Many consider Paracelsus (1493–1541) as the father of modern toxicology.
The introduction of the dose–response concept might have been his most important contribution to toxicology, meaning that everything is toxic at the right dose (even oxygen and water).
Dabigatran (Pradaxa), an antithrombin medication, was discussed in an earlier pearl and thought I would play devil's advocate and explain the possible concerns:
Toxicology Mantra: You never want to be the first person or the last person to use a drug
The Rumack-Matthew nomogram is a well studied and validated tool to help assess the potential for liver toxicity following acute acetaminophen poisoning. Here is a brief review of when it is best utilized.
Outside-the-box situations:
Naloxone is the epitomy of an antidote with complete reversal of opioid toxicity within 60 seconds of administration. Remember your clinical endpoint should be respiratory effort. If you utilize "the vial" of either 0.4mg or 2mg and there is a higher probability of withdrawal and for acute lung injury. Here are some tips for administration:
1) IV Access: Try 0.1 mg or even 0.05 mg - anesthesiology typically doses naloxone in micrograms. Reversal is slower so you have to be patient. It is also not as dramatic so closely monitor respirations to see if you have improvement, that may be all that you get. These are probably patients that you don't want that awake anyways.
2) No IV Access: advantage of naloxone is it is bioavailable IV, intranasal and even by nebulizer. Here you want the dose to be 0.4mg to start for intranasal. Nebulizer is difficult to measure and probably safe to start with 2mg in the nebulizer container.
There is a difference when you know it is an opioid overdose and are reversing apnea versus a diagnostic administration to determine if it is opioid toxicity. In the latter instance you can rationalize the large dose - just be ready and be sure you are not in line of the possible projectile vomiting.
When you think of an acid or base causing a burn, you usually think of the local damage but there is one particular acid that causes systemic illness. Hydrofluoric Acid, found in your local Home Depot in brick/stone cleaning products, can cause severe illness despite a small total body surface area burn and exposure. A recent case report came out that illustrates how deadly HF can be. The reason is that this acid enters the body and chelates cations like calcium and potassium. The abstract is below but essentially hypocalcemia, hypokalemia leading to asystole 16hrs after exposure all from a 3% TBSA Burn - very impressive.
The answer was fomepizole would be the treatment for life-threatening disulfiram reaction. Blocks Alcohol Dehydrogenase and ironically prevent metabolism of ethanol and prolong intoxication.
I forgot how many see the pearls and the response was overwhelming. That was great and cost a me a little more. There were two winners:
Katie Baugher, PGY-1
Ari Keslter
Please email me how to best send you the gift certificate.
There are medications, if taken with ethanol, will cause a disulfiram reaction. This reaction results from inhibition of aldehyde dehydrogenase, the enzyme in ethanol metabolism that breaks acetaldehyde to acetic acid. The increase in acetaldehyde results in nausea, vomiting, diarrhea, flushing, palpitations and orthostatic hypotension. So if you prescribe a patient with any of these medications you must make certain to tell them NOT to drink any ethanol - that includes cough/cold preparations that have ethanol:
Antibiotics: Metronidazole(Flagyl), Trimethoprim-sulfamethoxazole (Bactrim)
Sulfonylureas: Chlorpropamide and tolbutamide
These have possible reactions: griseofulvin, quinacrine, procarbazine, phentolamine, nitrofurantoin
Bonus Question: $10 Starbuck's Gift Card for first person that emails me with the answer to this question
What treatment could you give to someone suffering from a life threatening disulfiram reaction that biochemically should cure him?
Most cases of normal anion gap metabolic acidosis result from either urinary (RTA) or gastrointestinal HCO3- losses (diarrhea). A number of xenobiotics can also cause this disorder:
Toxic Holiday Plants
Of the three plants listed, which is NOT poisonous?
1. Holly plant
2. Poinsettia
3. Mistletoe
Poinsettia plants were once thought to be very poisonous. Contrary to popular belief, poinsettias are safe to have in the home during the holidays.
Although there are reported cases of death with ingestion of Holly plants in older literature, recent experience shows gastrointestinal effects in small doses, and serious toxicity such as CNS depression in large ingestions.
Mistletoe ingestion of few of the berries would, at most, produce mild gastroenteritis; however, ingesting concentrated extracts of the plant, including the berries, may produce serious effects such as seizures, mental confusion, drowsiness, and hallucinations.
