PoCUS – Dilated Aortic Root

Medical Student Clinical Pearl

James Kiberd

Class 2019 Dalhousie Medicine

Reviewed and Edited by Dr. David Lewis


Case:

A 66 year-old female presented to the Emergency Department with shortness of breath and back pain. She had a known dilated aortic root, which was being followed with repeat CT scans. Given the nature of her presenting complaint, a PoCUS was performed to assess her aorta.

 

 

 

Long Axis Parasternal View:

PoCUS for Cardiac imaging has been studied in the acute care setting; focusing on the assessment for pericardial effusion, chamber size, global cardiac function, and volume status, and cardiac arrest.1

In the setting of acute aortic dissection, further evaluation is often recommended depending on the practitioner’s skill level.2 There have been case reports where ultrasound has been used to assess both Type A and Type B aortic dissections.3–5

In order to assess the aortic root, have the patient in a supine position. Either the phased array or the curvilinear probe can be used depending on examiner’s preference. The probe should be positioned with the marker towards the patient’s right shoulder on the anterior chest to the left of the patient’s lower left sternal border. By tilting the transducer between the left shoulder and right hip, long axis views are obtained at different levels with the goal of identifying four main structures; the aorta, the left atrium, and the right and left ventricles. The parasternal long axis view of our patient is shown in Figure 1, where her aortic root measured 3.83cm.

 

Figure 1: Parasternal Long Axis View of Heart: Patient’s root diameter was found to be 3.83cm.

More generally, this view can be used to assess left ventricular contractility and the presence of pericardial effusion, which were not present in this patient. She went on to have a confirmatory CT scan where her aortic root was found to be unchanged from her last scan and was 3.8 cm in diameter as assessed by PoCUS.

In Summary:

Although not rigorously studied to assess aortic root dilatation at the bedside, we present a case where PoCUS was reliable in the assessment of the aortic root. There have been other cases of aortic dissection identified by ultrasound in the emergency department setting, however confirmatory studies (either CT scan or formal echocardiography) are still recommended.


References:

  1. Labovitz AJ, Noble VE, Bierig M, et al. Focused cardiac ultrasound in the emergent setting: A consensus statement of the American society of Echocardiography and American College of Emergency Physicians. J Am Soc Echocardiogr. 2010;23(12):1225-1230. doi:10.1016/j.echo.2010.10.005.
  2. Andrus P, Dean A. Focused cardiac ultrasound. Glob Heart. 2013;8(4):299-303. doi:10.1016/j.gheart.2013.12.003.
  3. Perkins AM, Liteplo A, Noble VE. Ultrasound Diagnosis of Type A Aortic Dissection. J Emerg Med. 2010;38(4):490-493. doi:10.1016/j.jemermed.2008.05.013.
  4. Bernett J, Strony R. Diagnosing acute aortic dissection with aneurysmal degeneration with point of care ultrasound. Am J Emerg Med. 2017;35(9):1384.e3-1384.e4. doi:10.1016/j.ajem.2017.05.052.
  5. Kaban J, Raio C. Emergency department diagnosis of aortic dissection by bedside transabdominal ultrasound. Acad Emerg Med. 2009;16(8):809-810. doi:10.1111/j.1553-2712.2009.00448.x.
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PoCUS – Pleural Effusion

Medical Student Clinical Pearl

James Kiberd

Class 2019 Dalhousie Medicine

Reviewed and Edited by Dr. David Lewis


Case: 

A 90 year-old male presented with worsening shortness of breath on exertion, crackles bilaterally at the bases on auscultation with known history of congestive heart failure. Bedside ultrasound was performed to assess for pleural effusion

Lung Views:

In order to perform ultrasound of the lungs, there are four views that are obtained (see Figure 1). Place the patient supine. The high frequency linear array transducer is often used, but either the phased array or curvilinear transducers can be used. The first views are taken at both right and left mid-clavicular lines of the anterior chest. With the marker of the transducer pointed toward the patient’s head, a minimum of 3-4 rib spaces should be identified. The next views are of the posterior-lateral chest. The patient can be supine or in the sitting position. It is these views where a pleural effusion can be identified.

Figure 1: Chest views with ultrasound. ‘A’ are anterior chest view positions and ‘B’ are posterolateral view positions

Pleural Effusion

Pleural effusion is assessed by ultrasound placing the transducer in the midaxillary line with the marker oriented toward the patient’s head. On the patient’s right side the diaphragm, the liver, and the vertebral line can be seen. On the left, the diaphragm, spleen, and vertebral line should be in view. In a patient without pleural effusion, one should not be able to visualize the lung as it is mostly air and scatters the sound produced by the transducer. However, in the presence of pleural effusion, the area above the diaphragm is filled with fluid and therefore will appear anechoic. In addition, the vertebral line will be present past the diaphragm as the fluid allows the sound waves to propagate and not scatter. This is known as the ‘spine sign’ (also known as the ‘V-line’). Finally, one is often able to see the atelectatic lung float and move with respirations in the fluid, this is known as the ‘sinusoid sign.’ These are the three criteria outlined by consensus statements in the identification of pleural effusions.1 Occasionally, the area above the diaphragm may look like spleen or liver, but this is known as ‘mirror image’ artifact and is normal.2 Figure 2 shows both the right and left views of our patient.

Figure 2: Pleural effusion showing anechoic pleural fluid, atelectatic lung, and ‘spine sign

Accuracy with Ultrasound

Ultrasound is more accurate than either chest x-ray or physical exam in the identification of small pleural effusions.3 For a chest x-ray to identify fluid there usually needs to be more than 200cc present.2 A meta-analysis found that ultrasound had a mean sensitivity of 93% (95%CI: 89-96%) and specificity of 96% (95%CI: 95-98%).4

 

Our patient went on to have a chest x-ray where he was found to have bilateral pleural effusions (see Figure 3).

