Tiny Tip: Anaphylaxis Treatment

Anaphylaxis is a common presentation to the emergency department requiring rapid treatment as death can occur within minutes. From 1986 – 2011, in Ontario, Canada alone there were 82 deaths from anaphylaxis (1). Epinephrine 0.5mg IM (1:1000) is the first line treatment for anaphylaxis and the only lifesaving treatment (2).

The other medications are for symptomatic control or can help prevent the biphasic reaction anywhere from 8-72 hours from the initial reaction. For the junior learner, remembering which medications to give and at what dose during an acute presentation can be daunting. Here are two rules to help remember the treatment of ADULT anaphylaxis easily:

ABCDsss – for the name of the intervention

Rule of 5s – each dose is in a multiple of 5

The Tiny Tip


  • Epinephrine 0.5mg IM for adults

Benadryl *

  • Diphenhydramine 50mg IV for adults

Corticosteroid *

  • Methyprednisolone 125mg IV

ranitiDine 50mg IV *

Supplemental O2 (5L via NP 15L via NRB)

Salbutamol (5mg via nebulizer)

Saline (500 mL or more)


*these treatments treatments are less useful during acute resuscitation and should be lowest on the priority list with a sick patient.


Don’t forget that the initial epinephrine administration for anaphylaxis is IM not IV!


These are the basics. Check out the awesome post on First 10 in EM for a much more comprehensive overview.


  1. Xu YS, Waserman S, Harada L, Kastner M. Anaphylaxis deaths in Ontario: a retrospective review of cases from 1986 to 2011. Allergy, Asthma, & Clinical Immunology 2012, 8(Suppl 1):A8
  2. Moore LE, Kemp AM, Kemp SF. Recognition, Treatment, and Prevention of Anaphylaxis. Immunol Allergy Clin N Am 35 (2015) 363-374
  3. Zilberstein J, McCurdy MT, Winters ME. Anaphylaxis. Journal of Emergency Medicine. Vol 47, No 2, pp. 182-287, 2014

Author information

Taft Micks

Taft Micks

Family Medicine Resident, Memorial University

The post Tiny Tip: Anaphylaxis Treatment appeared first on BoringEM and was written by Taft Micks.

A Boring guide to Spinal Cord Syndromes

Spinal cord syndromes? I love those, and never forget them!” – Said nobody, ever. Despite the fact that spinal cord syndromes can be difficult to remember, they are important to recognize and can yield a significant amount of clinical information. We seek to break SC syndromes into an easy to digest and understand discussion.

The basis of this discussion is highlighted by the importance of remembering the anatomy, and once you recall this simple diagram, the syndromes become significantly easier to recall:




The spinothalamic tract is intentionally drawn on the opposite side of the cord, to represent that those nerve fibres crossover in the cord, providing contralateral pain and temperature sensation.

On the opposite side of the cord, the dorsal column carries ipsilateral proprioception/vibration, while the corticospinal tract contains ipsilateral motor function.

Anterior Cord Syndrome

Anterior cord syndrome often occurs as a result of flexion injury, or due to injury to the anterior spinal artery. This may occur as a result of vascular or atherosclerotic disease in the elderly, or iatrogenic secondary to cross clamping of the aorta. These patients have preserved function of their posterior column, and so their proprioception and vibration sense is intact. However, the anterior portion of their cord is affected, and therefore they tend to have bilateral loss of motor function, light touch, pain and temperature below the level of the lesion.




Central Cord Syndrome:

Remember MUD-E!

Motor > Sensory

Upper extremity > Lower extremity

Distal > Proximal

Extension injury

The classic mechanism is the elderly patient who falls, and hits their chin – causing an extension injury of the neck. Distal upper extremity motor function is most medial in the spinal cord, these are the areas that are typically most effected with patchy sensory loss.

Central cord syndrome can often be missed in the ED, as the imaging in these patients is often unremarkable, and their sensory deficits can be patchy. Because it is a clinical diagnosis, it is important for the emergency physician to consider this entity during their assessment, particularly in trauma patients, where this may be overlooked.




