Podcasts about physostigmine

Contributor: Taylor Lynch MD Educational Pearls: Anticholinergics are found in many medications, including over-the-counter remedies Medications include: Diphenhydramine Tricyclic antidepressants like amitriptyline Atropine Antipsychotics like olanzapine Antispasmodics - dicyclomine Jimsonweed Muscaria mushrooms Mechanism of action involves competitive antagonism of the muscarinic receptor Symptomatic presentation is easily remembered via the mnemonic: Dry as a bone - anhidrosis due to cholinergic antagonism at sweat glands Red as a beet - cutaneous vasodilation leads to skin flushing Hot as a hare - anhidrotic hyperthermia Blind as a bat - pupillary dilation and ineffective accommodation Mad as a hatter - anxiety, agitation, dysarthria, hallucinations, and others Clinical management ABCs Benzodiazepines for supportive care, agitation, and seizures Sodium bicarbonate for TCA toxicity due to widened QRS Activated charcoal if patient present < 1 hour after ingestion Temperature monitoring Contact poison control with questions Physostigmine controversy Acetylcholinesterase inhibitor Black box warning for asystole and seizure Contraindicated in TCA overdoses Crosses blood-brain barrier, so useful for TCA overdoses Indicated only in certain anticholinergic overdose with delirium Disposition Admission criteria include: symptoms >6 hours, CNS findings, QRS prolongation, hyperthermia, and rhabdomyolysis ICU admission criteria include: delirium, dysrhythmias, seizures, coma, or requirement for physostigmine drip References 1. Arens AM, Shah K, Al-Abri S, Olson KR, Kearney T. Safety and effectiveness of physostigmine: a 10-year retrospective review. Clin Toxicol (Phila). 2018;56(2):101-107. doi:10.1080/15563650.2017.1342828 2. Nguyen TT, Armengol C, Wilhoite G, Cumpston KL, Wills BK. Adverse events from physostigmine: An observational study. Am J Emerg Med. 2018;36(1):141-142. doi:10.1016/j.ajem.2017.07.006 3. Scharman E, Erdman A, Wax P, et al. Diphenhydramine and dimenhydrinate poisoning: An evidence-based consensus guideline for out-of-hospital management. Clin Toxicol. 2006;44(3):205-223. doi:10.1080/15563650600585920 4. Shervette RE 3rd, Schydlower M, Lampe RM, Fearnow RG. Jimson "loco" weed abuse in adolescents. Pediatrics. 1979;63(4):520-523. 5. Woolf AD, Erdman AR, Nelson LS, et al. Tricyclic antidepressant poisoning: An evidence-based consensus guideline for out-of-hospital management. Clin Toxicol. 2007;45(3):203-233. doi:10.1080/15563650701226192 Summarized by Jorge Chalit, OMSIII | Edited by Jorge Chalit  

