Category Archives: CQI

EM Reflections December 2020 – Pelvic Trauma

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Big thanks to Dr. Joanna Middleton for leading discussions this month.

All cases are theoretical, but highlight important discussion points.

Authored and Edited by Dr. Mandy Peach

Case

A 46 yo male is transported to the ED via EMS after sustaining multiple injuries in a motorcycle accident. He was helmeted and driving on a community street, he estimates at 70km/hr, when he hit a patch of water and hydroplaned off the road into a ditch. He was not ambulatory on scene and a bystander called EMS. On arrival in the trauma bay his vitals are: BP 100/62 HR 115 Sat 100% on NRB, T 37.2

You begin your primary survey. His airway is patent and he is speaking full sentences. He complains primarily of chest pain with breathing and pain in his hips and legs. His helmet was removed on scene by EMS and is in good condition. He was collared as a precaution. He has obvious bruising over the anterior chest, you suspect from hitting the handlebars, but normal chest rise bilaterally with breathing. He has decreased air entry bilaterally to the bases, PoCUS reveals normal lung slide. You move on to circulation. There is no sign of arterial bleeding. FAST exam shows negative RUQ and LUQ views, however it is indeterminate as the patient was placed in a pelvic binder on scene and you can’t visualize the pelvic views.

Do you remove the pelvic binder to access for pelvic injuries?

No – pelvic ring injuries can result in massive venous hemorrhage. This patient is hypotensive and tachycardic, given the mechanism a pelvic injury is quite likely – therefore removing the binder could stop any tamponade of vessels, leading to move blood loss and an unstable patient.

If a patient is externally hemorrhaging from a source thought to be under the binder than the binder can be transiently removed to control the bleeding1 .

You decide to leave the binder in place and get portable XRs as you work through your trauma survey. XR’s confirm a pelvic ring fracture – you suspect open book that has been ‘closed’ with the binder.

This patient has a pelvic injury, other than hemorrhage what other injuries/complications is this patient at risk of 2,7,8?

Intraabdominal: 16%
Rectal injury – considered open fracture
High risk of infection/sepsis if missed

Urologic injury: <5%
More common in men (10X more likely)
Consider in anterior pelvic fractures

Gynecologic injury (if patient were female): 2-4%
Vaginal injury – considered open fracture

Neurological: 10-15%
Sacral plexus injury
The worsening instability of fracture = higher neurological risk
Cauda equina

Thoracic aortic rupture: 1.4% in pelvic fracture compared to 0.3% in blunt trauma without pelvic fracture

Imagine this patient was dropped off at the door by his friends who lifted him in, instead of being assessed by EMS – what injuries on visual exam would be concerning for pelvic injury3?

Perineal/scrotal bruising or hematomas

Blood at the urinary meatus or vaginal introitus or rectum

Malrotation of the lower limbs

Is a DRE warranted in this patient? In every trauma patient 4?

Rectal exam changes the management in 1.2% of trauma cases.

3 situations where a rectal exam is warranted

Spinal cord injury to access for sacral sparing

Pelvic fracture to determine if fracture is open

Penetrating abdominal trauma to assess for gross blood.

*Consider vaginal exam if consider genital injury as well.

What would be a contraindication to foley insertion?

Concern for genitourinary injury5
– Blood at the urethral meatus
– Penile/scrotal ecchymosis
– Gross hematuria or
– Patient unable to urinate

If possible, insert foley before application of pelvic binder if no contraindications. But in the field foley insertion does not delay the application of a pelvic binder.

If you were concerned about pelvic injury do you want to confirm with XR before placing a binder4?

No – if any concern for pelvic injury bind immediately.
Consider foregoing the pelvic exam and just place the binder on spec if mechanism of injury is concerning for pelvic injury.

If I do examine the pelvis – what is the best approach 4?

Do not place outward pressure or assess for vertical instability
Do not rock the pelvis.
Apply an inward pressure of the iliac wings once to assess for any movement.

Movement felt? Hold that inward pressure and immediately apply a pelvic binder.

How do you place a binder6?
This video reviews both the use of a commercial binder and using a bedsheet if you’re in a ‘bind’.

Remember that the binder goes over the greater trochanters (even though it is called a ‘pelvic’ binder). You can also internally rotate the legs and tape them together at the ankles to decreased anatomic bleed space4

 

Now imagine you are working a peripheral ED and the patient can’t be transported immediately due to mass casualty event at the nearest trauma center. The patient has been stabilized and will likely be in your department for hours.

Other than vitals, monitoring of symptoms and PoCUS assessment, what else should be part of your reassessment for a patient in a pelvic binder?

“Circumferential compression provided by pelvic binders should be released every 12 hours to check skin integrity and provide wound care as required1”

The patient had pulmonary contusions and other superficial injuries on exam in additional to an unstable pelvic fracture. He went on to have a successful OR and recovery.

 

References & further reading:

  1. NB Trauma Program (2015). Consensus statement: Pelvic Binders. https://nbtrauma.ca/wp-content/uploads/2018/02/Consensus-Statement-Pelvic-Binders-December-2015.pdf
  2. Thomas (2016). Crackcast Ep 055: Pelvic Trauma. CanadiaEM https://canadiem.org/crackcast-e055-pelvic-trauma/
  3. Nickson (2020). Pelvic Trauma. Life in the fast lane. https://litfl.com/pelvic-trauma/
  4. Helman, A. Bosman, K. Hicks, C. Petrosoniak, A. Trauma – The First and Last 15 Minutes Part 2. Emergency Medicine Cases. January, 2019. https://emergencymedicinecases.com/trauma-first-last-15-minutes-part-2. Accessed Jan 12 2021.
  5. Lipp (2016). Genitourinary Trauma. https://canadiem.org/crackcast-e047-genitourinary-trauma/
  6. How to Apply a Pelvic Binder. CoreEM https://www.youtube.com/watch?v=tWLBZKeWEkg&ab_channel=CoreEM
  7. Fiechtl (2020). Pelvic trauma: Initial evaluation and management. Uptodate. Retrieved Jan 12, 2020.
  8. Li, P., Zhou, D., Fu, B. et al. Management and outcome of pelvic fracture associated with vaginal injuries: a retrospective study of 25 cases. BMC Musculoskelet Disord 20, 466 (2019). https://doi.org/10.1186/s12891-019-2839-y

Pelvic image from: Govaert, Geertje & Siriwardhane, Mehan & Hatzifotis, Michael & Malisano, Lawrence & Schuetz, Michael. (2012). Prevention of pelvic sepsis in major open pelviperineal injury. Injury. 43. 533-6. 10.1016/j.injury.2011.12.002.

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EM Reflections Nov 2020 – A Case of Atrial Fibrillation/Flutter

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Big thanks to Dr. Paul Page for leading discussions this month.

All cases are theoretical, but highlight important discussion points.

Authored and Edited by Dr. Mandy Peach

Reviewed by Dr. Kavish Chandra

Atrial fibrillation

• Review risk factors and complications
• Features of primary vs secondary arrythmia
• Risk stratifying a patient for stroke
• CHADS-65
• Sedation and cardioversion

Case

A 45 yo male presents to the ED feeling unwell for 2 days. He has a known history of atrial fibrillation but doesn’t consistently take rate control medications. He describes feeling like his heart is racing and he has trouble breathing that ‘comes and goes’. He currently complains of palpitations for 4 consecutive hours. He denies any chest pain or shortness of breath.
His vitals: BP 125/76, HR 134, RR 18, O2 98% RA, T 37.2
His ECG:

He appears to be in atrial flutter.

 

If this patient didn’t have a known history of arrhythmia, what are some risk factors for atrial fibrillation/flutter 1?

 

What are the life threatening complications with atrial fibrillation and their mechanisms?

Stroke – formation of clots in the atria secondary to blood stasis that embolize
Acute Coronary Syndrome – rapid rate decreases coronary blood flow
Pulmonary edema/heart failure – increased pulmonary arterial pressures secondary to increased afterload in atria2

The patient is brought in and attached to cardiorespiratory monitoring. The nurse applies pads and asks if you would like to immediately cardiovert.

 

What are the indications to immediately cardiovert a patient with any tachycardia? Does this patient require cardioversion?

Any sign of clinical instability:
• New severe hypotension (SBP < 90 mmHg) or signs of hypoperfusion
• Chest pain or ST depression > 2mm on ECG
• Acute heart failure2 – shortness of breath, hypoxia, clinical findings on exam

Your patient is experiencing palpitations, has a stable blood pressure and has no shortness of breath. He does not require cardioversion.

 

Is it common for atrial fibrillation to cause instability as the primary arrhythmia? What presentations make secondary arrhythmia more likely?

No – generally there will be a secondary cause for the arrhythmia that should be addressed.

The differential can include:
• ACS
• PE
• Heart failure
• Bleeding
• Sepsis3

Presentations that would make it more likely that this is a secondary cause with an underlying medical condition are:
• Insidious onset onset with no palpitations
• Known atrial fibrillation on previous ECGs and currently on anti-coagulation
• No history of cardioversion
• HR < 150
• Fever, shortness of breath, pain3.

On further history you discover that the patient has presented 2 previous times to the ED and required cardioversion. He has known atrial fibrillation and is on anticoagulation. His previous transthoracic echocardiogram does not indicate a valvular cause You screen him for multiple secondary causes and come up empty. You feel this is a primary arrhythmia.