Brown-Sequard Syndrome

Brown-Sequard is a hemi-cord injury, typically noted in the setting of penetrating trauma.

The patient will have injury to their dorsal column, corticospinal tract and spinothalamic tract – therefore causing ipsilateral loss of motor function, and proprioception/vibration. Since the spinothalamic tract crosses over, they will have contralateral loss of pain and temperature.



Spinal shock vs Neurogenic shock

These two terms are often erroneously used interchangeably, however, they apply to two distinct concepts.

Spinal shock is not a true ‘physiologic shock’, and should be thought of more as a ‘spinal concussion’. It is manifested by a flaccid areflexia post spinal cord injury. As edema around the cord resolves, symptoms will improve over a period of days to months, noted by return of the bulbocavernosus reflex (anal sphincter contraction in response to tugging on a foley catheter).

Neurogenic shock is a true distributive shock, in which the patient becomes hypotensive and bradycardic, usually noted with lesions above T6. It is typically a manifestation of decreased vascular resistance and increased vagal tone secondary to autonomic disruption.

Management is focused around optimizing perfusion to the spinal cord, thereby preventing secondary cord injury and ischemia. No great evidence here, but expert opinion suggests targeting a MAP of 85-90.

Bradycardia may be treated with atropine or pacing, while hemodynamic therapy is supportive with fluids and vasopressors to help increase perfusion. There is a potential risk of reflex bradycardia with the use of phenylepiprhine, but this is considered theoretical, and a recent CAEP position statement suggests any vasopressor should be used just to optimize perfusion to the cord. If available, norepinephrine is probably your best option.

Steroids in spinal cord injury remains controversial, with conflicting evidence. The Congress of Neurological Surgeons has suggested that steroid therapy “should only be undertaken with the knowledge that the evidence suggesting harmful side effects is more consistent than any suggestion of clinical benefit”. The Canadian Association of Emergency Physicians is now recommending against the use of high dose steroids as standard of care. Therefore, the administration of steroids should be undertaken in consultation with local neurosurgeons/established protocols.



Bracken MB, Shepard MJ, Hellenbrand KG, et al. Methylprednisolone and neurological function 1 year after spinal cord injury. Results of the National Acute Spinal Cord Injury Study. J Neurosurg. 1985 Nov. 63(5):704-13.

Bracken MB, Shepard MJ, Holford TR, et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA. 1997 May 28. 277(20):1597-604.

Bracken MB. Steroids for acute spinal cord injury. Cochrane Database Syst Rev. 2002. CD001046.

Djogvic D, MacDonald S, Wensel A, Green R, Loubani O, Archambault P, Bordeleau S, Messenger D, Szulewski A, Davidow J, Kircher J, Gray S, Smith K, Lee J, Benoit JM, Howes D. Vasopressor and Inotrope use in Canadian Emergency Departments: Evidence Based Consensus Guidelines. Canadian Journal of Emergency Medicine. 2015; 17(S1)1-16.

Hadley MN, Walters BC, Grabb PA, et al. Pharmacological therapy after acute spinal cord injury.Neurosurgery. 2002. 50 Suppl:63-72.

Hurlbert RJ, Hamilton MG. Methylprednisolone for acute spinal cord injury: 5-year practice reversal. Can J Neurol Sci. 2008 Mar. 35(1):41-5.

Jia X, Kowalski RG, Scuibba DM, Geocadin RG. J Intensive Care Med. 2013 Jan;28(1)12-23.
Levi L, Wolf A, Belzberg H. Neurosurgery. 1993; 33(6)1007.

Nesathurai S. Steroids and spinal cord injury: revisiting the NASCIS 2 and NASCIS 3 trials. J Trauma. 1998 Dec. 45(6):1088-93.

Vale FL, Burns J, Jackson AB, Hadley MN. J Neurosurg. 1997;87(2)239


Author information

Shahbaz Syed, MD

Shahbaz Syed, MD

Senior Emergency Medicine resident at the University of Ottawa, undertaking a fellowship in Digital scholarship and #FOAMed.