Figure 3: Bilateral pleural effusions seen on chest radiography in our patient.

In Summary

Three criteria are used to identify pleural effusion on ultrasound; anechoic fluid above the diaphragm, the ability to visualize the spine above the diaphragm (‘spine sign’), and atelectatic lung moving with respirations (‘sinusoid sign’). Lung ultrasound for the detection of pleural effusion is more reliable to identify small effusions in comparison to both radiography and physical exam.


References:

  1. Volpicelli G, Elbarbary M, Blaivas M, et al. International evidence-based recommendations for point-of-care lung ultrasound. Intensive Care Med. 2012;38(4):577-591. doi:10.1007/s00134-012-2513-4.
  2. Liu RB, Donroe JH, McNamara RL, Forman HP, Moore CL. The practice and implications of finding fluid during point-of-care ultrasonography: A review. JAMA Intern Med. 2017;177(12):1818-1825. doi:10.1001/jamainternmed.2017.5048.
  3. Wong CL, Holroyd-leduc J, Straus SE. CLINICIAN ’ S CORNER Does This Patient Have a Pleural Effusion ? PATIENT SCENARIO. Jama. 2010;301(3):309-317. doi:10.1001/jama.2008.937.
  4. Grimberg AI, Carlos Shigueoka DI, Nagib Atallah III Á, et al. Diagnostic accuracy of sonography for pleural effusion: systematic review Acurácia diagnóstica da ultrassonografia nos derrames pleurais: revisão sistemática
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CAEP 2019 – Crowded House?

CAEP 2019, Halifax, May 26-29, 2019

CAEP By The Ocean – Crowding Track – May 26th 1pm


Are you concerned about ED Crowding? After a busy shift do you ever “..dream it’s over”? Do you work in a “Crowded House”?



Come to the Crowded House Track at CAEP19 on May 26th 1pm. International and Canadian experts present their experience and we discuss possible solutions.

Including Dr. Taj Hassan (President Royal College of Emergency Medicine UK), Dr. Alecs Chochinov (President CAEP), Dr. Judy Morris and Dr. David Lewis.

Join in the debate – “are redirection strategies better than accommodation strategies” – should we invest all our energy in redirection to alternative services or should we accept that we can’t stem the tide and bring all these services under one roof?


Register for CAEP19 – CAEP By The Ocean. https://caepconference.ca/registration/

Crowded House – Don’t Dream It’s Over

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PoCUS – Pneumothorax

Medical Student Clinical Pearl

Vlad Kovalik
MD Candidate, 2019
Dalhousie University Faculty of Medicine

Reviewed and Edited by Dr. David Lewis


A 90-year-old female presented to the emergency department after a fall. Her vitals were stable and a chest x-ray demonstrated three posterior rib fractures. She was keen to be managed at home and had the necessary supports in place. She was discharged with a prescription for analgesics and instructions to return to the ED if her condition changed.

4 days later, the same patient returned to the emergency department with shortness of breath and increased work of breathing. Auscultation revealed decreased air entry on the left. A pneumothorax was at the top of the differential.

PoCUS for Pneumothorax

Lung ultrasound has been found to be more sensitive than chest x-ray for detecting pneumothorax.1 To begin scanning, it is best to have the patient in a supine or semi-recumbent position. The high frequency linear array transducer provides excellent near-field imaging and may be used to better appreciate Lung Sliding, however both the phased array or curvilinear probe may also be used. The probe should be positioned in the longitudinal orientation, with the marker towards the patient’s head, on the anterior chest. Scanning through various rib spaces on both sides completes the exam.

In a normal healthy lung, the visceral and parietal pleura slide against each other creating a distinct shimmering effect known as Lung Sliding. The presence of Lung Sliding rules out pneumothorax with nearly 100% sensitivity in the area directly under the probe.2 *

Lung sliding


Absent lung sliding

Comet-tails are another normal feature of a healthy lung. This is an artifact caused by the reverberation between the parietal and visceral pleura. Comet-tails are seen as bright, vertical lines that fade quickly. The detection of comet tails allows you to rule-out pneumothorax.3

The Seashore Sign is a normal finding in M-mode of a healthy lung. The sliding of the parietal and visceral pleura creates a sand like pattern directly deep to the pleural line. In a pneumothorax, there is air between the parietal and visceral pleura and thus the ultrasound beam is scattered deep to the parietal pleura. In this case, an artifact known as the Barcode Sign may be seen where a reflection of the chest wall is seen below the parietal pleura.5 *

The most specific finding of pneumothorax is the Lung Point Sign. This is the point where the visceral pleura begins to separate from the parietal pleura indicating the boundary of the pneumothorax. Although pathognomonic for pneumothorax it is not always present – the sensitivity is 66%.4

Lung Point

In summary

PoCUS for pneumothorax can be performed quickly at the bedside and is more sensitive than chest x-ray. Look for the absence of Lung Sliding, the absence of Comet-tails and try to locate the Lung Point Sign.

