Tiny Tips: weakness MADE NICER

Editor’s Note: This is a great mnemonic developed by two Canadian medical students Anali Maneshi and Matthew Cherian. This tool serves as a framework for an approach to a common ED presentation. If you have a tiny tip for us please consider sending it along by following our author instructions here

Geriatric patients make up 20% of all visits to Canadian EDs (1). General weakness, which can have a large differential, is a common chief complaint expressed by geriatric patients in the ED (2). A good mnemonic to remember common etiologies for weakness in the elderly is:  “The elderly are MADE NICER.” A consistent framework allows students to produce a comprehensive list of differential diagnoses and focus their history and physical exam.

This mnemonic recognizes that most geriatric patients in the ED do not distinguish between true muscle weakness and generalized fatigue/malaise when using the word ‘weak.’

Medications

  • Glucocorticoids, statins, antipsychotics, diuretics, magnesium supplementation, insulin overdose and colchicine among others are commonly known to induce weakness. Make note of recent increases or decreases in dosages of medications such as benzodiazapenes, narcotics, neuroleptics…etc that can be culprits! Medication error, side effects, interactions and changes often result generalized weakness but can also present as true myopathies.

Anemia

  • Due to occult bleeding, chronic disease, malignancies, and nutritional deficiencies.

Dehydration

  • Hypovolemia, often secondary to diarrhea, diuretics, or vomiting, can manifest as fatigability, postural dizziness, lethargy and/or confusion.

Endocrine

  • Hypoglycemia secondary to insulin overdose, poor nutritional intake or adrenal insufficiency
  • Hyperglycemia causing diuresis and electrolyte abnormalities
  • Hypothyroidism

Neurological conditions

  • A large spectrum of neurological disorders such as: stroke (ischemic or hemorrhagic), subarachnoid hemmorrhage, spinal cord lesions, peripheral nerve disease, plexopathies, neuromuscular junction disease, myopathies, multiple sclerosis, migraines with neurological features, Parkinson’s/ Parkinsonism and postictal paralysis.

Infection

  • Epidural abscess can compress the spinal cord resulting in true weakness.
  • Sepsis can manifest as malaise
  • Other viral and bacterial infections can cause generalized weakness

Cardiac

  • Presyncope can be described as weakness. It is important to identify any cardiac causes for presyncope in the ED.
  • Myocardial infarction or unstable angina can manifest as malaise instead of chest pain in the elderly
  • Congestive Heart Failure can be perceived as weakness due to reduced physical activity and/or deconditioning.

Electrolyte imbalance

  • Can lead to generalized or focal muscle weakness. These include hypo/hyperkalemia, hypo/hypercalcemia, hypomagnesemia, and hypophosphatemia.

Rheumatological 

  • SLE, polymyalgia rheumatica, and temporal arteritis.

References

1. Melady, D. CAEP 2015 oral presentation: “Is it fit for your grandma?” Found here

2. Wadman MC1, Lyons WL, Hoffman LH, Muelleman RL. Assessment of a chief complaint-based curriculum for resident education in geriatric emergency medicine.  West J Emerg Med. 2011. Nov;12(4):484-8

If you are interested in learning more about Geriatric Care in the ED. Visit Geri-EM an: http://caep.ca/Geri-EM, which fills a training gap in the emergency care of older people.  

photo from flickr

Author information

Anali Maneshi

Anali Maneshi

Anali is a third year medical student at McGill University.

The post Tiny Tips: weakness MADE NICER appeared first on BoringEM and was written by Anali Maneshi.

Welcoming our new Senior Editors

Over the past two years BoringEM has grown in a way that I never could have imagined. The cute little blog with the quirky name has developed an editorial process and attracts >300,000 views each year. This growth is largely attributable to the core editorial staff and the increasingly frequent contributions of its readers. Over time, BoringEM has developed a niche as a FOAM website that is operated by learners and fosters the contributions of learners.

In keeping with that niche, there have been several changes occurring on the editorial board as Dr. Teresa Chan and I continue our transition into Faculty roles. Teresa and I have scaled back our editorial responsibilities to make room for Drs. Eve Purdy and Sarah Luckett-Gatopoulos to transition into Senior Editors. While we will be readily available to provide them with advice and assistance whenever it is needed, Eve and Luckett will be running the day-to-day operations of BoringEM and deserve all credit for the ongoing evolution of this website. We have every confidence in their abilities and believe that this transition will allow BoringEM to best meet its objectives of “Bringing the Boring to EM” while at the same time fostering the writing and editorial skills of the next generation of academic emergency physicians. At the same time, the frequency of posts on BoringEM will be decreasing to 1/week (Mondays) for the foreseeable future to ensure that our new editorial staff are able to juggle their new roles and clinical responsibilities.