 

What is one primary arrhythmia that causes instability that should be ruled out and why? What are the ECG features?

Atrial fibrillation/flutter + rapid ventricular pre-excitation (Wolff-Parkinson-White).

In WPW there is an accessory pathway that bypasses the AV node, causing early activation of the ventricles and leading to a tachyarrhythmia. Up to 20% of these patients can also have atrial fibrillation where there are multiple areas of the atria firing at different times as well. It is imperative to recognize this pattern as the use of AV blocking medications will cause more rapid conduction through the accessory pathway – leading to ventricular fibrillation or ventricular tachycardia.4

“Rate > 200 bpm

Irregular rhythm

Wide QRS complexes due to abnormal ventricular depolarization via accessory pathway

QRS Complexes change in shape and morphology

Axis remains stable unlike Polymorphic VT

Atrial Flutter results in the same features as AF in WPW except the rhythm is regular and may be mistaken for VT.”4

 

How do you control this patient’s heartrate?

The patient is stable, you have some time. First consider their risk of stroke.

LOW RISK 3
• onset < 48 hours AND no high risk factors OR
• On anticoagulation ≥ 3 weeks AND
• < 2 risk factors according to CHADS-65

HIGH RISK 3
• No anticoagulation/inadequate (< 3 weeks) AND
• Onset > 48 hours (or unknown) OR
• Onset < 24 hours but ≥ 2 risk factors according to CHADS-65 OR
• Stroke/TIA within 6 months OR
• Valvular heart disease

CHADS-65

You review with your patient and his CHADS-65 is 1 – he has history of hypertension. So based on the fact that he has been anticoagulated long term (and has been med compliant), his time with symptoms is 2 days with clear onset within 4 hours, and he scores < 2 on CHADS-65 you consider him LOW RISK.

LOW RISK

These patients can be treated with rhythm or rate control, however rhythm control is preferable in this population3. Their symptoms resolve immediately, they leave the ED faster and often happier as they don’t have to be admitted to hospital.

You discuss with the patient and decide to do a cardioversion as he is low risk, opting for rhythm control. He is agreeable.

 

What should I use to cardiovert – electricity or pharmacology?

Really either – it’s physician and patient dependent.

The RAF2 trial compared both electricity + pharmacology to electricity + placebo. Both were effective: procainamide followed by electricity had a 97% success rate in converting the patient to sinus rhythm, while the placebo infusion followed by shock was 93% effective. 97% of patients in the trial were discharged from the ED and on follow up 2 weeks later, 95% were still in sinus rhythm5.
Regardless of the method, rhythm control is a good option unless there is a patient preference.

Still not sure what to pick? Whatever worked in the past for the patient.

Our patient has previously had successful electrical cardioversion, so you decide to go with electricity.

You let the team know you will be proceeding with electrical cardioversion so they can prepare the room and patient. RT is on their way and the nurse is asking what drugs to draw up.

 

What are options for sedating a patient for electrical cardioversion? At what dose?

Many options – a systemic review in 2015 looked at studies including IV agents (ie. propofol and etomidate), inhaled agents (ie. Isoflurane) and benzodiazepines (ie. Midazolam) for electrical cardioversion. The primary outcome was adverse events: hypotension, apnea and patient awareness – unfortunately there is little high quality data available to suggest one drug over another6.

In a retrospective chart review from a Canadian ED the most common medications used were fentanyl, propofol, midazolam and ketamine in descending order. Practitioners primarily used combination drugs at that particular facility. The most commonly combined sedatives were propofol and fentanyl followed by midazolam and fentanyl. Adverse outcomes were rare overall. Apneic episodes were similar between these two combinations (both < 1%), as was hypotension (1.3% overall).7 Although a helpful study, this site had very few single agent sedatives, like ketamine, to compare to.

Here is a chart of suggested medications for procedural sedation for painful procedures like cardioversion 8:

 

 

Really it comes down to your comfort with your drug of choice. Even though adverse events seem to be rare, still consider the potential for increased risk of apnea and hypotension when combining sedatives and analgesia. 

You gather your team, give the plan with your drug of choice, consent the patient and complete an appropriate airway assessment. You are ready to begin.

 

Does pad placement matter?

No – anterior-lateral vs anterior-posterior placement is not deemed to be a critical factor in cardioversion for atrial fibrillation/flutter9

You successfully convert the patient to normal sinus rhythm. He is discharged from the department and advised to continue his anticoagulation (a NOAC) as previously prescribed.

 

What if this was a first presentation of atrial fibrillation – would he require anticoagulation for long term stroke prevention?

We go back to our CHADS-65. This patient had a score of 1.

If CHADS-65 positive : anticoagulation

If CHADS-65 negative: no anticoagulation

If CHADS-65 negative with stable CAD, PVD or aortic vascular disease – add ASA 81 mg3

According to the CCS guidelines for Atrial fibrillation anticoagulation is required for ALL patients undergoing cardioversion, regardless of risk factors, for 4 weeks.10 This is not based on strong evidence. Therefore,

 

Anticoagulation and the decision to start should involve shared decision making with the patient.

 

For details on rate control and treatment of high risk patients please see the CAEP Acute Atrial Fibrillation/Flutter Best Practices
Checklist

References and further reading:

  1. Cichon, C (2019). PIRATES illustration on twitter @DocScribbles
  2. Smarandache (2020. The Simple Guide to Management of Non-Valvular Atrial Fibrillation in the ED. CanadiaEM https://canadiem.org/the-simple-guide-to-management-of-non-valvular-atrial-fibrillation-in-the-ed/
  3. Stiell, Scheuermeyer, Vadeboncoeur, Angaran, Eagles, Graham et al. (2018). CAEP Acute Atrial Fibrillation/Flutter Best Practices Checklist. CJEM 20 (3): 334-342
  4. Burns (2020). Pre-excitation syndromes. Life in the fast lane. https://litfl.com/pre-excitation-syndromes-ecg-library/. Accessed Dec 9, 2020.
  5. Helman, A. Swaminathan, A. Juurlink, D. Long, B. Stiell, I. Morgenstern, J. Klaiman, M. Lloyd, T. EM Quick Hits 7 – Status Epilepticus, Codeine Interactions, Anticoagulants in Malignancy, Atrial Fibrillation rate vs rhythm control, Peripheral Vasopressors, Motivational Interviewing. Emergency Medicine Cases. August, 2019. https://emergencymedicinecases.com/em-quick-hits-august-2019/. Accessed Dec 9, 2020].
  6. Lewis, Nicholson, Reed, Kenth, Alderson & Smith (2015). Anaesthetic and sedative agents used for electrical cardioversion (review) Cochrane Database of Systematic Reviews , Issue 3. Art. No.: CD010824
    https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD010824.pub2/epdf/full
  7. Campbell, Magee, Kovacs, Petrie, Tallon, McKinley et al. (2006). Procedural sedation and analgesia in a Canadian adult tertiary care emergency department: a case series. Can J Emerg Med ;8(2):85-93
  8. Scheirer (2018). Procedural Sedation and Analgesia. CanadiaEM https://canadiem.org/crackcast-e195-procedural-sedation-and-analgesia/
  9. Kirkland, Stiell, AlShawabkeh, Campbell, Dickinson & Rowe (2014). The efficacy of pad placement for electrical cardioversion of atrial fibrillation/flutter: a systematic review. Acad Emerg Med Jul;21(7):717-26
  10. Andrade, Verma, Mitchell, Parkash, Leblanc, Atzema & al. (2018) Management of Atrial Fibrillation: Complete CCS Guidelines Listing. Canadian Cardiovascular Society. https://www.ccs.ca/images/Guidelines/Guidelines_POS_Library/2018%20AF%20Update_Supplement_Final.pdf

 

 

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EM Reflections Nov 2020 – Chest pain; expand the differential!

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Authored and Edited by Dr. Mandy Peach

 

Big thanks to Dr. Paul Page for leading the discussions in November.

All cases are imaginary, but highlight learning points that have been identified as potential issues during rounds.

Chest pain is a huge topic – this is not a deep dive, but hopefully a helpful review of some useful information for on shift. This post assumes a basic knowledge of bedside ultrasound.

Chest Pain

  • The ‘don’t miss’ diagnoses
  • The ultrasound findings that can be helpful in shortening the differential
  • The evidence for ultrasound in some chest pain diagnoses
  • Select decision rules in chest pain
  • D-dimer and troponin and their uses
  • Ultrasound findings of cholecystitis

Case

48 yo male presents to the ED with 4 hours of substernal CP. He describes the pain as sudden onset and waking him from sleep overnight. He feels sweaty and has had 2 episodes of nausea/vomiting. He denies any fever or diarrhea. He had a similar episode last week that spontaneously resolved after 3-4 hours. He has no history of exertional chest pain. His cardiac risk factors include hypertension and his father died of ‘heart problems’ in his late 60’s.

An ECG is completed:

On exam his vital signs are within normal limits. He appears slightly diaphoretic and uncomfortable. Cardiorespiratory exam is unremarkable.

 

What are the BIG can’t miss diagnoses for chest pain? What bedside tool can be helpful in diagnosing some of these conditions?