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Basic ECG Interpretation

Bare Bones Basics of ECG Interpretation from a First Year Medical Student Perspective

Medical Student Clinical Pearl – October 2018

Victoria Kulesza – Med I Class of 2021, Dalhousie Medicine New Brunswick 

Reviewed and Edited by Dr. David Lewis


Physiology

Electrical Events and Corresponding Waves and Lines on a Standard ECG

Basic Interpretation

Common Arrhythmias

Summary

Suggested Resources

References


Physiology

Cardiac cells are electrically polarized in their resting state, with the inside holding a negative charge in comparison to the outside.1,3 Membrane pumps maintain this electrical polarity through the regulation of ions including potassium, sodium, chloride and calcium.1 Depolarization is the key electrical event of the heart that occurs spontaneously in some cells and is initiated by the arrival of an electrical impulse carrying positively charged ions in other cells.1 There are 3 key cells involved in the electrical and mechanical activities that occur within the heart:

 

The sequential depolarization of cells creates a wave of depolarization that transmits across the entire heart, representing a flow of electricity that can be detected by the electrodes placed on the surface of that patient’s body. The waveforms visible on the ECG represent the electrical activity of the myocardial cells, the cells making up the vast majority of the heart.1 At the end of the depolarization process, cardiac cells are repolarized through membrane pumps reversing the flow of ions. Both the depolarization and repolarization are represented as the wave forms on the ECG.1


Electrical Events and Corresponding Waves and Lines on a Standard ECG

P Wave

The heartbeat is initiated in the sinoatrial node located in the posterior wall of the right atrium.4 After the sinus node fires, the atrial myocardium is depolarized in a wave-like fashion causing the atrial contraction. This depolarization and contraction of the atrial myocardial cells results in the first P wave.1 The wave of depolarization does not immediately pass through to the ventricles, the atrioventricular node located at the floor of the right atrium, slows the conduction of the electrical impulse to allow the atria to fully complete their contraction. 1,4 The contraction of the atria forces blood from the atria through the atrio-ventricular valves, known as the tricuspid and mitral valves, into the ventricles.3

PR Interval

This interval is the time that is required for the electrical impulse to travel from the atria, through the AV node, bundle of His, bundle branches and Purkinje fibers to the point where the ventricular myocardium begins its depolarization.5 As blood flows through the AV valves the physiologic pause in electrical conduction is represented on the EKG as the flat line following the initial P wave. The ventricular conduction system is composed of 3 parts including the Bundle of His, Bundle Branches and the Terminal Purkinje Fibers.1 The ventricular depolarization is rapidly transmitted through the Bundle of His which emerges from the AV node and subsequently bifurcates into the left and right bundle branches which carry the impulse down the interventricular septum to their terminating fascicles in multiple Purkinje fibers.1,3 Once this current is delivered to the ventricular myocardium the depolarization causes ventricular contraction visible on the ECG as the QRS complex.1

PR Segment

A straight line between the end of the P wave and the start of the QRS complex reflects the time between the end of atrial depolarization and the start of ventricular depolarization.1

QRS Complex

The QRS complex consists of 3 individual waves in a normal conduction1,3:

  • Q Wave: first deflection downward
  • R Wave: first upward deflection
  • S Wave: first downward deflection subsequent to an upward deflection

A complete QRS complex represents ventricular depolarization as well as the initiation of ventricular contraction.1,3 The use of the term QRS Interval describes the duration of the QRS complex alone indicating the duration of ventricular depolarization specifically.1

ST Segment

A straight line between the end of the QRS complex and the beginning of the T wave known as the ST segment measures the time from the end of ventricular depolarization to the beginning of repolarization.1

T Wave

Following the depolarization of the myocardial cells, there is a short refractory period and subsequent recovery phase identified as the T wave on the ECG.1,3,5 This is phase of ventricular repolarization that begins after the QRS and is completed at the end of the T wave.3,5 Repolarization is a slower process than the depolarization which is illustrated by the broader nature of the T wave in comparison to the QRS.1,5

QT Interval

This interval includes the QRS complex, ST segment as well as the T wave which allows for the measurement of time between the beginning of ventricular depolarization to the end of ventricular repolarization.


 

Basic Interpretation

The most effective way to ensure clinically significant abnormalities are not missed on ECG is to develop a consistent order of analysis. One suggested order is as follows:

 

A. Determine Rate:

  1. Sinus Tachycardia = >100 BPM
  2. Sinus Bradycardia = <60 BPM
  3. Three Ways to Determine Rate:
    • Identify an R wave that falls on or near one of the heavy lines of the ECG strip, count the number of large squares between this first R wave and the beginning of the subsequent wave. Divide 300 by the number of large squares between the R waves to determine the number of cardiac cycles per minute. Counting the number of small squares between R waves and dividing 1500 by this number would identify with greater accuracy the heart rate.1
    • Identify the series of small pink indicators above the rhythm strip that identify 3 second intervals and count the number of cycles between two 3 second intervals – multiply this number by 10 to identify the number of beats per minute.1
    • In the event of an irregular heartbeat identify the number of QRS complexes and multiply this number by 6. Each started ECG paper reads at 25mm/s therefore 1 ECG represents 10 seconds of activity.2

Thaler 2015

 

B. Intervals:

Identify the length of the PR and QT Intervals as well as the width of the QRS complexes

Normal Interval Lengths5:

  1. PR = 0.12 – 0.20 sec
  2. QT = varies with overall heart rate
  3. QRS = 0.05 – 0.10 sec

 

 

 

 

 

 

 

C. Rhythm5:

  1. P waves present and normal?
  2. QRS complexes wide or narrow? General pattern – regular, regularly irregular or irregularly irregular?
    1. Wide = >0.12 sec
    2. Narrow = <0.12 sec
  3. Relationship between P waves and QRS complexes
  4. Overall rhythm regular or irregular?