The post A Boring guide to Spinal Cord Syndromes appeared first on BoringEM and was written by Shahbaz Syed, MD.

Medical Concept: Abdominal Pain Labs

A 40 year-old woman presents to your emergency department with a chief complaint of abdominal pain. Unfortunately, she does not speak English and there is no interpreter available. It is clear that she is in a lot of pain, and she is not able to cooperate with your physical exam. You know that abdo labs are going to be important in understanding this patient’s complaint. Before reviewing with your staff, you wonder which laboratory investigations will be most helpful.

The Question

Which laboratory investigations are useful in patients with undifferentiated acute abdominal pain?

The Big Picture: Sick or Not Sick?

The most important factor in the emergency department management of abdominal pain is the distinction between sick and not-so-sick patients. The c-reactive protein (CRP) and white blood cell count (WBC) are useful laboratory investigations.

CRP is correlated with the likelihood of serious pathology on abdominal CT scan [1]  and  hospital admission [2]. It is also associated with more urgent diagnoses [3].

Like the CRP, a high white blood cell count is associated with hospital admission and more urgent pathology [2,3]. The white blood cell count differential can also provide clues to the etiology of abdominal pain. Neutrophilia (>9×109/L) combined with lymphopenia (<1.4×109/L) and eosinopenia (<0.04×109/L) is 95% specific, though insensitive, for an infectious or surgical cause for acute abdominal pain [4].

The combination of elevated CRP and white blood cell count should ring alarm bells. A patient with a CRP of greater than 50 mg/L and a WBC of greater than 15 has an 85% of having an urgent diagnosis [3]. Be warned that these tests are not sensitive. In other words, there are many things that don’t cause an elevated CRP or an elevated white blood cell count but are dangerous.

There is one other big picture test worth highlighting: All pre-menopausal women should have a urine or serum beta-HCG test. A negative pregnancy test rules out some life-threatening pathologies, and a positive one may mean a critical difference in subsequent management.

The Specifics

How good are lab tests for pancreatitis?

The two abdo lab tests commonly used to rule in or rule out pancreatitis are serum lipase and serum amylase. Amylase is secreted both by the pancreas and the salivary glands, and lipase is only secreted by the pancreas, This may explain why the lipase is, statistically, the better test; elevated serum lipase is both more specific (95-99%) [5] and more sensitive (see below) than elevated serum amylase for acute pancreatitis. Ordering both tests doesn’t improve sensitivity or specificity over lipase alone. Some estimates of lipase sensitivity are as low as 67%, so a normal lipase doesn’t exclude pancreatitis with certainty.

Use serum amylase and lipase with caution in a patient with chronic pancreatitis. Some of these patients have chronically elevated levels, and it is important to interpret the results in the context of the patient’s baseline, if you know it.

How good are lab tests for biliary tract disease?

The classic lab findings of biliary tract disease vary with the pathology. Biliary colic, with obstruction limited to the gallbladder itself, typically has no abnormal lab findings. Leukocytosis is often seen in acute cholecystitis as the gallbladder becomes inflamed. Acute cholangitis, with obstruction of the biliary tract, classically shows elevated bilirubin levels due to impaired excretion; elevated alkaline phosphatase and gamma-glutamyl transpeptidase (GGT) are also seen as they are released from damaged liver cells. Elevated AST and ALT are sometimes seen as well, but are not part of the classic “obstructive pattern”.

In practice, there aren’t great studies on the sensitivity and specificity of these tests. The authors of one review of diagnostic tests [6] found that bilirubin, AST/ALT, and alkaline phosphotase were not statistically useful tests for diagnosing acute cholecystitis. Only an elevated WBC was statistically significant, and this has very limited clinical use because it is so non-specific. Good data on the sensitivity and specificity of lab values for acute cholangitis are not available, but consider this diagnosis if there is elevated bilirubin, alkaline phosphatase, GGT, AST, or ALT in the setting of abdominal pain.

How good are lab tests for hepatic disease?

