Dip, Chew, and Snuff: A Case of Nicotine Toxicity

Authors: Tim Montrief, MD MPH and Mehruba Anwar Parris, MD FAAEM
AAEM/RSA Publications & Social Media Committee and Common Sense Assistant Editor 
Originally published: Common Sense May/June 2019

Case
A 25-year-old Caucasian male with no significant known past medical history presented to a community emergency department via EMS with palpitations and altered mental status while on vacation at a friend’s bachelor party. Per the patient’s friend, he had been drinking alcohol all day and accidentally ingested a large amount of smokeless tobacco one hour prior to arrival, with subsequent nausea, vomiting, and excessive salivation. His friend denied any co-ingestions or drug use. The patient was found to be somnolent but arousable to voice, without any focal neurologic deficits and normal point of care blood glucose. The initial physical exam was remarkable for new-onset atrial fibrillation with a heart rate in the 160’s, blood pressure of 102/56 mmHg, respiratory rate of 16 breaths per minute, and saturating 100% on room air. Aside from atrial fibrillation with rapid ventricular response, the electrocardiogram was unremarkable (Figure 1). Additionally, the chest X-ray showed no evidence of cardiopulmonary pathology. Further testing revealed normal troponin, T4, and TSH levels. He had an elevated serum alcohol level of 191 mg/dL, and a negative urine drug screen. Initial cotinine and nicotine levels were not available. The patient was given a diltiazem bolus and drip, as well as four liters of lactated ringers, with subsequent heart rates in the low 100’s, with corresponding blood pressures in the 120’s/80’s. The patient was admitted to the ICU, and spontaneously converted back to a normal sinus rhythm within 24 hours of his initial presentation. The patient was discharged the next day with close outpatient follow-up.

The Utility of Intravenous Lipid Emulsion Therapy in the Management of Acute Calcium Channel Blocker Overdose

Image Credit: Wikipedia

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Author: Mary E. Blaha, DO
Indiana University School of Medicine
AAEM/RSA Publications and Social Media Committe

Calcium channel blocker (CCB) overdose is a potentially lethal toxicity with multiple management options available. Intravenous lipid emulsion (ILE) therapy is a potential treatment that is being used with more frequency. This review will discuss the management of CCB overdose focusing on the available ILE literature.

CCB Toxicity Overview
CCBs are commonly prescribed to manage hypertension and arrhythmias. When implicated in accidental or intentional overdose, CCBs carry a high potential for toxicity that can ultimately lead to severe cardiovascular injury.[1,2] Specificlly, dihydropyridine CCBs, which include amlodipine and nicardipine, act primarily on arterial smooth muscle L-type calcium channels, which can lead to reflex tachycardia. Nondihydropyridine CCBs, which include diltiazem and verapamil, act primarily on cardiac myocyte L-type calcium channels, which can lead to cardiogenic shock.

Marine Envenomations

Image Credit: Pexels

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Authors: Grant Barker, MS4
University of Miami Miller School of Medicine

Tim Montrief, MD MPH
Jackson Memorial Health System/University of Miami
AAEM/RSA Publications and Social Media Committee Member

Case
While spearfishing for lionfish off the coast of Key West during one of our yearly excursions, my father was unfortunate enough to graze a lionfish’s spines with his thumb. Within the next ten minutes, he was hyperventilating and in extreme pain. On our small boat with just a rudimentary first aid kit, thirty miles from shore, we had minimal interventions at our disposal. What would your next step in treatment?

Bark Scorpion Stings

Image Credit: Flickr

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Author: Ashley Grigsby, DO, PGY-3
Indiana University combined Emergency Medicine/Pediatrics

Centruroides sculpturatus, also known as the bark scorpion, is a type of venomous scorpion found in the Southwestern United States, i.e. Arizona, Nevada, New Mexico and Texas. The majority of these stings occur in Arizona, with a reported 3,498 emergency department (ED) visits in 2010.[1] The bark scorpion’s venom is a neurotoxin that works at axonal sodium channels causing excessive acetylcholine release in the neuromuscular junction. The clinical syndrome is most pronounced in young children, especially under 10 years old, who are most susceptible to the toxin. From 2005-2015, there were 185,000 scorpion calls to the poison centers nationally, 68% from Arizona.[1] Multiple other southwestern states were included in these calls; however, Arizona had the highest rate of neurologic and respiratory symptoms, and hospital admission.

