Interprofessional Health Research Day 2017 – Devon McLean

ULTRASIM: ULtrasound in TRAuma SIMulation. Does the use of ultrasound improve diagnosis during simulated trauma scenarios?

Point of care ultrasound (US) is a key adjunct in the management of trauma patients, in the form of the extended focussed assessment with sonography in trauma (E-FAST) scan. This study assessed the impact of adding an edus2 ultrasound simulator on the diagnostic capabilities of resident and attending physicians participating in simulated trauma scenarios.

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Interprofessional Health Research Day 2017 – Fiona Milne and Kalen Leech-Porter

Combatting sedentary lifestyles; can exercise prescriptions in the Emergency Department lead to a behavioural change in patients?

Patients with chronic diseases such as COPD, coronary artery disease, depression and anxiety are known to benefit from exercise. They also frequently visit the emergency department (ED). Despite the large therapeutic window and evidence supporting its role in disease management, there are few studies examining prescribing exercise in the ED. We asked: Is exercise prescription in the ED feasible and effective?

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Interprofessional Health Research Day 2017 – Janeske Vonkeman

Determining ED staff documentation practice, awareness, and knowledge of intimate partner violence questioning and documentation tools

Domestic violence (DV) rates in smaller cities have been reported to be some of the highest in Canada. It is highly likely that emergency department staff will come across victims of intimate partner violence (IPV) in their daily practice. The purpose of this study is to better understand current practices for detecting IPV, staff awareness and knowledge surrounding IPV, available screening tools, and barriers to questioning about IPV. in the emergency department (ED). Finally, we will determine whether ED staff would be willing to implement a brief 3-question IPV screening tool, the Partner Violence Screen (PVS) in their daily practice.

 

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Welcome Block 10

Dr. A. Sundaram

March 8- April 3

PGY1 Ophthalmology
“I go by Aish. I am a first year Ophthalmology resident. I am originally from Alberta and did my undergrad in medical sciences and business at University of Western Ontario. I subsequently did my medical school at University of Alberta.”


Dr. F. MacKay

March 8- April 3

PGY1 FM

“Hi there. My name is Fraser. I live across the street. I am an alumni of Dal, U of T, Holland College, and the mean streets of many a Canadian city. I am a Family Medicine Resident. For now, when not developing my Doctoring skills, I am busy training my daughters to be astronauts and/or circus acrobats.”


Dr. D. Rollo

March 8- April 3

PGY1 FM

“Born, raised and refined in Western Canada. Home grown in Okotoks AB then borrowed a degree in biochemistry from UBC in Kelowna before I finally landed on Vancouver Island to learn medicine. From West to East, quite the jump and quite the adventure!”


Clinical Clerks

Sean Casey

March 6 – March 26

3rd DMNB

 

 

 

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ED Rounds – Lyme Disease – Dr Paul Frankish

Lyme Disease: Update and recent controversies

Presented by Dr Paul Frankish

 

 


 Link to NB Health Lyme Disease Information


Transmission

  • Borrelia burgdorferi
  • Tick-borne spirochetal bacteria
  • Ixodes scapularis and Ixodes pacificus
  • Field mice, birds and white-tailed deer

Discovered in Lyme, Connecticut  by Dr. Burgdorfer, investigating an abnormal cluster of juvenile RA. Other common tick-borne illnesses are transmitted through the lone star tick (Amblyomma americanum) and the American dog tick (Dermacentor variabilis) that transmit ehrlichiosis and Rocky Mountain spotted fever, respectively.  The ticks serve as the vector between the animal population and humans.  Deer are the preferred host for ticks, and the tick population is highest when deer are present, but the actually pick up the Borrelia from small mammals mostly.


Identification

A) is an Argasid (soft tick, Ornithodoros turicata)

B) has a scutum, long body butshort mouth parts (dog tick, Dermacentor variabilis)

C) is Ixodes scapularis(!)