 

D. Axis

  1. The ECG electrodes record the average direction of flow of electrical current within the heart.
  2. Lead I is the zero reference point, any axis lying below is deemed positive while those lying above are deemed negative.
  3. When the wave of depolarization begins, any lead that views this wave as moving towards it will record this as a positive deflection on the ECG paper.
  4. Assessment of P Wave Axis:
    • Atrial depolarization begins at the sinus node in the right atrium and follows a right to left and inferior direction. This depolarization of the right to left atria should demonstrate a positive deflection in leads aVL, I, II and aVF.
  5. Assessment of QRS Complex Axis:
    • As the wave of depolarization moves through the interventricular septum the current moves in a left to right direction. This wave may not be visible on the ECG but when apparent appears as a negative deflection in leads I, aVL (V5 and V6). As a result of the increased size of the left ventricle in comparison to the right, the remainder of the QRS complex vector of flow is directed leftward and is demonstrated as the positively deflected R wave in most left lateral and inferior leads. The aVR lead will record a deep negative deflection based on the direction of flow being away from this lead.

 


 

Common Arrhythmias1

1. Sinus Tachycardia

  • HR >100 bpm
  • Can be normal or pathologic, strenuous exercise can cause HR above 100.

 

2. Sinus Bradycardia

  • HR <60 bpm
  • Can be normal or pathologic, many well-conditioned athletes maintain a resting HR below 60.

 

3. Paroxysmal Supraventricular Tachycardia

  • HR 150-250 bpm
  • Narrow complex QRS
  • Very common, sudden onset, sudden termination.
  • Clinical Symptoms: palpitations, shortness of breath, dizziness. Possibly induced by alcohol, caffeine or extreme excitement.

 

4. Atrial Flutter

  • P waves 250-350 bpm
  • Atrial depolarization occurs so rapidly that discrete P waves are indiscernible.
  • Leads II and III demonstrate a prominent saw-tooth
  • AV node cannot handle the number of atrial impulses therefore there is an unequal number of P waves to QRS complexes – some electrical impulses from the sinus node bump into a refractory node and go no further, this is called AV Block. 2:1 block is most common while 3:1 and 4:1 are also frequently observed.
  • Clinical Symptoms: shortness of breath, angina type discomfort.

 

 

5. Atrial Fibrillation

  • AV Node may receive >500 impulses per minute
  • More common than atrial flutter, most commonly sustained arrhythmia.
  • No true P waves are discernible, AV node allows occasional impulses to pass through to the ventricles, creating an irregularly irregular ventricular rate often in the range of 120-180 bpm.
  • Clinical Symptoms: some patients experience no symptoms, others experience shortness of breath, chest pain, palpitations and dizziness.

 

6. Premature Ventricular Contractions

  • Most common ventricular arrhythmia.
  • Retrograde P wave or no P wave prior to the QRS.
  • Wide QRS of at least 0.12 seconds in majority of the leads often followed by a compensatory pause before the subsequent beat.
  • Often occur randomly and rarely require treatment unless an isolated PVC is noted in the setting of acute MI as it may trigger ventricular tachycardia or ventricular fibrillation.
  • When to worry:
    • Frequent PVCs
    • Consecutive runs, 3+ in a row
    • Multiform – demonstrating variation in the site of origin
    • Occurring on the T wave – “R-on-T” phenomenon
    • PVC in the setting of an acute MI

 

 

7. Ventricular Tachycardia

  • Rate 120-200 bpm
  • Wide complex QRS
  • A run of 3+ consecutive PVCs.
  • Prolonged ventricular tachycardia is an emergency requiring immediate treatment to prevent cardiac arrest.
  • May be uniform or polymorphic, uniform being more closely associated with healed infarctions and polymorphic waveforms more commonly associated with acute coronary events.

 

8. Ventricular Fibrillation

  • Spasmodic tracings or coarse ventricular fibrillation or fine ventricular fibrillation without any true QRS complexes.
  • Heart generates no cardiac output, CPR and defibrillation are required immediately.
  • Most common arrhythmia in adults who experience sudden death.
  • Common predisposing factors:
    • Myocardial ischemia/infarction
    • Heart failure
    • Electrolyte disturbances
    • Hypoxemia or hypercapnia
    • Hypotension or shock
    • Overdoses of stimulants especially when used in combination with others

 


 

Summary

 


 

 


 

Suggested Resources

Teaching Medicine – Rhythm Strip Interpretation Practice

ECG Guide Mobile Smartphone App

  • Available through itunes app store

The Only EKG Book You’ll Ever Need

  • PDF available online through Dalhousie Library

 

References

  1. Thaler, M. S. (2015). The Only EKG Book You’ll Ever Need (9th ed.). Lippincott, Williams & Wilkins.
  2. Andrade, J. (2013). ECG Guide [Mobile application software]. Retrieved from http://itunes.apple.com
  3. Dubin, D. (2000). Rapid interpretation of EKG’s: An interactive course (6th ed.). Tampa, Fla.: Cover Pub.
  4. McKinley, M. P., OLoughlin, V. D., Harris, R. T., & Pennefather-O’Brien, E. E. (2015). Human anatomy (4th ed.). New York, NY: McGraw-Hill Education.
  5. Khan, M. (2008). Rapid ECG interpretation (3rd ed., Contemporary cardiology (Totowa, N.J). Totowa, N.J.: Human Press.
  6. Thomas, V. (n.d.). Premature Ventricular Contractions Treatment Cape Town. Retrieved from https://cardiorhythm.co.za/premature-ventricular-contractions/
  7. https://inside.fammed.wisc.edu/medstudent/pcc/ecg/axis.html
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Fall ECCU Conference Workshop – 28th September

We still have availability for delegates wanting to attend the Fall ECCU Conference Workshop on the 28th September at the beautiful Algonquin Resort in St. Andrews, New Brunswick.