Toxicology Review: Chronic Salicylate Poisoning

Image Credit: Flickr

Author: Pollianne Ward, MD
Temple University Hospital
Originally Published: Modern Resident January 2013

A 46-year-old female presented to an urban emergency department with complaints of a fall and altered mental status per family. It was reported that the patient had begun to experience nausea and vomiting followed by somnolence one day prior. She had no medical problems and did not take any medications regularly. Vital signs were heart rate 125, BP 130/86, temperature 99.6˚ F, respiratory rate 22 and oxygen saturation 99% on room air. The patient had some minor facial fractures from a fall, but no other injuries after trauma evaluation. EKG showed a sinus tachycardia with a widened QRS and peaked T waves. Basic metabolic panel revealed creatinine 8.5, potassium 7.3, and an anion gap metabolic acidosis. Treatment of hyperkalemia was initiated. A comprehensive drug screen was sent, which showed a salicylate level of 75mg/dl.

Salicylate overdose is a not uncommon chief complaint that emergency physicians encounter. Either intentional or accidental, acute toxicity is usually easily recognizable with symptoms of nausea, vomiting, tinnitus, tachypnea and lethargy in a known or suspected ingestion. However, chronic toxicity can often be indolent and present with non-specific symptoms.

Tox Talks: Bath Salts

Author: Meaghan Mercer, MSIV
Western University of Health Sciences
AAEM/RSA Medical Student Council President '11-'12


Originally Published: Modern Resident October/November 2011




Walking onto my shift a few days ago, I heard shrieking coming from my pod, and I knew this would be an interesting night. I rushed over to find a female restrained by four police officers screaming that demons were out to get her. Witnesses reported that after snorting an unknown substance, the patient began running down the street, topless, yelling that something was after her. It required all four officers to control her and get her to the ED. She was agitated and combative, unwilling to answer questions, with a HR: 130, RR: 20, BP: 190/115, temp: 103, and an O2 saturation of 95% on room air. This was it, what I have been hearing so much about ... a bath salt ingestion.

There has been a recent insurgency of patients presenting to emergency departments across the country in an agitated delirium caused by a new designer drug called bath salts. On October 21st, the DEA issued a temporary one-year ban on methylenedioxypyrovalerone (MDPV), the main component of bath salts, classifying it as a schedule 1 substance. Manufacturers evade the restriction with minor alterations in the chemical structure, and bath salts are still available in gas stations, head shops and online.[1]

Board Review: Toxic Alcohols

Image Credit: Dr. Wanner

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Authors: Gregory Wanner, DO
Emergency Physician/Clinical Faculty
Christiana Care Health System
@gregwanner

Paul Kolecki, MD
Associate Professor, Emergency Medicine
Medical Toxicologist
Thomas Jefferson University

An 18-year-old male presents to the emergency department (ED) stating, “Doc, I’m really drunk.” He and a friend were drinking in the friend’s garage. The patient drank one “very strong” sweet-smelling drink, which was prepared by his friend. He began to feel sick and nauseated and rode his bike home (with difficulty due to this intoxication, but without any falls or trauma). He vomited twice and his mother referred him to the ED. Attempts to contact the friend were unsuccessful.

How would you evaluate this patient? 

