Here is a short quiz on toxicity related to essential oils.
Quizes based on Goldfrank’s Toxicologic Emergencies 11e and other sources when cited in answer explanation.
Flashcards aid in memory repetition of difficult to memorize things that may show up on boards and in-service exam. This list will grow as I distill my readings and notes into only the highest yield memorization points.
note: all images used are public domain, unless otherwise cited within the flashcard
Iron(II,III) hexacyanoferrate(II,III)
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The IUPAC name for Iron(II,III) hexacyanoferrate(II,III) is Prussian Blue. This form of Prussian blue is insoluble and administered orally.
Enhances elimination of cesium (Cs) from the GI tract, which is useful for radioactive fallout.
Prussian blue is also the treatment for thallium (Th) toxicity, via a similar mechanism.
Constipation is also commonly reported, and stools may be blue in color. The medication should be taken with food to enhance biliary secretion of Cs.
Adult dosing is 3 grams PO taken 3 times a day with food.
Although pregnancy category C, pregnant patients should likely still be treated as the benefits likely outweigh the risks.
Iron(II,III) hexacyanoferrate(II,III)
Toxicology of the Pancreatic Beta Cell
Describe the cellular mechanism of sulfonylureas, octreotide, and calcium channel blockers on the pancreatic beta cell.
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- Toxicology of the pancreatic beta cell, demonstrating the effect of sulfonylureas, octreotide, and calcium channel blockers. PDB file = 1zni
Toxicology of the Pancreatic Beta Cell
tear gas
Active ingredient? Mechanism? Treatment?
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- -Aerosolized liquids or solids (not actually a gas), 2-chlorobenzalmolonotrile is an example, but there are many other related compounds.
- -Activates TRP receptors and induce substance P release leading to pain and mucosal irritation
- -Complications include ocular irritation, keratitis. Requires very high concentrations to cause life threatening injury.
- -Extraction from environment, decontamination and supportive care?
tear gas
Phosgene
- -Mechanism of action? Structure? Clinical effects? Treatment? History?
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- -Causes a delayed ARDS type picture and respiratory irritation (typically around ppm>4.8).
- -Causes acylation of cells in the alveoli as well as formation of ROS. It is not readily water soluble so production of HOCl is less likely.
- -Supportive care, high dose steroids, ARDS net protocol, but theoretically antioxidant support with NAC maybe of benefit, ECMO for complete lung failure
- -History: chemical weapon used during World War 1
Phosgene
Serum Osmolarity
What is the formula to calculate serum osmolarity?
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normal is < 10
Serum Osmolarity
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Use this calculator to estimate the initial dose of xenobiotic, assuming taken at 1 time, and the serum sample is at tmax. It is not a perfect calculator, but can give the clinician a rough estimate. Future mathematical modeling will involve incorporating approximate metabolism and give variable for time of ingestion and kinetic order. Please note that µg/mL = mg/L.
D=C_0*V_d*Wt
This calculator will let you estimate a theoretical xenobiotic serum concentration at the Tmax using a reported dose . Use this with a grain of salt because in massive overdose, standard kinetics no longer apply. Please note that µg/mL = mg/L.
D=C_0*V_d*Wt
C_0=\cfrac{D}{{(V_d*Wt)}}
TEG learning case:
We had a patient on warfarin and plavix who had a GI bleed and was found to have INR>9.9. Prior to the start of my shift, her vital signs were stable so the decision overnight was to give vitamin K because she did not have yet have a diagnosed life threatening bleed. However, she became increasingly altered, and subsequent head CT showed spontaneous subarachnoid hemorrhage. By this time nearly 8 hours had passed and her INR was about 4. We ran a TEG platelet mapping assay before she received any reversal agents, which utilizes a green top (heparinized tube).
You can see the HKH (heparinized kaolin heparinase) TEG tracing in pink has a prolonged R time, indicating severe hypocoagulability. Furthermore, even though the patient was reported to be on plavix, you can see that the maximum amplitude (MA) of the platelet ADP tracing in green and the MA of the HKH tracing are approximately the same; both the green and pink curves approximate an MA of 60 mm. This indicates that she does not have significant antiplatelet effect.
For whatever reason, the TEG machine does not report R time as a numerical value on the platelet mapping assay; however, you can see it is just under 15 minutes (pink tracing), and is far outside of reference values, which are posted on the wall by the machine.
She then got 4 factor PCC, and we gave DDAVP anyway given the life threatening nature of her bleed. However, I would not rush to transfuse platelets given her normal platelet mapping assay.
2 hours after she got 4 factor PCC and DDAVP, we then ran a standard TEG (CK, CRT, CKH, CFF), which uses a blue top tube. We ran this test because we already knew her platelet function from the previous assay. Here you see that that R time has now normalized. The MA is high normal and the functional fibrinogen (CFF) channel is high normal. This indicated to us that our reversal during the resuscitation was sufficient. She definitely does not need more factors, lest she become hypercoagulable. 
She had stable hematocrit and stable interval head CT and was subsequently dispositioned.
Thanks for reading !
One reason I know that I went into the right speciality is that we HAVE to know about Ebola. Virology is uber fascinating, and we aim to hammer out everything the EP provider needs to know regarding this Ebola virus disease (EVD).
Aside from being an interesting topic, there is currently a budding outbreak of ebola in the congo. See news article below.