D) has a scutum, but has a short and stout body – it also has a “lone star” on its body (lone star tick, Amblyomma americanum)


Erythema Migrans Pearls

  • Often just a macule with no central clearing (20-30%)
  • Classically 1-2 weeks from time of tick bite, but anywhere from 3-30 days
  • Some patients may either not have it or notice it
  • May have multiple lesions
  • Rashes within 2 days are usually an immune reaction to tick saliva


Clinical Pearls

  • Always take clinical context into consideration
  • If IgM positive and IgG negative greater than 4 weeks since infection, likely false positive
  • Do not use the test in the setting of EM rash
  • Consider testing if all satisfied:
    • Lyme endemic area
    • Risks for exposure
    • Any features of disseminated or late disease

Testing


Prophylaxis

  • Common ED presentation
  • If attached less than 36 hrs or not Ixodes scapularis, then risk is very low
  • Criteria for prophylaxis (need all)3:
    • Ixodes scapularis
    • Attached longer than 36 hrs
    • Prophylaxis within 72 hrs of removal
    • Greater than 20% local tick infection rate
  • Single dose of Doxycycline 200 mg or 4mg/kg for children greater than 8 years old
  • Children < 8yrs
    • Not sufficient evidence to recommend any other regimes
    • A “watch and wait” approach is recommended in these cases

Full Presentation with Notes

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NB Health Lyme Disease Update Jan 2017

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RCP – Awake Intubations: “Alone we can do so little, together we can do so much”

Awake Intubations: “Alone we can do so little, together we can do so much”

Resident Clinical Pearl (RCP) – January 2017

Kalen Leech-Porter, PGY2 iFMEM, Dalhousie University, Saint John, New Brunswick

Reviewed by Dr. David Lewis

 

Case Example:

A healthy 60 year old man arrives at the Emergency Department (ED)3 hours after his camp caught fire.  He complains of shortness of breath and he has a hoarse voice. Vitals BP 140/90, HR 95, RR 24, Oxygen saturation 96%, afebrile.  GCS 15. You note he has facial and trunk burns. He is alert, scared but cooperative. How would you definitively manage his airway?

Picture 1.


Introduction:

RSI has gained much popularity in the ED for endotracheal intubation.  While there is good reason for this, there is still a role for awake intubation; with awake intubations the patient continues to breathe for themselves and will maintain and protect their airways.  This can be critically important in a situation where there is an anticipated difficult intubation and difficult bag mask ventilation.  The patient does have to be somewhat cooperative for awake intubation, but with proper explanation this might be the best option in a difficult situation.

Indications:

  • Predicted difficult airway anatomy (intubation AND maintaining oxygenation with BMV)
  • Variations of normal anatomy (ie Mallampati 4, obese, small mandible)
  • Pathologic distortion or obstruction: (ie burns, angioedema, stridor)
  • Predicted difficult physiology
  • Hemodynamic instability- (may still be able to do RSI- using appropriate agents and fluid bolus, but awake intubation is an option)
  • High minute volume – awake intubation will allow them to breathe at their current desired rate until intubation facilitated

Requirements:

  • Patients is awake, cooperative

Advantages of awake Intubation

  • Patient protects/maintains airways
  • Patient breathes spontaneously
  • Less risk of hypoxemia/hypercarbia with transition to positive pressure ventilation
  • May help with intubation: tissue movement/bubbles may indicate glottis opening in obscured airways

Disadvantages

  • Potentially uncomfortable
  • Requires cooperation
  • Procedure can be prolonged

 

Back to our case:

………….the hoarse voice and burns suggest airway edema.  This patient will likely both a difficult intubation and difficult to bag mask ventilate.  However, he is cooperative.  Following the AIME approach to tracheal intubation pathway (below), this patient would be a candidate for awake intubation (red arrow).

AIME approach to tracheal Intubations pathway decision making

 

Generic Approach to awake oral intubation:

  1. Supplemental O2 – consider high flow nasal prongs
  2. Prep:
    1. monitors, O2, BVM, suction, ETTs, stylet, laryngoscope, blades, drugs, alternative intubation options, rescue devices, mark cricothyroid membrane,
    2. Psychologically prepare the patient: tell them rationale and explain procedure
  3. Topical Airway Anesthesia +/- light sedation
  4. Awake intubation
  5. Confirm Tube location
  6. Additional Sedation

More Detailed:

Topical Airway Anesthesia
  1. Consider drying agent to reduce secretions and allow better working of topical anesthesia on mucous membranes: glycopyrrolate 5 micrograms/kg IV
  2. Lidocaine application -don’t add epi
    1. 5% lidocaine ointment with tongue depressor to back of tongue
    2. Gargle and swish 4% liquid lidocaine
    3. Then spray (soft palate, posterior pharynx, tonsillar pillars) as you go with either:
      1. Lidocaine 10% endotracheal spray
      2. 4% lidocaine atomizing device
    4. 4% nebulized lidocaine takes 10-12 mins but is another alternative
  3. Do not exceed toxic dose: 5 mg/kg (use less if elderly or cardiac/liver impairment)