Episode 105: Antidotes to toxidromes. Some poisonings share common signs and symptoms and may be treated with antidotes without laboratory confirmation of the offending agent. Dr. Francis discussed with Dr. Arreaza some of those toxidromes and how to treat them. Written by Aida Francis, MD. Participation by Hector Arreaza, MD. Definitions: • Antidotes are substances given as a remedy that inhibit the effects of another drug of abuse or poison. Most are not 100% effective and fatality is still possible after administration. • Toxidrome is a constellation of signs and symptoms caused by an overdose or exposure to chemicals or drugs that interact with neuroreceptors. Toxidrome is the combination of the word “toxin” and “syndrome”. Management strategies of toxidromes are determined by the signs and symptoms even when the causative agent has not been identified. A little bit of Background: The World Health Organization reported that 13% of deaths caused by poisonings are children and young adults. Intentional poisoning attempts are more frequent among adolescent women than men. It is difficult to evaluate poisoned patients because they are too altered to provide history and there is often not enough time to perform a physical exam or obtain serum studies prior to life-saving interventions. To diagnose a toxidrome clinically, you need three elements: pupil size, temperature, and bowel sounds. For example: Pinpoint pupils with hyperactive bowel sounds point to cholinergic toxidrome, and dilated pupils with high temperature, and hypoactive bowel sounds point to anticholinergic (see details below). Pinpoint pupils -> Bowel sounds -> Hyperactive: CHOLINERGIC -> Hypoactive: OPIOIDS Normal or dilated pupils -> Temperature -> High -> Bowel sounds -> Hyperactive: SYMPATHOMIMETIC -> Hypoactive: ANTICHOLINERGIC -> Normal or Low -> Bowel sounds -> Hyperactive: HALLOCUNOGENIC -> Hypoactive: SEDATIVE-HYPNOTICS Anticholinergic Toxidrome and the Physostigmine antidote: • Anticholinergics inhibit the binding of acetylcholine to the muscarinic receptors in the central nervous system and the parasympathetic nervous system. Examples of anticholinergics include atropine and tiotropium. Other substances that may cause anticholinergic toxidrome include antihistamines (especially first-generation: diphenhydramine), antipsychotics (quetiapine), antidepressants (TCAs, paroxetine), and antiparkinsonian drugs (benztropine). Symptoms of toxicity include tachycardia, non-reactive mydriasis, anhidrosis, dry mucous membranes, skin flushing, decreased bowel sounds, and urinary retention. Neurological symptoms include delirium, confusion, anxiety, agitation, mumbling, visual hallucination, and strange behavior. Neurological symptoms last longer because of the anticholinergic lipophilic properties which cause them to distribute into fatty organs and tissues like the brain. “Mad as a hatter, red as a beet, blind as a bat, hot as a hare, dry as a bone” [Spanish: loco como una cabra, rojo como un tomate, ciego como un topo, seco como una piedra, caliente como el infierno] • The antidote for anticholinergic toxidrome is physostigmine. It is an acetylcholinesterase inhibitor and prevents the metabolism of acetylcholine. This increases the level of acetylcholine in both the central nervous system and peripheral nervous system. Physostigmine can cause seizures and arrhythmia, so close monitoring in the hospital is required during treatment. Cholinergic toxidrome and its antidotes atropine and pralidoxime: Acetylcholine is part of the parasympathetic nervous system and cholinergic substances can induce a parasympathetic response. Some of these substances include pesticides, organophosphates, carbamate, and nerve gas. Chlorpyrifos had been used to control insects in homes and fields since 1965. It has been used in our crops in Bakersfield, and the most recent mass exposure was in May 2017. it was banned on food crops in the US in August 2021. It has been banned for residential use for a longer period. Repeated exposure to chlorpyrifos causes autoimmune disorders and developmental delays in children and fetuses. The symptoms of cholinergic toxidrome can be summarized with the SLUDGE/ “triple” BBB acronym. This includes salivation, lacrimation, urination, defecation, gastrointestinal cramping, emesis, bradycardia, bronchorrhea, and bronchospasm. There can also be muscle fasciculations and paralysis. • The antidote is Atropine. Pralidoxime is used for organophosphates only because it cleaves the organophosphate-acetylcholinesterase complex to release the enzyme to degrade acetylcholine. Pralidoxime should be used in combination with atropine, not as monotherapy. It requires hospital admission, and a note for organophosphate, remember that the patient needs external decontamination (shower). Let's go to part 2 of our discussion, environmental exposure. Carbon Monoxide Toxidrome and the antidote oxygen: Carbon monoxide intoxication is