Acute Myocardial Infarction (MI)

Pulmonary Embolism (PE)

Tension Pneumothorax

Aortic Dissection

Cardiac Tamponade

Esophageal Rupture

 

The ECG is unremarkable for ischemic change. You order a cardiac work up, including a CXR. While you await these results, you reach for your nearest ultrasound probe. You perform a cardiac and lung scan:

Figure 1 – normal subxiphoid view of the heart

Figure 2: Normal lung slide with visible A lines

You do not see any large pericardial effusion and on an eyeball observation the heart appears to have grossly normal form and function. The lung scan appears unremarkable with no sign of pneumothorax after viewing multiple rib spaces anteriorly and laterally.

 

How accurate is ultrasound at helping you rule in/out some of the major chest pain diagnoses?

Cardiac tamponade – Trained emergency physicians using beside ultrasound are quite effective at identifying significant pericardial effusions with a sensitivity of 96% and specificity of 98%1.

Figure 3: Large pericardial effusion with collapsing of RV

 

Pneumothorax – Lack of lung sliding and comet tails has a specificity of over 90% in ruling in pneumothorax. Time constraints? 1 view has comparable sensitivity to 4 views in picking up a clinically significant pneumothorax2

Figure 4: Absence of lung sliding or comet tails indicating pneumothorax

 

Pulmonary Embolism – Although no one finding is pathognomonic for PE, signs of RV dysfunction in the right clinical context is certainly suggestive of acute PE. Findings of:

  • RV enlargement equal or greater to that of the LV
  • RV systolic dysfunction (RV free wall hypokinesis) or
  • bowing of the RV into LV

have a 99% specificity for PE3.

Figure 5: Enlarged RV with free wall hypokinesis at the apex (McConnell’s sign)

Figure 6: Bowing of RV into LV in parasternal short view “D sign”

For advanced scanners, in patients with abnormal vitals (tachycardiac and hypotensive):

  • normal TAPSE
  • normal RV size
  • absence of RV flattening
  • absence of McConnell’s sign

significantly decreases the post-test probability for PE4

 

Aortic dissection – very specific findings – if you see a dissection flap you found it! If not, it’s still a high risk diagnosis you wouldn’t want to miss. There is evidence that when getting advanced cardiac views, suprasternal notch views and visualizing the abdominal aorta the sensitivity of POCUS is 86%5, however this did not translate into mortality benefit and is likely of more benefit for advanced scanners.

 

With normal vitals and ultrasound findings you feel confident there is no pneumothorax or tamponade. The probability of PE seems quite low given the history. Is there an objective way to risk stratify your patient for PE risk?

 

Apply the PERC rule 6 in the targeted low risk patients like this one where your physician gestalt of likelihood of PE < 15% . In the appropriate population this tool has a sensitivity of 96%;

The probability of him having a PE is < 2%.

 

You revisit the history and physical exam keeping in mind your remaining diagnoses of aortic dissection and esophageal rupture.

Are there any tools I can use to help decide if my patient is high risk for aortic dissection?

This tool is for low-moderate risk patients where dissection is in the differential.  When this rule was applied to a retrospective population only 4% of dissections were missed. When adding a normal CXR the miss rate decreased to 2.7%. Each feature equals 1 point. Essentially the absence of any high risk feature essentially rules out aortic dissection7. If more than 1 high risk feature, proceed to CT-A. If ≤ 1 this tool suggest ordering d-dimer.

Does d-dimer help rule out aortic dissection?

It’s controversial. If your patient is low risk and dissection isn’t high on your differential, a normal d-dimer doesn’t really add any value. If you order anyways and it is positive, it may lead to unnecessary testing. It certainly should not be used in isolation. The above tool combined with d-dimer had a sensitivity of 98.8% in one study, however this has not been externally validated8 – proceed with caution.

Your patient has no high risk features for aortic dissection.

 

Your patient did have episodes of vomiting – could they have a ruptured esophagus (Boerhaave syndrome)?

Mackler’s triad – vomiting, chest pain and subcutaneous emphysema – is present in 14-25% of cases so certainly not reliable. Patients can present with mediastinitis and abnormal vitals.9 CXR findings include 10:

With a normal CXR and normal vitals this is less likely.

 

So, you’ve considered the major diagnoses for chest pain and cardiac ischemia is left to consider – your first troponin result just become available – it is within normal range.

 

Can you use a single troponin to rule out a cardiac event?

You are now 4 hours from the onset of the event. Over his visit you have ordered a second ECG which is also normal. The troponin is  normal – you feel more reassured.  But your patient does have some risk factors for cardiac disease. You need to decide how at risk your patient is. You use the HEART score 11to help stratify:

Your calculated heart score is 3 which is low risk.

“A single undetectable hs-troponin after 3 hours of symptom onset or a delta 2-hr hs-troponin T <4ng/L plus normal serial ECGs and a HEART score of 0-3 rules out acute MI and lowers 30-day MACE to well below 1%, a threshold below which ancillary testing may cause more harm than benefit12.”

You feel quite confident your patient has no acute life-threatening cause of chest pain. You settle the pain and nausea in the ED and feel his is safe to go home. You suspect gastritis.

3 days later on shift you recognize the same patient – he again is complaining of chest pain, but today he looks much worst. You grab his chart – he is mildly tachycardiac, but otherwise vitals are normal. ECG again looks normal.
Today the patient describes having worsening nausea, fatigue and chest pain. His pain is more persistent and is not relieved with OTC medication at home. When you ask him to point to the pain he points towards his epigastric area – not substernal as he previously complained of.

This visit you complete an abdominal exam and find significant RUQ tenderness.

 

What are some other causes of chest pain, that although not immediately life threatening, should be considered13?

 

You grab your ultrasound probe as you suspect cholecystitis, what are the ultrasound findings?

Thickened gb wall > 3.5mm and fluid surrounding the gallbladder as seen above14.

You confirm cholecystitis and consult surgical service. On formal imaging the radiologist is concerned for potential perforation of the gallbladder.

Bottom line – chest pain has a broad differential! Grab your ultrasound probe and use some evidence based tools to help narrow your differential. Once life threatening causes ruled out consider other causes that can still affect patient morbidity.

 

References and further reading:

  1. Mandavia, Hoffner, Mahaney, Henderson (2001). Bedside echocardiography by emergency physicians. Annals of Emergency Medicine, Vol 38 (4); 377-382
  2. Michael Prats, MD. Comparison of Four Views Versus Single View for Pneumothorax. Ultrasound G.E.L. Podcast Blog. Published on November 07, 2016. Accessed on December 07, 2020. Available at https://www.ultrasoundgel.org/6.
  3. Pulmonary Embolism. The Evidence Atlas, The POCUS Atlas https://www.thepocusatlas.com/ea-echo
  4. Michael Prats. Focused Echo for Pulmonary Embolism in Patients with Abnormal Vital Signs. Ultrasound G.E.L. Podcast Blog. Published on February 17, 2020. Accessed on December 07, 2020. Available at https://www.ultrasoundgel.org/86.https://www.ultrasoundgel.org/posts/KsPSovvURE1CN7eZYELz1w
  5. Michael Prats. Return of the Aortic Dissection – POCUS Accuracy and Time. Ultrasound G.E.L. Podcast Blog. Published on August 31, 2020. Accessed on December 05, 2020. Available at https://www.ultrasoundgel.org/97.
  6. https://www.mdcalc.com/perc-rule-pulmonary-embolism
  7. Ohle, McIsaac, Atkinson (2019). How do I rule out aortic dissection? Just the Facts. CJEM 21(2): 34-36
  8. Nazerian, Mueller, Soeiro, Leidel, Salvadeo, Giachino et al. (2017). Diagnostic Accuracy of the Aortic Dissection Detection Risk Score Plus D-Dimer for Acute Aortic Syndromes: The ADvISED Prospective Multicenter Study. Circulation 137 (3): 250-258
  9. Cadogan, M. Boerhaave syndrome. Life in the Fast Lane. Published on Nov 3, 2020. https://litfl.com/boerhaave-syndrome/
  10. Diaz, G (2018). Boerhaaeve Syndrome. https://www.grepmed.com/images/5441/diagnosis-boerhaave-syndrome-signs
  11. Heart Score https://www.heartscore.nl/
  12. Low Risk Chest Pain and High Sensitivity Troponin – A Paradigm Shift. EM Cases. Published July 30, 2019. https://emergencymedicinecases.com/low-risk-chest-pain-high-sensitivity-troponin/
  13. Chest Pain. CanadiEM. Published June 1, 2020. https://canadiem.org/crackcast-e214-chest-pain/
  14. Flemming, Lewis, Henneberry. PoCUS – Measurements and Quick Reference. SJRHEM. Published 2017. https://sjrhem.ca/pocus-measurements-quick-reference/

All ultrasound gifs from The PoCUS Atlas https://www.thepocusatlas.com/

 

 

 

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EM Reflections October 2020 – Spinal Cord Injury

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Big thanks to Dr. Joanna Middleton for leading the discussions in October

All cases are imaginary, but highlight learning points that have been identified as potential issues during rounds.

