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The Tox Cave by Gregory S. LaSala, MD; 
Rita G. McKeever, MD; & Jolene Yehl, MD




​The Tox Cave dissects interesting ED cases from the perspective of a toxicologist, focusing on applying up-to-date management of the poisoned patient. The name Tox Cave was coined by a former toxicology fellow to describe the authors' small office space, likening it to the Bat Cave. The Tox Cave is where Drexel toxicology fellows and attendings have gathered to discuss the nuances of toxicology over the years.

Please share your thoughts about the Tox Cave's posts.


Wednesday, May 1, 2019

A 37-year-old man presented to the ED with thigh pain. He said his e-cigarette battery exploded in his pants pocket after he placed his keys in the pocket. He said he took his pants off immediately and noted that the battery had melted.

His initial vital signs were a temperature of 98.7°F, heart rate of 112 bpm, blood pressure of 159/95 mm Hg, and pulse oximetry of 98% on room air. He had a large area of burns of different degrees on his right thigh. Total body surface area of nine percent with first-, second-, and third-degree burns was noted.

may tox cave vaping leg.jpg

may tox cave vaping leg 2.jpg

E-cigarette use, or vaping, has risen significantly in the past 10 years. The device heats up a nicotine-containing solution that is inhaled. They may also be used to deliver other drugs like marijuana. The vast majority of these devices are powered by lithium ion batteries. These batteries are more typically used because they are lightweight and store more energy than other batteries, but they are also susceptible to thermal runaway, a condition involving overheating and spontaneous explosion. Circumstances that can lead to explosions include improper storage and charging, modifications of the device, and defective or poor-quality devices.

Reported e-cigarette explosion injuries include flame burns, chemical burns (alkali), blast injuries, inhalation injuries, and fractures. Patients have presented with injuries to the face (20%), hands (33%), and thigh and groin (53%).

How Should These Burns be Managed?

  • Wounds should be carefully irrigated and debrided to remove residual material.
  • Pain control
  • Many of these require consultation with appropriate specialists, depending on the injury, and transfer to a burn center.

What Tests Should be Done?

Most of these batteries are made of lithium-cobalt or lithium-manganese oxides. These metals may leak onto the skin and have the potential to be absorbed systemically. Lithium, manganese, and cobalt levels could be considered, but results may not be readily available.

The patient's lithium, manganese, and cobalt levels were sent. His clothes were removed, and the area was decontaminated. Due to the extent and nature of his burns, the patient was transferred to a burn center for further management.


  • Brownson EG, Thompson CM, et al. Explosion injuries from e-cigarettes [letter]. New Engl J Med. 2016;375(14):1400;
  • Kumetz EA, Hurst ND, et al. Electronic cigarette explosion injuries. Am J Emerg Med. 2016;34(11):2252.
  • Nicoll KJ, Rose AM, et al. Thigh burns from exploding e-cigarette lithium ion batteries: First case series. Burns. 2016;42(4):e42.
  • Maraqa T, Mohamed M, et al. Too hot for your pocket! Burns from E-cigarette lithium battery explosions: A case series. J Burn Care Research. 2018;39(6):1043.
  • Jones CD, Ho W, et al. E-cigarette burn injuries: Comprehensive review and management guidelines proposal. Burns. 2018 Nov 12; pii: S0305-4179(18)30279.
  • Treitl D, Solomon R, et al. Full and partial thickness burns from spontaneous combustion of e-cigarette lithium-ion batteries with review of literature. J Emerg Med. 2017;53(1):121.

Monday, April 1, 2019

A 50-year-old man presented to the emergency department complaining of ringing in his ears and difficulty understanding what people were saying. He was concerned that he was having a stroke. A full neurological exam was unremarkable aside from decreased hearing, but his hearing deficits appeared to be equal bilaterally. Otoscopic exam demonstrated a normal tympanic membrane, and the rest of his physical exam was unremarkable. The patient's past medical history was significant for hypertension and hypercholesterolemia, for which he took lisinopril and atorvastatin. He was recently treated with a 10-day course of doxycycline for cellulitis of his left arm.

Mechanisms of Drug-Induced Ototoxicity

The outer hair cells and the stria vascularis are targets for ototoxicity. The outer hair cells in the organ of Corti are responsible for converting mechanical waves into neural signals, while the stria vascularis in the cochlea is responsible for the electrochemical gradient that drives sound transduction.

Drugs associated with tinnitus include salicylates, quinine, streptomycin, neomycin, indomethacin, doxycycline, furosemide, metals, and caffeine. Ototoxicity at therapeutic dosing of most of the drugs listed below is unlikely. The risk of ototoxicity may increase with higher or prolonged dosing, individual susceptibilities (i.e., genetic predispositions), or synergistic effects with other ototoxic agents.