usually due to smoke inhalation injury. Carbon monoxide is a silent gas produced by carbon-containing fuel or charcoal. Carboxyhemoglobin (COHb) forms in red blood cells when hemoglobin combines with carbon monoxide, reducing the binding and availability of oxygen at the tissue level. It's like CO falls in love with hemoglobin and hemoglobin cheats on Oxygen by binding to CO instead, and neglects oxygen delivery to tissues. Carbon monoxide also causes direct cellular toxicity. The symptoms and signs of poisoning include headache, altered mental status, nausea, vomiting, visual disturbance, Cherry-red lips, coma, and seizure. You can also see lactic acidosis and pulmonary edema. Neurological symptoms can be chronic, so it's important to follow up. The blood COHb level must be used to confirm the diagnosis because standard pulse oximetry (SpO2) and arterial partial oxygen pressure (PaO2) cannot differentiate COHb from normal oxygenated hemoglobin. You must obtain a serum COHb level. • The antidote is 100% oxygen or hyperbaric oxygen therapy and close follow-up. Consider intubating if there is edema of the airways due to inhalation injury. Cyanide Toxidrome which include sodium nitrite, sodium thiosulfate, and hydroxocobalamin In combination with Carbon Monoxide poisoning Cyanide poisoning can simultaneously be caused by inhalation of smoke or colorless hydrogen cyanide or ingestion of cyanide salts or prolonged use of sodium nitroprusside (ICU for hypertensive emergency). Symptoms are very similar to carbon monoxide poisoning. There may be long-term neurologic deficits and Parkinsonism. Diagnosis is clinical and waiting for serum cyanide levels can cause treatment delay. However, serum lactate levels over 10 mmol/L suggest cyanide poisoning. • Since cyanide poisoning resembles carbon monoxide poisoning and both toxidromes typically present simultaneously in the pathognomonic fire victim, treat simultaneously with sodium nitrite, sodium thiosulfate, and hydroxocobalamin as well as oxygen as mentioned with carbon monoxide poisoning. Hypnotic and sedative substances (antidote: flumazenil) Examples of hypnotic or sedative substances are alcohol, benzodiazepines, or zolpidem. Signs and symptoms of toxicity include slurred speech, ataxia, incoordination, disorientation, stupor, and coma with mild and rare hypoventilation and bradycardia. • The antidote is flumazenil which is a competitive antagonist at the benzodiazepine receptor. After treatment monitor patients for seizures in case of TCA poisoning, arrhythmia, or epilepsy. Opioid toxidrome (antidote: naloxone) Examples of opioid intoxication in children would be heroine in adolescents or accidental ingestion of pain medication in young children. Signs and symptoms are similar to the sedative toxidrome except for the pathognomonic finding of miosis or “pinpoint pupils” on physical exam. There will also be respiratory depression, hyporeflexia, bradycardia, muscle rigidity, and absent bowel sounds or constipation. Hypoventilation is severe and can cause death. • The antidote is naloxone which is a synthetic opioid receptor antagonist that can diagnose and treat opioid poisoning. It is indicated if the respiratory rate is less than 12. It has a short half-life and is repeatedly administered every 3-5 minutes until the respiratory drive is restored in order to avoid rebound respiratory depression and intubation. It has a rapid onset so the patient must be observed for 24 hours for opioid withdrawal symptoms. Summary: It is important to be able to recognize a toxidrome and antidote early. Once the antidote is administered, you should observe the patient 24 hours for symptoms of rebound toxicity or withdrawal. Consider repeat administration of the antidote if rebound symptoms occur and treat withdrawal symptoms as needed. Don't forget to consider multidrug poisoning if symptoms are non-specific. Thank you for having me on your podcast to review this topic. ____________________________ Conclusion: Now we conclude our episode number 108, “Antidotes to Toxidromes.” Remember you can start treatment of a patient with typical signs and symptoms of specific toxidromes, especially in patients who are unstable. We hope you enjoyed this episode. We thank Hector Arreaza, Aida Francis, and Arianna Lundquist. Audio Edition by Adrianne Silva. Even without trying you go to bed being a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. If you have any feedback, contact us by email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________ References: 1) Jaelkoury, CC BY-SA 3.0 , via Wikimedia Commons. 2) Hon KL, Hui WF, Leung AK. Antidotes for childhood toxidromes. Drugs Context. 2021;10:2020 11-4. Published 2021 Jun 2. doi:10.7573/dic.2020-11-4, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8177957/. 3) Royalty-free music used for this episode: Space Orbit by Scott Holmes, downloaded on July 20, 2022 from https://freemusicarchive.org/music/Scott_Holmes/.