Edited by Dr. Mandy Peach

Spinal Cord Injury

  • Recognition of various patterns of spinal cord injury
  • Reviewing EMS record can be helpful for progression of symptoms and baseline exam
  • A normal CT does not rule out spinal cord injury in a patient with neurological deficits
  • Importance of detailed neurological exam and clear communication with consultant
  • Importance of clear documentation of exam – consider using ASIA

Case

A 72 yo female presents complaining of bilateral arm weakness ongoing for 1 day. She has no other symptoms concerning for stroke. She denies any direct trauma to head or neck, but did say she was pushed from behind by a large dog and her neck ‘snapped back’ the day prior. Incidentally she says she also hasn’t urinated in over 8 hours. Her vital signs are within normal limits.

 

You are concerned about a spinal cord injury – what are the various cord syndromes? What in the history predisposes to a particular spinal cord syndrome?

4 Classification of spinal cord syndromes

This woman is elderly, likely with underlying cervical spondylosis, and has a hyperextension injury – predisposing her to a central cord syndrome. This is the most common type of incomplete spinal cord injury. Often these patients are asymptomatic from their spondylosis before the event and the mechanism of injury is usually not severe5.

Central cord syndrome involves both motor and sensory pathways and has a variable presentation. Typically one sees motor weakness in the hands and forearms with sensory preservation. Bladder dysfunction and sexual dysfunction can be seen in severe cases5. A helpful mnemonic is MUD-E6.

 

MUD-E

  • Motor loss > sensory loss
  • UE > LE
  • Distal > proximal
  • Extension type injury

 

You complete a detailed neurological exam and find she does have upper limb weakness distally. A bladder scan confirms urinary retention with 850 cc of urine in her bladder.

You decide to order a CT C -spine to assess for bony injuries. The CT scan is unremarkable.

Does this rule out a spinal cord injury in this patient?

No – normal CT does not rule out SCI in a patient with ongoing neurological deficits. In fact, in elderly patients there is often no bony injury, but the narrowed spinal canal can predispose to buckling of the ligament flava, leading to injury of the spinal cord.

You review EMS notes and nursing documentation – there are subtle differences throughout in how the exam is performed and recorded.

What is one tool that can improve your documentation in terms of accuracy and clarity?

ASIA (American Spinal Injury Association) Classification

You document your findings on ASIA, which allows for clearer communication and documentation with the attending neurosurgeon.

 

References for further reading:

4 Perron & Huff (2010). Chapter 104 Spinal Cord Disorders. Rosen’s Emergency Medicine: Concepts and Clinical Practice. pp 1389-1397. Philadephia, PA

5  Douglas, Nowak et al. (2009). Review article: Central Cord Syndrome. Journal of the American Academy of Orthopedic Surgeons. 17: 756-765

6 A boring guide to spinal cord syndromes. CanadiamEM. https://canadiem.org/a-boring-guide-to-spinal-cord-syndromes/

 

Authored and Edited by Dr. Mandy Peach

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EM Reflections October 2020 – Acute Urinary Retention

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Big thanks to Dr. Joanna Middleton for leading the discussions in October

All cases are imaginary, but highlight learning points that have been identified as potential issues during rounds.

Edited by Dr. Mandy Peach

 

Acute Urinary Retention (AUR)

  • Categorized as obstructive, infectious/inflammatory, neurological, medication related
  • Physical exam should include a DRE and neurological exam
  • Investigations should include a U/A +/- C&S, creatinine, electrolytes +/- CBC
  • Consider a renal US if any renal impairment
  • PSA – defer at least 2 weeks, as acute urinary retention can cause elevation
  • Consider risk factors for post-obstructive diuresis

Case

A 60 yo male presents to the emergency department with inability to void over 8 hours, despite feeling urgency. He complains of increasing lower abdominal discomfort. He denies any infectious symptoms or new medications. He denies any back pain or recent injury. He does have a history of hesitancy and poor urine stream. He has never had a prostate exam and has no family doctor. His vital signs are within normal limits. He has a significantly distended bladder on physical exam.

Indications to insert a catheter1:

  • Inability to pass urine > 10 hours
  • Abdominal discomfort with bladder distention
  • Signs of acute kidney injury secondary to obstruction
  • Infectious cause of retention
  • Overflow incontinence

You decide to insert a urinary catheter. What else should you consider as part of your physical exam?

Consider the 4 main causes of urinary retention:

In this male patient it is pertinent to do a prostate exam to check for enlargement as well as a thorough neurological exam.

On exam you palpate a large, firm prostate. You are suspicious of prostate cancer – do you do a prostate specific antigen (PSA)?

No – acute urinary retention can transiently elevate PSA measurements up to 2 fold, this can persist for up to 2 weeks2. Defer PSA testing until after this time.

The U/A is negative for infection. The electrolytes are normal but the patient has an acute AKI with an elevated creatinine. Does this patient require renal imaging?

Consider renal imaging in any patient with AUR and abnormal renal function to assess for anatomical cause.

2 hours has passed and you reassess the patient – 1L of urine has drained upon insertion. A minimal amount has been draining since. The post-void residual is now 20 cc.

Is this patient at risk of post-obstructive diuresis?

Risk factors:

  • Abnormal electrolytes or acute creatinine elevation
  • Volume overload
  • Uremic
  • Acutely confused

Although the patient does have an abnormal creatinine, clinically he does not show signs of post-obstructive diuresis which is defined as urinary output > 200 mL for at least 2 hours after urethral catheter insertion, or > 3L in 24hrs AFTER the initial emptying of the bladder. Patients with any risk factors for post-obstructive diuresis should be observed in the ED for 4 hours.

After an appropriate observation period you discharge the patient with an urgent referral to urology given the acute presentation and abnormal prostate exam. You are sending the patient home with an indwelling catheter.

What is the optimum duration of catheter insertion? Does this patient require antibiotics?

Trials are contradictory. Some found increased likelihood of spontaneous voiding after 7 days, while an observational study found improved success if insertion was less than 3 days3.

Expert opinion from urology suggests duration of 7 days to avoid risk of re-catheterization1.

Routine antibiotics are not recommended unless the cause is thought to be infectious. However, if prostatic enlargement is thought to be the cause an alpha-blocker like tamsulosin can be beneficial1

 

 

References for further reading:

1 Ep 143 Priapism and Urinary Retention: Nuances in Management. Emergency Medicine Cases. https://emergencymedicinecases.com/priapism-urinary-retention/

2 Aliasgari, Soleimani, Moghaddam (2005).The effect of acute urinary retention on serum prostate-specific antigen level. Urology journal. Spring 2005;2(2):89-92

3 Acute Urinary Retention. Uptodate. https://www.uptodate.com/contents/acute-urinary-retention?search=post%20obstructive%20diuresis&source=search_result&selectedTitle=1~5&usage_type=default&display_rank=1#H537553020

 

Authored and Edited by Dr. Mandy Peach

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Trauma Reflections – October 2020

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Big thanks to Sue Benjamin for her efforts in putting these reviews together!

 

Major points of interest:

 

A) Kudos – Trauma Codes for qualifying cases has improved!

May – September 2020, for cases qualifying for trauma team activation, the rate of calling ‘Trauma Codes’ has improved to 84%. RN trauma note is 93% for the activations.

Many of the missed activations are transfers from peripheral sites

 Please review the attached updated simplified activation criteria – notable changes are:

1/ Removal of minor head injuries without signs or symptoms on anticoagulants under “D”

2/ Addition of pulseless extremity under “C”

 

B) Chest Tubes in trauma – 5 year review

Chest tubes are placed infrequently (~ 1 per month) in our departments.

Review of post procedure x-rays (thanks J ‘Mek1’) showed there was less than optimal tube positioning 60% of the time.

Tube position and function must be critically reviewed post procedure.

Chest tube discussion/demonstration with Dr Russell will take place at next Trauma case review  (January 2021)

C) Oh, that patient is just here for Plastics..

‘Distracting’ injuries are called that for a reason. It is hard to look past deformed limbs, but always perform a head to toe assessment (including FAST) to identify associated injuries to others systems.

Trauma transfers should be re-assessed by ED physician at receiving hospital, to also determine if there are any other concerning injuries that have been missed.

Trauma cases being transferred to consultants, outside of NB trauma line, should be identified by charge MD when taking report.

 

D) “Penetrating neck trauma is en route”

Those words will wake you up in a hurry.

Keys to management are early notification (pre-arrival) of consultants (ENT +/- vascular) and clear airway plans that include a ‘double set’ up for potential need for surgical airway.

 

E) What kind of monster would order a ‘Panscan’ on a child? 

One that can weigh the risks (missed injuries) vs. benefits (minimizing radiation exposure).

Panscans in pediatric patients should never be ordered routinely, but should be considered in cases with high risk for clinically significant multi-system injuries (head, spine, thorax, abdomen).

 

F) Blunt traumatic cardiac arrest

This population has a grave prognosis.

Airway management, continuous chest compressions, rapid fluid/blood resuscitation and consideration for procedural interventions (thoracostomies, pericardiocentesis) are usual steps in care.

Epinephrine has no role unless medical cause for arrest is suspected.

A more in-depth review will be topic of upcoming SJRH ED rounds.

 

G) What did this guy have for supper?

Pizza and beer, and lots of it.

Ducanto catheters – large bore suction catheters – are available on all airway carts in the top drawer. They are much more efficient at decontaminating airways soiled with semi-solid material when compared to Yankauer.

 

H) Updated Trauma checklist:

“SJRH ED Trauma Process Checklist” is in trauma note package in room 19 and is a very useful prompt (see below). K/ T- L spine Traumatic Spine Injury Guidelines also below.