(note: I wrote this for a departmental memo in 2018)
Now the outbreak is worsening: https://www.apnews.com/49fcb435740b4c5b88bab2a1c873b763
So it is even more important for the EP to keep this disease on their radar.
If you recall from the last outbreak, there were several notable US cases, one of which received treatment in NYC.
It is thought that there is animal reservoir (likely fruit bats) and the animal to human transmission of the virus may come from individuals handling bushmeat.
Ebola is a filovirus (meaning it looks like a string). It is a negative sense single stranded RNA virus.
Below is a colorized scanning electron microscope image of the virus (curtesy wikimedia commons)
Transmission is via contact of viral particles to mucus membranes or broken down skin.
Incubation time is 9-11 days.
The ebola virus is one of the most infectious agents known to man. A single ebola virion is enough to be infectious. This is in stark contrast to most other infectious agents which typically require a large inoculum to cause clinically significant disease.
Symptoms typically develop by infection day 5:
- -fever, fatigue
- GI upset: vomiting, watery diarrhea, abdominal pain
- this can progress to seizures and cerebral edema
- renal failure
- hepatic failure
- ecchymoses and petechial rash are also possible
- hemorrhage is uncommon, but reported in 18% of patients (typically GI)
Patients with severe disease typically die within 6-16 days. Mortality rate in west Africa was ~40-70%. Of 27 patients treated in the United States, the fatality rate was 18.5%.
The mechanism for the hemorrhagic fever is thought to be massive activation of macrophages and other immune cells causing a cytokine storm, which then leads to break down of the vascular endothelium and results in leaking. Other research suggests the virus itself has proteins which lead to endothelial dysfunction and leakage.
You can utilize ELISA, PCR, or virus isolation to test for the disease. These tests are only available in consultation with a governmental health agency.
Mainstay of treatment is supportive. However, you can transfuse convalescent serum from recovered and now immune individuals. A more elegant and certainly more expensive treatment is ZMapp, which is a mix of “3 humanized monoclonal antibodies” against Ebola. There also several vaccines including rVSV-ZEBOV which have been experimentally deployed in west Africa.
As per the CDC, travelers from endemic outbreak regions should self monitor their health for 21 days. Febrile patients who may had contact with ebola, should be placed on contact precautions and NYDOH should be immediately contacted.
Hopefully this is something we never see. But preparedness is critical for our specialty. Thank you for taking the time to read and have a great day.
References:
Bah EI, Lamah MC, Fletcher T, et al. Clinical presentation of patients with Ebola virus disease in Conakry, Guinea. N Engl J Med. 2015;372(1):40-7.
Cantoni D, Rossman JS. Ebolaviruses: New roles for old proteins. PLoS Negl Trop Dis. 2018;12(5):e0006349.
https://www.cdc.gov/vhf/ebola/healthcare-us/preparing/clinicians.html
https://commons.wikimedia.org/wiki/File:Ebola_virus_virion.jpg
Sanford guide, app on iOS
Zwart MP, Hemerik L, Cory JS, et al. An experimental test of the independent action hypothesis in virus-insect pathosystems. Proc Biol Sci. 2009;276(1665):2233-42.
I put together is piece as part of collaboration with Department of Toxicology at Mother Theresa hospital in Skopje, MK (Болница Мајка Тереза, Скопје МК). It features Cyrilic script reading Toxicology in Macedonian (Токсикологиа), the caduceus, a laboratory flask and the ekg rhythm strip. This version is a lowish quality version to save on web space and also has my signature on the bottom (the original does not).
There is, after all, an art to medicine as well. Regardless, it prints quite nice at 40 cm x 30 cm.
I have been tinkering around with some dose calculators, my own code of course!
input measured serum etoh and body weight, the output will be approximate to the dose if the patient had taken a 1 time chug of etoh and ended up in your ED. Derivations are also available below for your own education.
D=C_0*V_d
now converting for units, here is the full equation resulting in g of EtOH
D=(C_o\;mg/dL)(0.72\:L/kg)(weight\;in\;kg)(10\;dL/1\;L)(1\;g/1000\;mg)
So, say now we have a patient with a toxic alcohol ingestions and no fomepizole is available. We need to get them drunk!
Modifying the previous equation we get:
D=\cfrac{(100\;mg/dL)(0.72\;L/kg)(10\;dL/1\;L)(1\;g/1000\;mg)}{(EtOH\;fraction)}
Inputting pt weight and the concentration of alcohol you have available (0.01-1) will give you appropriate loading dose.
I plan to expand this to include steady state elimination over a number of hours so that you can calculate estimated times of metabolization, allowing for redosing if appropriate.
references:
Cowan JM, Weathermon A, Mccutcheon JR, Oliver RD. Determination of volume of distribution for ethanol in male and female subjects. J Anal Toxicol. 1996;20(5):287-90.
Mcmartin K, Jacobsen D, Hovda KE. Antidotes for poisoning by alcohols that form toxic metabolites. Br J Clin Pharmacol. 2016;81(3):505-15.
Use this infographic on your peds shifts to teach about measles. There is a current outbreak originating near to where I live in Brooklyn. We have seen several cases at our hospital. Given the high infectivity and crowding in our inner city ED’s, it is critical to become familiar with the natural course of the disease.
https://www.cdc.gov/measles/cases-outbreaks.html