On behalf of Teresa and I, I would like to thank our readers and the FOAM community for the support that they have given us over the past year. There is no way that we could have kept this project going without your engagement and support. While we are taking a step back from BoringEM, we are beginning work on a new, bigger project that we hope to be able to tell you about soon. It’s very Canadiem.

Sincerely,

Brent Thoma MD MA
Editor-in-Chief, BoringEM

Author information

Brent Thoma

Brent Thoma

Editor in Chief at BoringEM

Emergency Medicine Resident at the University of Saskatchewan, wannabe Medical Educator, Blogging Geek.
+ Brent Thoma

The post Welcoming our new Senior Editors appeared first on BoringEM and was written by Brent Thoma.

Boring Question: What is the role of xanthochromia in ruling out SAH?

The Case

Your first patient of the shift is a 19-year-old male with “the worst headache ever.” His mother states she’s quite worried because he “never gets headaches.”  He had some slight nuchal rigidity, but is afebrile.  And as such, you arranged a non-contrast CT Head, which was found to have a normal without signs of intracranial hemorrhage.  Now, 12 hours after onset of his headache, and after discussing the risk and benefits of a lumbar puncture to this patient, he and his mother ask, “So what happens if my spinal tap is not normal?”

You pause, and reflect on the evidence…

Search Strategy

Using Pubmed, three separate searches were performed:

(1) “xanthochromia”

(2) “lumbar puncture”

(3) “subarachnoid hemorrhage”

From the results of this literature search you find:

One study showed that out of 660 samples to be analyzed, 28 patients were found to have CSF with xanthochromia, 5 of these 28 had a subarachnoid hemorrhage [1] . Three other studies found xanthochromia to have a PPV of 6.8%, 8.3%, and 8.7% respectively, with a 100% NPV [2,3,4]. A fifth study looked at 15 patients with positive findings for xanthochromia found on CSF spectrophotometry who also received a CT angiogram of their brain.  Nine of these fifteen CTA’s were found to be normal, and one CTA had a coincidental unruptured aneurysm.  Thus, even spectrophotometry only had a PPV of 33% [5].

With that said, many labs do not use spectrophotometry to measure xanthochromia- including my own.  This is important, as there is not an insignificant amount of intra-observer disagreement amongst individual samples, with one study finding disagreement among 19.2% of samples[6].

So how long does it take for us to detect xanthochromia?

The release of oxyhemoglobulin from lysed red blood cells in CSF can be detected within 4-10 hours of a bleed on spectrophotometry, while the conversion of oxyhemoglobulin to bilirubin has been reported to be 9-10 hours. The conversion to bilirubin gives xanthochromia its yellow color. It has been thought that one must wait 12 hours for xanthochromia to develop based off one study of 111 patients in which an LP was not performed for at least 12 hours who all had xanthochromic CSF [7. An additional study showed xanthochromia persisted in 32/32 patients at 2 weeks from onset, 20/22 patients at 3 weeks, and 10/14 patients at 4 weeks [8].

Take-Home Point

You walk away for a minute to review the evidence.  You then explain to the patient that the LP is a screening tool. If it is normal, we push the probability of a diagnosis that has significant morbidity and mortality to extremely close to zero.  An abnormal LP increases the probability of the diagnosis, but only to about 8% – but this is certainly high enough to warrant further investigation given the potential diagnosis.

Resolution of the Case

Fortunately, after metoclopramide, they feel well, and their LP revealed no WBC’s, no xanthochromia, their CSF lactic acid level was normal, and they are happy to be safely discharged.

