Creating Visually Stunning and Effective Presentations!

Part 1: Background on Lecturing

People have been giving lectures for thousands of years in the form of storytelling. However, the use of PowerPoint as the new norm for lecturing in the past couple of decades. Lecturing new material has been shown to be most beneficial when using visual and oral stimulation together. While PowerPoint as a lecture style may offer this, it often creates a dangerous situation bysplitting the learner’s attention.


In the book Brain Rules, by John Medina, he showed that retention of knowledge increases up to 65% when using visual and oral representation of data as opposed to 10% retention for oral only and 35% for visual only.


Richard Mayers, a scientist studying multimedia learning, created the theory of Dual Channel Processing to explain how oral and visual data combine to form memory. He stated that oral stimulation and visual stimulation (including text and images) use separate pathways to form memories. If the two pathways complement each other, this leads to enhanced learning. However, the pathways work at different speeds – people generally read faster/understand quicker by visualizing something as opposed to hearing something. As a result, If the two stimuli come at the same time and cause a split in the receiver’s attention, then you get what is called ‘Cognitive Overload’ and an overall decrease in retention.


Therefore, in order to maximize retention and use both channels of processing to their fullest, we should present visuals that support the oral presentation, instead of competing with it. Using careful design of lecture visuals, we can thwart the dangerous pitfalls inherent to PowerPoint presentations.


Part 2: Understanding the learner’s poor attention span


It is well known that learners in general have poor attention spans, amplified by the typical learning environment provided by lecture halls (dimly lit, warm, comfortable seats, etc.). Many studies have shown that during lectures, our best attention lasts for 10-15 minutes after which our retention of information plummets.


Here we see that by about 10 minutes into a lecture, the learner’s retention of the information decreases to about 70%. The learner’s retention drops significantly and only recovers briefly at the lecture conclusion. The overall average amount of a lecture that is retained ends up being about 20%.


Studies looking at how to keep the learner’s attention and increase retention have shown that this can be achieved by introducing breaks every 10-15 minutes. Breaks as short as 25 seconds, for example, polling the audience or audience participation, have been shown to be effective at increasing overall retention.

Lastly is the concept that a leaner can only learn so much within a given time frame. If we, as lecturers, try to teach too much, this leads to an overall decreased retention of information. Therefore, it is better to pick a smaller scope of discussion, simplifying the lecture as much as possible, and really honing down on the important learning objectives. The general rule of thumb is to cut down material to 75% for an allotted time (for example, an hour-long lecture should have 45 minutes of lecture material). This will leave room for questions and explanations and minimize the risk of too much information.


Part 3: Building your story


Humans are wired to listen to stories, which are the preferred way to both be entertained and acquire information. Nancy Duarte discusses that we as lecturers should build our presentations like a story in that we should have a beginning, middle, and an end.



To accomplish this, we should begin by setting the stage for why the learner should care about the information. Like a story, we give the background about the world as the learner knows it and then introduce what will be discussed and why it is important.



Here is where we actually give the information.



We should finish by bringing it back around, reminding the learner what they had just learned, and what you want them to get out of the lecture. Inspire them as to why this new knowledge will be beneficial for them.


Another important element of stories is to keep familiar/comforting themes. Here are four ways to accomplish this:

  1. Keep a consistent feel – avoid using different fonts, backgrounds, or color schemes, and try to make the lecture feel like it remains consistent throughout.
  2. Be mindful of topic transitions – transitions between different topics should be smooth and logical, as opposed to jumping around with no clear path of where the lecture is headed.
  3. Use brain memory tricks for structure – Humans prefer to learn things in sets of 3, rule of 10s, or memorizing numbers in series of 7.
  4. Sign posting of slides, a trick by Scott Weingart (EMCrit) – these are images or text (such as a header or slide number) on each slide that orients the audience to where they are in the talk.


Part 4: Tips and tricks for having good visuals

The most important tip for improving lecture slides is to use less text, which has been universally shown to be an ineffective way to provide visual information during a lecture. If you must use text, try to avoid using bullet points, which encourages filling the slides with text rather then images. However, if choosing to use bullets, limit them to 3 or 4 bullets added sequentially to the screen as you are talking about each point. Furthermore, keep bullet points short, avoiding full complete sentences and only using short key phrases, numbers, important terms, and definitions.