  • International PoCUS experts from South Africa, USA and Canada
  • PoCUS hot topics and updates
    • PoCUS in Rural Health
    • Why aren’t you doing THIS with PoCUS?
    • How to be a leader in PoCUS
  • Top PoCUS research
  • IP2 Diagnostic stream lectures
  • Hands-on scanning workshops


  • Choose your own workshop
    • Pediatrics, Cardiac, Lung, IVC, DVT, Gallbladder, DVT, Aorta, FAST, Obstetric
  • CPoCUS approved
  • CCFP CME approved
  • Bring the family and stay for the weekend
    • Top golf resort, whale watching, explore the islands

 

Click Here for More information and Booking

 


 

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PoCUS and Clavicle Fractures

Using PoCUS to diagnose clavicular fractures

Medical Student Clinical Pearl – May 2018

Danielle Rioux – Med III Class of 2019, Dalhousie Medicine New Brunswick 

Reviewed by Dr. Mandy Peach and Dr. David Lewis

Case: A 70 year-old man presented to the emergency department with pain in his left shoulder and clavicular region following a skiing accident. He slipped and fell on his left lateral shoulder while he was on skis at the ski hill. He has visible swelling in his left shoulder and clavicular region, and was not able to move his left arm.

On exam: The patient was in no sign of distress. He was standing and holding his left arm adducted close to his body, supporting his left arm with his right hand. There was swelling and ecchymosis in the left clavicle, mid-shaft region, with focal tenderness. On palpation, there was crepitation, tenderness, swelling, and warmth in this region. He was unable to move his left shoulder due to pain. His neurovascular exam on his left arm was normal. Auscultation of his lungs revealed normal air-entry, bilaterally and no adventitious sounds.

Point of Care Ultrasound (PoCUS): We used a linear, high-frequency transducer and placed it in the longitudinal plane on the normal right clavicle (see Image 1.), and the fractured left clavicle (see Image 2.). Image 3 shows the fractured clavicle in the transverse plane.

Image 1. PoCUS of normal right clavicle along the long axis of the clavicle (arrows depict the hyperechoic superficial cortex with deep acoustic shadowing).

Clip 1. PoCUS of normal right clavicle along the short axis of the clavicle. The transducer is moving from the lateral to medial, note the visible hyperechoic curved superficial cortex and the subclavian vessels at the end of the clip. 

Image 2. PoCUS of normal right clavicle along the short axis of the clavicle (arrows depict the hyperechoic superficial cortex with deep acoustic shadowing).

Image 3. PoCUS of a fracture in the left clavicle along the long axis of the clavicle

Clip 2. PoCUS of a fracture of the left clavicle, viewed in the long axis of the clavicle. Compare this view with image 1.

Clip 3. PoCUS of a fracture in the left clavicle viewed in the short axis of the clavicle. Compare this view with Clip 1. Note the fracture through the visible cortex and the displacement that becomes apparent halfway through the clip.

Radiographic findings: Radiographic findings of the left clavicle reveal a mid-shaft spiral clavicular fracture.  (Image 4).

Image 4. Radiographic image of fractured left clavicle.

 

Take home point: Research has shown that Ultrasonography is a sensitive diagnostic tool in the evaluation of fractures (Chapman & Black, 2003; Eckert et al., 2014; Chen et al., 2016).

This case provides an example of how PoCUS can be used to diagnose clavicle fractures in the emergency department. In a rural or office setting where radiography is not always available, PoCUS can be used to triage patients efficiently into groups of those with a fracture and those with a low likelihood of a fracture. This would enable more efficient medical referrals while improving cost-effectiveness and patient care.

References:

Chapman, D. & Black, K. 2003. Diagnostic musculoskeletal ultrasound for emergency physicians. Ultrasound, 25(10):60

Eckert, K., Janssen, N., Ackermann, O., Schweiger, B., Radeloff, E. & Liedgens, P. 2014 Ultrasound diagnosis of supracondylar fractures in children. Eur J Trauma Emerg Surg., 40:159–168

Chen, K.C., Chor-Ming, A., Chong, C.F. & Wang, T.L. 2016. An overview of point-of-care ultrasound for soft tissue and musculoskeletal applications in the emergency department, Journal of Intensive Care, 4:55

This post was copyedited by Dr. Mandy Peach

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SJRHEM @Calgary CAEP 2018

Congratulations to all our researchers presenting at CAEP Calgary 2018. This year we have had a total of 13 research abstracts accepted for either oral or poster presentation, 2 invited presentations and 1 track chair. We are also involved in a number of administrative, academic and research committee meetings across the conference.


Last years presentations (CAEP Whistler 2017) can be viewed here


Q-Code Link to this page

 

 

 

 

 

 


Download (PDF, 144KB)

 


 

Training first-responders to administer anaphylaxis publicly available epinephrine – a randomized study – Presenter – Robert Dunfield

Download (PDF, 1.08MB)

 


 

Emergency Critical Care Ultrasound (ECCU) paramedical course: A novel curriculum for training paramedics in ultrasound – Presenter – David Lewis

Download (PDF, 702KB)

 


 

Critical Dynamics Study of Burnout in Emergency Department Health Professionals in New Brunswick: Revisiting  5 years later – Presenter – Felix Zhou

Download (PDF, 585KB)

 


 

Do electrocardiogram rhythm findings predict cardiac activity during cardiac arrest? A SHoC series study. – Presenter – Paul Atkinson

Oral Research Presentation – Track 5 – Sunday May 27th 15:50hrs

 


 

Introduction of extracorporeal cardiopulmonary resuscitation (ECPR) into emergency care: a feasibility study – Presenter – Derek Rollo

Download (PDF, 673KB)

 


 

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

Download (PDF, 803KB)

 


 

Development of a predictive model for hospital admissions by utilizing frequencies of specific CEDIS presenting complaints – Presenter – David Lewis

Oral Research Presentation – Track 4 – Wednesday May 30th 12:45hrs

Admission Prediction


 

