic metabolism causing a profound lactic acidosis > 8
•  Impaired peripheral oxygen delivery and utilization can cause “arterialization” of venous blood (cherry red skin), in which the concentration of venous oxygen resembles that of arterial blood 
• Clinical effects are profound but nonspecific, most frequently reported include unresponsiveness, respiratory failure, hypotension, cardiac arrest, and seizure
• There are no pathognomonic clinical symptoms or diagnostic blood tests for cyanide poisoning (good correlation of carboxyhemoglobin levels >10 with cyanide toxicity, lactate level >10), clinical suspicion is required
• Rapid administration of antidote is crucial. Survival is determined by timing of exposure, rapid recognition, and administration of antidote and supportive treatment. 

The preferred first line antidote is hydroxycobalamin (vitamin B12) available as Cyanokit, which has higher affinity for cyanide than cytochrome oxidase and binds to form harmless cyanocobalamin and is renally excreted. Limited studies reveal good survival rates in noncardiac arrest patients. Hydroxycobalamin has minimal side effects (red skin and urine, increased BP) and is well-tolerated with safer and simpler mechanism of action than Nithiodote (original antidote), containing sodium nitrite (CN preferentially binds methemoglobin to form cyanomethemoglobin) and thiosulfate (provides sulfur to convert cyanide to thiocynate for excretion). Sodium nitrite has numerous adverse effects causing hypotension and methemoglobin (contraindicated in smoke inhalation victims due to concern for carbon monoxide poisoning, G6PD deficiency, preexisting amenia), and hypersensitivity reactions. Sodium thiosulfate has less side effects and augments cyanide excretion but is considered less effective due to its slow onset, short half-life, low volume of distribution, and poor intracellular penetration.  

As of August 2025, the American Society of Health -System Pharmacists (ASHP) Drug Shortage lists Cyanokit as “limited availability” in the U.S. as manufacturing was suspended due to investigation of ongoing quality defect with concern for sterility and endotoxin content. Impacted batches were released and their numbers are listed in an FDA bulletin (see references). Healthcare providers should weigh the potential benefit of using Cyanokit against the risk of infection. Infusion set with 0.2 micron in line filter can be temporarily used for administration of Cyanokit 5 mg hydroxycobalmin to prevent potential infection.

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Question

A 3 year old is bitten by a spider on his right ear which is causing him intense pain, tachycardia, and muscle cramping. Identify the spider.  What is the treatment?

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Volatile inhalants such as glue, lighter fluid, spray paint are abused by "sniffing" (from container), "huffing" (poured into rag), or "bagging" (poured into bag). "Dusting" is the abuse of canned air dust removal products. These inexpensive easliy accessible products are so dangerous  that manufacturers include product warnings regarding lethal consequences from misuse and even may indicate that a bitterant is added to discourage use. Common duster gases include the halogenated hydrocarbons, 1,1-difluoroethane or 1,1,1-trifluroethane which are highly lipid soluble and rapidly absorbed by alveolar membranes and distributed to CNS. Desired effect of euphoria and disinhibition rapidly occur but unwanted side effects include confusion, tremors, ataxia, pulmonary irritation, asphyxia and, rarely, coma.

"Sudden sniffing death" is seen within minutes to hours of use and is due to ventricular arrhythmias and cardiovascular collapse. Available experimental evidence postulates the following mechanisms: Inhibition of cardiac sodium, calcium, and repolarizing potassium channels hERG and I(Ks) causing reduced conduction velocity and altered refractory period leading to reentry arrythmias or myocardial "sensitiization" to catecholamines resulting in after depolarizations and enhanced automaticity. Treatment should include standard resuscitation measures but refractory arrythmias to defibrillation have been reported and use of amiodarone and beta blockers should be considered.

Bottom Line:

• Volatile Inhalant Abuse is common and dangerous 
• SSD can occur even with first use
• Ventricular arrythmias can be refractory to electricity. Consider amiodarone and beta blockers.