Welcome all to IS PHARMACOLOGY DIFFICULT Podcast! I am Dr Radhika Vijay. In today's episode I will be setting up the verbal conference about drug details, all reversible anticholinesterases like Physostigmine, Neostigmine, Pyridostigmine, Rivastigmine, Galantamine, Edrophonium, Ambenonium, Distigmine, Tacrine, Donepezil.... All sea waters gonna be touched and splashed like basic characteristics, derivation, chemical nature, half life, pharmacodynamics, pharmacokinetics, and as the discussion proceeds, drugs will be compared and evaluated as per their pros and cons too! All in all , a good thorough knowledge storm filling up the sky of curiosity and learning!! Are you ready, if yes, its your cup of tea, if you do not find it, it is advised that stay tuned and soon it gonna be in your cup :) For all the updates and latest episodes of my podcast, please visit- www.ispharmacologydifficult.com where you can also sign up for a free monthly newsletter of mine. It actually contains lot of updates about the medical sciences, drug information and my podcast updates also. You can follow me on different social media handles like twitter, insta, facebook and linkedin. They all are with same name "IS PHARMACOLOGY DIFFICULT". If you are listening for the first time, do follow me here, whatever platform you are consuming this episode, stay tuned, do rate and review on ITunes, Apple podcasts, stay safe, stay happy, stay enlightened, Thank you!! You can access various links via- https://linktr.ee/ispharmacologydifficult

