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

This post was peer reviewed.
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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: 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]

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.