Several intoxicants can cause similar symptoms. While ethanol is the most likely cause, in patients with unclear ingestions other alcohols should be considered as well. The following is a brief summary of the alcohols often tested on in-service and board exams; a summary table is included at the end:

Tox Talks: Lithium Toxicity

Author: Kaitlin Fries, DO PGY1
Doctors Hospital
Originally Published: Modern Resident, December 2015/ January 2016

Lithium is often a first line treatment for bipolar disorder and major depressive disorder, and is commonly present on many emergency department patients’ medication lists. Studies have shown that as many as 75-90% of patients taking lithium long-term develop toxicity at some point throughout their treatment.[5] This is primarily due to the fact that lithium has a very narrow therapeutic index. In 2008, the American Association of Poison Control Centers received over 6,000 reports of potential lithium toxicities and four reported deaths.[5] While lithium toxicity is not as commonly seen as some other toxidromes in the emergency department, it is still very relevant to daily practice.

Synthetic Cannabinoids, a NEW Problem

Image Credit: Image from
Lance Cpl. Damany S. Coleman

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   Author: Nishma Sachedina, MD
   Emergency Medicine Resident
   University of Chicago
   AAEM/RSA Publications Committee Member

In the 1980s, scientists developed synthetic cannabinoids as a means to study the endocannabinoid system.[1,2] While some earnest chemists characterized cannabinoid receptors, more entrepreneurial chemists created a novel market of NEW drugs—nontraditional emerging web-based drugs.[3] Synthetic cannabinoids (SCs) are one varietal of these NEW drugs, and their use has been growing exponentially since they were first recognized as drugs of abuse in Europe in 2000.[4]

When SCs came to the USA in 2008, they flourished because of a lack of legislation against them and because they evaded standard medical toxicology screening tests.[1] Sold over the internet, in head shops, and in even in gas stations and convenient stores, SCs are often marketed as “legal highs.”[1] They can be consumed in a number of ways, from adding the compound to plant materials to dissolving the compounds in liquid for use in e-cigarettes or beverages.

Diphenhydramine Overdose in the ED

Image Credit: Flickr Andrew Ranta

Author: Kaylinn Dokken, OMSIV
Western University of Health Sciences

You are just at the beginning of your shift when paramedics call in and notify you that they are bringing in a 35 year old female who reports that she took 3,000 mg of diphenhydramine in a suicide attempt. Her BP is 145/80, her pulse is 160 beats per minute (bpm) with sinus tachycardia on the monitor, and her respiratory rate is 24 breaths per minute. Upon presentation, the patient is disoriented, continuously writhing, and having intermittent myoclonic jerks. An initial EKG is obtained and is shown below.

Local Anesthetic Systemic Toxicity – Is Fat The New “Wonder Drug?”

Image Credit: Photo by NIH: https://flic.kr/p/nQg4F7

Author: Jonathan Morgan, MSIV
Lake Erie College of Osteopathic Medicine-Bradenton

The provision of local and regional anesthesia is a core part of emergency medicine. Toxicity as a result of the administration of local anesthetics is exceedingly rare, but it does occur, and may even be more common than malignant hyperthermia.[1] Many outpatient facilities provide local or regional anesthesia and may not be prepared to handle severe toxicity. Emergency physicians should be prepared to deal with this rare but catastrophic outcome if it occurs following anesthesia either in their own department or in another setting.

Local Anesthesia Systemic Toxicity

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Local anesthetic systemic toxicity (LAST) can result from administration of any of the local anesthetics and can be difficult to identify. Classic descriptions include CNS toxicity (altered mental status, agitation, sedation, or seizures) preceding respiratory or cardiac arrest, but the presentation can be quite variable and the first symptom of LAST may be cardiac arrest. Symptoms may appear within a minute, but can also appear more than 5 minutes after injection of an anesthetic. There is a classic prodrome of auditory changes and metallic taste, but one review found that this was present in less than 20% of cases.[2,3]

Peds Tox Talk: Liquid Nicotine

Photo by Lindsay Fox

Author: Ashley Grigsby, DO PGY-1
Indiana University Emergency Medicine/Pediatrics

Originally Published: Modern Resident, June/July 2015 

Nicotine toxicity is a well-described clinical entity that often occurs in children who accidentally ingest cigarette buds or nicotine patches. However, a new form of nicotine has the potential to cause serious clinical symptoms, including death.

