UMEM Educational Pearls - Toxicology


US, Canadian and European critical care and toxicology societies recently published a consensus recommendation is the management of CCB poisoning.

Bottom line:

1. First line therapy remains unchanged: IV calcium, atropin, high-dose insulin (HIE) therapy, vasopressor support (norepinephrine and/or epinephrine).

2. Refractory to first line therapy: increase HIE, lipid-emulsion, transvenous pacemaker

3. Refractory shock, periarrest or cardiac arrest: Above (#1 & #2) plus ECMO if available.

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Category: Toxicology

Title: "Leaves of 3 let them be"

Keywords: Poison Ivy, Toxicodendron, Urushiol (PubMed Search)

Posted: 10/6/2016 by Kathy Prybys, DO (Emailed: 10/7/2016) (Updated: 10/7/2016)
Click here to contact Kathy Prybys, DO


Fall clean up = Poison Ivy, oak, sumac (Toxicodendron species) which is ubiquitous in North America but it can also be found in British Columbia, Mexico and in parts of Asia. These plants are truly the scourge of outdoor enthusiasts and agricultural workers responsible for up to 40 million cases of miserable often temporarily incapacitating rashes annually.

Fast Facts:

  • Grows as plant, vine, or shrub with leaves ranging in color from light or glossy green to red and yellow in fall.
  • Exposure by direct contact with plant, indirectly from oil resin on objects, clothes, pets, or airborne from burning plant.
  • Urushiol toxin induced type IV hypersensitivity allergic contact dermatitis. This oily resin toxin is excreted from all parts of plant (stems, leaves, flowers, roots, vines). and is extremely stable staying active even after plant dies.
  • Intensely itchy blistering rash starts 12-72 hours after contact and lasts up to 21 days. Characterized by red streaks or linear configuration where skin brushed up against plant sap. Inflammation (redness, swelling, hives, blistering) to thick leathery plagues depending on severity and vulnerability of skin location. Intense inflammation can mimic cellulitis.
  • Rash is Not contagious but spread of oil on clothes, pets, tools, objects is!
  • Delayed reaction accounts for seemingly "spread" of rash. Eruption rate depends on thickness of skin and dose of urushiol oil.

Treatment Tips:

  • Prevention. Avoidance and universal precautions when gardening. Clusters of 3 leaves each trio growing on their own stem, hairy vines, no thorns, white berries.
  • Cover skin to prevent exposure and if known contact immediately wash skin, clothes, objects.
  • Hot water relieves itch as does cool compresses.
  • Domeboro or witch hazel are astringents can reduce inflammation.
  • External analgesics (e.g., benzocaine, lidocaine, benzyl alcohol) can help itching.
  • Highly viscous or granular cream surfactant washes bind urushiol and can reduce exposure. Zanfel, Mean green, Gojo orange, various generic poison ivy removal scrubs now available. (Zanfel works wonders used every few hours and may alleviate need for steroids but is $$$ and several tubes are required).
  • In severe cases, Steriod burst followed by 2-3 week taper to prevent relapse flare.

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Naloxone has been used to reverse opioid-induced respiratory depression for decades. The “standard” dose of opioid intoxication has been 0.4 mg.  However, over the past decade, initial naloxone dose for opioid intoxication has evolved to recommend a lower initial dose (0.04 – 0.05 mg).


A recent article by Connors et al. reviewed 25 medical resources (internet, medical texts and study guides) of different medical specialties (internal medicine, medical toxicology, emergency medicine, pediatrics, anesthesiology, pain medicine and general medicine)



  • 12 medical resources (48%) recommend using 0.05 mg or less IV as an initial dose.
  • 9 medical resources (36%) recommend using 0.4 – 0.5 mg or higher as an initial dose.
  • Maximum dose also ranged widely from 2 to 20 mg.


Recent editions of emergency medicine text (Rosen’s and Tinitinalli) recommend using 0.04 – 0.05 mg IV in ED patients with history of opioid dependence. Higher doses of naloxone are recommended for non-opioid dependent/apneic patients.


However, history of opioid dependence is difficult to obtain in patients with opioid induced CNS/respiratory depression.