Changes in situational awareness of emergency teams in simulated trauma cases using an RSI checklist – Presenter – James French

Download (PDF, 937KB)

 


 

Interprofessional airway microskill checklists facilitate the deliberate practice of surgical cricothyrotomy with 3-D printed surgical airway trainers – Presenter – James French

Download (PDF, 3.9MB)

 


 

How aware is safe enough? Situational Awareness is higher in safer teams doing simulated emergency airway cases – Presenter – James French

Download (PDF, 760KB)

 


 

Interprofessional airway microskill checklists facilitate the deliberate practice of direct intubation with a bougie and airway manikins – James French

Download (PDF, 3.83MB)

 


 

Lung ultrasound – Presenter – Paul Atkinson

Invited Oral Presentation – Track 1 – Sunday May 27 10:15hrs

 


Design is Devine – Presenter – James French

Invited Oral Presentation – Track 1 – Sunday May 27 10:15hrs

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Great ideas and making things better

I heard Dr. Dylan Blacquiere speaking on the radio while driving home after one of those busy D2 shifts on Friday, and it really cheered me up to hear him describe how we all in Saint John are leading the way in managing acute stroke care. http://www.cbc.ca/player/play/1152508483846
From EMS, through Emergency Medicine, diagnostic and intervention radiology, internal medicine and neurology, Saint John Regional Hospital (probably more appropriately Saint John University Hospital) provides a world class service for stroke patients in New Brunswick.
This got me thinking about many of the other innovations and ideas that we continue to push forward locally, especially relating to emergency medicine, and how important it is not to let ourselves become disillusioned by busy shifts, perceived administrative inertia, perceived injustices, crowding and many of the negatives we face, and will likely continue to face for sometime.
To name but a few, we can be proud of the integrated STEMI program we have from EMS to Cath Lab, the Point of Care Ultrasound program that leads in this nationally and beyond, the new Trauma Team leadership program, the patient wellness initiatives such as the photography competition corridor that make things just a little brighter for patients, the regionally dominant and growing simulation program, the regional and local nursing education programs, the nationally unique and hugely popular 3 year EM residency program, the impact of our faculty on medical education at DMNB, the leading clinical care provided by a certified faculty of emergency physicians, our website, our multidisciplinary M&M and quality programs, many of the research initiatives underway including development of an ECMO/ECPR program with the NB Heart Centre, improving detection of domestic violence, innovations around tackling crowding, preventing staff burnout, better radiology requesting, encouraging exercise prescriptions, and much more.
I was particularly impressed how Dylan explained the integrative approach that was required to improve stroke care, and how that was achieved here. There are many other areas that we can also improve, innovate and lead in. Every day we see ways to make things better.
I hope that at this point in our department’s journey, we can continue to make the changes that matter, for patients, our departmental staff, physicians, nurses and support staff alike.
I encourage all of us to think of one area we can improve, to plan for change and for us all to support each other to achieve those improvements. Some of our residents are embarking on very interesting projects, such as designing early pregnancy clinic frameworks, models to improve performance under stress, and simulating EMS ECPR algorithms – all new innovations, not just chart reviews of what we are already doing. I encourage us all to support them, and others with these projects, and to begin to create innovation priorities for the department.
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Urinary Tract Infections

Urinary Tract Infections


Medical Student Clinical Pearl

Rob Hanlon, Med 1

Dalhousie Medicine New Brunswick, Class of 2021

Reviewed by: Dr David Lewis


Urinary tract infections (UTIs) are common in both the inpatient and outpatient settings. As such, it is important to understand the etiology, pathogenesis, and treatment of such infections. This post will focus primarily on uncomplicated UTIs, bacteriology and pathogenesis, treatment options with consideration for drug resistance.

Types of UTIs: 

The term UTI encompasses different infections. These include asymptomatic bacteriuria, acute uncomplicated cystitis, recurrent cystitis, complicated UTI, catheter-associated asymptomatic bacteriuria, catheter-associated UTI, prostatitis, and pyelonephritis. 1 There are two broad classifications: uncomplicated and complicated.

Uncomplicated UTIs refer to infections occurring in individuals with normal urinary tracts; meaning they have no structural or neurological issues, such as neurogenic bladder. These are differentiated into lower (bladder and urethra) and upper (ureters and kidneys) urinary tract infections; cystitis and pyelonephritis respectively. 2 Typical symptoms of cystitis include dysuria, urinary frequency and urgency, suprapubic pain, and hematuria. Symptoms of pyelonephritis include fever, chills, flank pain, costovertebral angle tenderness, and nausea/vomiting. 3

Risk factors of uncomplicated UTIs include being female (proximity of urethral opening to anus), frequent sexual intercourse, history of recurrent UTIs, use of spermicide-coated condoms, diaphragms, obesity, and diabetes. 3 Menopause also increases the risk for UTIs as the decrease in estrogen causes the walls of the urinary tract to thin, which decreases resistances to bacteria. 4 Uncomplicated UTIs do occur in men; albeit, less frequently than women. Risk factors in men include anal intercourse (fecal bacteria), lack of circumcision, and benign prostatic hyperplasia. 5

Complicated UTIs refer to infections that are typically more severe and difficult to treat. This type of infection can be seen in people with structural abnormalities impairing the flow of urine, catheter use or other foreign bodies, renal transplantation, and kidney/bladder dysfunction.4

Bacteriology and Pathogenicity:

It is important to note that recently the urinary tract has been found to be colonized by a normal microbiome, similar in concept to the gut and vaginal lumens. The urinary tract has traditionally been thought to be a sterile lumen. Changes in the bacterial make-up may contribute to a disease state in the urinary tract.6 There is more research needed to fully appreciate how changes to the normal bacteria contribute to disease and specifically to UTIs. There is ongoing research to determine how the microorganisms become pathological and if the normal flora can be a source of a pathological process.6 There is research indicating possible alternative treatments such as probiotics and dietary modifications that can impact urinary tract diseases.6 The impact of antibiotics on the normal urinary tract bacteria is also a current research topic.6 Clinically, the presence of UTI symptoms would indicate that there is a pathological process present and, when indicated, antibiotics as first-line treatments are still recommended.