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Drug-induced hypoglycemia is an important cause of hypoglycemia which should be considered in any patient presenting with altered mental status. In one study, drug-induced hypoglycemia represented 23% of all hospital admissions attributed to adverse drug events. Risk factors for developing hypoglycemia include older age, renal or hepatic insufficiency, concurrent use of insulin or sulfonylureas, infection, ethanol use, or severe comorbidities. The most commonly cited drugs associated with hypoglycemia include:

• Quinolones
• Sulfonylureas* either alone or with a potentiating drug 
• Insulin
• Pentamidine
• Quinine
• B-blockers
• ACE Inhibitors
• Tramadol**

*In Glipizide users, there was 2-3 fold higher odds of hypoglycemia with concurrent use of sulfamethoxale-trimethoprim, fluconazole, and levofloxacin compared with patients using Cephalexin.

**Tramadol potentially induces hypoglycemia by effects on hepatic gluconeogenesis and increasing insulin release and peripheral utlizilation. Was seen in elderly at initiation of therapy within first 30 days.

BOTTOM LINE:

Take care in prescribing drugs known to increase risk of hypoglycemia in elderly patients, with comorbidities, or those already taking medications associated with hypoglycemia. 

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Scromboid (histamine fish poisoning) can be easily misdiagnosed since its' clinical presentation can mimic that of allergy. Seen most frequently in the summer and occurring with Scombroideafish (tuna, mackerel, bonito, skipjack) but also with large dark meat fish (sardines and anchovies) and even more commonly with nonscromboid fish such as mahi mahi and amber jack. In warm conditions when fish is improperly refrigerated, bacterial histidine decarboxylase converts muscle histidine into histamine which quickly accumulates. Histamine is heat stable and not destroyed with cooking. 

• Clinical features: Intense flushing of face, neck, and upper torso, urticaria, abdominal cramps, headache, palpitations, diarrhea, nausea, vomiting, burning of the mouth and throat.
• Symptoms begin within minutes of ingestion and typically last several hours
• Self limiting condition. Mainstay of treatment is H1 blockers (antihistamines) and good supportive care. If bronchospam present steroids and inhaled B2 agonists should be administered.

Bottom Line:

Scromboid poisoning is due to histamine ingestion and is often misdiagnosed as allergic reaction. It is preventable with proper fish storage.

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The primary tenet of poisoning treatment is to separate the patient from the poison. Gastric decontamination has been the cornerstone of poisoning treatment throughout history and methods include induced emesis, nasogastric suctioning, EGD or gastrostomy retrieval, activated charcoal, and whole bowel irrigation. Current guidelines for gastic decontamination are limited to few clinical situations. The detection of residual life threatening poisons in the stomach would be of value in predicting who might benefit from gastric decontamination in overdose.

Plain radiographs have variable sensitvity in detecting radioopaque pills. Computed tomography (CT) has been successful and gained wide acceptance in the detection of drug in body packers. In a recent study, authors studied the usefulness of non-contrast abdominal computed tomography for detection of residual drugs in the stomach in patients  presenting over 60 minutes from acute drug overdose:

• 140 patients were included in this study
• Median ingested drug amounts were 28 tablets or capsules
• Median time until CT scan was performed after drug ingestion was 4 hours
• Multiple types of drugs were ingested in 53.6%
• Sustained-release drugs  were ingested in 17.1 %
• Gastric lavage and WBI were performed on 32.9% patients
• Drugs were detected in 25.7% in the non-contrast CT scan performed over 60 min after ingestion.
• Total duration of hospital stay was significantly longer in the “presence of drugs” group

BOTTOM LINE:

Non-contrast CT may help to predict which patients would benefit from gastric decontamination in acute life-threatening drug poisonings.

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Most clinicians are familiar with use of methylene blue for the treatment of methemoglobinemia, as a urinary analgesic, anti-infective, and anti-spasmodic agent, or for its use in endoscopy as a gastrointestinal dye, but this compound also has a role as a rescue antidote in life threatening poisonings causing refractory shock states and other shock states.