Administering 0.4 mg or higher dose may/can acute agitation or opioid withdrawal symptoms that can utilize more ED resources to calm agitated patient/management of withdrawal. Thus it may be prudent to use low-dose strategy (0.04 mg IV with titration) to minimize the risk of precipitating naloxone-induced opioid withdrawal/agitation.


Bottom line:

In opioid-induced respiratory depression/apneic patients:

  1. Ventilate with bag-valve mask for apnea/hypoxia
  2. Administer naloxone: 0.04 mg IV every 2 – 3 min until reversal of respiratory depression/hypoxia is achieved.

To make 0.04 mg naloxone solution:

  • Dilute 1 mL of 0.4 mg naloxone with 9 mL normal saline in 10 mL syringe. 


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Category: Toxicology

Title: Atypical antipsychotics: are they truly safer than typical antipsychotics?

Keywords: atypical antipsychotic toxicity (PubMed Search)

Posted: 9/8/2016 by Hong Kim, MD, MPH (Updated: 5/29/2023)
Click here to contact Hong Kim, MD, MPH

Antipsychotic as a class has diverse range of toxicity. The atypical (2nd generation) antipsychotics are considered to possess less toxicologic manifestation compared to the typical (1st generation) antipsychotics - lower K channel blockade and minimum Na channel blockade properties. However, select atypical antipsychotics overdose can results in significant morbidity in addition to sedation.


Alpha-1 blockade (hypotension)

  • Clozapine
  • Olanzapine
  • Quetiapine
  • Risperidone
  • Ziprasidone


Antimuscarinic effect (anticholinergic toxicity)

  • Clozapine
  • Olanzapine
  • Quetiapine


Delayed rectifier K channel blockade (QT prolongation)

  • Ertindole
  • Ziprasidone


Bottom line:  Although lethal overdose from atypical antipsychotics are rare, they can result in significant clinical toxicity when ingested alone or in combintation with other classes of medications.



Category: Toxicology

Title: Lethal in small dose or single pill in pediatric population (age < 5 years old)

Keywords: One pill killers, pediatric (PubMed Search)

Posted: 8/17/2016 by Hong Kim, MD, MPH (Emailed: 8/18/2016) (Updated: 8/18/2016)
Click here to contact Hong Kim, MD, MPH

In pediatric population, small dose or single pill ingestion can potential result in severe or lethal toxicity.

Clinicians should be mindful of potential toxicity following xenobiotic exposure (below) in pediatric population, especially under the age of 5 years old, even if the patient may initially appear asymptomatic.

  • Benzocaine
  • B-adrenergic antagonist (sustained release)
  • Calcium Channel blockers (sustained release) 
  • Camphor
  • Clonidine
  • TCAs
  • Diphenoxylate/atropine (Lomotil)
  • Toxic alcohol (methanol or ethylene glycol)
  • Methylsalicylate
  • MAO-Is
  • Opioids
  • Phenothiazines
  • Quinine or chloroquine
  • Sulfonylureas
  • Theophylline


Suspected ingestion of above medications/xenobiotics may warrent observation up to 24 hours in asymptomatic pediatric population.



Drug-induced hypoglycemia is an often severe and symptomatic. It is a potentially preventable cause of significant morbidity. In one large study, it accounted for 23% for hospital admissions due to adverse drug events and 4.4% of overall admissions. The majority of hypoglycemic events occur with insulin and sulfonylureas. However, multiple drugs can affect glucose homeostasis and have been cited to cause hypoglycemia in therapeutic dose alone or in combination with other medications or illness. Factors that predispose to low blood sugar include reduced food intake, age, hepatic and renal disease, and severe infection. Beware of the possibility of inducing hypoglycemia in patients taking the following:

  • Ethanol
  • Insulin
  • Pentamidine
  • Quinine
  • Quinolones (Gatifloxin others rare)
  • Sulfonylureas

Agents with lesser quality evidence as predisposing medications or illnesses were present:

  • Ace Inhibitors (with diabetic agents)
  • Propanolol ( less likely in other beta blockers)
  • Trimethoprim/sulfamethoxazole (in renal compromise)
  • Salicylates (high dose or intoxication)

Drugs induced hypoglycemia should always be considered in the differential diagnosis of every patient presenting with low blood glucose. Octreotide antagonizes pancreatic insulin secretion and should be considered for first-line therapy in the treatment of sulfonylurea-induced hypoglycemia particularly when glucose levels cannot be maintained by dextrose infusions. Octreotide is administered 50 mcg subcutaneously (1-10 mcg in children) every 12 hours.