References

1. Goyale A, O'Shea J, Marsden J, Keep J, Vincent RP. Analysis of cerebrospinal fluid for xanthochromia versus modern computed tomography scanners in the diagnosis of subarachnoid haemorrhage: experience at a tertiary trauma referral centre. Ann Clin Biochem. 2015. PMID: 25766384

2. Hann A, Chu K, Greenslade J, Williams J, Brown A. Benefit of cerebrospinal fluid spectrophotometry in the assessment of CT scan negative suspected subarachnoid haemorrhage: a diagnostic accuracy study. J Clin Neurosci. 2015; 22(1): 173-9. PMID: 25439758

3. Wallace AN, Dines JN, Zipfel GJ, Derdeyn CP. Yield of catheter angiography after computed tomography negative, lumbar puncture positive subarachnoid hemorrhage [corrected]. Stroke. 2013; 44(6): 1729-31. PMID: 23619131

4. Ahmed F, Gibbons S, El-Kadiki A. CSF xanthochromia: correlation with brain imaging and its usefulness as an out-of-hours test. J Clin Pathol. 2014; 67(8): 736-8. PMID: 24839296

5. Rana AK, Turner HE, Deans KA. Likelihood of aneurysmal subarachnoid haemorrhage in patients with normal unenhanced CT, CSF xanthochromia on spectrophotometry and negative CT angiography. J R Coll Physicians Edinb. 2013; 43(3): 200-6. PMID: 24087797

6. Marshman LA, Duell R, Rudd D, Johnston R, Faris C. Intraobserver and interobserver agreement in visual inspection for xanthochromia: implications for subarachnoid hemorrhage diagnosis, computed tomography validation studies, and the Walton rule. Neurosurgery. 2014; 74(4): 395-9; discussion 399-400. PMID: 24448178

7. Williams A. Xanthrochromia in the cerebrospinal fluidPractial Neurology. 2004; 4: 174-175.

8. Vermeulen M, Hasan D, Blijenberg BG, Hijdra A, van Gijn J. Xanthochromia after subarachnoid haemorrhage needs no revisitation. J Neurol Neurosurg Psychiatry. 1989; 52(7): 826-8. PMID: 2769274

Author information

Patrick Bafuma

Patrick Bafuma

The post Boring Question: What is the role of xanthochromia in ruling out SAH? appeared first on BoringEM and was written by Patrick Bafuma.

Phone a Friend: the fantastic pharmacist

Editor’s Note: This series was created by third year medical student Gerhard Dashi and will highlight the important work that our interprofessional colleagues do. This week’s post was co-authored by Emily Wiener. Keep your eye open for more “Phone a Friend” articles and if you would like to be featured or know a colleague that should be highlighted follow this link to complete the questions on a google form. 

Background on the “Phone a Friend” Series

As I progress through medical school, I notice a common thread drawing me to Emergency Medicine and events like the “National Health Care Team Challenge” or the “Simulation Olympiad”.  That thread is that I love working with an array of talented and fascinating healthcare professionals. Just like doctors, these nurses, pharmacists, paramedics and other health experts belong to professions with intriguing histories, rich cultures, ambitious goals, and unique skills. These distinctive characteristics shine through as soon as you meet these experts, even during the stages of their training.

Their indispensable roles within the ED guide care from the minute patients walk in the door until they leave the department. Multiple decisions, including acuity determination, initial course of care, and long-term follow-up strongly involve input and expertise from these indispensable team members.

At every “Pearls of Wisdom” session (in which a clerk, resident, doctor, or program director gives advice to medical students) I hear “Be nice to the [non-MD specialists]. They know everything.” Interprofessional contributions are especially important in the Emergency Department, where we often work with partial information in a fast-paced, over-stimulating environment.

Therefore, we would like to give these health professionals an opportunity to tell BoringEM readers what they do, what they’ve been through, what you should know about them and, most importantly, how you can be a good colleague to them.

Although we have sent requests to some of our favorite professionals, we would love to hear from you or someone you know. Please send us the questions you would like answered or your own answers to the following questions. We hope to feature your responses on upcoming posts.

The Fantastic Pharmacist

Dr. Bryan Hayes (@PharmERToxGuy) completed his undergraduate degree in Chemistry. He conducted pharmaceutical research in lab for a number of years before heading back to school to obtain his PharmD. After completion of his PGY-1 pharmacy residency, he completed a 2-year clinical toxicology fellowship (not common for pharmacists) and started working in the ED at the University of Maryland, Baltimore. He currently holds dual Clinical Associate Professor appointments at the School of Pharmacy and the School of Medicine (also not common for pharmacists).

Profession/current job title: Clinical Pharmacy Specialist, Emergency Medicine & Toxicology

Years of practice: 7

Country of practice: US

Practice setting: Baltimore- academic medical center in the ED. 800 bed facility.