Welcome all to IS PHARMACOLOGY DIFFICULT Podcast! I am Dr Radhika Vijay.In today's episode I will be setting up the verbal conference about drug details, all reversible anticholinesterases like Physostigmine, Neostigmine, Pyridostigmine, Rivastigmine, Galantamine, Edrophonium, Ambenonium, Distigmine, Tacrine, Donepezil....All sea waters gonna be touched and splashed like basic characteristics, derivation, chemical nature, half life, pharmacodynamics, pharmacokinetics, and as the discussion proceeds, drugs will be compared and evaluated as per their pros and cons too!All in all , a good thorough knowledge storm filling up the sky of curiosity and learning!!Are you ready, if yes, its your cup of tea, if you do not find it, it is advised that stay tuned and soon it gonna be in your cup :)For all the updates and latest episodes of my podcast, please visit-  www.ispharmacologydifficult.com  where you can also sign up for a free monthly newsletter of mine. It actually contains lot of updates about the medical sciences, drug information and my podcast updates also.You can follow me on different social media handles like twitter, insta, facebook and linkedin. They all are with same name "IS PHARMACOLOGY DIFFICULT". If you are listening for the first time, do follow me here, whatever platform you are consuming this episode, stay tuned, do rate and review on ITunes, Apple podcasts, stay safe, stay happy, stay enlightened, Thank you!!You can access various links via- https://linktr.ee/ispharmacologydifficult

Welcome all to IS PHARMACOLOGY DIFFICULT Podcast! I am Dr Radhika Vijay.In today's episode, I will be discussing Introductory aspects of Anticholinesterases, these are the inhibitors of Acetylcholine esterase enzyme which hydrolyses Acetylcholine in the synapse! It is all in all a new runway to land our plane of episode today…After discussing structural aspects, slight differences, common features, binding sites, mechanisms.I will be heading over to broadly classify these agents and today will be the celebrated day to name the Reversible Anticholinesterases like Physostigmine, Pyridostigmine, etc.With a motivation push in the end, I hope this information is good enough to set in motion your awaited endeavours, talk to you all in the next episode!For all the updates and latest episodes of my podcast, please visit - https://www.ispharmacologydifficult.com where you can also sign up for a free monthly newsletter of mine. It actually contains a lot of updates about the medical sciences, drug information and my podcast updates also.You can follow me on different social media handles like twitter, insta, facebook and linkedin. They all are with same name "IS PHARMACOLOGY DIFFICULT". If you are listening for the first time, do follow me here, whatever platform you are consuming this episode, stay tuned, do rate and review on ITunes, Apple podcasts, stay safe, stay happy, stay enlightened, Thank you!!You can access various links via- https://linktr.ee/ispharmacologydifficult