• Nitric Oxide plays an important role in the regulation of vascular tone.
• Metylene blue inhibits the NO-cGMP pathway which decreases vasodilitation and increases responsiveness to vasopressors.
• Several case reports document hemodynamic improvement in recalcitrant shock states form calcium channel and beta blockers despite multiple therapies including vasopressors, glucagon, high dose insulin, and fat emulsion therapy.
• Dosing is 1-2 mg/kg (0.1-0.2 ml/kg) of 1% solution given IV over 5 minutes folllowed by continuous infusion.

Bottom Line: 

Methylene blue should be considered when standard treatment of distributive shock fails. 

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• History of regular cannabis use at least weekly for any duration of time.
• Compulsive hot water bathing multiple times per day for symptom relief which is mediated by the TRPV capsaicin receptors.
• Resolution of symptoms with cannabis cessation.
• Prior nonrevealing extensive diagnostic work up.

CHS Treatment:

• Definitive and most effective treatment is to stop cannabinoid use which provides complete relief within 7–10 days.
• Temporary relief occurs with hot water bathing, Capsaicin topical cream, Haldol administration, and fluid resuscitation.

Bottom line: Patient education should be provided on the paradoxical and recurrent nature of the symptoms of CHS to discourage relapse of use often stemming from false preception of beneficial effects of cannabis on nausea. 

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Question

A 19 year old male presents confused and very agitated complaining of seeing things and stomach pain. His friends report he ingested a naturally occurring plant to get high a few hours ago but is having a "bad trip".  His physical exam :

Temp 100.3, HR 120, RR 14, BP 130/88. Pulse Ox 98%.

Skin: Dry, hot , flushed

HEENT: Marked mydriasis 6mm

Lungs: Clear

Heart: Tachycardic

Abdomen: Distended tender suprapubic with absent bowel sounds,

Neuro: Extremely agitated pacing, no muscular rigidity.

What has he ingested and what is the treatment?

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 A 68 year old male presents to the ED complaining of weakness to his legs. He states today his yard chores took him over 2 hours to complete instead of the usual 15-20 minutes due need to take frequent breaks for rest due to leg pain. He denied any chest pain or shortness of breath. Past medical history included hypercholesteremia, HTN,  and CAD. He is taking aspirin and recently started on rosuvastatin.

His physical exam was unremarkable.

Results showed normal EKG and CBC. Bun was 70, Creatinine was 3.4, and CPK of 1025.

This patient has statin induced rhabdomyolysis and acute renal failure.

Take Home Points:

• Rhabdomyolysis is characterized by muscle necrosis which causes the release of myoglobin into the bloodstream.
• Clinical manifestations can range from asymptomatic elevation of CPK to life-threatening cases with extremely high CPK levels, electrolyte imbalance, and acute renal failure.
• Classic triad is: muscle aches and pains, weakness, and tea-colored urine.
• Numerous recreational drugs, pharmaceuticals, and toxins can alter myocyte function. Ethanol, statins, and cocaine in particular have high risk to cause rhabdomyolysis.
• 50% of cases of statin-induced-rhabdomyolysis were due to drug interactions.

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Sulfonylureas are commonly used oral hypoglycemic agents for type II diabetes. Agents on the market include glipizide (Glucotrol), glyburide (Micronase, Glynase, Dibeta) and glymepiride (Amaryl). These agents exert their effect by stimulation of insulin release from the pancreatic beta islet cells. Following overdose, hypoglycemia is usually seen within a few hours of ingestion and can be prolonged and profound. First line treatment for rapid correction of severe hypoglycemia is administration of an intravenous bolus of concentrated dextrose. However, use of dextrose infusion in attempt to maintain euglycemia is problematic as it can cause further release of insulin and rebound hypoglycemia. Octreotide ia a long acting synthetic somatostain analogue, blocks insulin secretion and has been shown to prevent recurrence of hypogylcemia better than placebo.