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Category: Toxicology

Title: Are synthetic opioids next novel designer drugs of abuse in the U.S?

Keywords: novel synthetic opioid, U-47700 (PubMed Search)

Posted: 8/1/2016 by Hong Kim, MD, MPH (Emailed: 8/3/2016) (Updated: 5/29/2023)
Click here to contact Hong Kim, MD, MPH

Recently, there have been several news reports regarding the emergence of synthetic opioids in the U.S. and Canada. There are multiple synthetic opioids that have been identified as potential agents of abuse including W-18, U-47700, fentanyl derivatives, AH-7921 and MT-45. These compounds share a similar story with synthetic cannabinoid where they were synthesized for research purpose or by pharmaceutical companies but were not marketed. They are often sold as “research chemicals” over the internet.

In July 2016, three case reports have been published regarding several cases of U-47700 intoxication in San Diego, CA and Dallas, TX.

  • Dallas, TX: A couple in their 20’s purchased U-47700 on the internet believing it to be “synthetic cocaine.” They both suffered CNS and respiratory depression after insufflation. Naloxone was not administered in both cases. The man was intubated while the woman was awake at time of presentation to the ED. U-47700 exposure was confirmed by liquid chromatography/tandem mass spectrometry.


  • San Diego, CA: a 22 year old man with history of heroin abuse was found unresponsive and apneic (4 breaths per minute and pulse oximetry of 60%). He received naloxone 2 mg IV which completely reversed his CNS and respiratory depression. He admitted to purchasing U-47700 on the internet and its use prior to being found unresponsive. U-47700 exposure was confirmed using liquid chromatography/mass spectrometry.


  • Central CA: 41 year old woman presented with CNS depression and pinpoint pupils after ingesting 3 tablets of “Norco” purchased from the street.  Her intoxication was completely reversed with naloxone 0.4 mg IV and discharged after 4 hour observation. Fentanyl and U-47700 was detected in serum blood test.

It is unknown if currently available heroin is cut with above mentioned synthetic opioids. Like other opioid receptor agonists, administration of naloxone will likely reverse the opioid toxidrome. But clinical experience in reversing synthetic opioids intoxication with naloxone is limited.  


Bottom line:

Irrespective of whether an ED patient is exposed to synthetic opioids or "traditional" opioids of abuse (prescription opioid pain medication or heroin), the management of opioid intoxication management remains unchanged for respiratory depression. 

  1. Airway management: bag-valve assisted ventilation if needed
  2. Naloxone administration (initial dose: 0.04 to 0.4 mg IV) with titration as needed. 
  • naloxone's clinical duration of effect ranges from 30 to 90 minutes.

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Category: Toxicology

Title: Laundry detergent pods exposure - the hidden danger.

Keywords: Pediatric exposure, laundry detergent pods (PubMed Search)

Posted: 6/23/2016 by Hong Kim, MD, MPH
Click here to contact Hong Kim, MD, MPH

Laundry detergent pods were introduced in 2012 to make washing clothes more "convenient." Since then, pediatric exposures to laundry detergent pods have increased as the use of these detergent pods have become more common in homes. Like other household chemical exposure, small, colorful candy like appearances of laundry detergent pods can attract the attention of < 3 years old children resulting in unintentional exposure due to curiosity or taste.

Most frequent clinical effects (2013 - 2014 national poison center data) from exposure to detergents in general (laundry detergent pods and nonpods & dishwasher detergent):

  • GI: nausea & vomiting: 29.1%
  • Cough/choking: 8.3%
  • Ocular irritation/pain: 5.6%
  • Red eye/conjunctivitis: 3.4%
  • Drowsiness/lethargy: 2.8%

Laundry detergent pod vs. nonpods:

  • Higher referral to health care facility: 17.4% vs. 4.7%
  • Higher odds of experiencing > 1 clinical effects (OR: 3.9; 95% CI: 3.7 4.1)
  • Higher odds of hospital admission (OR: 4.8; 95% CI: 4.0 5.8)
  • Higher odd of intubation (OR: 6.9; 95% CI: 3.5 13.6)

Laundry detergent pods (only) also resulted in following:

  • Coma: 17 cases
  • Respiratory arrest: 6 cases
  • Pulmonary edema: 4 cases
  • Cardiac arrest: 2 cases

Cases of caustic exposure-like injuries have also been reported (corneal abrasion and esophageal injury)

Bottom line:

Pediatric laundry detergent (nonpods) exposures usually have self-limited symptoms. However, laundry detergent pod exposure can cause more serious clinical effects that may require hospitalization.