Drugs that can result in hearing loss include diuretics (furosemide, acetazolamide), NSAIDs, salicylates, aminoglycosides (reported risk of ototoxicity for gentamicin and tobramycin is five to eight percent), cisplatin (most ototoxic of antineoplastics and effects are often irreversible), and solvent abuse (toluene, styrene).

Occupation-Related Impairment

The most common cause is exposure to high-intensity or prolonged noise. This is generally preventable and typically results from prolonged cumulative exposure. Duration of exposure, intensity, individual characteristics, and additive effects with exposure to certain ototoxic chemicals contribute to the risk of damage. Chemical exposures associated with hearing impairment include solvents (styrene, toluene, xylene), metals (arsenic, lead and mercury), and nitriles and asphyxiants (carbon monoxide, hydrogen cyanide).

Non-toxicologic Causes of Hearing Loss

These include Ménière's disease, autoimmune disease, perilymphatic fistula, encephalitis, demyelinating disease, vestibular schwannoma, and degenerative changes associated with aging.

A CBC, CMP, and head CT were done for our patient, all of which were unremarkable. His salicylate level was negative. After further discussion with the patient, it was found that he had been taking large doses of ibuprofen while taking his doxycycline because of the pain associated with his cellulitis. The patient was discharged home with reassurance that his hearing would return, and was told to avoid all NSAIDs. He was told to follow up with his PCP. At one-month follow-up, the patient's hearing had returned and he only had intermittent bouts of tinnitus.


  • Campo P, Morata TC, Hong O. Chemical exposure and hearing loss. Dis Mon 2013;59(4):119;
  • Cunningham LL, Tucci DL. Hearing loss in adults. N Engl J Med 2017;377(25):2465.
  • Durrant JD, et al. American Academy of Audiology position statement and clinical practice guidelines: ototoxicity monitoring. American Academy of Audiology. October 2009;
  • Lewin NA, et al. Goldfrank's Toxicologic Emergencies, 9e. New York: The McGraw-Hill Companies; 2011.

Friday, February 1, 2019

A 32-year-old man presented to the emergency department complaining of eye pain and decreased vision. He worked for the city and was removing rust and graffiti from a wall with a power washer when the spray ricocheted off the surface and into his eye. He presented with a bottle of the chemical he used, which contained hydrofluoric acid (HF) and other chemicals. He rinsed his eyes with tap water, but experienced persistent decreased vision and pain in both eyes. His exam was remarkable for bilateral injected conjunctiva and excessive tearing.

More than 7,000 ocular exposures were reported to U.S. poison control centers per month from 2000 to 2016. (Ophthalmic Epidemiol 2018:1. doi: 10.1080/09286586.2018.1521982.) The highest rate of exposures was among children younger than 6 years old and lowest among adult patients 20 or older. The majority of these exposures were mild, with less than one percent needing hospital admission, but these injuries may cause significant and permanent damage to the patient. Most exposures were from household cleaning products (22%), followed by cosmetics, personal care products, and pesticides. These patients generally present with severe pain and complaints of vision changes or loss.

Routes of Ocular Exposure

  • Direct ocular injury from a liquid chemical such as household cleaning products being splashed into the eye
  • Exposure to chemical vapors, i.e., chlorine gas exposure
Exposure to topical ophthalmic medications such as accidental overdose of beta-blocker eye drops for glaucoma

Management of Ocular Exposures

If a patient presents with the complaint of a chemical coming into contact with his eye, immediate irrigation with normal saline or lactated ringers is necessary. Irrigation should not be delayed for a complete ophthalmic examination or review of the chemical's information. Local anesthesia such as tetracaine or proparacaine may be used to aid in the patient's comfort while irrigating. This will also allow for placement of a Morgan Lens for proper irrigation. After the Morgan Lens is placed, the affected eye should be irrigated with a minimum of 1 L of fluids. Continue irrigation of the eye if the patient's burning or painful sensation persists.

While weaker acids or bases may only require 1-2 L of irrigation, industrial chemicals may need hours of irrigation. The endpoint of irrigation should be reducing pain and neutralizing the pH of the affected eye. After irrigation, each affected eye should be tested with the goal of a neutral pH. It is important to wait for a minimum of one minute after irrigation before checking the pH to ensure that the pH being tested is the eye and not the solution used to irrigate it. After irrigation, visual acuity testing, eye inspection, and slit lamp examination should be performed.

Patient Disposition

Disposition depends on the extent of the injury:
  • Patients with baseline vision and no pain or corneal injury seen on exam can be discharged with good return precautions and follow-up as needed.
  • Patients with signs of globe perforation or rupture should receive emergent ophthalmologic consultation.
Patients with signs of corneal injury can be further subdivided into patients with conjunctival injection or minimal corneal haziness or injury who can safely be discharged with topical antibiotics, systemic analgesics, and ophthalmology follow-up within 24-48 hours and those with severe corneal haziness or opacification who should receive immediate ophthalmologic consultation.