Download (PDF, 98KB)

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EM Reflections – September 2020

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Thanks to Dr. Paul Page for leading the discussions this month

All cases in this series are imaginary, but highlight learning points that have been identified as potential issues during rounds

Edited by Dr David Lewis 

Discussion Topics

  1. Incomplete Abortion

    • Unstable patients require staff to staff direct communication. OBGYN staff are always in house.
    • Patients remain responsibility of EM attending staff during and after consult. Transfer of care occurs at admission.
    • Be aware of the pitfalls of handover and possible need to reassess patient depending on clinical situation

  2. Cardiac Arrest – Pulmonary Embolism

    • Be aware of bias when seen patient in low acuity area
    • Alway consider and document a ‘top 3’ differential diagnosis
    • CPR must be extended after thrombolysis for suspected / confirmed PE
    • Consider following a standardized VTE pathway

 

Incomplete Abortion

Case

A 30yr old female presents with a profuse PV bleeding. She is 7 weeks pregnant by dates. She presents with abdominal pain, palor and is hypotensive and tachycardic. During fluid resuscitation, PV exam confirms the presence of blood and clots, the os is open and contains tissue. This is removed. The bleeding appears to stop. CBC identifies a low hemoglobin. The patient is transfused. What are the potential pitfalls in the management of this case?

 

Threatened abortion

Bleeding before 20 weeks’ gestation in the presence of an embryo with cardiac activity and closed cervix

Spontaneous abortion

Spontaneous loss of a pregnancy before 20 weeks’ gestation

 Complete abortion

Complete passage of all products of conception

 Incomplete abortion

Occurs when some, but not all, of the products of conception have passed

 Inevitable abortion

Bleeding in the presence of a dilated cervix; indicates that passage of the conceptus is unavoidable

 Septic abortion

Incomplete abortion associated with ascending infection of the endometrium, parametrium, adnexa, or peritoneum

 

First Trimester Bleeding – American Family Physician

Patient Information Leaflet

 

Management of Unstable Patients with 1st Trimester Bleeding

  • Urgent Consult to OBGYN
  • Management is similar to all unstable bleeding patients (resus room, monitors, vascular access, IV fluid +/- unmatched O neg blood, foley).
  • Investigate for DIC.
  • Tranexamic acid (1g IV) +/- oxytocin (40U by IV in 1L NS at 150cc/hour) can be given to slow bleeding before definitive management (in the OR).
  • **In an unstable patient with massive vaginal bleeding, a pelvic exam is indicated to identify a source and to look for and extract tissue found in the cervix.**
  • Any unstable patient who presents with 1st trimester bleeding and requires blood transfusion should be admitted, even if they stop bleeding in ED and the low Hb is corrected. There is potential for rebleed over next 24 hrs especially if products are retained.

Episode 23: Vaginal Bleeding in Early Pregnancy

Further Reading:

CanadiEM Frontline Primer – Early Pregnancy – First Trimester Bleeding

 

 

 

Cardiac Arrest – Pulmonary Embolism

Case

A 68 yr old male is brought into the emergency department with chest pain and shortness of breath. The patient is diaphoretic and hypotensive. They report a 5 day history of progressive leg swelling prior to these new symptoms. During the initial assessment the patients has a cardiorespiratory arrest. What is the differential diagnosis? What is the management of cardiac arrest when PE is suspected

 

A retrospective study published in Arch Intern Med  – May 2000, found that PE was found as the cause in 60 (4.8%) of 1246 cardiac arrest victims over an 8 year period.The initial rhythm diagnosis was pulseless electrical activity in 38 (63%), asystole in 19 (32%), and ventricular fibrillation in 3 (5%) of the patients. Thrombolysis resulted in significantly higher rate of ROSC, however survival to discharge was very low.

Diagnosis of PE in cases of cardiac arrest is often difficult to establish. Clinical suspicion of PE as a cause of cardiac arrest remains the key in timely diagnosis and treatment. In this study sudden dyspnea and syncope were the most suggestive reported symptoms. Deep vein thrombosis is known to be an important risk factor for PE, but clinical signs of deep vein thrombosis are rare and nonspecific. Right bundle-branch block was present in 67% of these cases, and this should induce a high suspicion for massive PE as cause of cardiac arrest. The authors recommend either transthoracic or transesophageal echocardiography be performed at the bedside in all cases to help establish the diagnosis of PE as the cause of a cardiac arrest.

 

 

Management of Cardiac Arrest in Suspected PE

  1. Commence CPR and follow the ACLS 2018 Algorithm
  2. Suspicion for PE as cause of cardiac arrest?
  3. Bedside Assessment to Increase Suspicion of PE as cause of cardiac arrest
  4. Thrombolysis
  5. VA ECMO + Interventional Radiology / Cardiovascular Surgery

1.  Commence CPR and follow the ACLS 2018 Algorithm

AHA ACLS 2018 Algorithms –  Update Highlights

2.  Suspicion for PE as cause of cardiac arrest?

  • Sudden onset dyspnoea or syncope prior to cardiac arrest
  • Right ventricular strain, new RBBB or other PE suggestive findings on ECG immediately prior to cardiac arrest
  • Initial non-shockable rhythm
  • History of immobilization prior to cardiac arrest (recent surgery, travel, injury)
  • History of thromboembolism
  • History of recent cancer diagnosis and treatment
  • Known hypercoagulation condition (e.g. Factor V Leiden)
  • No history of cardiac disease
  • Age less than 50yrs
  • Female
  • Pregnancy or Birth Control
  • Clinical signs of recent DVT (swollen leg, history of swollen/painful leg)

Improving identification of pulmonary embolism-related out-of-hospital cardiac arrest to optimize thrombolytic therapy during resuscitation

3.  Bedside Assessment to increase likelihood of PE as cause of cardiac arrest

  • Clinical exam for signs of DVT
  • Clinical assessment to exclude other reversible causes of cardiac arrest (5H’s and 5T’s)
  • DVT PoCUS
  • Transthoracic Echo PoCUS – RV dilatation, TV regurge, visible clot, dilated IVC (must not delay CPR)
  • Transesophageal Echo PoCUS – RV dilatation, TV regurge, visible clot, dilated IVC (superior images, does not interfere with CPR)

 

4.  Thrombolysis

An retrospective study published in Chest in 2019 analysed thrombolysis in PE related out-of-hospital-cardiac arrest. They found that thrombolysis was associated with increased 30 day survival but that a good neurological outcome was rare and not significantly improved. This 2019 systematic review and meta-analysis concluded that systematic thrombolysis during CPR did not improve hospital discharge rate.

Despite a weak evidence base, both the European Resuscitation Council (ERC) as well as the American Heart Association (AHA) have recommend the use of fibrinolytic therapy when PE is either known or suspected as the cause of cardiac arrest.

AHA Recommendations – in refractory cardiac arrest where PE has either been confirmed or is suspected, thrombolysis is a reasonable emergency treatment option:

  • Alteplase 50mg peripheral IV bolus
  • Option to repeat the bolus at 15 mins
  • Continue CPR for 30-60 minutes after lytic administration

EMCrit 261 – Thrombolysis during Cardiac Arrest

 

5.  VA ECMO + Interventional Radiology / Cardiovascular Surgery

Interventional and surgical procedures cannot be performed during CPR.

Several studies have concluded that ECMO can be beneficial in patients with PE related cardiac arrest

Extracorporeal membrane oxygenation in life-threatening massive pulmonary embolism

Use of extracorporeal membrane oxygenation in patients with acute high-risk pulmonary embolism: a case series with literature review

Resuscitation of prolonged cardiac arrest from massive pulmonary embolism by extracorporeal membrane oxygenation

Massive Pulmonary Embolism as a Cause of Cardiac Arrest: Navigating Unknowns in Life After Death

 

The consensus seems to be that in order to see benefit from the use of ECMO to bridge patients with massive PE / cardiac arrest a protocolized approach is required, including a standby ECMO team and predetermined pathways.

 

Further Reading

Submassive & Massive PE

 

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Trauma Reflections – June 2020

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Thanks to Dr. Andrew Lohoar and Sue Benjamin for leading the discussions this month

 

Major points of interest:

 

A) How are we doing with calling Trauma Codes for qualifying cases?

In the past year, for cases qualifying for trauma team activation, the rate of calling ‘Trauma Codes’ has fallen to 66%.

If a Trauma Code was called, RN trauma note use increased to 85% and time to disposition to an ICE setting was significantly decreased.

 

Please review the attached updated simplified activation criteria – notable changes are:

  • Removal of minor head injuries without signs or symptoms on anticoagulants under “D”
  • Addition of pulseless extremity under “C”

B) ECMO in trauma

MVC victim survived after being submerged x 20 minutes – CPR (with LUCAS) and then managed further with ECMO.

Key to successful outcome will be EARLY recognition of cases that may benefit and early alert/consultation with CV surgery.

Best evidence for ECMO is for re-warming severe hypothermic patients.

 

 C) Significant MOI + spine pain = CT

Obtaining spine x-rays in cases with moderate probability of bony injury inevitably leads to another trip down the long hallway to visit our diagnostic imaging colleagues (and delay to definitive diagnosis).

If your patient needs a CT, order a CT.

See attached consensus guideline.