There are two mechanism by which bacteria enter the urinary tract, these are ascending infections and haematogenous infections. The ascending mechanism occurs when perineal/fecal bacteria enter the urethra and travel up towards the bladder/kidneys. The haematogenous route occurs when bacteria from the blood enter the kidneys.7

Bacteria causing UTIs are termed uropathogens. The common UTI causing organisms are gram negative Klebsiella spp., Escherichia coli, and Proteus spp., and gram positive Enterococci spp. and Staphylococcus saprophyticus. E. coli being the most common uropathogen; seen in 80% of cases. More opportunistic organisms can be isolated in complicated UTIs, such as Pseudomonas spp. and fungal Candida spp.4 8

Uropathogenic E. coli (UPEC) strains contain virulence factors that allow them to colonize the urinary tract. Fimbriae are filamentous cell surface extensions that allow the bacteria to adhere to the uroepithelium and promote invasion into the tissue. Other surface molecules include flagella that allow the bacteria to mobilize up the urinary tract. 9 UPEC also produce toxins such as haemolysin, which damage epithelial cells and induce inflammatory responses (causing UTI symptoms). Factors allowing adherence of UPEC to uroepitehlium are paramount, as urine could wash away the bacteria. Other virulence factors allow the bacteria to thrive and grow. 7

Klebsiella spp. and Proteus spp. are other gram negative uropathogens that also produce fimbriae. Klebsiella produce polysaccharide capsules that prevent host defense phagocytosis.7  It also produces an enzyme called urease, produced by Proteus spp. as well, which hydrolyzes urea into ammonia and CO2. The bacteria use ammonia as a source of nitrogen for metabolism. The enzymatic process also increases the pH of the urinary tract and leads to the formation of renal stones. 10

Proteus

Pseudomonas aeruginosa is a gram-negative commonly associated with nosocomial acquired UTIs, especially when catheters are in place. Its major virulence factor is the production of biofilms, which protect it from host defenses and many antimicrobials. 7 Staphylococcus saprophyticus is a gram-positive bacterium that also produces biofilms, as well as a specific epithelial adhesion protein called lipoteichoic acid. 11

Although some of these uropathogens have similar virulence mechanisms, it is important to understand the different types of pathogens and their virulence factors because different antimicrobials target specific parts of the bacteria and the bacteria can be resistant to specific treatment options.

Treatment with Consideration for Antimicrobial Resistance

Multiple factors must be considered when choosing treatment options for UTIs in order to determine the risk of increased drug resistance. Patients are considered to be at a higher risk of drug resistance if, within the last three months, they have been found to have a multidrug resistant strain in their urine, they have been admitted to a hospital or other care facility, used broad-spectrum antibiotics, or have a travel history to areas known for resistant strains. 3

For low risk patients, treatments for uncomplicated cystitis include nitrofurantoin, trimethoprim-sulfamethoxazole, and fosfomycin. Choosing which drug depends on the individual’s allergies, local rates of resistance, and availability. If the patient has used one of these drugs within the last three months, the remaining two drugs are possible options. 3 If first-line treatments are not an option, then an oral beta-lactam, such as amoxicillin-clavulanate is appropriate. If allergic to this, then a fluoroquinolone such as ciprofloxacin can be used.3

Table 1: Drugs and dosages for empiric treatment of uncomplicated cystitis. 3

For higher risk patients, a urine culture and antimicrobial susceptibility testing should be ordered. First-line treatments (see above) can be used as empiric treatments until test results are obtained. However, if the patient is unable to take these treatments, test results should be obtained prior initiating treatment. 3

For complicated UTIs, such as catheter infections, treatment depends on the severity of the illness. Urine culture and susceptibility testing should be performed. In the case of a catheter infection, it should be removed and a sample from the catheter should be cultured. 12 If the catheterized patient requires treatment prior to obtaining test results, treatment should cover gram-negative bacilli. Third-generation cephalosporins can be used in this case. Critically ill patients should be put on broad spectrum antibiotics such as carbapenems and vancomycin, in order to cover pseudomonas and methicillin-resistant Staphylococcus aureus infections respectively. 13

Local (New Brunswick, Canada) Information on Antimicrobial Treatment of UTIs can be found here:

NB Antibiotic Guidelines and Resources

This is not an exhaustive description of infection types, treatments, or resistance mechanisms. This post focused on uncomplicated UTIs and their treatments because they are commonly seen in the clinical setting. An in-depth patient history is crucial for understanding the possible causes of a UTI and for developing a differential diagnosis. These should be included alongside test results when evaluating treatment options.