On the other hand, the best way to improve slides is to use more high definition images. One caveat is to be careful that the images you choose provide a useful purpose and do not distract from your overall message. It also is important to use images created for creative commons in order to avoid plagiarizing other people’s works. The easiest place to start is by using Google Images. Under ‘Tools’, there is a section, which you can change to “Labeled for reuse” (See below), showing images safe to use. You can also search by size, picking out only large photos that are high resolution, which will look nice when stretched on the big projector screen.



There are many websites online that provide free or cheap stock photos. Here are a few:


Cheap Photo Banks


Free Photo Banks



Once the picture is selected, you should crop out all the unnecessary sections of the photo. If the photo has a distracting or unappealing background color, then PowerPoint has an option to fix this under the formatting section for a selected photo titled ‘Remove Background.’ By using this feature you can select what part of the image is the background, and the program will remove it, making the main image look transparent and visually pleasing on a slide (See below how I made the Hermes staff with a white box become transparent).

If using multiple images or words that you would like to maneuver around the screen in unison, you can select all the images and right click them. This will bring up an option labeled ‘Grouping,’ which will allow you to group the images together, making them easier to move around the slide.


Matching the color of text, shapes, and symbols could be useful in giving a consistent and cohesive feel to the slides. You can match colors for these objects to anything else on the slide by going into the color palette for the desired text/shape, and clicking ‘pick a color,’ which turns your cursor into an eyedropper. You can then click on anything on the screen (such as an image you found online), and PowerPoint will match the color to the image color.


As far as font size, it is important to use a size no smaller then size 24 in order to be legible in an auditorium. However, the optimal font size is around 32, with fonts in the 40s being most visible. Furthermore, the preferred font type for PowerPoint presentations is San Serif, which is the font without the small lines capping off the ends of the characters. The top three preferred San Serif fonts for presentations are usually Arial, Calibri, and Tahoma.


Difficult Lectures: Lectures on journals, cases, and M&Ms

In medicine, we frequently have to give lectures heavy in data, graphs, and clinical information. These are often difficult to improve with pictures. While this may seem difficult, spending some extra time could improve the lecture immensely. Avoid falling into the classic trap of copying and pasting confusing graphs or taking a poor quality screenshot of the chart.


Spend the time to remake charts and graphs, focusing on only the important parts you want to highlight. If copying a graph/chart, crop out the unnecessary information and blow it up, highlighting the important parts with boxes or arrows. For case presentations, it is helpful remake vital signs and try to provide parts of the history and physical using images or short phrases instead of sentences.


Part 5: Perfecting your lecture performance

The best way to perfect your performance is to rehearse, rehearse, and rehearse!! Give the lecture to anyone who will listen such as friends/family and perform it in front of a mirror or record yourself using a camera. This will help you perfect the kinks and find out the “Umms” or nervous ticks you have during performance. This will also help you to memorize all of your slides, so that you can perform the lecture without looking at them.


Come early to the lecture auditorium, and come prepared. Have multiple ways to upload your lecture (email, google drive, flash drive, etc), and try to upload and go through your slides before your presentation. This will allow you to see if there are any issues with their computer or projector specs and possibly fix them before your lecture. Avoid bringing anything with you to the stage, such as keys or cellphones, which could be a distraction during the presentation.


Use of laser pointers should also be avoided, as they are often hard to see, and encourage you to face away from the audience. Furthermore, most people have difficulty keeping the pointer straight, since we often are jittery after coffee. Some people recommend using your hands to point to the screen or using a stick, or even using the computer cursor. You can change the cursor into a pen by clicking ctrl p during the lecture. To erase it, click ctrl e. To bring back a cursor arrow, press ctrl a.


You should use the front area as your stage during the performance. Avoid turning your back or reading your slides. You don’t want to hide all the way to the side behind the podium. Try to use the space in the front and engage with the audience. Some people recommend marking your stage at a couple places, which you can walk back and forth to, preventing you from being stagnant. Try to use good eye contact with some audience members, scanning the room back and forth in a ‘Z formation’.