How does your work impact patient care? 

I would say that optimizing antimicrobial therapy and medication oversight of all medical emergencies are my two biggest clinical roles as a pharmacist. Education (for patients, nurses, and providers) has to come in a close third, as this is what ultimately leads to practice change. Fourth, my involvement with Academic Life in EM has been an outstanding way to disseminate my practice pearls and experience worldwide.

What is the most common misperception about your role in the ED? 

Probably that the pharmacist is there just to second-guess a provider’s order (although not within my department).

How can the ED utilize your skills more effectively? 

My skills are best utilized in a prospective manner. In other words, involving the pharmacist while seeing patients and developing a plan together is more beneficial for patients than the pharmacist reviewing orders retrospectively.

What is your favourite part about working in an interprofessional environment? 

I can’t really pinpoint one particular favorite. I love all aspects of my job, particularly working with an interdisciplinary team to improve patient safety. As much as we all hate committees, we have developed our own ED patient safety committee as well as an ED resuscitation committee to help optimize both of those areas. I also love how we all bring different perspectives to patient care. I’m always looking for potential adverse drug events, drug interactions, or possible unintentional overdose as a cause for a patient’s presentation while the physicians are usually focused on other parts of the differential diagnosis. As a team, we cover it all together.

What is the most difficult aspect of working in the ED? 

For me, the most difficult thing is that even after education, the same mistakes happen over and over again. Part of that has to do with having to teach the same concept to new trainees each year and it is hard to target everyone all at once.

What can be done to improve interprofessional practice in the ED?

As much as computer order entry systems have positively impacted patient care, they certainly promote less verbal communication between ED team members. We really need to communicate better with other team members to let them know the ‘why’ behind what we do. This helps educate all involved team members at the bedside and prevents the silos from forming between the different professionals.

What is your biggest pet peeve when you are working in the ED? 

Routinely seeing medication doses prescribed incorrectly (particularly antibiotics) even after intense education about what is correct.

What is the aspect of your job that you are most proud of?

I’ve been very blessed to work where I do as my first job out of fellowship. The U of Maryland EM faculty have provided me with numerous opportunities to teach (locally, regionally, and nationally) and perform research. The department of pharmacy I work for has provided me with flexibility to be able to pursue all of my passions (clinical, teaching, and research). What I’m most proud of are three things:
1. The education I’ve been able to provide through Academic Life in EM
2. The “To-Go Meds” program we created to reduce ED return visits
3- National speaking opportunities at SMACC, AAEM, ASHP, the Teaching Course, and the Crashing Patient Conference

Can you provide an example of an optimal patient interaction (e.g. one in which you used all of your training to positively impact the outcome for a patient)?

There are many, but the one that comes to mind is an incredibly sick DKA patient who was also hypokalemic (not common). Before I was involved, an insulin bolus was administered, without having a potassium value resulted yet. This patient required intense resuscitation, optimized insulin administration, and repletion of potassium.

I worked closely with the nurse and physician team to work outside of our institutional guidelines to resuscitate the patient. Educating the team about how to manage the patient outside standard treatment regimens while rapidly providing treatment is the reason I think I’m here and why a pharmacist is needed in the ED. I truly feel my role helps fill the gap between nurses and physicians.

Additional information

A good resource for pharmacy students/residents interested in pursuing a career in EM pharmacy can be found by clicking here.

Author information

Gerhard Dashi

Gerhard Dashi

Gerhard Dashi is a second year medical student at Queen’s University with growing interests in Emergency Medicine, mentorship, interprofessional teamwork, and #FOAMed.

The post Phone a Friend: the fantastic pharmacist appeared first on BoringEM and was written by Gerhard Dashi.

Could my patient have an Aortic Dissection?

“List top 5 worrisome diagnoses for chest pain” – we’ve all asked this question to junior learners and medical students, and one answer that should always come up is aortic dissection (AD).

As emergency physicians we are well versed in the entity, workup and management of AD, but as a fairly challenging diagnosis, I have often found it difficult to decide who needs to be worked up for dissection. During my training I have observed significant staff variation when considering this condition; with some rarely investigating for AD, while others regularly order CT scans.

As with any disease entity, when considering our workup we need to evaluate our pretest probability to drive investigations and management. The current standard of care for AD workup is a CT scan of the chest and abdomen with contrast. A dissection protocol scan has a significant contrast and radiation load, so one must employ sound clinical judgment with his/her diagnostic decisions.