+/- Light Sedation
  1. No sedation is reasonable
  2. Consider ketamine, or midazolam +/- fentanyl in small doses (pros and cons not discussed in this pearl)

Awake intubation using DL

Intubation may be performed with bronchoscopy, glidescope, blind nasotracheal intubation. Below is an abridged description of key points of direct laryngoscopy during awake intubation.

  1. Perform in semi-sitting or sitting position – physician may need to stand on a stool/chair
  2. Use “precision laryngoscopy”, slowly walking the blade in avoiding as many structures as possible
  3. Warn patients they will feel some pressure then compress tongue to visualize epiglottis
  4. Place blade in valleculla and perform appropriate lift to visualize cords
  5. Pass the ETT through the cords while the patient inspires

Picture 2

Post Intubation:

Don’t forget to confirm tube location, and provide sedation if the patients hemodynamics tolerate the sedation!

 

References:

Airway Management in Emergencies: Second Edition.  George Kovacs, J. Adam Law. 2011.

Picture 1

Picture 2

 

 

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Resident Clinical Pearl – No Bullus Paediatric DKA

No Bullus Paediatric DKA

Resident Clinical Pearl – December 2016

Luke Taylor, PGY1 iFMEM, Dalhousie University, Saint John, New Brunswick

Reviewed by Dr. David Lewis

 

An altered 2yr old female child presents to your Emergency Department with a BP of 80/50 and a ++high point-of-care blood glucose…….anxiety provoking for all concerned right?

With a presentation like this, the best thing to do according to the House of God…is to “check your own pulse.”  Hopefully after reading this RCP you won’t need to and please don’t waste time recognising that this is severe DKA and this child needs appropriate emergency management.

Key Point – DO NOT BOLUS Fluid and DO NOT BOLUS Insulin

Paediatric DKA (P-DKA) was deemed by a TREKK (TRanslating Emergency Knowledge for Kids) Needs Assessment to be to be an area in which general EDs wished to improve management. A lack of awareness that optimum P-DKA management is different from that of adult DKA was a major driver. In particular, recognition that P-DKA can be complicated by cerebral edema in up to 1.5% of cases.

Management

Is the child in Decompensated Shock? Systolic BP less than (70+(2*age in yrs) for a child >1yr.

If Decompensated? = Bolus 5-10cc/kg over 1-2hrs and reassess after each bolus

 

If not Decompensated? = Correct slowly

Max fluid = 2x maintenance of Normal Saline

Time: Calculate to correct fluid deficit over 48hrs, most are 4-8% dehydrated in moderate DKA

**DKA develops over days (most of the time), therefore slow correction**

Fluid alone, over first 1-2hrs, then Fluid + insulin infusion at 0.05-0.1U/kg/hr

 

Cerebral Edema (CE)

Risk factors:

  • <5yrs old
  • new onset DM
  • ++acidosis
  • longer duration of symptoms
  • severe dehydration

Symptoms of CE:

**Generally 3-12hrs after initiation of therapy

  • headache
  • vomiting
  • confusion
  • GCS<15
  • irritability

Treatment of CE:

  • ABCs
  • restrict IV fluid to maintenance
  • elevate head of bed
  • Mannitol (0.5-1gm/kg IV over 20min) and/or 3% NaCl (5-10ml/kg IV over 30min)

Bottom line

Always:

Use paediatric specific protocol

Like this: http://sjrhem.ca/guideline/dka-pediatrics/

or http://www.bcchildrens.ca/endocrinology-diabetes-site/documents/dkaprt.pdf

And: contact local paediatric diabetes specialist

DO NOT: BOLUS


References

EM Cases Paediatric DKA: https://emergencymedicinecases.com/pediatric-dka/ (Great podcast!)

Lifeinthefastlane DKA: http://lifeinthefastlane.com/ebm-diabetic-ketoacidosis/

Diabetes Ther. 2010 Dec; 1(2): 103–120. The management of diabetic ketoacidosis in children – Arlan L. Rosenbloom

TREKK: http://trekk.ca/

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In case you missed it, 2016…

Don’t touch – from colon to screen.