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Category: Toxicology

Title: Loperamide high more than a fix for diarrhea.

Keywords: loperamide, opioid alternative, cardiac toxicity (PubMed Search)

Posted: 6/15/2016 by Hong Kim, MD, MPH (Updated: 5/29/2023)
Click here to contact Hong Kim, MD, MPH

Loperamide is a peripheral mu-opioid receptor agonist that is found in over the counter anti-diarrheal medication. Following the trend of opioid abuse epidemic, loperamide has been promoted on online drug-use forum as a treatment for opioid withdrawal and as a possible alternative to methadone.  At the same time, recreational use of loperamide has been increasing as an opioid alternative. Unlike therapeutic use of loparamide (2 – 4 mg), loraparmide abusers take supratherapeutic doses (e.g. 50 – 100 mg) to penetrate the CNS to produce opioid effects.  


In published case reports, loperamide caused cardiac Na channel blockade (similar to TCA and bupropion) and K channel blockade, resulting in EKG changes including QRS interval > 100 msec with terminal R wave in aVR and QTc prolongation, respectively. Loperamide associated death has also been reported (autopsy finding), although the exact cause of death was not determined.


It is unclear if administration of NaHCO3 can reverse the cardiac Na channel blockade as in TCA and bupropion as the clinical experiences have been limited.


Bottom line:

  • Clinicians should be aware of potentially lethal cardiac toxicity of loperamide abuse (Na and K channel blockade).

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Category: Toxicology

Title: Ketamine for Prehospital Agitation - Prospective Study Results

Keywords: ketamine, agitation, prehospital, haloperidol (PubMed Search)

Posted: 6/7/2016 by Bryan Hayes, PharmD (Emailed: 6/9/2016) (Updated: 6/27/2016)
Click here to contact Bryan Hayes, PharmD

Ketamine is gaining traction as a prehospital option for managing severe agitation or excited delirium syndrome. Previous reports have mostly been case series, but a new prospective study adds some important information that may help delineate ketamine's role in this setting. [1] The study and an accompanying commentary are both open access. [2]

What They Did

Open-label before-and-after prospective comparison of haloperidol (10 mg IM) versus ketamine (5 mg/kg IM) for the treatment of acute undifferentiated agitation.

What They Found

  • Ketamine demonstrated a statistically and clinically significant difference in median time to sedation compared to haloperidol, 5 min vs. 17 min (p < 0.0001, 95% CI: 9 15)
  • Complications: ketamine, 49%; haloperidol, 5%
    • Ketamine complications: hypersalivation (38%), emergence reaction (10%), vomiting (9%), and laryngospasm (5%)
  • Intubation rate: ketamine, 39%; haloperidol, 4%

Appliation to Clinical Practice

  • Ketamine works for prehospital agitation (and more rapidly)
  • Ketamine has a higher complication and intubation rate
  • Though this study did not find a dose relationship between ketamine and intubations, future studies should evaluate further and potentially use lower ketamine doses
  • At our institution, we start with 2-3 mg/kg IM and repeat if necessary after 5 min. Most patients have not required a second dose and none have been intubated. This allows time to place an IV line and initiate additional treatment.

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Category: Toxicology

Title: Bupropion Toxicity

Keywords: Bupropion, Seizure, Cardivascular instability (PubMed Search)

Posted: 6/2/2016 by Kathy Prybys, DO (Emailed: 6/3/2016) (Updated: 6/3/2016)
Click here to contact Kathy Prybys, DO

Bupropion (Wellbutrin, Zyban) is one of the most frequently prescribed antidepressants and smoking cessation agents. A lesser incidence of undesirable side effects such as weight gain and sexual dysfunction when compared to other antidepressants lends to its popularity. Bupropion's mechanism of action is only partially understood but it is known to be a norepinephine dopamine reuptake inhibitor and anticholinergic receptor blocker at certain nicotinic receptors. Bupropion has a monocyclic structure similar to amphetamines. Seizures are a major concern in overdose. When first released, Bupropion was initially withdrawn from the market due to its narrow therapeutic window with seizures occurring at doses as low as 450 mg.