After reading this post, you will be able to take your lecture to the next level of excellence!



  • Anderson C. How to give a killer presentation. Harvard Business Review. org. From June 2013 Issue.
  • Bavolck R. Adult Learners/ Novice/Expert Students. 2016-2017 ACEP Teaching Fellowship
  • Duarte N. Structure Your Presentation Like a Story. Harvard Business Review. org. From 11/31/2012
  • Collins J. Education techniques for lifelong learning: giving a PowerPoint presentation: the art of communicating effectively. Radiographics : a review publication of the Radiological Society of North America, Inc 2004;24:1185-92.
  • Fisher R. Ross Fisher‘s approach to presentation (p cubed presentations), com. Taken on 3/15/2017
  • Harolds JA. Tips for giving a memorable presentation, Part I – VI. Clinical nuclear medicine 2012;37:669-70.
  • Issa N, Mayer RE, Schuller M, Wang E, Shapiro MB, DaRosa DA. Teaching for understanding in medical classrooms using multimedia design principles. Medical education 2013;47:388-96.
  • Issa N, Schuller M, Santacaterina S, et al. Applying multimedia design principles enhances learning in medical education. Medical education 2011;45:818-26.
  • Lex J. Death by Bullet Points. The Teaching Course Podcast, released 11/15/2015
  • Mayer, R.E. (2005) The Cambridge Handbook of Multimedia Learning. New York: Cambridge University Press.
  • Medina, J. (2008). Brain rules: 12 principles for surviving and thriving at work, home, and school. Seattle, WA: Pear Press.
  • Pillow T. Poznanski S. Lin M., Tubbs R, Presentation Design for Medical Educators: A Missing Piece of Faculty Development. 2014 CORD Academic Assembly
  • Prince, M (2004) Does Active Learning Work? A Review of the Research. J Engr. Education, 93(3), 223-231
  • Swaminathan A., Rezai S. How to build a talk – part 1. The Teaching Course Podcast, released 8/1/2015
  • Weingart S. Powerpoint and Meth, Emcrit Podcast, Podcast episode 192. Updated on 2/6/2017

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So Bored I Saw Floaters – Retinal Detachment

It’s always a balancing act of knowing when to eat on shift. You’re hypoglycemic, but you just saw a patient with gastroenteritis. You’ve got to wash your hands and grab a quick snack before you syncopize or get gastro! On a particularly busy shift, I was starting to see spots from being so hungry. I took a few bites of my bagel with egg whites and cheese, chugged a Dunkin’ Donuts coffee, threw it all in my bag before the head nurse could see, and then ran in to see my next patient.

90 year-old female brought in by EMS for sudden painless loss of vision in her right eye. What is your differential?

-Central retinal artery occlusion

-Central retinal vein occlusion


-Posterior uveitis

-Optic neuropathy

-Retinal Detachment

What is retinal detachment?

The posterior segment of the eye is a large cavity filled with vitreous gel. Natural aging causes contraction of vitreous gel and separation from the posterior wall of the eye. However, when vitreous pulls the retina enough to cause a defect in the retinal attachment, fluid will accumulate and cause the retina to slowly peel off, leading to retinal detachment (RD).

What are the causes of RD?

The origin of most retinal detachments is a retinal tear, caused by:

-Normal aging process

-Severe nearsightedness

-Posterior vitreous detachment

-Prior eye trauma or surgery

What are the signs and symptoms of RD?

-Flashes of light/photopsia caused by retinal tugging (unilateral in affected eye)

-Floaters (shadows cast by vitreous gel)

-Painless monocular vision loss

-A dark veil or curtain in the peripheral field of vision that progresses to the center over hours to weeks

-Decreased peripheral and/or central visual acuity

-Blurry vision


Back to your differential diagnosis:

What other conditions present with floaters?

-Posterior vitreous detachment

-Proliferative diabetic retinopathy


What other conditions present with flashes?