Bottom Line:

• Octreotide is the antidote of choice for sulfonylurea poisoning. Its use greatly simplifies management by avoiding the need for a central line, prolonged ICU admit, and frequent monitoring.
• Bolus 50 μg IV followed by an infusion of 25–50μg/h or give100 mcg subcutaneously with additional doses at 6-12 hour intervals for recurrent hypoglycemia. Octreotide has similar bioavailability by SC and IV route. It's duration of action can extend from 6 to 12 hours with SC use.
• After stopping Octreotide monitor for 12-24 hours for rebound hypoglycemia.

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Methylene Blue is a dye that was synthesized in the late 1800s as an antimalarial drug. After the emergence of chloroquine its use loss favor partly due to unpopular side effects of temporarily turning the urine, other body fluids, and the sclera blue. Methylene blue is primarily known as a highly effective fast acting antidote for methemboglobinemia. Over the past few years, it has become an important therapeutic modality with expanding uses in cardiac surgery and critical care.  As a potent inhibitor of nitric oxide mediated guanylate cyclase induced endothelium vascular smooth muscle relaxation, it has been shown to be effective in increasing arterial blood pressure and cardiac function in several clinical states, such as septic shock and calcium channel blocker poisoning.

BOTTOM LINE:

• Methylene blue should be considered for treatment of refractory shock from calcium channel and beta blocker poisoning.

• Clinical improvement in refractory hypotension and reduction of vasopressor dose has been described in several poisoning cases. 

• Recommended dose is 1–2 mg/kg injection with effects seen within 1 hour.

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Despite initial excitement for the use of intravenous lipid emulsion (ILE) therapy as an antidote for serious poisonings due to lipohphilic drugs there remains an absence of evidence combined with an incomplete understanding of its efficacy, mechanisms of action, safety, and analytical interferences to recommend its use except in a few clinical scenarios.

The lipid emulsion workgroup performed a comprehensive analysis of four systematic reviews and based recommendations from consensus of expert panelists from the American Academy of Clinical Toxicology, the European Association of Poison Centres and Clinical Toxicologists, the American College of Medical Toxicology, the Asia Pacific Association of Medical Toxicology, the American Association of Poison Control Centers, and the Canadian Association of Poison Control Centers. Toxins evaluated had to have a minimum of three human cases reported in the literature.They concluded that ILE could be indicated for the following clinical situations:

•  In Bupivacaine poisoning resulting in cardiac arrest or life threatening toxicity (dysrhythmias, VTach  with compromised organ perfusion, VFib, status epilepticus, and/or hypotension with organ compromise defined as  increased lactate concentration, acute kidney injury, increased troponin, altered mental status, or decreased capillary refill) ILE is recommended after standard ACLS is started  and if other therapies fail or as last resort.

• In life-threatening toxicity due to other local anesthetics,  ILE recommended if other therapies fail/in last resort

• In cardiac arrest due to toxicity from Amitriptyline (or other tricyclic antidepressants), lipid soluble and non-lipid soluble Beta-receptor antagonists,  Bupropion, Calcium channel blockers (diltiazem, verapamil and dfihydropyridines), Cocaine, Diphenhydramine, Lamotrigine,  Baclofen, Ivermectin and other Insecticides, Malathion and other Pesticides, Olanzapine and other Antipsychotics, and SSRIs.

• Most common regimen of ILE was a bolus of 1.5 mL/kg of ILE 20% followed by infusion of 0.25 mL/kg/min

• The use of ILE with extracorpeal membrane oxygenation may cause fat deposition in the circuit and increase blood clot formation causing malfunction and limitation of use of this potentially life saving modality. This should be considered if VA-ECMO is a treatment option.

The Bottom Line:

The use of Intravenous Lipid Emulsion in severe poisoning is recommended only for a few poisoning scenarios and was based on very low quality of evidence, and consideration of risks and benefits, adverse effects, laboratory interferences as well as related costs and resources.