Potential Systemic Toxicity

Systemic toxicity may occur via transcorneal absorption of eye drops, nasal mucosal absorption from nasolacrimal drainage, and absorption through the conjunctival capillaries and lymphatics. (Clin Ophthalmol 2016;10:2433;

Topical beta-adrenergic antagonists (timolol, levobunolol, carteolol) may cause bradycardia, hypotension, syncope, and bronchospasm.

In cases of ocular exposure to hydrofluoric acid (in rust removers, cleaners, or glass etching) and the corrosive effects of the hydrogen ion, fluoride ions have the potential to penetrate tissues deeply to cause local damage and systemic toxicity. (Int J Ophthalmol 2015;8[1]:157; Fluoride complexes with calcium and magnesium ions lead to hypocalcemia and associated cardiac dysrhythmias.

Our patient's eyes were anesthetized with tetracaine, and irrigation was initiated. Because he had been exposed to an industrial chemical, his eyes were irrigated for two hours. A total of 6L of normal saline were used for each eye, after which the patient no longer complained of pain but only a mild irritation. His vision returned to baseline, and the slit lamp examination demonstrated superficial corneal abrasions. A CBC and BMP were done because patients can develop hypocalcemia after HF exposure. They were, however, unremarkable for our patient. Ophthalmology was consulted and recommended no further irrigation but advised erythromycin ointment and follow-up within 24 hours.

tox cave ocular exposure.jpg

Monday, December 3, 2018

A 3-year-old boy presented to the ED after ingesting a liquid in an unmarked bottle. His parents said he vomited a few times before ED arrival. His initial vital signs were a blood pressure of 92/54 mm Hg, heart rate of 114 bpm, respiratory rate of 20 bpm, and pulse oximetry of 98% on room air. The parents reported that he may have ingested a cleaning solution known to contain aluminum hydroxide.

The patient was breathing comfortably, and his airway was monitored closely in the ED. He had no oropharyngeal edema or erythema, and his lung sounds were clear. His mother said she did not think he drank too much of the fluid. The patient was given a PO challenge, and he reported pain with drinking and did not want to drink more.

About 5,000 cases of caustic ingestions are reported annually in the United States, mostly unintentional ingestions in children. Common household corrosive agents may contain ammonia (jewelry or metal cleaners), hydrochloric acid (metal cleaners), sodium hydroxide (detergents, drain and oven cleaners), sodium hypochlorite (bleach), hydrogen peroxide (antiseptic, hair bleach, "food grade" homeopathics), sulfuric acid (drain cleaners), other alkaline substances (hair relaxer), and laundry detergent pods. Reviewing the product's online safety data sheet may be helpful if the ingredients are not listed on the packaging.

Caustics cause a direct chemical injury. The extent of damage depends on the pH, concentration, and volume of the substance ingested and the duration of exposure. Acids cause a coagulation necrosis, and eschar forms, limiting further damage. Acids tend to affect the stomach more than the esophagus. Damage from alkali ingestions occurs due to liquefactive necrosis. There is no eschar formation, so damage continues. This usually affects the esophagus more than the stomach. Other caustic agents work as oxidizing or reducing agents or by defatting and denaturing mechanisms.

Symptoms of a corrosive ingestion include oral pain and burns, drooling, nausea, vomiting, odynophagia, and abdominal pain. The presence or absence of intraoral burns is not reliable about whether damage occurred more distally. Gastrointestinal perforation and sepsis are potentially life-threatening consequences. Symptoms of airway compromise include progressive stridor, voice changes, and respiratory distress.

Some corrosive agents also have systemic effects:

  • Hydrofluoric acid and ethylene glycol may cause a profound hypocalcemia.
  • Barium salts can be found in some soaps and lubricants, and may cause a severe hypokalemia.
  • HCl and formaldehyde may cause a severe metabolic acidosis.
  • Concentrated hydrogen peroxide may cause air emboli.
  • Boric acid, aside from causing blue-green emesis, may lead to CNS depression and kidney failure.

Gastric decontamination is not recommended in most cases. Activated charcoal will limit the use of endoscopy by interfering with visibility. Induced emesis is contraindicated because it will lead to re-exposure and cause more damage.

Endoscopy is recommended in all patients with intentional ingestions to assess for esophageal injury and provide prognostic information. Also perform an endoscopy for patients with unintentional ingestions if they have stridor and two or more of the following symptoms: vomiting, pain, and drooling.

It is important to remember that endoscopy should be performed within 12 hours of ingestion and no later than 24 hours post-ingestion because the risk of perforation increases after this time. Those patients who are asymptomatic and tolerate liquids after a few hours of observation can safely be discharged with no further intervention.