In order to interpret how to utilize this information, it is important to have a good understanding of pretest probability and likelihood ratios (LHR’s). For a refresher, check out this previous BoringEM post on interpreting likelihood ratios.

The only decision rule to date that has been validated is the AHA Aortic Dissection decision rule, which has a reasonable sensitivity of 91%, but a low specificity of 40%1,2, so its utility as a bedside assessment tool is questionable. The decision rule is based on three main components3:

  1. High risk conditions
    • Marfan Syndrome
    • Connective tissue disease
    • Family history aortic disease
    • Known aortic valve disease (ie: bicuspid aortic valve)
    • Recent aortic manipulation
    • Known thoracic aortic aneurysm
  1. High Risk pain features
    • Chest, back or abdominal pain described as the following:
      • Abrupt onset/severe in intensity AND
      • Ripping/Tearing/sharp or stabbing in quality
  1. High risk exam features
    • Evidence of perfusion deficit:
      • Pulse deficit
      • Systolic BP differential
      • Focal neurologic deficit
    • Aortic insufficiency murmur
    • Hypotension or shock state

Risk stratification based on the above criteria:

Low Risk:

  • Patient has no features from any category above.
  • In this population, the AHA suggests if an alternative diagnosis is identified you can stop there (in regards to AD workup).
  • Unexplained hypotension or widened mediastinum on CXR suggests you should pursue advanced imaging.
  • AHA also suggests to pursue imaging in patients who you are suspicious for AD based on the clinical scenario, regardless of their risk stratification.

Intermediate risk:

  • Patient has any one feature from the categories above.
  • AHA suggests to seek an alternative diagnosis on CXR and ECG, but if none is identified you should proceed with CT scan of the chest.

High Risk:

  • Patient has more than one feature
  • AHA suggests that all these patients need advanced imaging.

As previously mentioned, the rule has a rather low specificity, and as a result far too many patients are scanned. In this discussion, we aim to another approach to which low risk patients may need to be worked up for AD, and which patients we can avoid imaging.

 

There are a few features that will help you to determine your pretest probability, with particularly important LHR’s highlighted below4,5.

 

History

  • Severe pain: sensitivity of 90% (This doesn’t help you differentiate any of the chest pain syndromes, it is often a given of the presentation).
  • Sudden onset chest pain, sensitivity of 84% (immediate, rather than crescendo pain):
    • Not necessarily helping in making the diagnosis, LHR of 1.6
    • But the LACK of sudden onset chest pain has a negative LHR of 0.3
    • Think of this as the ‘thunderclap headache’ of the chest.
  • Tearing or ripping pain has a LHR of 1.2-10.8.
  • Migratory pain carries a LHR of 1.1-7.6.
  • Past medical history of hypertension has a LHR of 1.4

 

 Physical Exam

  • Diastolic murmur has a LHR of 1.4
  • Pulse Differential or deficits has significant diagnostic variability, LHR: 2.4-47.0
    • Note this is significantly different from blood pressure differential in two arms, which has a poor sensitivity of 15%.
  • Focal neurologic deficit has a high LHR of 6.6-33.0.
  • Hypertensive in the ED: poorly studied, but considered a significant risk factor by expert opinion6.
    • Hypertension is concerning when it is unexplained within the clinical context, or persists despite appropriate analgesia.
    • As a refresher; recall that according to the Stanford Classification for aortic dissections, type A involve the ascending aorta, while type B dissections involve the descending aorta.
    • Typically, type A dissections have a worse prognosis, and tend to be sicker patients, while Type B often have reasonable prognosis if detected. They are more likely to be hypertensive, and won’t have many typical findings, such as neurological deficits, pulse differentials and murmurs7.

 

FeaturePositive LHRNegative LHR
Immediate onset chest pain1.60.3
Ripping/Tearing quality1.2-10.80.4
Migratory pain1.1-7.60.6
History of Hypertension1.40.5
Diastolic murmur1.41.2
Pulse differential2.4-47.00.7
Focal Neurological deficit6.6-33.00.9
Abnormal CXR(+)/Normal CXR(-)2.00.3

Investigations

  • “Abnormal” CXR has a LHR of 2.0, while normal CXR has a negative LHR of 0.34.
    • Utility of CXR is to help further lower your pretest probability in the low risk patient.
    • An abnormal CXR is defined by having a widened mediastinum or abnormal aortic contour, but incorporates other findings that one classically considers in aortic dissection (pleural effusion, loss of AP window, etc.).