Am J Infect Control. 2016 Mar 1;44(3):358-60.

Gerba et al. compared the occurrence of opportunistic bacterial pathogens on the surfaces of computer touch screens used in hospitals and grocery stores. Clostridium difficile and vancomycin-resistant Enterococcus were isolated on touch screens in hospitals and in MRSA in grocery stores. Enteric bacteria were more common on grocery store touch screens than on hospital computer touch screens. So don’t snack while you shop over the holidays. The keywords say everything…

Clostridium difficile; Coliforms; Computer touch screen; Methicillin-resistant Staphylococcus aureus; Vancomycin-resistant enterococcus

 

It hurts, it’s tender, but it’s not appy!

J Pediatr Gastroenterol Nutr. 2016 Mar;62(3):399-402.

Siawash at al. remind us about anterior cutaneous nerve entrapment syndrome (ACNES), a frequently overlooked condition causing abdominal pain. They carried out a cross-sectional cohort in a population 10 to 18 years of age consulting a pediatric outpatient department with new-onset AP during a 2 years’ time period. History, physical examination, diagnosis, and success of treatment were obtained in patients who were diagnosed as having ACNES. Twelve of 95 adolescents were found to be experiencing ACNES. Carnett sign was positive at the lateral border of the rectus abdominus muscle in all 12. Altered skin sensation was present in 11 of 12 patients with ACNES. Six weeks after treatment (1-3 injections, n = 5; neurectomy, n = 7), pain was absent in 11 patients.

BUT WHAT IS CARNETT’S SIGN? Have them tense the abdominal wall (by pulling their legs or head off the bed) and if the pain gets worse or stays the same- it is not intra abdominal.

 

Is there a good REASON to stop CPR?

Gaspari R, Weekes A, Adhikari S, Noble VE, Nomura JT, Theodoro D, Woo M, Atkinson P, Blehar D, Brown SM, Caffery T, et al. Resuscitation. 2016;109:33-9.

Some clinicians use a lack of cardiac activity on ultrasound as a reason to terminate resuscitation efforts. We at the Saint John Regional Hospital Emergency Department (ED) participated in this prospective observational study at 20 EDs across North America. We assessed the association between cardiac activity on point of care ultrasound (PoCUS) during advanced cardiac life support (ACLS) and survival to hospital discharge in patients with pulseless electrical activity (PEA) or asystole. Of 793 patients with out-of-hospital cardiac arrest enrolled, 26% had ROSC, 14% survived to hospital admission, and 1.6% survived to discharge. Among 530 patients without cardiac activity on PoCUS, only 0.6% survived to discharge (compared with 3.8% of those with cardiac activity).

There is always an argument that the association between dismal survival and lack of cardiac activity is just a self-fulfilling prophecy, if absence of cardiac activity led to early termination of salvageable resuscitations. In this study, resuscitation had to continue until at least 2 scans were completed. So, unless there are very special circumstances, such as significant hypothermia, or post defibrillation, it seems safe to terminate resuscitation for most patients with asystole on ECG and without cardiac activity on ultrasound.

 

 

SIRS, I’m not sure what you mean? The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)

JAMA. 2016;315(8):801-810.

Singer et al. lay out the new definitions for sepsis and septic shock. SIRS is out. Sepsis should be defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Quantify as a SOFA score of 2 points or more, which is associated with an in-hospital mortality greater than 10%. Patients with septic shock can be clinically identified by a vasopressor requirement to maintain a mean arterial pressure of 65 mm Hg or greater and serum lactate level greater than 2 mmol/L  in the absence of hypovolemia. This combination is associated with hospital mortality rates greater than 40%. In emergency department, adult patients with suspected infection can be rapidly identified as being more likely to have poor outcomes typical of sepsis if they have at least 2 of the following: quickSOFA (qSOFA): respiratory rate of 22/min or greater, altered mentation, or systolic blood pressure of 100 mm Hg or less. These updated definitions and clinical criteria should replace previous definitions, and facilitate earlier recognition and more timely management of patients with sepsis or at risk of developing sepsis.

 

NSAIDs and Lasix – best of friends.

Eur J Intern Med. 2015 Nov;26(9):685-90.