  • Seizures are dose dependent and all types can occur. Incidence increases dramatically with higher doses. Benzodiazepines are first-line therapy.
  • Most patients experience seizure within 8 hours however, seizures can occur up to 24 hours after ingestion even without preceding symptoms.
  • Longer acting forms: SR, XL, ER cause prolonged toxicity and activated charcoal should be administered in the absence of contraindications (depressed mental status, lack of airway protection, seizure).
  • Myocardial sodium channel blocking properties occur and sodium bicarbonate should be administered when this occurs.
  • Cardiovascular effects including tachycardia, prolonged QT interval, QRS widening, arrhythmia, and cardiovasular collapse.
  • Bupropion is extremely lipid soluble and intravenous lipids should be considered in severe poisonings. Intralipid has been successfully used in several cases of Bupropion poisoning with cardiovascular instability or severe CNS symptom with good outcomes.

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Category: Toxicology

Title: Does Digoxin Immune Fab Work in Chronic Digoxin Poisoning?

Keywords: digoxin, chronic, poisoning, immune Fab (PubMed Search)

Posted: 5/9/2016 by Bryan Hayes, PharmD (Emailed: 5/12/2016) (Updated: 5/12/2016)
Click here to contact Bryan Hayes, PharmD

Patients with chronic digoxin toxicity generally have multiple co-morbidities such as renal failure, dehydration, and cardiac failure. Sick patients with chronically high digoxin levels may have more than just digoxin toxicity as the cause of illness.

A New Study

Prospective observational study with the primary objective to investigate changes in free digoxin concentrations and clinical effects on heart rate and potassium concentrations in chronic digoxin poisoning when digoxin immune Fab are given.

What They Found

One to two vials of digoxin immune Fab initially bound all free digoxin confirming Fab efficacy. However, this was associated with only a moderate improvement in HR (49 to 57 bpm) and potassium (5.3 to 5.0 mmol/L).

Application to Clinical Practice

  • Elevated digoxin concentrations alone may not be solely responsible for bradycardia and hyperkalemia in the chronic setting.
  • Digoxin immune Fab is not a magic bullet in chronic digoxin poisoning.

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Category: Toxicology

Title: ECMO for Severely Poisoned Patients

Keywords: Extracorporeal Membrane Oxygenation, ECMO, toxicology, poison (PubMed Search)

Posted: 4/13/2016 by Bryan Hayes, PharmD (Emailed: 4/14/2016) (Updated: 4/14/2016)
Click here to contact Bryan Hayes, PharmD

The American College of Medical Toxicology's ToxIC Registry is a self-reporting database completed by medical toxicologists across 69 insitutions in the US.

  • Over a 3 year period, just 10 cases in the database received ECMO: 4 pediatric, 2 adolescent, and 4 adults (individual cases presented in the table below)
  • Time of initiation of ECMO ranged from 4 h to 4 days, with duration from 15 h to 12 days
  • Exposures included carbon monoxide/smoke inhalation (2), bitter almonds, methanol, and several medications including antihistamines (2), antipsychotic/antidepressant (2), cardiovascular drugs (2), analgesics (2), sedative/hypnotics (2), and antidiabetics (2)
  • Overall survival rate was 80%

Application to Clinical Practice

In settings where ECMO is available, it may be a potential treatment option in severely poisoned patients. From the limited data, ECMO was generally administered prior to cardiovascular failure and might be of benefit particularly during the time the drug is being metabolized.