D) Pelvic binders are not used to ‘treat’ the pelvic fracture

They are used to treat any hemodynamic instability caused by the fracture. If a patient is stable or has a pelvic fracture that is not likely causing significant bleeding, the binder can likely be loosened or removed.

A pelvic binder can exacerbate some fractures, such as lateral compression fractures. Orthopedics should be assisting with this decision.

 

E) That intubated transfer patient just waved at me!

There is a reason trauma transfers should be assessed on arrival.

Consultants are expected to attend to these patients ASAP, but timely review by emergency MD is expected to assess/treat priorities (ventilatory status, analgesia need, sedation etc.)

 

F) The patient is on warfarin…how quaint!

Do you remember when anticoagulants could be reversed? In the event you do meet a trauma patient on warfarin, early correct dosing of vitamin K and PCC may be crucial.

Review of such charts in past 2 years has our dosing all over the map.

Easy dosing regime is:

 

Vitamin K – 10mg IV and PCC – 2000IU if INR unknown,

If INR known: PCC – 3000IU if INR > 5, PCC – 2000IU if INR 3-5, PCC – 1000 if INR < 3.

 

G) Trauma checklist:

“SJRH ED Trauma Process Checklist” is in trauma note package in room 19 and is a very useful prompt (see below).

H/ High MOI Knee injuries are at risk for deterioration in department

Vascular status may change, compartment syndrome may develop.

Consider repeating physical exams, early orthopedic consultation and low threshold for CT with vascular studies.

 

I/ Where is this guy bleeding?

Maybe he isn’t. Failure to respond to resuscitation suggests continued hemorrhage or non-hemorrhagic cause for shock. With neurogenic shock, loss of sympathetic tone may cause hypotension without tachycardia or vasoconstriction.

Consideration should be made to start vasopressors in patients with spinal cord injury with persistent hypotension after attempted resuscitation and no evidence of hemorrhagic shock. Aim for a SBP of 90-100. Avoid overzealous fluid administration.

 

J/ NB Trauma Traumatic Brain Injury Consensus statement – May 2020

See attached

Download (PDF, 1.32MB)

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EM Reflections – June 2020

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Thanks to Dr Joanna Middleton for leading the discussions this month

Edited by Dr David Lewis 

Discussion Topics

  1. Antiviral Toxicity

    • Always adjust dosing in patients with renal impairment

  2. Necrotising Fasciitis

    • Difficult clinical diagnosis
    • Should be on the differential for all soft tissue infections
    • Delayed definitive care always results in poor outcomes

  3. Epidural Abscess

    • Thorough detailed neurological examination required
    • Isolated leg weakness is rare in Stroke
    • Progressive development of symproms and mixed UMN/LMN signs suggests spinal cord compression.

 

Antiviral Toxicity

Case

A 70yr old male presents with a typical zoster rash in the left L1 dermatome. He has a past medical history of chronic renal insufficiency. He is started on Valacyclovir 1000mg TID. He represents 3 days later with hallucinations including a feeling that he was occupying a dead body. What is the differential diagnosis?

 

Varicella Zoster Encephalitis vs Valacyclovir Toxicity

VZV and antiviral toxicity can present with similar symptoms

Two main risk factors increase the risk for VZV

  • age greater than 50 years old
  • immunocompromised due to reduced T cell-mediated immunity

The main risk factor for antiviral toxicity is renal insufficiency

Differentiation

  • Timing
    • Toxicity presents within 1-3 days of starting drug (vs 1-2 weeks)

 

  • Symptoms – both can present with confusion and altered LOC
    • Encephalitis – fever, HA, seizures, more likely with Trigeminal nerve (V1) or disseminated zoster
    • Toxicity – Visual hallucinations, dysphasia, tremor/myoclonus
    • Toxicity – Cotard’s syndrome…

Cotard’s Syndrome

“le délire des négations”

(delirium of negation)

https://en.wikipedia.org/wiki/Cotard_delusion

  • Described in 1880 by neurologist Jules Cotard
    • “patient usually denies their own existence, the existence of a certain body part, or the existence of a portion of their body”
  • Seen in schizophrenia, psychosis and…
  • ….acyclovir toxicity (felt to be due to metabolite CMMB (9-carboxymethoxymethylguanine) crossing BBB)

Further Reading

Varicella Zoster Encephalitis case report and outline

Valacyclovir Toxicity case report and outline

Cotard’s Syndrome

Drug Dosing in Chronic Kidney Disease

 

 

 

Necrotising Soft Tissue Infections (NSTI)

Case

A 28yr old female presents pain, redness and swelling over the right thigh. She has a past medical history of type 2 diabetes. She is managed as an outpatient with intravenous ceftriaxone q24hrs. Her symptoms failed to respond on follow up. What is the concern now? Are there any red flags? What condition needs to be considered in patients with soft tissue infections that fail to respond to antibiotics?

NSTI first described by Hippocrates 5th century BC

“[m]any were attacked by the erysipelas all over the body when the exciting cause was a trivial accident…flesh, sinews, and bones fell away in large quantities…there were many deaths.”

 

Necrotizing fasciitis is characterized by rapid destruction of tissue, systemic toxicity, and, if not treated aggressively, gross morbidity and mortality. Early diagnosis and aggressive surgical treatment reduces risk; however, it is often difficult to diagnose NF, and sometimes patients are treated for simple cellulitis until they rapidly deteriorate.

Infection typically spreads along the muscle fascia due to its relatively poor blood supply; muscle tissue is initially spared because of its generous blood supply.

Infection requires inoculation of the pathogen into the subcutaneous tissue or via hematogenous spread.

Classification

  • Type 1 – polymicrobial – older/diabetics/EtOH/IC/PVD
  • Type 2 – monomicrobial – usually group A beta-hemolytic strep (often hematogenous) – healthy people of all ages

Early signs and symptoms of NSTI are often identical to those seen with cellulitis or abscesses potentially making the correct diagnosis difficult

‘Classic’ Signs / Symptoms

(1) the presence of bullae
(2) skin ecchymosis that precedes skin necrosis
(3) crepitus
(4) cutaneous anesthesia
(5) pain out of proportion to examination
(6) edema that extends beyond the skin erythema
(7) systemic toxicity
(8) progression of infection despite antibiotic therapy or rapid progression

First 4 are “hard” signs

  • Erythema (without sharp margins; 72 percent)
  • Edema that extends beyond the visible erythema (75 percent)
  • Severe pain (out of proportion to exam findings in some cases; 72 percent)
  • Fever (60 percent)
  • Crepitus (50 percent)
  • Skin bullae, necrosis, or ecchymosis (38 percent)

Streaking lymphangitis favours the diagnosis of cellulitis over necrotizing fasciitis

Diagnosis

  • There is no set of clinical findings, lab test results and even imaging that can definitively rule out necrotizing fasciitis
    • “Surgical exploration is the only way to establish the diagnosis of necrotizing infection”.
    • “Surgical exploration should not be delayed when there is clinical suspicion for a necrotizing infection while awaiting results of radiographic imaging other diagnostic information”
  • But what if you really aren’t sure?  Or if you get pushback?
  • CT is probably the best test – esp Type 1 (gas forming)
    • Findings – gas, fluid collections, tissue enhancement, inflammatory fascial changes
  • Finger test…
    • “After local anesthesia, make a 2-3 cm incision in the skin large enough to insert your index finger down to the deep fascia. Lack of bleeding and/or “dishwater pus” in the wound are very suggestive of NSTI. Gently probe the tissues with your finger down to the deep fascia. If the deep tissues dissect easily with minimal resistance, the finger test is + and NSTI can be ruled in.”  (emergencymedicinecases.com)
  • But what about PoCUS????

PoCUS

Diagnosis of Necrotizing Faciitis with Bedside Ultrasound: the STAFF Exam

Findings – “STAFF”

ST – subcutaneous thickening
A – air
FF – fascial fluid

Ultrasound video demonstrating Subcutaneous Thickening, Air, and Fascial Fluid (STAFF).

 

Soft tissue ultrasound findings are significantly different when compared to normal soft tissue ultrasound

Bottom Line: Limited data, but basically PoCUS is not sufficient to rule-in or rule out, but might be helpful in raising suspicion level for necrotising fasciitis for physicians who routinely scan all soft tissue infections.

 

LRINF Score

The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) Score: A Tool for Distinguishing Necrotizing Fasciitis From Other Soft Tissue Infections

Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) Score.  2004, retrospective – score >6 negative predictive value of 96.0% and a positive predictive value of 92%.

 

A validation study looking only at patients with pathology-confirmed necrotizing fasciitis showed that a LRINEC score cutoff of 6 points for necrotizing fasciitis only had a sensitivity of 59.2% and a specificity of 83.8%, yielding a PPV of 37.9% and NPV of 92.5%. However, the study did show that severe cellulitis had a LRINEC Sscore ≥ 6 points only 16.2% of the time.  Therefore, the available evidence suggests that the LRINEC score should not be used to rule-out NSTI.

Bottom Line: Doesn’t rule-out…… or rule-in

 

Suggested Algorithm – UpToDate

 

EM Cases Review

BCE 69 Necrotizing Fasciitis

 

Further Reading

Necrotizing fasciitis – Can Fam Physician. 2009 Oct; 55(10): 981–987.