E-cigarettes use a form of liquid nicotine of varying concentrations that come in individual vials. E-cigarette use is on the rise across the United States, and unfortunately, the liquid nicotine is both easily accessible and appealing to young children. These liquid cartridges are often packaged in a tempting way, with one such cartridge described as having a cartoon monkey holding grapes on the front. The packaging is not regulated by the FDA and therefore has no child proof regulations for packaging. The liquid itself is also appealing for young children, and flavors include cotton candy, bubble gum, fruit, mint and chocolate.[1,2]

The CDC reported a significant increase from 2010 to 2014 of calls to poison centers regarding nicotine exposure. They also reported that e-cigarette exposure compared to regular cigarette exposure was about 1.5 times more likely to cause an adverse health effect.[1] Among the calls to poison centers during this time period, 51% involved young children.[2]

Treatment of Diphenhydramine Cardiotoxicity

Source: Flickr

Author: Teng Lu, MD
Emergency Medicine Resident
Stanford-Kaiser Emergency Medicine Residency

This post was peer reviewed.
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Case
A 16 year old girl was brought in by family for ingestion of an unknown amount of diphenhydramine (Benadryl®) in a suicide attempt. Initial vitals were remarkable for sinus tachycardia at a rate of 120. Her mental status was sleepy but responsive to speech with occasional coherent answers. On EKG her QRS interval was noted to be mildly widened at 108 msec. She was given multiple doses of sodium bicarbonate in the emergency department. Around 45 minutes after arrival, she had a witnessed generalized tonic clonic seizure which self-resolved. She was admitted to the pediatric intensive care unit for neurologic and cardiac monitoring.

Pearls
Diphenhydramine is a first generation antihistamine that also has anticholinergic properties (competitive antagonist at muscarinic receptors). Because of its lipophilic structure, it easily crosses the blood brain barrier. General anticholinergic symptoms include paradoxical agitation, hallucinations, seizures, cerebral edema, rhabdomyolysis, tachycardia, hypertension, hyperthermia, flushed/dry skin, urinary retention, and mydriasis.

The severity of symptoms increase with dose ingested:

• 0.05-0.2 mg/day: therapeutic dose
• 0.6-1.0 g: Minor symptoms – somnolence, tachycardia (<160/min), nausea/vomiting, 
• 1.0-1.5 g: Moderate symptoms - agitation, confusion, hallucinations, ECG disturbances 
• >1.5 g: Severe symptoms - delirum/psychosis, seizures, coma

Deaths occur due to cardiac toxicity, as diphenhydramine has type IA sodium channel blockade properties.

ECG changes are similar to tricyclic antidepressant (TCA) cardiotoxicity:

• wide complex tachycardia
• R’ in aVR 
• S wave in leads I, aVL

Treatment for cardiac toxicity is sodium bicarbonate (just like TCA toxicity), however much of the evidence regarding treatment is based on case reports. Case reports also suggest some benefit with intralipid use in severe cardiac or neurotoxicity. As always involve Poison Control Center early at 1 (800) 222-1222.


References:

Abdelmalek D, Schwartz ES, Sampson C, Halcomb SE, McCammon C, Arroyo-Plasencia A, Stenger A, Krehbiel N, Mullins ME. Life-threatening diphenhydramine toxicity presenting with seizures and a wide complex tachycardia improved with intravenous fat emulsion. Am J Ther. October 3 2013; Epub ahead of print.

Pragst F, Herre S, Bakdash A. Poisonings with diphenhydramine – a survey of 68 clinical and 55 death cases. Forensic Sci Int. 2006 Sep;161(2-3):189-97.

Radovanovic D, Meier PJ, Guirguis M, Lorent JP, Kupferschmidt H. Dose-dependent toxicity of diphenhydramine overdose. Hum Exp Toxicol. 2000 Sep;19(9)489-95.