Table from the Case Series

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Category: Toxicology

Title: Ketamine for Severe Undifferentiated Acute Agitation

Keywords: Ketamine, Benzodiazepines (PubMed Search)

Posted: 4/7/2016 by Kathy Prybys, DO (Emailed: 4/8/2016) (Updated: 4/8/2016)
Click here to contact Kathy Prybys, DO


[CORRECTION]: Versed dose is 2-2.5 mg total not mg/kg

Patients with severe agitation present a unique challenge to the emergency department. Acute delirium is often due to psychostimulants such as cocaine, amphetamines, PCP, or synthetic cannabinoids, alcohol, or psychiatric illness. These patients require urgent evaluation necesssitating the use of physical and chemical restraints, not only for their own safety but also the hospital staff's. Fingerstick glucose, pulse oximetry, and vital signs must be expeditiously obtained. Severely agitated combative patients who are physically restrained are at high risk for morbidity from asphyxiation, hypermetabolic consequences (acidosis, hyperthermia, rhabdomyolysis), and death can occur.

Ketamine is phencyclidine derivative that causes dissociative state between the cortical and limbic systems which prevents the higher centers from preceiving visual, auditory, or painful stimuli. Ketamine has a wide safety profile and has been used worldwide for many years with few complications. It possesses ideal characteristics for rapid sedation of agitated patients:

  • Rapid onset of action 1-3 minutes
  • Preservation of airway reflexes
  • Lack of respiratory or cardiac depression or QT prolongation
  • Short half-life of 30-40 minutes
  • Safe in situations with minimal to no monitoring
  • Dose: Intravenous =1.5-2 mg/kg Intramuscular = 5-6 mg/kg (maximum 400 mg)

Experience with Ketamine in patients with excited delirium has shown good initial control of agitation however, patients often require additional medications for deeper or longer duration of sedation. Benzodiazepines are recommmended as second line agents particularly intravenous or intramuscular Midazolam 2-2.5 mg /kg.




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Category: Toxicology

Title: Treatment of Acute Cocaine Cardiovascular Toxicity

Keywords: cocaine, toxicity, cardiovascular (PubMed Search)

Posted: 3/9/2016 by Bryan Hayes, PharmD (Emailed: 3/10/2016) (Updated: 3/12/2016)
Click here to contact Bryan Hayes, PharmD

Acute cocaine toxicity can manifest with several cardiovascular issues such as tachycardia, dysrhythmia, hypertension, and coronary vasospasm. A new systematic review collated all of the available evidence for potential treatment options. Here is what the review found (there is also an 'other agents' section for medications with less published reports):

  • Benzodiazepines and other GABA-active agents: Benzodiazepines may not always effectively mitigate tachycardia, hypertension, and vasospasm from cocaine toxicity.

  • Calcium channel blockers: Calcium channel blockers may decrease hypertension and coronary vasospasm, but not necessarily tachycardia.

  • Nitric oxide-mediated vasodilators: Nitroglycerin may lead to severe hypotension and reflex tachycardia.

  • Alpha-adrenoceptor blocking drugs: Alpha-1 blockers may improve hypertension and vasospasm, but not tachycardia, although evidence is limited.

  • Alpha-2-adrenoceptor agonists: There were two high-quality studies and one case report detailing the successful use of dexmedetomidine.

  • Beta-blockers and alpha/beta-blockers: No adverse events were reported for use of combined alpha/beta-blockers such as labetalol and carvedilol, which were effective in attenuating both hypertension and tachycardia.

  • Antipsychotics: Antipsychotics may improve agitation and psychosis, but with inconsistent reduction in tachycardia and hypertension and risk of extrapyramidal adverse effects.

  • Sodium bicarbonate: Twelve case reports documented treatment of dysrhythmia with IV sodium bicarbonate, with seven reporting successful termination.

The authors note that "publication bias is a concern, and it is possible that successful treatment and/or adverse events have not been reported in some of the publications, and in general."

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Category: Toxicology

Title: Super Potent Opioid Street Drugs

Keywords: Fentanyl, W-18, Clandestine (PubMed Search)

Posted: 3/4/2016 by Kathy Prybys, DO
Click here to contact Kathy Prybys, DO

Pure opioid agonists such as Morphine, Hydromorphone, and Fentanyl stimulate opioid receptors and are the most potent analgesics. Fentanyl and fentanyl analogues are up to 100 times more powerful than morphine and 30-50 times more powerful than heroin.

  • Fentanyl abuse is causing significant problems worldwide. In the U.S., age-adjusted rate of death involving Fentanyl has increased 80% in 2014.
  • Sources include production in illicit clandestine labs or diversion from legitimate pharmaceutical sales.
  • 12 different analogues of Fentanyl have been identified in the U.S. drug traffic market.
  • Commonly laced in heroin or cocaine or sold as fake Oxycodone or OxyContin tablets.