-Posterior vitreous detachment

Ophthalmic migraines with or without aura (binocular)

-Optic neuritis

-Postural hypotension (binocular)

-Vasovagal reactions (binocular)



What is the most common location for a retinal tear?

Peripheral retina (where retina is thinner). This is not visualized on a direct fundoscopic examination!

How do we diagnose it in the ED?

Bedside ultrasound (US) with a high frequency linear probe is the fastest method for diagnosis in the ED. The eye is circular and hypoechoic on US. The detached retina will be seen as a hyperechoic stripe at the bottom of the screen floating in the anechoic posterior chamber. See this ALiEM blog post for more info.

What is the treatment?

-If retinal detachment is diagnosed in the ED by ultrasound or clinical presentation, refer the patient to an Ophthalmologist within 24 hours for prompt surgical repair.


How do we know the difference between benign flashes and floaters vs. retinal detachment?

You can have flashes and floaters without retinal detachment, but you cannot have retinal detachment without flashes and floaters. Prompt ophthalmologic evaluation is therefore important to differentiate benign from pathologic. So next time you see a patient with floaters and flashes of light, be sure to ask about timing and any changes, especially in the context of vision loss. Any new flashes and floaters with vision changes should be alarming.


-Retinal tears and retinal detachment usually affect the elderly, but they can occur in severely nearsighted young people

-Bedside ultrasound in the ED is the fastest and most accurate method for diagnosis

-Time is of the essence. The faster the recognition of a retinal tear, the sooner you can refer to a specialist for treatment, and the more likely that vision can be preserved.



Tintinalli, Judith E., J. Stephan Stapczynski, O. John Ma, Donald M. Yealy, Garth D. Meckler, and David M. Cline. Tintinalli’s Emergency Medicine a Comprehensive Study Guide. New York: McGraw-Hill Education, 2016. Print.


Rosh Review—Practice-Management/Focus-On–Ultrasound-for-Acute-Retinal-Detachment/

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Special K for breakfast: A solution for sickle cell pain?

It’s 4am in the emergency department, and you’ve finally reached a lull in the onslaught of patients after having finally successfully bailed out the flood from the afternoon. An individual very familiar to you and the rest of the department pops up on the board. Despite the risk of crashing your computer due to the enormous size of this patient’s chart, you assign yourself and take the plunge. Chief complaint: Sickle cell pain.


You approach the patient, who tells you her pain is mostly in her back and legs. No, she hasn’t been short of breath, and no, she hasn’t had a fever. She answers your questions patiently but eventually cuts to the chase, “Can I have my dose of 6mg Dilaudid and 50 mg of Benadryl?”


We’re all aware of opioid epidemic that’s currently raging, presumably as a result of patient satisfaction metrics and the medical community’s heavy-handed prescribing over the past few decades. While this is a problem for the treatment of acute and chronic conditions across the board, the nature and course of sickle cell disease predisposes these patients to dependence and makes it complicated to address responsibly. We all know to start with NSAIDS, but for patients who have been prescribed opioids from a young age, this sometimes doesn’t cut the mustard.


Is there another way?

There are many alternatives for acute pain control: IV lidocaine, IV acetaminophen, propofol, and even dexmedetomidine (See Dr. Nguyen’s excellent lecture). One emergency department in New Jersey has even employed “energy healing and a wandering harpist” to avoid opioid prescriptions. Although these are all reasonable regimens, the medications listed above are administered intravenously, which may be a challenge in sickle cell patients with notoriously difficult venous access. (And there’s a certain lack of evidence that energy healing and the harp are effective as monotherapy.)

Easing suffering one chord at a time.

Ketamine, however, has been tested intranasally (IN) and found to be effective. One double-blinded RCT on 90 trauma patients in the ED compared either 1 mg/kg IN ketamine, 0.1 mg/kg IV morphine, or 0.15mg/kg IM morphine and found that the three regimens had similar onset and effectiveness at relieving pain. No adverse events were reported.[1] Although a small study, IN ketamine’s utility in treating acute pain in the ED has been corroborated by other observational studies.[2],[3]


Another RCT on 20 patients on opioid maintenance therapy for chronic pain found self-administered IN ketamine to be more effective at placebo at controlling breakthrough pain1; in this population, no patients receiving ketamine required their ‘normal’ rescue opioid medication. However, 35% of the placebo group had to reach for additional opioids. No adverse events were reported. If you consider sickle cell pain to be acute-on-chronic, ketamine may be something to consider.