The most commonly used tests to look for hepatic injury are the transaminases, alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Both are fairly sensitive tests for liver damage, but AST is found in non-hepatic tissue more than ALT and so is less specific [7]. Rises of up to 300 IU/L are non-specific, but levels above 1000 IU/L are most commonly due to viral hepatitis, toxin or drug induced hepatitis, or ischemic injury [7], though actual levels don’t have much prognostic significance.

While AST and ALT can give an idea of how much damage has been done, they don’t show how well the liver is functioning. For that, the INR is the most commonly used test. Clotting factor VII has a half-life of six hours, and falling serum levels if hepatic production is failing will show as a rising INR[7].

How good are lab tests for renal colic?

A urine dip and/or urinalysis is often ordered if renal colic is suspected. Among adult patients presenting with flank pain, blood on a urine dip has been estimated to have a positive predictive value of 54% and a negative predictive power of 66%[8]. In the same population, a cutoff of 5 RBCs per high power field on urinalysis has a 65% positive predictive value and 68% negative predictive value[8]. These tests may point you in the right direction, but they aren’t nearly specific enough to be relied on without a solid history suggestive of renal colic.

How good are lab tests for appendicitis?

In short, laboratory tests for appendicitis are not useful. Much of the traditional teaching about appendicitis has stressed the role of leukocytosis[9]. The literature, however, is equivocal. The authors of one large metaanalysis[10]found that higher white blood cell counts were indeed correlated with appendicitis, but as a single test it was of limited use. Very high values of leukocytosis (>15×109) only had a positive likelihood ratio of 3.5, and low cut-off values (10×109) had a negative likelihood ratio of 0.3. In other words, normal WBC values couldn’t exclude appendicitis, and high values could not confirm it. The combination of a normal WBC and a normal CRP may seem reassuring, but the use of these tests to rule out appendicitis has not been well established[10].

What about ALL the other causes of abdominal pain?

Besides the pancreas, gallbladder, liver, and ureter, the organs that might be causing acute addominal pain don’t have any organ-specific or pathology-specific lab test. There is a long and sobering list of pathologies that can cause abdominal pain with no specific lab findings: peptic ulcer disease (with or without perforation), gastritis, small bowel obstruction, acute mesenteric ischemia, diverticulitis, cecal volculus, ruptured abdominal aortic aneurism, pyelonephritis, pelvic inflammatory disease, ruptured ectopic pregnancy, inflammatory bowel disease … you get the idea.

Undifferentiated abdominal pain is a presentation where the history and physical exam are absolutely crucial, and laboratory tests are confirmatory. Some experts advise against the use of standard panels of “belly labs”[11], as there is no evidence they are useful for the undifferentiated patient, and may add diagnostic confusion. Instead, rely on your history, physical exam wherever possible.

Back to the case

You go on a laboratory spree and send off the works: urinalysis (including beta HCG), CRP, lipase, bilirubin, AST, ALT, GGT, alkaline phosphatase, and the standard CBC, electrolytes, urea and creatinine. The labs come back normal except for a borderline white blood cell count at 10.5. In desperation, you send the patient for an abdominal ultrasound. The radiologist identifies acute cholecystitis. The patient has a laparoscopic cholecystectomy the next day, and recovers well.


The Bottom Line

  • All pre-menopausal women should have a beta HCG test.
  • The white blood cell count and CRP are correlated with illness severity, but cannot be relied upon in isolation to rule in or out serious disease.
  • Elevated serum lipase is specific for pancreatitis, but not sensitive enough to rule it out conclusively.
  • Biliary colic and acute cholecystitis do not have sensitive or specific laboratory findings. The sensitivity and specificity of the classic laboratory findings of acute cholangitis haven’t been thoroughly studied.
  • Liver enzymes are reasonably sensitive and specific (especially ALT) for hepatic injury, but hepatic injury itself has a long differential diagnosis.
  • Hematuria is associated with renal colic, but is of limited usefulness in isolation.
  • The history and physical exam are key in determining the cause of acute undifferentiated abdominal pain.