References:

  1. Kalpana Gupta, Larissa Grigoryan, Barbara Trautner. Urinary tract infection. Annals of Internal Medicine. 2017;167(7). https://search.proquest.com/docview/1975585404.
  2. Ana L Flores-Mireles, Jennifer N Walker, Michael Caparon, Scott J Hultgren. Urinary tract infections: Epidemiology, mechanisms of infection and treatment options. Nature Reviews. Microbiology. 2015;13(5):269. http://www.ncbi.nlm.nih.gov/pubmed/25853778. doi: 10.1038/nrmicro3432.
  3. Hooton T, Gupta K. Acute uncomplicated cystitis in women. Retrieved from: https://www.uptodate.com/contents/acute-uncomplicated-cystitis-in-women?source=see_link. Updated 2017.
  4. Harvey S. Urinary tract infection. University of Maryland. Retrieved from: http://www.umm.edu/health/medical/reports/articles/urinary-tract-infection. Updated 2012.
  5. Hooton T. Acute uncomplicated cystitis in men. Retrieved from: https://www.uptodate.com/contents/acute-uncomplicated-cystitis-in-men?source=see_link. Updated 2017.
  6. Aragón IM, Herrera-Imbroda B, Queipo-Ortuño MI, et al. The urinary tract microbiome in health and disease. European Urology Focus. 2016. doi: 10.1016/j.euf.2016.11.001.
  7. Walsh C, Collyns T. The pathophysiology of urinary tract infections. Surgery (Oxford). https://www.sciencedirect.com/science/article/pii/S0263931917300716. doi: 10.1016/j.mpsur.2017.03.007.
  8. Beyene G, Tsegaye W. Bacterial uropathogens in urinary tract infection and antibiotic susceptibility pattern in jimma university specialized hospital, southwest ethiopia. Ethiopian journal of health sciences. 2011;21(2):141. http://www.ncbi.nlm.nih.gov/pubmed/22434993. doi: 10.4314/ejhs.v21i2.69055.
  9. Bien J, Sokolova O, Bozko P. Role of uropathogenic escherichia coli virulence factors in development of urinary tract infection and kidney damage. International journal of nephrology. 2012;2012:681473. http://www.ncbi.nlm.nih.gov/pubmed/22506110. doi: 10.1155/2012/681473.
  10. Schaffer JN, Pearson MM. Proteus mirabilis and urinary tract infections. Microbiology spectrum. 2015;3(5). http://www.ncbi.nlm.nih.gov/pubmed/26542036.
  11. Raul Raz, Raul Colodner, Calvin M. Kunin. Who are you: Staphylococcus saprophyticus? Clinical Infectious Diseases. 2005;40(6):896-898. http://www.jstor.org/stable/4463165. doi: 10.1086/428353.
  12. Fekete T. Catheter-associated urinary tract infection. Retrieved from: https://www.uptodate.com/contents/catheter-associated-urinary-tract-infection-in-adults?source=see_link#H123172989. Updated 2016.
  13. Hooton T, Gupta K. Acute complicated urinary tract infection (including pyelonephritis) in adults. Retrieved from: https://www.uptodate.com/contents/acute-complicated-urinary-tract-infection-including-pyelonephritis-in-adults?source=see_link#H12414288. Updated 2017.
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SJRHEM Journal Club Report Oct 2017

SJRHEM Journal Club Report Oct 2017

Allyson Cornelis, R1 iFMEM

Hosted by Dr Andrew Lohoar


Abstract:

Idarucizumab for Dabigatran Reversal — Full Cohort Analysis

Charles V. Pollack, Jr., M.D., Paul A. Reilly, Ph.D., Joanne van Ryn, Ph.D., John W. Eikelboom, M.B., B.S., Stephan Glund, Ph.D., Richard A. Bernstein, M.D., Ph.D., Robert Dubiel, Pharm.D., Menno V. Huisman, M.D., Ph.D., Elaine M. Hylek, M.D., Chak-Wah Kam, M.D., Pieter W. Kamphuisen, M.D., Ph.D., Jörg Kreuzer, M.D., Jerrold H. Levy, M.D., Gordon Royle, M.D., Frank W. Sellke, M.D., Joachim Stangier, Ph.D., Thorsten Steiner, M.D., Peter Verhamme, M.D., Bushi Wang, Ph.D., Laura Young, M.D., and Jeffrey I. Weitz, M.D.

N Engl J Med 2017; 377:431-441August 3, 2017DOI: 10.1056/NEJMoa1707278

 

BACKGROUND
Idarucizumab, a monoclonal antibody fragment, was developed to reverse the anticoagulant effect of dabigatran.

METHODS
We performed a multicenter, prospective, open-label study to determine whether 5 g of intravenous idarucizumab would be able to reverse the anticoagulant effect of dabigatran in patients who had uncontrolled bleeding (group A) or were about to undergo an urgent procedure (group B). The primary end point was the maximum percentage reversal of the anticoagulant effect of dabigatran within 4 hours after the administration of idarucizumab, on the basis of the diluted thrombin time or ecarin clotting time. Secondary end points included the restoration of hemostasis and safety measures.

RESULTS
A total of 503 patients were enrolled: 301 in group A, and 202 in group B. The median maximum percentage reversal of dabigatran was 100% (95% confidence interval, 100 to 100), on the basis of either the diluted thrombin time or the ecarin clotting time. In group A, 137 patients (45.5%) presented with gastrointestinal bleeding and 98 (32.6%) presented with intracranial hemorrhage; among the patients who could be assessed, the median time to the cessation of bleeding was 2.5 hours. In group B, the median time to the initiation of the intended procedure was 1.6 hours; periprocedural hemostasis was assessed as normal in 93.4% of the patients, mildly abnormal in 5.1%, and moderately abnormal in 1.5%. At 90 days, thrombotic events had occurred in 6.3% of the patients in group A and in 7.4% in group B, and the mortality rate was 18.8% and 18.9%, respectively. There were no serious adverse safety signals.

CONCLUSIONS
In emergency situations, idarucizumab rapidly, durably, and safely reversed the anticoagulant effect of dabigatran. (Funded by Boehringer Ingelheim; RE-VERSE AD ClinicalTrials.gov number, NCT02104947.)

 

http://www.nejm.org/doi/full/10.1056/NEJMoa1707278

 


SJRHEM Journal Club Report

 

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