It is worth noting that although we’ve concentrated on IN route above because of its implications for patients with difficult vascular access (i.e. sickle cell patients), IV ketamine at 0.1 mg/kg – a subdissociative dose – has been shown to be effective for pain in the ED when given IV compared to morphine at a dose of 0.3 mg/kg.[4] A meta-analysis and review by Motov et. al. on the subject supports its use at this dose.[5]


Sickle Cell Specifics

Before you pull the trigger on ordering that ketamine and get the inevitable call from pharmacy (and then explain its indication to the nurse), has it been studied in sickle cell disease, specifically?

Unfortunately, there is really no consensus on how to manage refractory pain in sickle cell patients – a Cochrane review from 2009[6] found that studies examining the correct pain regimen were underpowered, and the authors were unable to provide a recommendation.

There’s a right way to administer intranasally. And then there’s the other way.


The data on sickle cell disease is confined to case reports,[7],[8],[9],[10],[11] mostly from inpatient teams that had success with ketamine when opioids failed. However, in combination with the data on its use in both acute and chronic pain, I would argue that it is a reasonable alternative to opioids. A pediatric anesthesia review[12] on the subject agrees.


But what about the abuse potential?
While it’s true ketamine is used recreationally, it’s important to note that we’re not currently in the throes of history’s greatest ketamine epidemic (unlike opioids). A 2016 review[13] acknowledges that ketamine abuse and tolerance does occur, but contrary to opioids, it tends to be more in the specific setting of recreational use, and users do not seem to develop the same level of dependence. The American Association of Poison Control Centers recorded only 327 exposures to ketamine in 2014, only 1 of which was fatal[14]. Furthermore, no formal withdrawal syndrome has been described.


Get ‘em while they’re young
As an editorial aside, many sickle cell patients seem to have developed tolerance to opioids as a result of frequent hospitalizations, many at a young age, resulting in dependence that may be related to but is separate from sickle cell disease itself. Perhaps there should be some discourse about the long-term consequences that these patients face as a result of opioid prescriptions – should we be encouraging the use of a regimen that utilizes more opioid-sparing agents for sickle cell patient at an younger age?

Less abuse potential than some alternatives


Wrap Up

Subdissociative-dose ketamine has been shown to be safe and effective at treating chronic and acute pain. Although specific evidence regarding its use in sickle cell disease is lacking beyond case reports, it has the advantage of intranasal (rather than parenteral) administration in the difficult venous access-patient and has a more favorable profile with regards to abuse. It requires adequate prospective study to reach a more concrete conclusion, but perhaps it’s time to consider 1 mg/kg IN ketamine in sickle cell patients as an opioid-alternative to reduce the risk of dependence.


[1] Shimonovich S, Gigi R, Shapira A, et al. Intranasal ketamine for acute traumatic pain in the Emergency Department: a prospective, randomized clinical trial of efficacy and safety. BMC Emergency Medicine 2016;16(1).


[2] Andolfatto G, Willman E, Joo D, et al. Intranasal Ketamine for Analgesia in the Emergency Department: A Prospective Observational Series. Academic Emergency Medicine 2013;20(10):1050–4.


[3] Shrestha R. Intranasal ketamine for the treatment of patients with acute pain in the emergency department. World Journal of Emergency Medicine 2016;7(1):19.


[4]Motov S, Rockoff B, Cohen V, Pushkar I, et. al.  Intravenous Subdissociative-Dose Ketamine Versus Morphine for Analgesia in the Emergency Department: A Randomized Controlled Trial. Annals of Emergency Medicine 2015; 66(3)222.