  1. Coyle, Joseph P, Cressida R Brennan, Shane F Parfrey, Owen J O’Connor, Patrick D Mc Laughlin, Sebastian R Mc Williams, and Michael M Maher. “Is Serum C-Reactive Protein a Reliable Predictor of Abdomino-Pelvic CT Findings in the Clinical Setting of the Non-Traumatic Acute Abdomen?” Emergency Radiology 19, no. 5 (October 2012): 455–62. doi:10.1007/s10140-012-1041-4.
  2. Chi, C H, S C Shiesh, K W Chen, M H Wu, and X Z Lin. “C-Reactive Protein for the Evaluation of Acute Abdominal Pain.” The American Journal of Emergency Medicine 14, no. 3 (May 1996): 254–56. doi:10.1016/S0735-6757(96)90169-2.
  3. Gans, Sarah L, Jasper J Atema, Jaap Stoker, Boudewijn R Toorenvliet, Helena Laurell, and Marja A Boermeester. “C-Reactive Protein and White Blood Cell Count as Triage Test between Urgent and Nonurgent Conditions in 2961 Patients with Acute Abdominal Pain.” Medicine 94, no. 9 (March 2015): e569. doi:10.1097/MD.0000000000000569.
  4. Deibener-Kaminsky, Joelle, Jean-François Lesesve, and Pierre Kaminsky. “Leukocyte Differential for Acute Abdominal Pain in Adults.” Laboratory Hematology : Official Publication of the International Society for Laboratory Hematology 17, no. 1 (March 2011): 1–5. doi:10.1532/LH96.10023.
  5. Butler, J. “Serum Amylase or Lipase to Diagnose Pancreatitis in Patients Presenting with Abdominal Pain.” Emergency Medicine Journal 19, no. 5 (September 1, 2002): 430–31. doi:10.1136/emj.19.5.430.
  6. Trowbridge, Robert L, Nicole K Rutkowski, and Patient Page. “Does This Patient Have Acute Cholecystitis?” Journal of the American Medical Association 289, no. 1 (2003).
  7. Pratt, Daniel S. “Evaluation of Liver Function.” In Harrison’s Principles of Internal Medicine., edited by Dennis L. Kasper, Anthony S. Fauci, Stephen L. Hauser, Dan L. Longo, J. Larry Jameson, and Joseph Loscalzo, 19th editi. McGraw-Hill Education, 2015. http://accessmedicine.mhmedical.com.proxy.queensu.ca/book.aspx?bookid=1130.
  8. Bove, P, D Kaplan, N Dalrymple, a T Rosenfield, M Verga, K Anderson, and R C Smith. “Reexamining the Value of Hematuria Testing in Patients with Acute Flank Pain.” The Journal of Urology 162, no. 3 Pt 1 (1999): 685–87. doi:10.1097/00005392-199909010-00013.
  9. Pines, Jesse M., Christopher R. Carpenter, Ali S. Raja, and Jeremiah D. Schuur. Evidence-Based Emergency Care: Diagnostic Testing and Clinical Decision Rules. 2nd ed. Chichester, UK: John Wiley & Sons, Ltd., 2013.
  10. Andersson, R. E. B. “Meta-Analysis of the Clinical and Laboratory Diagnosis of Appendicitis.” British Journal of Surgery 91, no. 1 (2004): 28–37. doi:10.1002/bjs.4464.
  11. Salem, T A, R G Molloy, and P J O’Dwyer. “Prospective Study on the Role of C-Reactive Protein (CRP) in Patients with an Acute Abdomen.” Annals of the Royal College of Surgeons of England 89, no. 3 (April 2007): 233–37. doi:10.1308/003588407X168389.

Author information

David Wonnacott

David Wonnacott

PGY-1 in Family Medicine at Queen's University

The post Medical Concept: Abdominal Pain Labs appeared first on BoringEM and was written by David Wonnacott.

Tiny Tips: Epinephrine Dosing

Epinephrine is a commonly used medication in the emergency department for the management of anaphylaxis and cardiac arrest. Administering this drug can be confusing as the dosage and concentration are different for each indication.