W-18 is a highly potent opioid agonist with a distinctive chemical structure which is not closely related to older established families of opioid drugs. While Fentanyl is approximately 100 times more powerful than Morphine, W-18 is about 100 times more powerful than Fentanyl.

  • First discovered at the University of Alberta in 1982 in hopes of producing a non-addictive analgesic, 32 compound series named from W-1 to W-32, with W-18 being the most potent.
  • Recently emerged on the streets of Canada when police in Calgary confiscated 110 green pills being sold as Fentanyl, known on the streets as "shady eighties" or "green beans pills" but chemical analysis revealed some pills containing W-18 instead.
  • W-18 has never been used clinically as drug companies did not pick the patent, which lapsed by 1992 so little clinical experience.
  • The effects of naloxone to reverse this synthetic opioid are unknown and higher doses are expected to to be required.
  • Illicit drug manufacturers research pharmacological history in search of the more powerful, exotic, and new opioids to circumvent current legal regulations.

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Colchicine is an alkaloid compound found in Colchicum autumnale that is often mistaken by foragers as wild garlic (Allium ursinum). Unintentional ingestion wild garlic or therapeutic misadventures among elderly population with history of gout often result in unintentional toxicity.


It is a potent inhibitor of microtubule formation and function involved in cell division and intracellular transport mechanism. Thus toxicity is related to diffuse cellular dysfunction of all major organs and results in significant morbidity and mortality.


Colchicine toxicity occurs in three phases:




Signs and symptoms



0 – 24 hr

·  Nausea, vomiting, diarrhea

·  Salt and water depletion

·  Leukocytosis

·  Antiemetic

·  GI decontamination

·  IV fluids

·  Observation for leukopenia


1 – 7 days

·  Sudden cardiac death (24 – 48 hr)

·  Pancytopenia

·  Acute kidney injury

·  Sepsis

·  Acute respiratory distress syndrome

·  Electrolyte imbalance

·  Rhabdomyolysis

·  Resuscitation

·  G-CSF

·  Hemodialysis

·  Antibiotics

·  Mechanical ventilation

   ·  Electrolyte repletion


>7 days

·  Alopecia (2-3 weeks later)

· Myopathy, neuropathy, myoneuropathy.




  • Primarily supportive care as no antidote is available.
  • ICU admission due to risk of sudden cardiac death in symptomatic patients.
  • Patients who does not manifest GI symptoms within 8 -12 hr are unlikely to be significantly poisoned.

Category: Toxicology

Title: Lipid use in poisoning: comprehensive systematic reviews now published

Keywords: lipid, intralipid, poisoning, local anesthetic, non-local anesthetic (PubMed Search)

Posted: 2/10/2016 by Bryan Hayes, PharmD (Emailed: 2/11/2016) (Updated: 4/2/2016)
Click here to contact Bryan Hayes, PharmD

In September 2013, an international group representing major societies in toxicology and nutrition support began collaborating on a comprehensive review of lipid use in poisoning. Six total papers will be published, with the most recent two made available online this week. Here are the available (and forthcoming) papers:

  1. Gosselin S, et al. Methodology for AACT evidence-based recommendations on the use of intravenous lipid emulsion therapy in poisoning. Clin Toxicol 2015;53(6):557-64. [PMID 26059735]

  2. Grunbaum AM, et al. Review of the effect of intravenous lipid emulsion on laboratory analyses. Clin Toxicol 2016:54(2):92-102. [PMID 26623668]

  3. Levine M, et al. Systematic review of the effect of intravenous lipid emulsion therapy for non-local anesthetics toxicity. Clin Toxicol. 2016;54(3):194-221. [PMID 26852931]

  4. Hoegberg LC, et al. Systematic review of the effect of intravenous lipid emulsion therapy for local anesthetic toxicity. Clin Toxicol. 2016;54(3):167-93. [PMID 26853119]

  5. Hayes BD, et al. Systematic Review of Clinical Adverse Events Reported After Acute Intravenous Lipid Emulsion Administration. Clin Toxicol. 2016 Apr 1. [Epub ahead of print] [PMID 27035513]

  6. The final paper, which is in process, is the consensus recommendations from the workgroup based on the 4 systematic reviews.