[5] Motov S, Rosenbaum S, Vilke G, Nakajima Y. Is there a role for intravenous subdissociative-dose ketamine administered as an adjunct to opioids or as a single agent for acute pain management in the emergency department? The Journal of Emergency Medicine 2016;6(51)752


[6] Dunlop R, Bennett KC. Pain management for sickle cell disease in children and adults. Cochrane Database of Systematic Reviews 2014


[7] Uprety D, Baber A, Foy M. Ketamine infusion for sickle cell pain crisis refractory to opioids: a case report and review of literature. Annals of Hematology 2013;93(5):769–71.


[8] Tawfic QA, Faris AS, Kausalya R. The Role of a Low-Dose Ketamine-Midazolam Regimen in the Management of Severe Painful Crisis in Patients With Sickle Cell Disease. Journal of Pain and Symptom Management 2014;47(2):334–40.


[9] Meals CG, Mullican BD, Shaffer CM, Dangerfield PF, Ramirez RP. Ketamine Infusion for Sickle Cell Crisis Pain in an Adult. Journal of Pain and Symptom Management 2011;42(3).


[10] Jennings CA, Bobb BT, Noreika DM, Coyne PJ. Oral Ketamine for Sickle Cell Crisis Pain Refractory to Opioids. Journal of Pain & Palliative Care Pharmacotherapy 2013;27(2):150–4.


[11] Zempsky WT, Loiselle KA, Corsi JM, Hagstrom JN. Use of Low-dose Ketamine Infusion for Pediatric Patients With Sickle Cell Disease-related Pain. The Clinical Journal of Pain 2010;26(2):163–7.


[12] Neri CM, Pestieau SR, Darbari DS. Low-dose ketamine as a potential adjuvant therapy for painful vaso-occlusive crises in sickle cell disease. Pediatric Anesthesia 2013;23(8):684–9.


[13] Sassano-Higgins S, Baron D, Juarez G, Esmaili N, Gold M. A Review Of Ketamine Abuse And Diversion. Depression and Anxiety 2016;33(8):718–27.


[14] Mowry JB, Spyker DA, Brooks DE, McMillan N, Schauben JL. 2014 Annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 32nd Annual Report. Clin Toxicol (Phila). 2015;53(10):962-1147

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Wednesday Wrap Up – 4/19/2017

Wrap up of our conference day focused on pediatrics and environmental emergencies.


Dr. Subramaniam on Venomous Land Animals


  • 9000 snake bites annually, with 1% mortality – highest in young children
  • DO: remove constricting clothing, transport to hospital immediately, establish IV access, immobilize and raise limb, and mark the leading edge of erythema/edema
  • DO NOT: incise the wound, use a venom suctioning kit, apply tourniquets, or apply ice or heat
  • In addition to the localized effect of pain from a bite, systemic events include hematologic and neurologic problems.
    • Cellulitis  and compartment syndrome are rare
    • Pain control with opiates
    • Give tetanus if not up to date
  • Venomous snakes in the US are either Crotalidae (“pit vipers”) or Elapidae (coral snakes).
    • Crotalids, aka pit vipers, include rattlesnakes, copperheads, and cottonmouths
      • Venomous crotalids have broad heads, elliptical pupils, pointy snouts, and heat-sensing pits on their face
      • More common to have hematologic effects
      • Can use Crofab antivenom for moderate to severe bites (use grading system)
    • Coral snakes are found in the southeastern US
      • “red on yellow kill a fellow” (these are venomous!)
      • “red on black venom lack” (not so much)
  • Call the Poison center and your local zoo or snake center (in NYC this is Jacobi Hospital)


  • Bark Scorpion in the Southwestern US and Mexico is venomous
  • Effects:Local injury / pain, cranial nerve dysfunction, neuromuscular hyperactivity, dysautonomia, and rarely pancreatitis or rhabdomyolysis
  • 20,000 bites per year, most lethal in children
  • Antivenom was discontinued but now made by Mexico, however your best bet is supportive intensive care (intubation, benzodiazepines, etc)