The “allergy epi” 1:1000 concentration is 10 times more concentrated than the “cardiac epi”. The “allergy epi” is delivered IM while the “cardiac epi” is delivered IV.

This difference leads to an increased risk of error as administering epinephrine. Administering epinephrine in the wrong dosage, concentration, or route can have disastrous consequences for patients including coronary dissection, infarction, and ventricular arrhythmias (1-3). Here is a little saying to easily remember the dosage and concentration of epinephrine in both anaphylaxis and cardiac arrest…


LESS (volume) is MORE (concentrated)

Less (0.5cc) is More (1:1000)

Use ½ ml of 1:1000 epinephrine and deliver it into the muscle (IM). This will deliver a total of 0.5mg of epinephrine IM.


This is the 1:1000 epinephrine to be given IM for anaphylaxis.

Cardiac Arrest

MORE (volume) is LESS (concentrated)

More (10cc) is Less (1: 10,000)

Use 10cc of 1: 10,000 epinephrine and give it intravenously (IV). This will deliver 1mg of epinephrine IV.

This is the box that has a preloaded 10cc syringe of 1:10,000 epi to be used IV in Cardiac arrest

This is the box that has a preloaded 10cc syringe of 1:10,000 epi to be used IV in Cardiac arrest



  1. Kanwar M, Irvin CB, Frank JJ, et al. Confusion about epinephrine dosing leading to iatrogenic overdose: a life-threatening problem with a potential solution. Ann Emerg Med. 2010. Apr;55(4):341-4
  2. Wood JP, Traub SJ, Lipinski C. Safety of epinephrine for anaphylaxis in the emergency setting. World J Emerg Med. 2013;4(4):245-51
  3. Campbell RL, Bellolio MF, Kuntson BD, et al. Epinephrine in anaphylaxis: higher risk of cardiovascular complications and overdose after administration of intravenous bolus




The ‘Top Five Changes’ Project: 2015 AHA guidelines on CPR + ECC update infographic series

Editor’s Note:

Last Wednesday was like the night before Christmas for the BoringEM team. We had trouble getting to sleep as we awaited the Thursday release of the 2015 ILCORAHA / Heart & Stroke Foundation of Canada guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiac Care (ECC)! We spent the prior week planning for how our team could help to translate and disseminate this material to our readers, the #FOAMed community, and around the world.

We are happy to share what we came up with today. By now, many of you have seen the results of our infographic campaign to disseminate the “Top Five Changes” from each section of the 2015 AHA Guidelines on Twitter and Facebook. Collectively, these resources have been shared and retweeted >500 times (!!) in just a few days. This blog post compiles the full collection in one place.

In keeping with our goal to help disseminate these changes as quickly as possible, we hope that you will share them either by passing this post along to your colleagues via email or social media or by printing the PDF version to paste on the walls of your hospital, ambulance bay, or hangar. 

Cardiac Arrest: Why everyone should care what the 2015 AHA guidelines say

In emergency medicine, we see the sickest patients in their sickest moments. Whether you’re a respiratory therapist, registered nurse, paramedic, or physician, you have likely wondered if your resuscitation efforts are worth it; worth the time, the commitment, the money, and the emotional drain. Whether it’s moaning when someone yells “I feel a pulse!” or groaning when the patch phone rings with a “VSA 10 minutes out”, at times we all question if what we are doing right.

It’s important for us to recognize how narrow our perspective is. Patients are often comatose and unstable after a successful resuscitation and it’s easy to assume death will follow shortly after admission. However, the numbers have become more encouraging than most of us realize.

Advanced cardiac life support efforts have been described as “heroic” since the 1960’s. Researchers have trialed therapies in dogs, pigs, and people searching for a “magic bullet” – a drug, a device, a technique – that can reverse death. While defibrillation and early, high-quality CPR are often cited as “the only things that work,” the survival rates for out of hospital cardiac arrest continue to climb as we refine the ACLS algorithm. While nailing down interventions supported by P-values and confidence intervals has proven elusive, these trends indicate that we are on the right path.