Welcome all to IS PHARMACOLOGY DIFFICULT Podcast! I am Dr Radhika Vijay. In today's episode, I will be discussing Introductory aspects of Anticholinesterases, these are the inhibitors of Acetylcholine esterase enzyme which hydrolyses Acetylcholine in the synapse! It is all in all a new runway to land our plane of episode today… After discussing structural aspects, slight differences, common features, binding sites, mechanisms. I will be heading over to broadly classify these agents and today will be the celebrated day to name the Reversible Anticholinesterases like Physostigmine, Pyridostigmine, etc. With a motivation push in the end, I hope this information is good enough to set in motion your awaited endeavours, talk to you all in the next episode! For all the updates and latest episodes of my podcast, please visit - https://www.ispharmacologydifficult.com where you can also sign up for a free monthly newsletter of mine. It actually contains a lot of updates about the medical sciences, drug information and my podcast updates also. You can follow me on different social media handles like twitter, insta, facebook and linkedin. They all are with same name "IS PHARMACOLOGY DIFFICULT". If you are listening for the first time, do follow me here, whatever platform you are consuming this episode, stay tuned, do rate and review on ITunes, Apple podcasts, stay safe, stay happy, stay enlightened, Thank you!! You can access various links via- https://linktr.ee/ispharmacologydifficult

Born in Montgomery, Alabama, the son of a railway mail clerk and the grandson of enslaved people. In an era when African Americans faced prejudice in virtually all aspects of life, not least in the scientific world, he succeeded against the odds. Inadequately prepared by his high school, he was accepted at DePauw University in Greencastle, Indiana, as a sub-freshman, meaning that he had to take high-school courses concurrently with his freshman courses. Majoring in chemistry, he graduated as valedictorian of his class in 1920. After graduation he taught chemistry at Fisk University for two years before winning an Austin Fellowship to Harvard University, where he completed a master's degree in organic chemistry. After Harvard he returned to teaching at West Virginia State College and Howard University. In 1929 Julian traveled to the University of Vienna, Austria, to begin doctoral studies on the chemistry of medicinal plants. Two years later, with degree in hand, he and a Viennese colleague, Josef Pikl, took positions back in the United States at Howard and two years later moved to DePauw. There they accomplished the first total synthesis of physostigmine, the active principle of the Calabar bean, used since the end of the 19th century to treat glaucoma. Physostigmine, an alkaloid, eases the constriction of outflow channels from the eye's aqueous humor to relieve high pressure there, which, if left untreated, damages the retina and eventually causes blindness. Meanwhile researchers in many countries were seeking innovative and cost-effective ways to synthesize steroids, including cortisone and the sex hormones. German chemists discovered that the steroid stigmasterol, which Julian had obtained as a by-product of the physostigmine synthesis but was also obtainable from soybeans, could be used in the synthesis of certain sex hormones, including progesterone, a female sex hormone that was important in helping pregnant women avoid miscarriages. In pursuit of this lead, in 1936 Julian wrote to the Glidden Company in Chicago, requesting samples of their soybean oil. Through a series of events he wound up being hired by Glidden instead, as their director of research in the Soya Division, where he set about figuring out ways to make new products from soybeans. In 1948 scientists at the Mayo Clinic announced their landmark discovery of cortisone, which had remarkable effects on rheumatoid arthritis, and Julian jumped into the exciting competition to synthesize cortisone inexpensively. Cortisone is a cortical hormone of the adrenal gland. In 1949 Julian developed a new synthesis for a related substance (called “Substance S”) also present in the adrenal cortex and differing from cortisone by only an oxygen atom. From this substance he was able to synthesize both cortisone and hydrocortisone. Hydrocortisone and its derivatives today are more widely prescribed than cortisone products, and most industrial syntheses still begin along the same route that Julian pioneered. Julian located a wild sweet potato in Guatemala. He figured out how to synthesize cortisone from yams, for pennies a gram. Julian remained at Glidden until 1954, when he founded his own company, Julian Laboratories of Franklin Park, Illinois, and Mexico City (which he eventually sold to Smith, Kline and French) for Millions of dollars. Throughout his life he was socially active in groups seeking to advance conditions for African Americans, helping to found the Legal Defense and Educational Fund of Chicago and serving on the boards of several other organizations and universities --- Support this podcast: https://anchor.fm/unlabeled/support