Happy holidays!
As we eat our turkey today and the myth that we are tired because of the tryptophan content is propagated further - nothing to do with the 2000kcals that we just ate - I would like to share an interesting and controversial study.
Use of stimulants and and sedatives by EM residents. Incidence is as follows:
In a study of 485 residents with 47% response rate:
Prescription Stimulants: 3.1%
Sleep Aids (all): 89%
Use of Nonbenzodiazepines (zolpidem): 14%
Use of Melatonin: 10%
Benzodiazepines: 9%
Difficult job with difficult hours. What is the appropriate medication or is there a medication that truly assists with performance? Are they doing harm to themselves? to patients?
Disrupted circadian rhythm, addiction tendencies and the hardship of a stressful nightshifts are the price we pay for this specialty. Awareness and education are needed for the residents as well as the attendings.
In the setting of a patient suffering from an anticholinergic overdose with hallucinations/agitation, it may be beneficial to administer the antidote: Physostigmine. Many hesitate simply because they have never administered before or there may be doubt in the diagnosis. Here is the skinny:
1) Anticholinergic OD seen in following meds: diphenhydramine (Benadryl), dimenhydrinate (Dramamine), scopolamine, benztropine (Cogentin), some plants like datura stromonium (thorn apple)
2) Physostigmine 1mg IV slowly over a REAL 5 min. Administer to fast and patient may seize. Maximum dose of 2mg IV.
3) Contraindications: suspicion of TCA OD (anectdotal and from old case report) - screening EKG should be done prior to administration of physostigmine. Also glaucoma, closed angle, obstructive uropathy.
Remember your clinical endpoint needs to be measurable, thus hallucinations and agitation should be reversed. No indication if the patient is only experiencing dry mouth or other more mild anticholinergic symptoms.
French LK, et al. Hydrogen peroxide ingestion associated with portal venous gas and treatment with hyperbaric oxygen: a case series and review of the literature. Clinical Toxicology 2010;48:533–38.
Dabigatran
When a patient presents to the ED with a recent ingestion of a wild mushroom there are three very specific questions you must ask:
1) Exactly what time did you eat the mushroom?
2) Exactly what time did you begin vomiting/diarrhea/GI Sx in general?
3) Are there are more mushrooms that can be brought to ED for identification?
The reason the first two questions are critically important is it determines the total time of onset of toxicity. As a very general rule of thumb, delayed GI symptoms >6hrs is predictive of a possible lethal ingestion of a cyclopeptide containing mushroom like Amanita Phalloides. Immediate symptoms < 6hrs and even more so if within 2 hrs usually indicates ingestion of a nonlethal mushroom that causes GI distress (many mushrooms like Clitocybe nebularis)
Website with pics of the most poisonous mushrooms:
http://scienceray.com/biology/botany/13-deadliest-mushrooms-on-the-planet/
There is a saying:
"There are old mushroom pickers and wise mushroom pickers but no old and wise mushroom pickers"
Emerging evidence supports using intravenous fat emulsion (Intralipid) therapy for various drug overdoses, particularly those that are lipophilic. Within seconds to minutes of administration, toxic cardiovascular effects are reversed, including return of spontaneous circulation in cardiac arrest patients. Central nervous system effects also tend to improve.
Lipophilic agents for which there has been success include:
Bottom line: Consider intralipid therapy early in the course of a hemodynamically unstable patient with suspected overdose. Give a bolus of 1.5 mL/kg of 20% lipid emulsion over 1-2 minutes.
Although we may not be able to eat as much shellfish after the oil spill, there are still some left that can cause some interesting toxicity here in the USA. Shellfish act as vectors for the bacteria, virus etc that produces toxin thus not specific to one species of shellfish. There is a map attached that shows where shellfish poisoning occurs most. In the picture CFP=ciguatera, PSP=Paralytic and ASP=AmnesticC. Surprising the distribution and it will be interesting how the oil spill affects the distribution. Treatment for all of these is supportive with no known antidote and incidence increases during Red Tide months:
A fentanyl patch contains 100-fold more fentanyl in the reservoir than what is posted on the patch. For instance, 100mcg/hr patch will have over 10mg - thats milligrams - of fentanyl. This provides a rather large source for potential abuse. Overdose and deaths have occurred by patients in the following ways:
It is the many