Check out another of our blog posts on scorpions: Bored Review in the Sonoran


Dr. Fernando - Marine Envenomations
  • Bites
    • Blue-Ringed Octopus – tiny but deadly, uses tetrodotoxin
    • Sea Snakes – 50 species: all are venomous, 7 are fatal.
  • Nematocysts (Jellyfish and Portugese Man o’ War
    • Use barb, spine, and thread to discharge into skin
    • Management
      • Remove nematocysts (shaving cream and credit card method) or warm saline water
      • Consider oral antihistamines and oral corticosteroids
  • Stings
    • Sea urchin, sea cucumber and starfish – no venom but cause local irritation
    • Stingrays – cause laceration and puncture envenomation – treat both!
      • Severe local pain
      • Syncope, weakness, nausea, vomiting, diarrhea, muscle fasciculations
      • Treatment: salt water immersion / irrigation, remove stinger, explore wound
    • Bony Fish – have spines with venom
  • Ciguatera Poisoning
    • From large fish that eat smaller reef fish that feed off of coral that hosts bacteria
    • Heat stabile, water soluble = you can’t cook it off
    • Clinical manifestations are:
      • GI (3-6 hours) – vomiting, diarrhea, abdominal pain
      • Neurologic (3-72 hours) – paresthesias, tooth discomfort, blurred vision *these can lasts for weeks!
      • Cardiovascular (hours) – bradycardia, heart block, hypotension
    • Treatment is supportive care, mannitol for very severe symptoms
  • Scromboid Poisoning
    • From dark meat, large fish (tuna, mackerel, swordfish, mahi-mahi)
    • Caused by bacterial overgrowth when fish is improperly stored (> 40° C) leading to production of histadine (converted to histamine)
    • Clinical manifestations are flushing, rash, diarrhea, headache, numbness (think histamine reaction)
    • Treatment is antihistamines and supportive care, most cases resolve within 12-48 hours
  • Pufferfish Poisoning – Tetrodotoxin
    • Not just pufferfish! Also found in frogs, salamanders, octopus, and crab eggs
    • Sodium cannel blockade leads to weakness, hypotension, paralysis and ultimately respiratory failure
    • Treatment is aggressive supportive care and GI decontamination

Lastly, check out this TOKC post reviewing fish-related poisoning.



Dr. Delgado Torres - Poisonous Plants
  • Most poisonous plant exposures are unintentional, small, asymptomatic, and from household plants
  • Get a thorough history including travel, time of exposure, quantity eaten and which part of plant
  • Problems for medical providers include misidentification, scant literature, and variable xenobiotics within a plant. Best bet is to observe your patient!
  • Types of Xenobiotics in plants, with examples
    • Alkaloids
      • Jimsonweed – anticholinergic toxicity through atropine
    • Gylcosides
      • Yellow oleander and foxglove – acts like digoxin toxicity
      • Cassava (from improperly prepared yucca) is cyanogenic
    • Terpenes and resins
      • Castor bean – one seed is toxic
      • Causes multi-organ dysfunction – use aggressive decontamination
    • Proteins, peptides and lectins
      • Ackee (official fruit of Jamaica) is toxic when not ripe, causes “Jamaican Vomiting Sickness” manifesting with severe hypoglycemia, vomiting, and seizures.
    • Phenols and phenylpropanoids
      • Capsaicin = pepper spray
  • Water Hemlock = most common cause of plant-related (ingestion) fatalities in the US
    • Cicutoxin, found in all parts of the plant
    • Cholinergic manifestations = vomiting, flushing, salivation, bradycardia, hypotension, seizures, and rhabdomyolysis


Heat Stroke
  • Definition = core temperature > 106° F with neurological dysfucntion
  • Exertional heat stroke – can be rapid, caused by sports/ athletics in the heat. You may see sweating!
  • Nonexertional heat stroke – most common in infants or children left in hot cars and elderly
  • Treatment
    • Cooling! Use evaporative cooling as cold water immersion can cause vasoconstriction making cooling more difficult.
    • Treat shivering with benzodiazapines +/- paralytics
    • Antipyretics (acetaminophen) not helpful
    • Mortality from electrolyte imbalance, cardiac arrhythmias, and multi-organ dysfunction
    • In pediatrics, must consider child abuse!