In this podcast, Dr. Cole Pueringer, a toxicology fellow with the Minnesota Poison Control System (Hennepin Healthcare), discusses various over-the-counter medications and their toxicological potential. Enjoy the podcast! Objectives:     Upon completion of this podcast, participants should be able to: List at least 3 potentially dangerous over-the-counter (OTC) medications. Discuss the basic clinical presentation and management of the following over-the-counter (OTC) medications: acetaminophen, diphenhydramine loperamide, ibuprofen, and dextromethorphan. CME credit is only offered to Ridgeview Providers & Allied Health Staff for this podcast activity. Complete and submit the online evaluation form, after viewing the activity.  Upon successful completion of the evaluation, you will be e-mailed a certificate of completion within approximately 2 weeks.  You may contact the accredited provider with questions regarding this program at  rmccredentialing@ridgeviewmedical.org. Click on the following link for your CME credit: CME Evaluation: "The Dose Makes the Poison: Over-the-Counter (OTC) Medication" (**If you are listening to the podcasts through iTunes on your laptop or desktop, it is not possible to link directly with the CME Evaluation for unclear reasons. We are trying to remedy this. You can, however, link to the survey through the Podcasts app on your Apple and other smart devices, as well as through Spotify, Stitcher and other podcast directory apps and on your computer browser at these websites. We apologize for the inconvenience.)  DISCLOSURE ANNOUNCEMENT  The information provided through this and all Ridgeview podcasts as well as any and all accompanying files, images, videos and documents is/are for CME/CE and other institutional learning and communication purposes only and is/are not meant to substitute for the independent medical judgment of a physician, healthcare provider or other healthcare personnel relative to diagnostic and treatment options of a specific patient's medical condition; and are property/rights of Ridgeview Medical Center & Clinics.  Any re-reproduction of any of the materials presented would be infringement of copyright laws.  It is Ridgeview's intent that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts. It is not assumed any potential conflicts will have an adverse impact on these presentations. It remains for the audience to determine whether the speaker’s outside interest may reflect a possible bias, either the exposition or the conclusions presented. Ridgeview's CME planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed that no conflict of interest exists with the presentation/educational event.    SHOW NOTES: Antihistamines:  Like so many other over-the-counter medications, the dose of antihistamines makes the poison. Sedation is the most common side effect in antihistamine overdose. Some, like diphenhydramine, are more toxic and have profound anticholinergic effects. Sinus tachycardia is one of the first presentations, but remember the phrases: Tachy as a tie, dry as a bone, mad as a hatter, red as a beet, hot as a hare and blind as a bat. Excitatory toxidromes can be confusing, but urinary retention, impaired bowel motility and the absence of diaphoresis will differentiate anticholinergic toxicity from the other excitatory toxidromes. the higher the dose, the more side effects seen, leading to seizures and cardiac toxicity. Physostigmine is an antidote for anticholinergic toxicity. Delirium is the main indication for physostigmine, but it can also be given to prevent intubation and at times to get a more accurate history from the patient. Physostigmine lowers the seizure threshold, so benzodiazepines are usually given prior administration. Most likely they have already been given to treat undifferentiated delirium and excitation. Of note, physostigmine is not the cure all for the toxidrome because it has a very short half life. In the setting of seizures in overdose, very few anticonvulsants are safe. Benzodiazepines are some of the safer GABAergic agents. GABA is our main CNS inhibitory neurotransmitter, it essentially "tones down the nerves". Propofol and some other GABAergic agents can also help with tachycardia and hyperthermia. In these settings, benzodiazepines are given in very high doses. Diphenhydramine causes sodium channel blockade, subsequently decreasing action potential. lowering calcium in the cells, and causing life threatening myocardial depression. Calcium is given in this circumstance, but the mainstay of treatment is sodium bicarbonate. It works by increasing overall sodium availability and the pH. The more acidotic the patient, the more of the drug becomes unbound and available. At higher pH levels, the sodium channel blockade weakens, and more of the drug becomes protein bound. What about other antihistamines? While overdose of other antihistamines will be uncomfortable, the life threatening seizures and cardiac toxicity is unique to diphenhydramine.  Acetaminophen:  Acetaminophen is the highest nationally in morbidity and mortality of all drug overdoses. Most often taken on it's own, it's also mixed into many over-the-counter remedies. In the first 24-hours post-ingestion, the symptoms can be minimal. It's metabolized in the liver, and a small portion is metabolized by CIP 2E1, resulting in the toxic metabolite NAPQI. Normally, glutathione will detoxify NAPQI, but in acetaminophen overdose, glutathione stores are depleted and the excess NAPQI creates havoc in the liver. In a reliable historian with an acute ingestion, the Rumack-Matthew nomogram is employed, and will help guide antidote therapy. Serum acetaminophen levels will not be helpful until 4 hours post-ingestion, unless something that slows GI transit time and absorption has been taken as well. N-acetylcysteine or "NAC", is the antidote for Tylenol. If given within eight hours of ingestion it can prevent any liver toxicity. It can also be started any time a serious ingestion is suspected. Keep in mind, delayed-release Tylenol, certain populations, and conditions can obscure the diagnosis and in those settings the Rumack-Matthew nomogram can no longer be used. Chronic alcoholics who have just stopped drinking and malnourished patients are at higher risk of toxicity. Subacute and chronic ingestion is also very common. Essential lab tests include serum acetaminophen levels, ALT and AST, and INR. One would expect any or all of these to be elevated in significant toxicity. If they are, NAC is given intravenously for nearly 24 hours. NAC won't reverse hepatotoxicity that has already occurred, but will prevent more from happening. Dextromethorphan:  Dextromethorphan, referred to sometimes as "robotripping" or "robo-frying". Taken in excess causes an individual to become disassociated. It is an NMDA antagonist, like ketamine, LSD and PCP. Expect to see the same clinical signs of serotonin excess, as well as dystonia. Patients can alternate dramatically between vacant blank stares, to incredibly violent outbursts. Patient and staff safety is a crucial element in treating this toxidrome. Rotatory nystagmus, a distinctive rapid "clock ticking" of the eyes is diagnostic of this type of ingestion. Loperamide:  When Loperamide, an over-the-counter antidiarrheal, is used in abuse it can lead to death. It acts similar to opioids, slowing down the GI tract but without the central effects, because it is actively expelled from the CNS. In large doses, however, it delivers an opioid-like high. Loperamide can cause respiratory depression, but also persistent arrhythmias. The lethal effects are due to loperamide's potassium channel blocker properties causing profound QT prolongation, sinusoidal waves and can lead to cardiac arrest. Potassium channel blockade is difficult to treat. ACLS drugs, electrolyte normalization like magnesium infusions, and even Narcan can be given, but more than likely these incredibly sick patients will need ECMO. Ibuprofen:  Ibuprofen is, overall, a safe drug. Large quantities of the drug have to be taken for toxic effects. If taking over 200mg/kg if Ibuprofen, a patient is likely to have some GI symptoms and possibly an acute kidney injury. treatment would include possible admission for antiemetics and IV fluids. Ibuprofen is metabolized as a propionic acid anion. If ore than 400mg/kg are taken, it will result in an anion gap metabolic acidosis. At over 600mg/kg, a whole constellation of symptoms results: seizures, hypotension, and cardiac shock. These patients are severely ill and may require ECMO for an extended period of time. At this dosage, a 100kg patient would need to take 300 pills. Which leads to the question, "How did they fit that many pills in their stomach?"  Activated Charcoal:  Finally, a note on activated charcoal. It works great for almost everything, except alcohol ingestion and metals, by binding drugs in the GI tract. Drug absorption is decreased by 60% if given within an hour. It should be avoided if the airway is compromised or if the patient is a risk for seizure. In an intubated patient with recent ingestion, it's given via nasogastric tube. Thank-you for listening.