 

Epidural Abscess

Case

A 40yr old female presents with left leg weakness. She has a complex recent past medical history including recently diagnosed pneumonia, previous renal colic and type 2 diabetes. Could this be a stroke? What are the other causes of leg weakness? How does the examination differentiate UMN from LMN lesions? When considering a diagnosis of epidural abscess what investigation is required? How soon should it be performed?

Only 4% of Strokes present with isolated or predominant leg weakness. (Brain. 1994 Apr;117 ( Pt 2):347-54.
doi: 10.1093/brain/117.2.347)

Common mechanisms of weakness:

  • Upper motor neuron lesions (Stroke, Tumour, Spinal Cord Compression, etc)
  • Lower motor neuron lesions ( Neuropathy, Disc Prolapse, Spinal Cord Compression, etc)
  • Neuromuscular junction lesions (Myasthenia, etc)
  • Neuropathies (Guillain-Barre, etc)
  • Muscle (Myopathies, etc)

Full review on Muscle Weakness from the Merck Manual here

Weakness that becomes severe within minutes or less is usually caused by severe trauma or stroke; in stroke, weakness is usually unilateral and can be mild or severe. Sudden weakness, numbness, and severe pain localized to a limb are more likely caused by local arterial occlusion and limb ischemia, which can be differentiated by vascular assessment (eg, pulse, color, temperature, capillary refill, differences in Doppler-measured limb BPs). Spinal cord compression can also cause paralysis that evolves over minutes (but usually over hours or days) and is readily distinguished by incontinence and clinical findings of a discrete cord sensory and motor level.

Unilateral upper motor neuron signs (spasticity, hyperreflexia, extensor plantar response) and weakness involving an arm and a leg on the same side of the body: A contralateral hemispheric lesion, most often a stroke

Upper or lower motor neuron signs (or both) plus loss of sensation below a segmental spinal cord level and loss of bowel or bladder control (or both): A spinal cord lesion

 

Epidural Abscess

Spinal epidural abscess (SEA) is a severe pyogenic infection of the epidural space that leads to devastating neurological deficits and may be fatal. SEA is usually located in the thoracic and lumbar parts of the vertebral column and injures the spine by direct compression or local ischemia. Spinal injury may be prevented if surgical and medical interventions are implemented early. The diagnosis is difficult, because clinical symptoms are not specific and can mimic many benign conditions. The classical triad of symptoms includes back pain, fever and neurological deterioration.

Spinal Epidural Abscess: Common Symptoms of an Emergency Condition – A Case Report

 

  • 75% are a delayed diagnosis
    • Usually hematogenous spread, usually S. aureus
  • Diagnosis
    • CRP has an sensitivity of 85%, specificity of 50%
    • MRI is gold standard
    • CT with contrast 2nd choice

 

Further Reading

Spinal epidural abscess

Episode 26: Low Back Pain Emergencies

 

 

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EM Reflections – May 2020

Posted on by

Thanks to Dr Paul Page for leading the discussions this month

Edited by Dr David Lewis 

Discussion Topics

  1. Seizure disorder and safe discharge 

    • Consider risk factors for adverse outcome of discharge for all patients with recurrent seizure disorder
    • Use a checklist

  2. Competency and Capacity

    • Multidisciplinary consultation is paramount in deciding capacity
    • Special circumstances include vulnerable adults and pregnancy

  3. Testicular Torsion

    • Time = Testicle viability
    • Do not delay definitive management

Seizure disorder and safe discharge 

Case

A patient presents with recurrent seizures. They have a past medical history of schizophrenia and mental health delay. Following appropriate ED management with complete resolution of seizures and full recovery of the patient – what is the recommended disposition?

Seizure disorder is a common presentation to the Emergency Department. This EM Cases post provides an excellent summary for the ED approach to resolved seizures:

Ep 132 Emergency Approach to Resolved Seizures

 

ED approach to resolved seizures – Summary pdf

In this study – Ethanol withdrawal or low antiepileptic drug levels were implicated as contributing factors in 177 (49%) of patients. New‐onset seizures were thought to be present in 94 (26%) patients. Status epilepticus occurred in only 21 (6%) patients.

73% of patients were discharged.

 

 

 

Disposition

Most authors recommend admission for patients presenting with FIRST Seizure Episode. Patients with a past medical history of recurrent seizure disorder are more likely to be discharged than admitted.

However – this EBMedicine article cites an incidence of 19% seizure recurrence rate within 24 hours of presentation, which decreased to 9% if patients with alcohol related events or focal lesions on CT were excluded. They suggest, that at present, there is insufficient evidence to guide the decision to admit. They recommend this decision be tailored to the patient, taking into consideration the patient’s access to follow-up care and social risk factors (eg, alcoholism or lack of health insurance). Patients with comorbidities, including age > 60 years, known cardiovascular disease, history of cancer, or history of immunocompromise, should be considered for admission to the hospital.

 

Considerations For Safety On Discharge

Patients and their families should be counseled and instructed on basic safety measures to prevent complications (such as trauma) during seizures. For example, patients should be advised to avoid swimming or cycling following a seizure, at least until they have been reassessed by their neurologist and their antiepileptic therapy optimized, if needed. A particularly important point for seizure patients is education against driving. Although evidence remains controversial on this issue, there is general agreement that uncontrolled epileptic patients who drive are at risk for a motor vehicle crash, with potential injury or death to themselves and others. For this reason, most states do not allow these patients to drive unless they have been seizure-free on medications for 1 year. According to population survey data, 0.01% to 0.1% of all motor vehicle crashes are attributable to seizures

Competency and Capacity

Case

A young female patient with a history of polysubstance drug abuse presents with a psychotic episode. She refuses treatment. What are the competency and capacity implications? She is also pregnant. Does this change the the competency and capacity implications?

This LitFL post provides and excellent outline for Competency and Capacity in the ED:

Capacity and Competence

This article published by the RCPSC provides a useful outline from a Canadian perspective – with the following objectives.

  1. To clarify the role of decisional capacity in informed consent
  2. To discuss problems associated with decisional capacity and addiction

RCPSC – Decisional Capacity

 

 

Capacity in Pregnancy

Recommendations from the American College of Obstetricians and Gynecologists

On the basis of the principles outlined in this Committee Opinion, the American College of Obstetricians and Gynecologists (the College) makes the following recommendations:

  • Pregnancy is not an exception to the principle that a decisionally capable patient has the right to refuse treatment, even treatment needed to maintain life. Therefore, a decisionally capable pregnant woman’s decision to refuse recommended medical or surgical interventions should be respected.
  • The use of coercion is not only ethically impermissible but also medically inadvisable because of the realities of prognostic uncertainty and the limitations of medical knowledge. As such, it is never acceptable for obstetrician–gynecologists to attempt to influence patients toward a clinical decision using coercion. Obstetrician–gynecologists are discouraged in the strongest possible terms from the use of duress, manipulation, coercion, physical force, or threats, including threats to involve the courts or child protective services, to motivate women toward a specific clinical decision.
  • Eliciting the patient’s reasoning, lived experience, and values is critically important when engaging with a pregnant woman who refuses an intervention that the obstetrician–gynecologist judges to be medically indicated for her well-being, her fetus’s well-being, or both. Medical expertise is best applied when the physician strives to understand the context within which the patient is making her decision.
  • When working to reach a resolution with a patient who has refused medically recommended treatment, consideration should be given to the following factors: the reliability and validity of the evidence base, the severity of the prospective outcome, the degree of burden or risk placed on the patient, the extent to which the pregnant woman understands the potential gravity of the situation or the risk involved, and the degree of urgency that the case presents. Ultimately, however, the patient should be reassured that her wishes will be respected when treatment recommendations are refused.
  • Obstetrician–gynecologists are encouraged to resolve differences by using a team approach that recognizes the patient in the context of her life and beliefs and to consider seeking advice from ethics consultants when the clinician or the patient feels that this would help in conflict resolution.
  • The College opposes the use of coerced medical interventions for pregnant women, including the use of the courts to mandate medical interventions for unwilling patients. Principles of medical ethics support obstetrician–gynecologists’ refusal to participate in court-ordered interventions that violate their professional norms or their consciences. However, obstetrician–gynecologists should consider the potential legal or employment-related consequences of their refusal. Although in most cases such court orders give legal permission for but do not require obstetrician–gynecologists’ participation in forced medical interventions, obstetrician–gynecologists who find themselves in this situation should familiarize themselves with the specific circumstances of the case.
  • It is not ethically defensible to evoke conscience as a justification to attempt to coerce a patient into accepting care that she does not desire.
  • The College strongly discourages medical institutions from pursuing court-ordered interventions or taking action against obstetrician–gynecologists who refuse to perform them.
  • Resources and counseling should be made available to patients who experience an adverse outcome after refusing recommended treatment. Resources also should be established to support debriefing and counseling for health care professionals when adverse outcomes occur after a pregnant patient’s refusal of treatment.

Further Reading:

Ethically Justified Clinically Comprehensive Guidelines for the Management of the Depressed Pregnant Patient

How Do I Determine if My Patient has Decision-Making Capacity?

 

Testicular Torsion

Case

A 12 year old boy presents with scrotal discomfort in the early hours of the morning. The department is very busy and the waiting time to be seen is 4 hours. What triage category is this presenting complaint? If a diagnosis of torsion is considered, how quickly should definitive management be initiated?