Sharma AN, Hexdall AH, Chang EK, Nelson LS, Hoffman RS. Diphenhydramine-induced wide complex dysrhythmia responds to treatment with sodium bicarbonate. Am J Emerg Med. 2003 May;21(3):212-5.

Tox Talks: Drug Induced Noncardiogenic Pulmonary Edema

Author: Ashley Grigsby, DO, Indiana University

Noncardiogenic pulmonary edema (NCPE) is a clinical entity consisting of alveolar fluid accumulation without evidence of cardiac cause.[1] Although there are many non-toxicologic causes of NCPE, both opiate overdose and salicylate toxicity are known to cause NCPE and should be part of one's differential diagnoses.

Opiate overdose induced NCPE was first recognized by William Osler in 1880.[2] It can occur with any opioid, including heroin and methadone. Although the pathophysiology of this phenomenon is not yet completely understood, it is believed that both direct drug toxicity and hypoxia induced alveolar permeability play a role in the development of pulmonary edema.[1,2] New users and males are more at risk to develop NCPE than other opiate users. Symptoms become clinically apparent within 24 hours of use, but usually manifest within four hours.[2,3] Treatment for NCPE in these patients is mostly supportive. In one case series, approximately 33% of patients required mechanical ventilation; fortunately, most are able to be extubated within 24 hours as the effects are short lasting.[1] Naloxone may be beneficial in these patients to reverse the opioid toxicity. Patients who present with respiratory failure from opiate overdose should be observed for development of pulmonary edema, even if reversed with naloxone.[2]

'Tis the Season to Investigate Holiday Plant Myths

Orignially Published: Modern Resident, Dec/Jan 2012

Original Authors:
Christopher DeClue, MS1
Veronica Tucci, MD JD
Michael Omori, MD FACEP
University of South Florida Emergency Medicine

Submitted by: Rachel Engle, DO Communications Committee Chair 

Contrary to popular belief, the poinsettia (Euphorbia pulcherrima) is not a toxic plant. This misconception began as an urban legend dating back to 1919 when the two year old son of an Army officer stationed in Hawaii reportedly died of poisoning from what was believed to be a poinsettia leaf.

Tox Talks

Originally Published: Modern Resident, Dec/Jan 2010

Submitted by: Saadiyah Bilal, Publications Committee, Co-Chair

Iron toxicity remains a common toxidrome in the emergency department and is the leading cause of pediatric overdose death under age 6. Its antidote, defuroxamine, was recently designated by the Antidote Summit Authorship Group (Ann Emerg Med, Sept. 2009) as a medicine recommended for availability within 60 minutes of every emergency department in the country.

Tox Talks: Toxic Alcohols

Originally Published: Modern Resident, Oct/Nov 2010 

Original Author: Neal Shelley, MD Georgetown/Washington Hospital Center Emergency Medicine

Submitted by: Saadiyah Bilal, Publications Committee, Co-Chair  

Just like ethanol, ethylene glycol and methanol cause inebriation and are often ingested by a desperate alcoholic or as a suicide attempt.

Board Review: Methadone Intoxication

Originally Published: Modern Resident, Jun/Jul 2010

Original Author: Dana Kindermann, MD Georgetown-Washington Hospital Center Dept. of Emergency Medicine

Submitted by: Saadiyah Bilal, Publications Committee, Co-Chair 


Case history:
56 y/o male BIBA, found in apartment by roommate with altered mental status x 24h, found lying in feces. Patient (pt) with multiple substance abuse related admissions and ED visits. On arrival, pt slow to respond, confused, A&O x 2, denies pain, takes 150mg PO methadone daily, denies other med/drug use. Initial EKG: QTc - 500ms, bigeminy. Pt loaded with IV Mg, IV fluids; all initial labs normal and pt transferred to floor. Three hours later, pt develops Torsades de Pointes (TdP).