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Rhythm Nation: March 2017 Answer

ECG: NSR @ 90 bpm, normal axis, S1Q3T3 pattern present



  • S1Q3T3 was first described in 1935 in JAMA by Drs. McGinn & White
  • They report a case series of 9 patients with pulmonary embolism (PE) and “acute cor pulmonale” and the ECG findings in 7 of those patients.
  • 5 of these ECGs demonstrated a constellation of findings that we now term the “S1Q3T3” pattern:
    • “(1) prominent S wave and low origin of the T wave in lead 1; ST segment starting slightly below the baseline,
    • (2) the gradual staircase ascent of the ST interval from the S wave to the T wave in lead 2,
    • and, especially, (3) the Q wave and definite late inversion of the T wave in lead 3.”
  • They concluded that: “Whether or not these electrocardiographic manifestations are pathognomonic for pulmonary embolism, the consistency with which they have been demonstrated in tracings taken soon after acute attacks of extensive pulmonary embolism has been striking.”


  • McGinn and White thought that these ECG findings would help clinicians differentiate between a myocardial infarction and a pulmonary embolism. They attributed the ECG changes to the acute occlusion of the pulmonary artery causing “dilatation and partial failure of the chambers of the right side of the heart.”
  • S1Q3T3 can be found in other states of acute cor pulmonale or right heart strain:
    • COPD and/or asthma exacerbation
    • Pneumothorax
    • Severe pneumonia
    • Upper airway obstruction


  • The incidence of S1Q3T3 in patients diagnosed with PE varies from as low as 10% to as high as 50%.
  • Thus, S1Q3T3 should not be thought of as being pathognomonic for acute PE

  • S1Q3T3 and other ECG findings become useful when they are applied together rather than separately – for instance, in the Daniel Score:
    • Maximum score of 21 and incorporates S1Q3T3
    • Scoring system to correlate with severity of pulmonary hypertension
    • Score of > or = 10 had: specificity of 97.7% and sensitivity of 23.5%

  • Shopp et al published a systematic review and meta-analysis of 10 studies, which included 3,007 patients with acute PE to determine the prognostic value of certain ECG findings that would help predict patients at risk for circulatory shock and death.
  • The ECG findings they reviewed included components of the Daniel score as well as ST elevation in aVR and atrial fibrillation.
  • In this meta-analysis, the most common ECG findings among patients with PE were tachycardia (38%) and T wave inversion in V1 (38%).
  • Despite it’s lower incidence, Shopp et al found that S1Q3T3 was one of six ECG findings that predicted hemodynamic collapse and death within 30 days of acute PE:
  1. Tachycardia
  2. S1Q3T3
  3. Complete RBBB
  4. Inverted T waves in V1-V4
  5. ST elevation in aVR
  6. Atrial Fibrillation
  • A constellation of these ECG findings or a Daniel score >5 can be used to risk stratify patient with RV failure secondary to PE and are at a higher risk for hemodynamic collapse.



  • The ECG in PE is often abnormal, but these findings are neither sensitive nor specific.
  • S1Q3T3 on an ECG does not automatically equal PE! It can be seen in other pathologies causing right heart strain such as pneumothorax, pneumonia, and bronchospasm.
  • It is more helpful when used in the appropriate clinical context with other ECG findings to identify patients at risk for shock.

Back to our patient…

  • He had a work-up including D-dimer, which was negative, and he was happily discharged home.



Chan TC, et al. Electrocardiographic manifestations: pulmonary embolism. Journal of Emergency Medicine. 2001;21(3): 263-270.
Daniel K, et al. Assessment from cardiac stress from massive pulmonary embolism with 12-lead ECG. Chest. 2001;120(2):474-81.
McGinn S, White Paul. Acute cor pulmonale resulting from pulmonary embolism: its clinical recognition. JAMA. 1935;104(17):1473-1480
Shopp JD, et. al. Findings From 12-lead Electrocardiography That Predict Circulatory Shock From Pulmonary Embolism: Systematic Review and Meta-Analysis. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 2015;22(10):1127-1137.

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