Ungprasert and co. look at the association between exacerbation of heart failure (HF) and use of non-steroidal anti-inflammatory drugs (NSAIDs). Their systematic review and meta-analysis looked at six studies where the use of conventional NSAIDs was associated with a significantly higher risk of development of exacerbation of HF. The excess risk was approximately 40% for conventional NSAIDs and celecoxib.

 

Dispelling the nice or naughty myth: retrospective observational study of Santa Claus

BMJ 2016; 355

Park et al. report their attempt to determine which factors influence whether Santa Claus will visit children in hospital on Christmas Day. They carried out an observational study in paediatric wards in the UK. They discovered that Santa Claus visited most of the paediatric wards in all four countries: 89% in England, 100% in Northern Ireland, 93% in Scotland, and 92% in Wales. The odds of him not visiting, however, were significantly higher for paediatric wards in areas of higher socioeconomic deprivation in England (odds ratio 1.31 (95% confidence interval 1.04 to 1.71) in England, 1.23 (1.00 to 1.54) in the UK). In contrast, there was no correlation with school absenteeism, conviction rates, or distance to the North Pole. The results of this study dispel the traditional belief that Santa Claus rewards children based on how nice or naughty they have been in the previous year. Santa Claus is less likely to visit children in hospitals in the most deprived areas. Potential solutions include a review of Santa’s contract or employment of local Santas in poorly represented regions. Clearly Santa likes everyone in Northern Ireland too! Merry Christmas and happy holidays!

 

PA Dec 2016

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Resident Clinical Pearl – A New Focus for PoCUS

A New Focus for PoCUS

Elective Resident Clinical Pearl – December 2016

Heather Flemming, PGY4 Emergency Medicine, Dalhousie University, Saint John, New Brunswick

Reviewed by Dr. David Lewis

 

A 70 year old female presents to the emergency department with central abdominal pain and one episode of vomiting.  Her vital signs are stable, but she appears uncomfortable.

You bring the ultrasound machine to the bedside to assess her abdominal aorta. Your exam is challenged by the presence of bowel gas, causing scattering of your ultrasound beam, but is ultimately negative for an abdominal aortic aneurysm. You note that the patient has a midline scar, which she states is from a remote hysterectomy. With increased suspicion for bowel obstruction, you move the curvilinear probe across the abdomen and generate the following images: (Video Below)

The images demonstrate dilated loops of bowel and alternating peristalsis (a ‘to and fro movements’ of bowel contents). This confirms your suspicion for a small bowel obstruction (SBO).

 

Discussion:

Bedside ultrasound is a useful tool in evaluating any patient with abdominal pain, and has shown to be more sensitive and more specific than abdominal xray in diagnosing SBO1. Additional advantages of ultrasound include lack of radiation to the patient, bedside availability and potential to improve ED flow2. Treatments, such as nasogastric tube insertion, and early consultation to general surgery can be expedited by rapid identification. In individuals with recurrent sub-acute SBO, PoCUS may become the investigation of choice, reducing radiation exposure for this group of patients.

 

Pearls for performing a bedside ultrasound for SBO:

Multiple regions of the abdomen should be assessed, including the epigastrium, bilateral colic gutters, and suprapubic regions2. (Image 2).

Image 2 (overlapping survey of all quadrants)

 

Typical SBO ultrasound finding include:

  • ≥3 bowel loops dilated >25mm (Measurements taken at 90° to bowel wall)
  • Transition point – dilated peristalsing small bowel visualized adjacent to non-peristalsing collapsed bowel
  • Increased intraluminal fluid
  • Abnormal peristalsis: Hyperdynamic, alternating or absent peristalsis
  • Abdominal free fluid may also be present

 

Credit: ACEP.org

 

References

  1. Jang, Timothy B. Schindler, Danielle. Kaji, Amy H. Bedside ultrasonography for the detection of small bowel obstruction in the emergency department. Emerg Med J 2011 28:676-678.
  2. Chao, Gharahbaghian. Tips and Tricks: Clinical Ultrasound for Small Bowel Obstruction – A Better Diagnostic Tool? https://www.acep.org/content.aspx?id=100218
  1. http://www.emdocs.net/ultrasound-small-bowel-obstruction/
  1. A video on Ultrasound in Small Bowel Obstruction by the Academy of Emergency Ultrasound can be found here: https://vimeo.com/69551555
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Resident Clinical Pearl – “Wellens ≠ well”

“Wellens ≠ well”

Resident Clinical Pearl – November 2016

Mandy Peach, PGY1 iFMEM, Dalhousie University, Saint John, New Brunswick

Reviewed by Dr. David Lewis

 

It’s 7:30 in the morning, you are just starting your shift as a new R1 (you haven’t had coffee yet) and a 69 yo male rolls into the ED with chest pain ongoing since 2am. He has no known cardiac history (hasn’t seen a doctor in years) and is on no medications other than multivitamins. He is an active guy, doesn’t smoke or drink and has no pertinent family history.

