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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.

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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;

Saturday, September 29, 2018

A 27-year-old man presented by EMS was agitated, confused, and combative. EMS said they had received a call for a patient who was minimally responsive lying on the sidewalk. They noted the patient with pinpoint pupils and decreased respirations. The concern was that he had been using heroin, so he was given 2 mg intranasal naloxone. This caused the patient to become acutely confused and combative. He was awake and alert but oriented x 0. His vital signs included a temperature of 99.1°F, a heart rate of 122 bpm, a respiratory rate of 26 bpm, and pulse oximetry of 97% on room air.

At least 160 people were admitted to Philadelphia hospitals over one weekend in July for overdose caused by an adulterated heroin named Santa Muerte. This drug was being sold as some of the last remaining "pure heroin" in the city. Naloxone reversed patients' somnolence but then made them agitated and confused. A sample of the seized drug was analyzed by GC/MS and was found to contain heroin, fentanyl, and 5F-ADB. 5F-ADB is a synthetic cannabinoid, which explains the severe agitation and confusion that ensued. ("Information Regarding 'Santa Muerte' Stamped Drug Seizures Causing Hospitalizations in the Greater Philadelphia Area." The Center for Forensic Science Research and Education. July 25, 2018.

This recent epidemic of overdoses from adulterated heroin is similar to another epidemic in 1995 when heroin adulterated with scopolamine led to 370 reported overdoses in New York City. Hamilton, et al., reported extreme agitation with anticholinergic symptoms when these patients were given naloxone for reversal of respiratory depression. (J Toxicol Clin Toxicol 2000;38[6]:597.)

tox cave-Santa Muerte.jpg

Initial reports about Santa Muerte said the heroin was adulterated with an anticholinergic agent. Other adulterants considered were K2, PCP, Thorazine, atropine, and Benadryl. Patients were described as being agitated, combative, and delirious and as having flushed skin and dilated pupils.

5F-ADB is a synthetic cannabinoid that binds to the cannabinoid receptors to produce sympathomimetic effects. Symptoms include agitation, psychosis, hallucinations, anxiety, and tachycardia.

Many drugs have been adulterated with other substances over the years. It is important that physicians are aware of this and that they manage patients according to their presentation.

Like other heroin overdoses, naloxone should be administered to maintain adequate respiration. It is difficult to tell if giving naloxone will unmask another drug. The physician should be prepared to manage agitation when the somnolence is reversed by naloxone. Benzodiazepines can be used as an adjunct to treat the agitation. The patient's airway must be closely monitored, especially in circumstances where several doses of benzodiazepines were administered.

Our patient's symptoms improved after he was given 2 mg intravenous Ativan; he also received IV fluids and was monitored closely in the ED. The patient became progressively more awake, alert, and was oriented x 3. He asked for food and tolerated eating, and he walked around the ED with a steady gait prior to discharge.

Friday, August 31, 2018

A 30-year-old woman was brought in by EMS tearful and reluctant to answer questions initially. Her mother was with her and stated that the patient had been depressed and may have taken some pills in a suicide attempt. Her initial vitals on presentation were a temperature of 99.1°F, heart rate of 128 bpm, blood pressure of132/92 mm Hg, and a respiratory rate of 26 bpm. She had clear lungs and sinus tachycardia on cardiac monitoring. She admitted to having taken "a lot" of aspirin.

Initial Labs

CBC: WBC of 14, hemoglobin of 14 g/dL, hematocrit of 42%, platelet count of 250,000

BMP: Sodium of 132 mEq/L, potassium of 4 mEq/L, Cl of 99 mEq/L, bicarbonate of 16 mEq/L, BUN of 30 mg/dL, creatinine of 1.2 mg/dL, glucose of 105 mg/dL