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Bradycardias caused by poisoning are due to the toxin's effects on cardiovascular receptors and cellular channels and transport mechanisms and are often refractory to standard ACLS drugs. The most common drug classes responsible for bradycardias are calcium channel and beta blockers and digoxin (cardiac glycosides). Sodium channel blockers, clonidine, and opiates also can cause bradycardias. Antidotes are as follows:

• Glucagon 5-10mg IV bolus followed by 1-5 mg/hr (Always pretreat with antiemetic) - Beta Blockers
• Calcium infusion 1-3 grams IV Bolus - Calcium Channel Blockers
• High Dose Insulin Euglycemic therapy of reg insulin 0.5-2 unit/kg Bolus (ie. 100 Units) with D50 IV bolus followed by reg insulin 0.5-1 units/kg/hr and dextrose 0.5 grams/kg/hr - Calcium channel and Beta Blockers
• **Intravenous Lipid Emulsion therapy bolus 1.5 mL/kg of ILE 20% followed by an infusion of 0.25 mL/kg/min-  Very small subset of toxins. See below.
• Atropine 2mg IV - Acetylcholinestrase inhibitors (Organophosphates)
• Sodium Bicarbonate 1-3 amps IV - Sodium Channel Blockers
• Digibind  for acute toxicity10 vials IV (20 Vials in cardiac arrest) and for chronic toxicity 2 vials and repeat as needed - Cardiac gylcosides
• Narcan 2 mg IV repeat boluses up to 10 mg- Opiates and Clonidine

** ILE is recommended only in life threatening poisonings where other accepted therapies have been use first or in cardiac arrest clinical scenarios. 

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A leading cause of cardiac arrest in patients 40 years and younger is due to drug poisoning.  Adverse cardiovascular events (ACVE) such as myocardial injury (by biomarker or ECG), shock (hypotension or hypoperfusion requiring vasopressors), ventricular dysrhythmias (ventricular tachycardia/fibrillation, torsade de pointes), and cardiac arrest (loss of pulse requiring CPR) are responsible for the largest proportion of morbidity and mortality overdose emergencies. Clinical predictors of adverse cardiovascular events in drug overdose in recent studies include:

• QTc prolongation on presentation ECG ( > 500 msec )
• Prior history of either coronary artery disease or congestive heart failure
• Metabolic acidosis (elevated serum lactate)

Bottom line:

Obtain ECG and perform continuous telemetry monitoring in overdose patients with above risk factors. Patients with two or more risk factors have extremely high risk of in-hospital adverse cardiovascular events and intensive care setting should be considered.

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Bupropion (Wellbutrin, Zyban) is unique monocyclic antidepressant and smoking cessation agent that is structurally similar to amphetamines.  Bupropion blocks dopamine and norepinephrine reuptake and antagonizes acetylcholine at nicotinic receptors.

• One of the most common causes of drug-induced seizures.
• Sinus tachycardia is the most frequently seen cardiac effects with overdose.
• QTc prolongation and ventricular dysrhythmias can occur in severe overdose. New evidence supports this is not related to cardiac sodium channel block but likely due to blockade of the delayed rectifying (ikr) potassium channel and gap junction inhibition in the myocardium simulating effects class IA effect.

Bottom line:

Bupropion is a common cause of drug induced seizures but in severe overdose can also cause prolonged QTc and wide complex ventricular dysrhythmia that may be responsive to sodium bicarbonate. All patients with an overdose of bupropion should have an ECG performed and cardiac monitoring to watch for conduction delays and life-threatening arrhythmias.

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Question

47 year old woman presents with cough, headache, weakness, and low grade fever. Her symptoms have been present for several days. Vital signs are temperature 99.9 F, HR 96, RR 16, BP 140/88, Pulse Ox 98%.  Physical exam is nonfocal. She is Influenza negative. She is treated with Ibuprofen and oral fluids.  Upon discharge she mentions she is having difficulty hearing and feels dizzy. Upon further questioning she admits to ringing in her ears. What tests should you order?

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