Show References

Category: Toxicology

Title: Activated Charcoal, Is it still useful?

Keywords: Activated Charcoal, Gastric decontamination, Antidote (PubMed Search)

Posted: 2/4/2016 by Kathy Prybys, DO
Click here to contact Kathy Prybys, DO


Throughout medical history one of the basic tenets of poisoning therapy is to remove the poison from the patient. For hundreds of years, gastric decontamination has been the cornerstone treatment for acute poisonings by ingestion. This commonsense approach endeavors to remove as much of the the ingested toxin as possible before systemic absorption and organ toxicity occurs. Multiple GI decontamination methods have been utilized including gastric emptying by lavage and ipecac, toxin binding by activated charcoal, and increasing GI transit time with cathartics and bowel irrigation. Numerous studies have been conducted to assess the effectiveness of GI decontamination including measurement of amount of toxin removed by gastric retrieval, reduction of bioavailability by measuring blood levels, and finally comparison of clinical outcomes of patients treated with and without GI decontamination. Controlled studies have failed to show conclusive evidence of benefit and have even demonstrated resultant harm especially with use of gastric lavage. Activated charcoal has a tremendous surface area capable of binding many substances. Although viewed as relatively safe it does have risks in certain subsets of patients, pulmonary aspiration the most common, and is no longer routinely recommended.

Considerations for use of Activated charcoal (AC) use in acutely poisoned patients:

  • AC does not bind alcohols, hydrocarbons, heavy metals
  • Contraindications include diminished level of consciousness, seizure, emesis, unprotected airway, and intestinal obstruction
  • Consider AC use in cases where there is potential for toxin to remain in the gut longer such as with delayed-release formulations or slowed gastric emptying
  • Consider AC use in cases of expected severe toxicity with lack of effective antidote

The decision to use activated charcoal is no longer standard of care but should be individualized to each clinical situation weighing the risk versus clinical benefits.

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Lead is a ubiquitous metal in the environment partly due to decades of using leaded gasoline (organic lead) and lead-based paint (inorganic lead). Outside of occupational exposure, children are disproportionately affected from environmental lead exposure.


Common route of exposure are:

  1. Ingestion (common in children): soil, water, lead-based paint chips, toys, certain folk remedies.
    • Absorption: adult: 3 – 10% vs. children: 40 – 50%
  2. Inhalation (mostly occupational exposure): lead dust
    • Absorption: 30 – 40%
  3. Dermal (minor): cosmetic products
    • Absorption: < 1%


Majority of the absorbed lead are stored in bone (years) > soft tissue (months) > blood (30-40 days) (half-life). Thus blood lead level does not accurately reflect the true body lead burden.


Incidence of elevated blood lead level (EBLL > 5 microgram/dL) in children increased from 2.9 to 4.9% in Flint, MI before and after water source change. In the area with the highest water lead level, the incidence increased by 6.6%.


Clinical manifestation in children

Clinical severity

Typical blood lead level (microgm/dL)


  • CNS: encephalopathy (coma, seizure, altered sensorium, ataxia, apathy, incoordination, loss of developmental skills, cranial nerve palsy, signs of increased ICP
  • GI: persistent vomiting
  • Heme: anemia

> 70 – 100

Mild to moderate

  • CNS: hyperirritable behavior, intermittent lethargy, decrease interest in play, “difficult” child
  • GI: intermittent vomiting, abdominal pain, anorexia

50 – 70


  • CNS: impaired cognition, behavior, balance, fine-motor coordination
  • Misc: impaired hearing or growth

> 10


Evaluation for lead poisoning

  1. Blood lead level (BLL)
  2. CBC: hypochromic microcytic anemia, basophilic stippling
  3. Imaging: abdominal XR – check for foreign bodies in GI tract; long-bone XR – lead lines


Management of children with EBLL

  1. Removal from exposure
  2. Environmental investigation/intervention (BLL: 15 - 44 ug/dL)
  3. Chelation
    • Asymptomatic (BLL: 45 – 69 ug/dL): Succimer (PO)
    • Symptomatic (BLL: > 70 ug/dL): Dimercaprol (IM) and CaNa2EDTA (IV)

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