Lactate: 2.6 mmol/L

Salicylate level: 62.2 mg/dL

Common Presentation of Salicylate Toxicity

  • Nausea, vomiting, gastric irritation
  • Tinnitus or hearing loss
  • Altered mental status: confusion, agitation, somnolence, coma
  • Seizures
  • Hypoglycemia
  • Tachypnea
  • Tachycardia
  • Acid-base disturbances: Central stimulation of the respiratory center results in hyperventilation, which leads to a respiratory alkalosis and a compensatory metabolic acidosis.
  • Hyperthermia because of the effects intracellularly of uncoupling oxidative phosphorylation
  • Cerebral and pulmonary edema

Acute v. Chronic Salicylate Ingestion

  • Acute ingestion:
    • Levels correlate with symptoms:
      • 30-45 mg/dL: Tinnitus and tachypnea
      • 45-60 mg/dL: Nausea and vomiting
      • 70-90 mg/dL: Tachycardia, altered mental status, and agitation
      • Toxic levels greater than 90-100 mg/dL are usually associated with severe toxicity.
  • Chronic ingestion:
    • The levels do not correlate with symptoms, and toxicity can occur at much lower levels.
    • Symptoms are generally more insidious and can appear similar to those of a septic patient.
    • The provider must have a greater index of suspicion because an unexplained anion gap acidosis may be the only indicator.

Risk Factors of Acute Respiratory Distress Syndrome (ARDS)

  • Cigarette smoking
  • Chronic salicylate toxicity
  • Presence of altered mental status

Management of Salicylate Overdoses?

  • Activated charcoal:
    • Be mindful of the time of ingestion.
    • Do not administer if a patient has a change in mental status because he may aspirate.
  • Alkalinize urine with sodium bicarbonate infusion (3 amps of sodium bicarbonate in D5W at 200 mL/hr) with the goal urinary pH between 7.5 and 8. It is important to keep potassium levels normal to promote urinary alkalinization. If the potassium is low, the patient will excrete hydrogen ions into the urine, acidifying it so that it can keep the potassium in the hydrogen potassium ATPase pump in the nephron.​
tox cave salicylate.jpg

  • Administer IV fluids to achieve euvolemia and ensure adequate urinary output.
  • Hemodialysis (HD):
    • Intermittent HD is the preferred modality of extracorporeal treatment (ECTR).
    • Indications:
      • If salicylate >7.2 mmol/L (100 mg/dL)
      • If salicylate >6.5 mmol/L (90 mg/dL) in the presence of impaired kidney function
      • In the presence of altered mental status
      • In the presence of new hypoxemia requiring supplemental oxygen
    • It is recommended to continue IV bicarbonate between ECTR sessions.
  • Check salicylate level and repeat every one to two hours until two sequential downward trending levels have been obtained.
  • Frequent blood gas monitoring.

Pearls and Pitfalls

If intubation becomes necessary, consider administering an intravenous bolus of sodium bicarbonate prior to RSI. Maintaining hyperventilation is important to avoiding respiratory acidosis, which can lead to rapid clinical deterioration. These patients will precipitously decline after intubation because patients on mechanical ventilation have difficulty maintaining a respiratory rate similar to native breathing. Exhaust all possibilities prior to intubating these patients.

  • Pharmacobezoars, aspirin-induced pylorospasm, and enteric-coated tablets can delay absorption.
  • Ensure correct interpretation of salicylate concentrations—labs report different units, including mg/dL, mg/L, and mmol/L.

The patient was immediately started on a bicarbonate infusion. She became more altered while in the ED, and had a repeat salicylate level of 92 mg/dL. Nephrology was consulted for immediate hemodialysis. She was diaphoretic and somewhat agitated at this point. A dialysis catheter was placed, and the patient was transferred to the ICU for hemodialysis. A repeat salicylate level was 54 mg/dL, and the patient's mental status began to improve. She required another session of dialysis, and a repeat level was 20 mg/dL. Repeat consecutive levels were checked and decreasing appropriately. She improved and was sent to a step-down unit, and psychiatry was consulted.


1. J Med Toxicol. 2015;11(1):149.

2. Ann Emerg Med. 2003 Apr 1;41(4):583.

3. Ann Emerg Med. 2015 Aug 1;66(2):165.