Widened mediastinum. With permission; Wikimedia commons.

  • There may be a role for point of care ultrasound in the bedside evaluation of a patient for aortic dissection; it is suggested that emergency physicians have a sensitivity of 67% and a specificity of 99-100%8 for detecting an intimal flap on POCUS. This is of course, very user dependent and requires some further investigation, but is a useful skill for the emergency physician to augment their clinical exam, if they have an appropriate pretest probability prior to doing ultrasound.
  • D-Dimer has been extensively studied in the past few years with controversial results, and let’s delve into this further:

There have been a few primary studies, and multiple meta-analyses questioning if a negative D-Dimer can rule-out aortic dissection. The most robust study was a meta-analysis that suggested that patients who are low risk according to AHA aortic dissection decision rule, and have a negative D-Dimer can safely have aortic dissection ruled out. Within this meta-analysis, they demonstrated sensitivity of 98.0%, but a rather poor specificity of 41.9%, and a false positive rate of 40.0%9,10,11.

When applied to low risk patients, it appears that a D-Dimer does not significantly change one’s pretest probability for AD; therefore its utility in the workup for dissection is questionable. This sentiment was echoed in a policy statement released by ACEP in January 201512:

 

“D-Dimer cannot be recommended for use in the evaluation of aortic dissection.”

 

Based on the current data available, in my mind, utilizing D-Dimer in AD would be akin to sending off a D-Dimer in patients who are already PERC negative, when considering PE.

 

Take Home points

AD is a rare disease, and as emergency physicians we should be screening patients for the potential to have this disease entity. It is therefore more useful to identify features to reassure us that a patient is indeed low risk, and negate the need for further investigations, which is why negative LHR’s are an important aspect of this diagnostic consideration.

 

How should you apply this information?

  • The AHA guidelines are too inclusive and result in the unnecessary scanning of patients.
    • The decision to perform a CT scan to investigate for AD depends on your pretest probability – which can be modified using the LHR’s of various historical and physical exam features.
    • Ultimately when your think that your patient is low risk, or you have a low pretest probability, you can probably stop there and consider an alternative diagnosis.
  • In the patient presenting without high risk features, lacking immediate onset chest pain, vascular pain/migratory features, a normal clinical exam and CXR – aortic dissection is highly unlikely and doesn’t warrant significant consideration.
  • With the exception of neurological findings, one individual historical or physical exam finding does not necessarily warrant investigation for AD, recognizing that this is a deviation from the proposed AHA guidelines, and therefore requires the clinician’s interpretation of the data available (i.e.: pretest probability).
  • BP differential between arms is not useful, and instead we should be looking for pulse differences amongst extremities.
  • D-Dimer adds very little to your workup of the patient with aortic dissection.
    • D-Dimer is not validated in those that are intermediate to high risk.
    • In low risk patients, it does not significantly change your pretest probability, and shouldn’t be utilized.