On speaking with him he says the pain has actually subsided en route in EMS. You are passed his ECG1

picture1

Your immediate concern is to look for ST changes to determine if this guy is having a STEMI requiring immediate catheterization…but you don’t see any.

However, T-wave inversions in V1-V5 catch your eye, and they are fairly deep. Just ischemic changes?

Your staff cleverly hints – “This guy isn’t well”.

 

Wellens Syndrome

This ECG pattern is indicative of critical stenosis of the proximal LAD. It is not an acute infarction, but it is a predictor of bad things to come – namely anterior wall MI, usually within days to weeks2. Patients with this level of stenosis require more than medical management, and stress-testing them may precipitate infarction and death3.  They require catheterization.

Criteria to diagnose Wellens includes1:

  • Biphasic T waves (Type A) or deeply inverted T waves (Type B) in V2-3 (may extend to V1-6)
  • Isoelectric or minimally-elevated ST segment (< 1mm)
  • No precordial Q waves
  • Preserved precordial R wave progression
  • Recent history of angina
  • ECG pattern present in pain-free state
  • Normal or slightly elevated serum cardiac markers

The reasoning behind the T-wave pattern is as follows1:

When our patient had the chest pain at 0200 it was likely transient ischemia secondary to occlusion of the LAD. By the time he arrived to the ER the clot had spontaneously lysed and he was pain free. No ST elevation was seen, but the reperfusion of the LAD caused T wave changes – usually first biphasic (Type A) that progress to deeply inverted T waves (Type B)1:

picture1

 

But don’t be fooled – the differential for deeply inverted T waves is extensive and includes several important and potentially life-threatening conditions including1:

Pulmonary Embolism1 http://i0.wp.com/lifeinthefastlane.com/wp-content/uploads/2011/10/ecg-wellens-syndrome-1.jpg

Brugada Syndrome1 http://i2.wp.com/lifeinthefastlane.com/wp-content/uploads/2009/09/Brugada-type-1.jpg

Hypokalemic1 http://i2.wp.com/lifeinthefastlane.com/wp-content/uploads/2011/02/U-waves-in-hypokalaemia.jpg

 

And let’s not forget other high risk ECG presentations of chest pain that shouldn’t be missed as they involve a considerable section of the left ventricle and thus require activation of the cath lab:  http://rebelem.com/five-ecg-patterns-you-must-know/

  1. First Diagonal Branch of the LAD occlusion
  2. De Winters – proximal LAD occlusion
  3. Left Main Coronary Artery Stenosis
  4. Posterior Wall MI

 

So what happened with our guy?

The patient in this case did go on to have cardiac catheterization that same morning, most likely preventing a catastrophic MI.

 

What can you do in ED?

  1. Recognize the pattern
  2. Immediate consult to interventional cardiology
  3. Treat as unstable angina – chewable ASA and load with anti-platelet therapy in anticipation of catheterization.

 

Take away point –  Wellens ≠ well. The money isn’t always on ST changes alone, always check the T waves in V2-V3 for biphasic pattern or inversion and consider high risk ischemic ECG patterns in absence of chest pain and cardiac marker abnormalities. Poor outcomes can be prevented in these patients by consulting Cardiology and admitting for early cath.

 

 

References:

  1. http://lifeinthefastlane.com/ecg-library/wellens-syndrome/
  2. De Zwaan, C., Bar, F., Wellens, H. (1982). Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. American Heart Journal, 103 (4): 730-736.
  3. Tandy, R., Bottomy, D., Lewis, J. (1999). Wellens’ Syndome. Annals of Emergency Medicine, 33 (3): 347-351.
  4. De Zwaan, C., Bar, F., Janssen, J., Cheriex E., Dassen W., Brugada P., Penn, O., and Wellens, H. (1989). Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. American Heart Journal; 117(3): 657-65
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