Ramachandra et al. demonstrated through multivariate analysis of the factors associated with testicular salvage, that duration of symptoms of less than 6 h was a significant predictor of testicular salvage. They found that the median duration of pain was significantly longer in patients who underwent orchiectomy versus orchidopexy. Similar findings were seen with respect to time to operating room from initial presentation. They concluded that time to presentation is in fact the most important factor in determining salvageability of the testicle in testicular torsion. If surgical exploration is delayed, testicular atrophy will occur by 6 to 8 h, with necrosis ensuing within 8 to 10 h of initial presentation. Salvage rates of over 90% are seen when surgical exploration is performed within 6 h of the onset of symptoms, decreasing to 50% when symptoms last beyond 12 h. The chance of testicular salvage is less than 10%, when symptoms have been present for over 24 h

Factors influencing rate of testicular salvage in acute testicular torsion at a tertiary pediatric center.

Ramachandra P, Palazzi KL, Holmes NM, Marietti S

West J Emerg Med. 2015 Jan; 16(1):190-4.

[PubMed]

 

 

This study (Howe et al). confirmed the relationship between duration of torsion and testicle viability and also found a relationship between the degree of torsion

 

 

AAFP Review of Testicular Torsion: Diagnosis, Evaluation, and Management

 

 

 

 

 

 

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EM Reflections – January 2020

Posted on by

Thanks to Dr Paul Page for leading the discussions this month

Edited by Dr David Lewis 

 

Discussion Topics

  1. Esophageal Perforation

  2. Neonatal Status Epilepticus

Esophageal Perforation – Boerhaave syndrome

A spontaneous perforation of the esophagus that results from a sudden increase in intraesophageal pressure combined with negative intrathoracic pressure (eg, severe straining or vomiting) otherwise known as Effort Rupture.

Difficult diagnosis in first few hours due to nonspecific early symptoms. But, delayed diagnosis results in significant mortality. Diagnosis and surgery within 24 hours carries a 75% survival rate but drops to approximately 50% after a 24-hour delay and approximately 10% after 48 hours.

25 to 45 percent of patients have no clear history of vomiting, and those that do are often confusing with pain sometimes preceding vomiting due to coexisting pathologies e.g gastroenteritis, gastritis, pancreatitis etc.

Clinical manifestations — The clinical features of Boerhaave syndrome depend upon the location of the perforation (cervical, intrathoracic, or intra-abdominal), the degree of leakage, and the time elapsed since the injury occurred. Patients with Boerhaave syndrome often present with excruciating retrosternal chest pain due to an intrathoracic esophageal perforation. Although a history of severe retching and vomiting preceding the onset of pain has classically been associated with Boerhaave syndrome, approximately 25 to 45 percent of patients have no history of vomiting. Patients may have crepitus on palpation of the chest wall due to subcutaneous emphysema. In patients with mediastinal emphysema, mediastinal crackling with each heartbeat may be heard on auscultation especially if the patient is in the left lateral decubitus position (Hamman’s sign). However, these signs require at least an hour to develop after an esophageal perforation and even then are present in only a small proportion of patients. Within hours of the perforation, patients can develop odynophagia, dyspnea, and sepsis and have fever, tachypnea, tachycardia, cyanosis, and hypotension on physical examination. A pleural effusion may also be detected.

Patients with cervical perforations can present with neck pain, dysphagia or dysphonia.  Patients may have tenderness to palpation of the sternocleidomastoid muscle and crepitation due to the presence of cervical subcutaneous emphysema.

Patients with an intra-abdominal perforation often report epigastric pain that may radiate to the shoulder. Patients may also report back pain and an inability to lie supine or present with an acute (surgical) abdomen. As with intrathoracic perforation, sepsis may rapidly develop within hours of presentation.

Laboratory findings — Laboratory evaluation may reveal a leukocytosis. While not part of the diagnostic workup for an esophageal perforation, pleural fluid collected during thoracentesis may contain undigested food, have a pH less than 6, or have an elevated salivary amylase level.

UptoDate

 

Chest X-ray  showing a pneumomediastinum (closed arrows) and silhouette sign over the right heart border (open arrow).

Case Presentation 1

Case Presentation 2

 

Take Home

  • The diagnosis of Boerhaave syndrome should be suspected in patients with severe chest, neck, or upper abdominal pain after an episode of severe retching and vomiting or other causes of increased intrathoracic pressure and the presence of subcutaneous emphysema (crepitus) on physical exam.
  • While thoracic and cervical radiography can be supportive of the diagnosis, the diagnosis is established by contrast esophagram or computed tomography (CT) scan
  • Delayed diagnosis is associated with high mortality
  • Radiological signs develop over time, repeat imaging is often useful when considering this diagnosis

 

Neonatal Status Epilepticus

When an altered few-day-old baby is brought into the ED, other than requesting immediate pediatric support, opening PediStat on you phone and trying to keep calm – consider the causes of altered LOC in pediatrics – Think VITAMINS:

V – Vascular (e.g. arteriovenous malformation, systemic vasculitis)

I – Infection (e.g. meningoencephalitis, overwhelming alternate source of sepsis)

T – Toxins (e.g. environmental, medications, contaminated breast milk)

A – Accident/abuse (e.g. non-accidental trauma, sequelae of previous trauma)

M – Metabolic (e.g. hypoglycemia, DKA, thyroid disorders)

I – Intussusception (e.g. the somnolent variant of intussusception, with lethargy)

N – Neoplasm (e.g. sludge phenomenon, secondary sepsis, hypoglycemia from supply-demand mismatch)

S – Seizure (e.g. seizure and its variable presentation, especially subclinical status epilepticus)

 

Altered Mental Status in Children

 

What elements are highly suggestive of true seizures?

  1. Lateralized tongue biting (high specificity)
  2. Flickering eyelids, deviation of gaze
  3. Dilated pupils with a blank stare
  4. Lip smacking
  5. Increased heart rate and blood pressure, desaturations in pulse oximetry during event

Management of Pediatric Seizures

Newborn Resuscitation

 

Elemental EM: Pediatric Intubation

 

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EM Reflections – December 2019

Posted on by

Thanks to Dr Joanna Middleton for leading the discussions this month

Edited by Dr David Lewis 

Discussion Topics

  1. Cardiopulmonary Resuscitation In Patients With Mechanical Circulatory Support

    • Patient with mechanical circulatory support devices have unique clinical signs of cardiac arrest
    • Understanding the function of these devices ids critical to the management of these complex cases

  2. Aortic Dissection

    • Remains a commonly missed or delayed diagnosis
    • Once diagnosed, meeting the therapeutic goals requires a careful and considered approach

Cardiopulmonary Resuscitation In Patients With Mechanical Circulatory Support

Case

A 70yr male presents with cardiac arrest. He has an LVAD. What are the implications for emergency management and cardiopulmonary resuscitation?

Introduction

Cardiac arrest in patients on mechanical support is a new phenomenon brought about by the increased use of this therapy in patients with end-stage heart failure.

It is important to understand the difference between blood flow and perfusion when assessing any patient with suspected cardiovascular hemodynamic instability, especially patients with an LVAD, in whom the peripheral arterial pulse is not a reliable indicator. Flow represents the forward movement of blood through the systemic circulation. It can be either adequate or inadequate to provide sufficient oxygen delivery to sustain tissue per- fusion. Assessment of adequate tissue perfusion is the most important factor in determining the need for circu- latory assistance such as chest compressions.

What is a Left Ventricular Assist Device?

With an LVAD, blood enters the device from the LV and is pumped to the central aortic circulation, “assisting” the heart.  The outflow cannula is typically anastomosed to the ascending aorta, just above the aortic valve. RA/RV still working

 

Blue Arrow – Important point as patients often present with iGel in place…

 

Unique Patient Properties

  • Pulses often absent
    • BP measured manually with a Doppler – MAP (50-90)
  • SpO2 may not be measurable
  • Anticoagulated
  • Need power!
  • Very reliant on RV function/preload
  • Leading cause of death – sepsis and stroke

Further Reading

Cardiopulmonary Resuscitation in Adults and Children With Mechanical Circulatory Support. A Scientific Statement From the American Heart Association

Aortic Dissection

Aortic dissection remains difficult to diagnosis with 1 in 6 being missed at the initial ED visit. Why? The diagnosis is rare with and incidence of only 2.9/100,000/year, and the presentation is often atypical mimicking other more common diagnoses such as ACS and stroke.

View The SJRHEM  – Aortic Dissection – Resident Clinical Pearl here:

Aortic Dissection

Diagnosis

The most common initial misdiagnoses are acute coronary syndrome, pulmonary embolism, and stroke. Patients with these suspected diagnoses should also be screened for high-risk features of acute aortic dissection. If none are present, they are unlikely to have an acute aortic dissection. If high-risk features are present, balance your clinical suspicion for an aortic dissection with the likelihood of an alternative diagnosis using an approach such as RAPID

How Do I rule Out Aortic Dissection – Just the Facts – CJEM

PoCUS

Early Screening for Aortic Dissection With Point‐of‐Care Ultrasound by Emergency Physicians

A total of 127 patients were enrolled: 72 in the US group and 55 in the control group. In the US group, compared with CTA, the sensitivity of EP POCUS was 86.4%, and the specificity was 100.0%.

 

 

Treatment Goals

From EMCases.com

 

Further Reading

Episode 92 – Aortic Dissection Live from The EM Cases Course

 

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