Our patient was admitted to the hospital, GI was consulted, and an endoscopy was performed, which showed a small grade 1 lesion. No further intervention was needed. The patient tolerated a PO trial, and was able to resume his normal diet.

Zargar Grading of Caustic Esophageal Injury

                                                                                        Risk of

Grade     Description                       Incidence             Stricture Formation

0             No injury evident                 11-57%                        0

I             Edema and erythema            11-88%                        0

              of mucosa

IIA          Superficial non-                   7-26%                        <5%

              circumferential erosions,

              ulcers, hemorrhage,


IIB          Deep or circumferential         13.6-28%                   71.4%


IIIA         Multiple scattered                0.5-12%                   ~100%

              ulcerations with patchy

              necrosis (brown, black,


IIIB         Extensive necrosis                0-1%

Thursday, November 1, 2018

A 32-year-old woman and her 36-year-old husband with no past medical history presented to the ED with palpitations, headache, a feeling of warmth all over, and a rash extending from their upper chests to their faces.

The blood pressures of the wife and husband were 91/56 mm Hg and 93/61 mm Hg, respectively. Both were mildly tachycardic with heart rates of 112 bpm and 108 bpm. The patients described intense pruritus, and they had patchy blanching and erythema over their chests and faces with mild eyelid edema. They reported that their symptoms started five to 10 minutes after sharing an ahi tuna poke bowl.

What Is the Differential Diagnosis?

Allergic reaction, MSG reaction, disulfiram reaction, tyramine reaction, and carcinoid syndrome.

What Is the Diagnosis?

The patients were diagnosed with scombroid fish poisoning. Onset is usually within minutes to hours. Patients present with findings similar to those of an allergic reaction, including flushing (face, neck, torso), urticaria, bronchospasm, angioedema, dizziness, palpitations, and hypotension. Other symptoms include abdominal cramping and diarrhea. They may last 12-24 hours if untreated.

What Is the Pathophysiology of Scombroid?

The poisoning is due to inadequate cooling and poor fish preservation. This occurs most commonly in mackerel, tuna, and yellowfin tuna. The reaction is due to histamine, which is formed from histidine from the histidine decarboxylase from bacteria found in dark-meat fish.

What Is the Management/Treatment?

Treatment is mainly supportive:

  • Use an antihistamine such as diphenhydramine.
  • Use IV fluids for hypotension.
  • Give albuterol for signs of bronchospasm.

Other Illnesses Caused by Marine Toxins





Toxin and Mechanism





Amnestic shellfish poisoningShellfish like mussels (Eastern Canada, northeastern and western United States)Domoic acid; stimulates glutamate receptorsGI symptoms onset <24 hours and neurologic onset <48 hours; may last yearsAmnesia, weakness, mental status changes, pain, visual disturbances; may have GI symptoms
CiguateraLarge reef fish like barracuda, snapper, grouper, and sea bass (tropical areas)Ciguatoxin (odorless, tasteless, heat-stable); opens sodium channelsThree to 30 hours, may recur later; can lasts for monthsFacial and perioral paresthesias, temperature reversal sensation, GI symptoms, dental pain
Diarrheic shellfish poisoningShellfishOkadaic acid; inhibits protein phosphatases30 minutes to 12 hoursDiarrhea, nausea, vomiting, abdominal cramps
Neurotoxic shellfish poisoningShellfish (Western Florida and the Caribbean)Brevetoxins; opens sodium channelsThree to six hours; may last up to 72 hoursSimultaneous GI and neurologic symptoms: paresthesias, hot/cold reversal, myalgia, vertigo
Paralytic shellfish poisoningShellfish (Northwest and northeast United States, southern Chile, North Sea, Japan)Saxitoxin; blocks sodium channels30 minutes, daysFacial and perioral paresthesias, headache, dizziness, muscular weakness, ataxia, dysmetria, respiratory depression
Tetrodotoxin Puffer fish (fugu), blue-ringed octopus, horseshoe crabs/legsBlocks sodium channelsMinutes to hoursGI symptoms, progressive paresthesias and weakness (bulbar), ataxia, ascending paralysis, respiratory depression

Select characteristics of syndromes caused by marine toxins. Adapted from Clin Infect Dis 2005;41(9):1290.

The patients were treated with intravenous normal saline and diphenhydramine 50 mg. Their symptoms dramatically improved, and they were discharged home after brief observation.

Suggested Readings:

Lavon O, Lurie Y, Bentur Y. Scombroid fish poisoning in Israel, 2005-2007. Isr Med Assoc J 2008;10(11):789;

Sobel J, Painter J. Illnesses caused by marine toxins. Clin Infect Dis 2005;41(9):1290;