References

  1. Rogers, A. M., Hermann, L. K., Booher, A. M., Nienaber, C. a., Williams, D. M., Kazerooni, E. a., … Eagle, K. a. (2011). Sensitivity of the aortic dissection detection risk score, a novel guideline-based tool for identification of acute aortic dissection at initial presentation: Results from the international registry of acute aortic dissection. Circulation, 123(20), 2213–2218. http://doi.org/10.1161/CIRCULATIONAHA.110.988568
  1. Nazerian, P., Giachino, F., Vanni, S., Veglio, M. G., Castelli, M., Lison, D., … Morello, F. (2014). Diagnostic performance of the aortic dissection detection risk score in patients with suspected acute aortic dissection. European Heart Journal. Acute Cardiovascular Care. http://doi.org/10.1177/2048872614527010
  1. Hiratzka, L. F., Bakris, G. L., Beckman, J. a, Bersin, R. M., Carr, V. F., Casey, D. E., … Williams, D. M. (2010). 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease: Executive Summary. Circulation, 121(13), 1544–1579. http://doi.org/10.1161/CIR.0b013e3181d47d48
  1. Upadhye, S., & Schiff, K. (2012). Acute Aortic Dissection in the Emergency Department: Diagnostic Challenges and Evidence-Based Management. Emergency Medicine Clinics of North America, 30(2), 307–327. http://doi.org/10.1016/j.emc.2011.12.001
  1. Braverman, A. C. (2011). Aortic dissection: Prompt diagnosis and emergency treatment are critical. Cleveland Clinic Journal of Medicine, 78(10), 685–696. http://doi.org/10.3949/ccjm.78a.11053
  1. Sharpe, B. a. (2002). Clinical manifestations of acute aortic dissection. JAMA : The Journal of the American Medical Association, 288(7), 828; author reply 828.
  1. Klompas, M. (2014). Clinician’s corner: Does This Patient Have an Acute Thoracic Aortic Dissection? Clinical Scenarios, 287(17).
  1. Williams, J., Heiner, J. D., Perreault, M. D., & McArthur, T. J. (2010). Aortic dissection diagnosed by ultrasound. The Western Journal of Emergency Medicine, 11(1), 98–99.
  1. Asha, S. E., & Miers, J. W. (2015). A Systematic Review and Meta-analysis of D-dimer as a Rule-out Test for Suspected Acute Aortic Dissection. Annals of Emergency Medicine, 1–11. http://doi.org/10.1016/j.annemergmed.2015.02.013
  1. Nazerian, P., Morello, F., Vanni, S., Bono, A., Castelli, M., Forno, D., … Grifoni, S. (2014). Combined use of aortic dissection detection risk score and D-dimer in the diagnostic workup of suspected acute aortic dissection. International Journal of Cardiology, 175(1), 78–82. http://doi.org/10.1016/j.ijcard.2014.04.257
  1. Cui, J., Jing, Z., Zhuang, S., Qi, S., Li, L., Zhou, J., … Yin, Y. (2015). D-dimer as a Biomarker for Acute Aortic Dissection. Medicine, 94(4), e471. http://doi.org/10.1097/MD.0000000000000471
  1. Diercks, D. B., Promes, S. B., Schuur, J. D., Shah, K., Valente, J. H., & Cantrill, S. V. (2015). Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients With Suspected Acute Nontraumatic Thoracic Aortic Dissection. Annals of Emergency Medicine, 65(1), 32–42.e12. http://doi.org/10.1016/j.annemergmed.2014.11.002

 

Author information

Shahbaz Syed, MD

Shahbaz Syed, MD

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

The post Could my patient have an Aortic Dissection? appeared first on BoringEM and was written by Shahbaz Syed, MD.

Thrombosis Infographic Series: NOACs in VTE

These infographics are a series of introductory tools for learners in the ED for thrombosis and hemostasis. The goal is to provide a visual guide to the how, when, and why of thrombosis and its treatment in the ED. We will use a mechanistic approach to help you build a conceptual framework to understand how these diseases work.

We will cover:

(1) hemostasis
(2) diseases of hemostasis including thrombo- and hemophilias
(3) antithrombotic treatments and how common agents work,
(4) treatment reversal strategies and how they work,
(5) hemostasis in trauma including fibrinolytics and acquired coagulopathies.

Why were these infographics developed

There are two common ways subspecialty knowledge of new topics in medicine are communicated: (1) word of mouth and experience, and (2) journal articles. Formal journal articles as we all know, are almost always next to useless for communicating the clinical relevance of a topic, and definitely always useless for learners. Experts don’t have a problem reading between the lines because they have experience and prefer these convoluted methods because they allow for communication of a ton of information at one time.

The problem is that this makes for a major barrier for translating new medical advances.

So why not break it down into small manageable pieces for people to digest? This series of tools are being developed because hemostasis and thrombosis is a field that is extremely relevant to the ED, but poorly understood by learners because of the reliance on classical methods of teaching.

Throughout my graduate schooling, I had to come up with easy ways to understand (and remember) all the nitty gritty biochemistry that is required in this field. This series outlines my approach for you which hopefully you’ll find useful. Please feel free to send me any feedback to improve future parts of this series!

NOACs in VTE Infographic:

This infographic is designed to give the ED learner an introduction to the key reasons why new oral anticoagulants are now being used. Due to the controversial status of these drugs, this piece also serves to lay out the major points of discussion as it pertains to the ED.

Click HERE download the complete Infographic (9.9 MB).

Otherwise, read on below.

VTE First Page

VTE Second Page

VTE 3rd Page

VTE 4th Page VTE 5th page

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 Thrombosis Infographic Series: NOACs in VTE appeared first on BoringEM and was written by Calvin Yeh.