Here are three points to consider the next time you’re faced with a patient in cardiac arrest:

  • Cardiac arrest survival is varies from 2% to 59% depending on the rhythm (shockable or nonshockable) and where you live.
  • Survival is increasing – everywhere. In Ontario, Canada survival has climbed from 4% to 10% in the last decade!
  • Prognostication is hard. The guidelines now recommend waiting 72 hours before initiating exams to determine futility. Decisions to withdraw life support in the emergency department should take into account our inability to accurately prognosticate post-cardiac arrest patients in the ED. Futility is not the rule.

While many succumb to cardiac arrest, we also have survivors with remarkable stories: Children with prolonged downtimes who recover fully; middle-aged snow-shovellers who make it home for the holidays; and elderly people who survive to see the birth of a grandson or the graduation of a granddaughter. These people are the reason we dedicate ourselves to advancing the science of resuscitation; translating knowledge into practice through education, mentorship, administrative actions, and policy work; and hitting the front lines armed with two hands, two pads, and good judgment.

How high can survival from cardiac arrest go? That’s one question science hasn’t yet answered!

The Top Five Changes Project

Infographic Series Picture

The BoringEM team believes strongly in the science and expert deliberations that resulted in the 2015 AHA guidelines. This series of infographics highlights the changes since the 2010 publication but are not meant to replace a sound understanding of the guidelines and literature, nor to fully communicate the nuances of best practices in resuscitation. We hope only that they spur those on the front lines to delve deeper into the medicine of resuscitation while hastening the translation of the best available evidence from guideline into practice.

Click on the links below to download PNG or PDF versions of each individual update infographic.

SectionPNG LinkPDF Link
Special CircumstancesPNGPDF
Post-Resuscitation CarePNGPDF

Or download all of the PDFs as a package by clicking here.

Top 5 PDF Packet Pic

Why did we do this?

At BoringEM, we know that educators can play a key role in translating the knowledge within the pages of medical journals into actions at the bedside by creating user-friendly resources. Traditionally, this has been done using lectures, workshops, and ACLS courses… but this year we were approached by Canadian EMS / Resuscitation guru Dr. Laurie Morrison and asked to use social media to spread the word. We hope this little initiative might inspire a new wave of knowledge translation efforts for important medical literature.

Thanks to our team

Projects like these are not possible without a great team. Special thanks should be given to our writers (Blair Bigham, Sarah Luckett-Gatopoulos, Brent Thoma, Ponn Benjamin, Teresa Chan), editors (Alim Pardhan, Michelle Welsford, Teresa Chan, Brent Thoma), and designers (Alvin Chin, Teresa Chan) for putting aside other projects to concentrate on this one. Our resuscitation guru and mentor, Dr. Laurie Morrison, also deserves credit for inspiring this project.

Author information

Blair Bigham

Blair Bigham

Blair Bigham is a flight paramedic, resident physician and wannabe astronaut in Ontario, Canada. He has spent the last decade balancing life as a clinician, educator and scientist. When not roaming the skies, wards, or recesses of his imagination he can found kayaking in Canada’s great white north.

The post The ‘Top Five Changes’ Project: 2015 AHA guidelines on CPR + ECC update infographic series appeared first on BoringEM and was written by Blair Bigham.

Thrombois Infographic Series: Thrombosis and Hemostasis

Editor’s note: This is the second in a series of infographics related to thrombosis. Check out the first one on NOACs in VTE! I know I am not the first medical trainee to be confused by the clotting cascades and mechanisms of anticoagulant/antiplatelet therapies. This visual representation is simply awesome.  

CHY 2015 Mechanisms of antithrombotics d2-2

Author information

Calvin Yeh

Calvin Yeh

Calvin is a MD/PhD student at McMaster University. Calvin completed PhD studies under Dr. Jeffrey Weitz at the Thrombosis and Atherosclerosis Research Institute. He focussed on the biochemical mechanism and regulation of the coagulation system in the context of anticoagulant drugs including the new (direct) oral anticoagulants.

The post Thrombois Infographic Series: Thrombosis and Hemostasis appeared first on BoringEM and was written by Calvin Yeh.