In this EM Quick Hits podcast we have Emily Austin on physostigmine for anticholinergic toxidrome, Walter Himmel on understanding nystagmus to differentiate central vs peripheral causes of vertigo, Rob Devins on the role of transesophageal echocardiogram in cardiac arrest, Jesse MacLaren on nuances in inferior MI ECG changes and aVL, Andrew Petrosoniak on a practical approach to blunt cerebrovascular injury and Reuben Strayer on choicebo... The post EM Quick Hits 11 Blunt Cerebrovascular Injury, Physostigmine, TEE in Cardiac Arrest, Understanding Nystagmus, Subtle Inferior MI, Choicebo appeared first on Emergency Medicine Cases.

Ready for some fright-night fun Rangers? PoisonBoy is joined by the Copperhead Kid himself, Jarratt Lark and our newest Ranger, the Blonde Widow, Dr. Morgan Smith to discuss all sorts of terrifying topics. Join us to learn why witches ride broomsticks and why brown recluse and black widow spiders are so misunderstood. It's all the Halloween horror without the sore teeth from eating all that chocolate, plus you might actually learn something. Or maybe not. Either way - you are guaranteed to have a good time, so what are you waiting for? 

In this episode of Tox in Ten ACMT Highlights, co-host Dr. Gillian Beauchamp sits down with Emergency Medicine Physician and Medical Toxicologist Dr. Spencer Greene to discuss the use of Flumazenil and Physostigmine. 

Physostigmine for Anticholinergic toxicity

We review this blog post by Bryan Hayes, an ED pharmacist (@PharmERToxGuy), on the use of physostigmine in anticholinergic toxicity. We then review anticholinergic toxidrome using Rosen's, Tintinalli's, and Goldfrank's as a guide. Thanks for listening! Lauren Westafer and Jeremy Faust

This week we delve into the anticholinergic toxidrome with a focus on management and the use of physostigmine. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_48_0_Final_Cut.m4a Download Leave a Comment Tags: Anticholinergic, Diphenhydramine, Physostigmine, TCA, Toxicology Show Notes Howland M. Antidotes in Depth (A12): Physostigmine Salicylate. In: Nelson LS, Lewin NA, Howland M, Hoffman RS, Goldfrank LR, Flomenbaum NE. eds. Goldfrank's Toxicologic Emergencies, 9e . New York, NY: McGraw-Hill; 2011. Velez LI, Feng SY: Anticholinergics, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen's Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2010, (Ch) 150: p 1970-5. Anticholinergic Infographic (B...

This week we delve into the anticholinergic toxidrome with a focus on management and the use of physostigmine. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_48_0_Final_Cut.m4a Download Leave a Comment Tags: Anticholinergic, Diphenhydramine, Physostigmine, TCA, Toxicology Show Notes Howland M. Antidotes in Depth (A12): Physostigmine Salicylate. In: Nelson LS, Lewin NA, Howland M, Hoffman RS, Goldfrank LR, Flomenbaum NE. eds. Goldfrank's Toxicologic Emergencies, 9e . New York, NY: McGraw-Hill; 2011. Velez LI, Feng SY: Anticholinergics, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen's Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2010, (Ch) 150: p 1970-5. Anticholinergic Infographic ...

This week we delve into the anticholinergic toxidrome with a focus on management and the use of physostigmine. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Episode_48_0_Final_Cut.m4a Download Leave a Comment Tags: Anticholinergic, Diphenhydramine, Physostigmine, TCA, Toxicology Show Notes Howland M. Antidotes in Depth (A12): Physostigmine Salicylate. In: Nelson LS, Lewin NA, Howland M, Hoffman RS, Goldfrank LR, Flomenbaum NE. eds. Goldfrank’s Toxicologic Emergencies, 9e . New York, NY: McGraw-Hill; 2011. Velez LI, Feng SY: Anticholinergics, in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2010, (Ch) 150: p 1970-5. Anticholinergic Infographic (BrianandKloss.com)

Sun, 1 Jan 1989 12:00:00 +0100 https://epub.ub.uni-muenchen.de/10304/1/10304.pdf Arbogast, Helmut; Arndt, H.