COVID-19 – SJRH and New Brunswick

This post is provided as an information resource specifically for HealthCare Professionals within the Saint John Region and New Brunswick Emergency Departments

This post will be updated continuously as required.

COVID-19 Clinical Management is posted HERE.

Internal Communication Daily Update Thread is posted HERE. Password has been emailed to all staff and is posted on Closed Group FaceBook SJRHEM Education page.


Public Health

WorkSafe New Brunswick

Infection Prevention and Control

SJRHEM Clinical Pathways

Academic Activity – News, Cancellations

National Organization COVID Resources

Staff Wellness

Dalhousie Medical Students – Volunteer Support


What is COVID-19

  • A novel betacoronavirus first reported in Wuhan, China on December 31st 2019
  • Symptoms for the novel coronavirus are similar to those for influenza or other respiratory illnesses.
  • New Brunswick Case Definition – see below– Note this continues to evolve
  • Current assumptions are that spread is via droplet and/or fomite to face
  • Infection Prevention and Control = Contact and Droplet precautions
  • Links to reliable COVID-19 Information: New Brunswick, Horizon, Canada, CDC, WHO
  • Other COVID -19 respected resources: EMCrit, RebelEM
  • COVID -19 Rounds – Dr. Duncan Webster (Infectious Disease Physician)

 


Active Screening for Emergency Physicians before Shift

At shift handover ask the following questions:

  • Do you have any Influenza Like Illness symptoms?
  • Have you reviewed the SJRHEM COVID webpage and Daily Updates?
  • Have you read the Donning-Doffing Posters?
  • Are you aware the Donning and Doffing requires a Buddy?


Personal Protective Equipment for COVID-19

PPE Evidence – Centre For Evidence Based Medicine Oxford – This paper reviews compares effectiveness of surgical mask to N95 effectiveness for coronavirus

 

PPE: What We Know, Conservation Strategies and Protected Code Blue – From EmergencyMedicineCases.com – a great summary on IP&C and how to use PPE.

Low Risk of Aerosolization 

  • Surgical mask
  • Gloves
  • Scrub hat,cap or bonnet
  • Visor or goggles
  • Gown

e.g pretriage screening walking patients

High or Unknown Risk of Aerosolization

  • N95 mask
  • Gloves
  • Scrub hat,cap or bonnet
  • Visor or goggles
  • Gown

Aerosol Generating Procedures = non-invasive positive pressure ventilation, high-flow nasal cannula, bag-mask ventilation, endotracheal intubation, cardiopulmonary resuscitation, bronchoscopy, open suction of respiratory tract, sputum induction, use of nebulizer therapy, high frequency oscillatory ventilation

 

 


Donning and Doffing PPE

  • When removing PPE, always start by first applying alcohol-based hand sanitizer to your gloves.
  • After fully removing PPE, sanitize hands and wrists with alcohol-based hand sanitizer again.

  • Note that we recommend also wearing a scrub hat,cap or bonnet to reduce risk of fomite transmission

 

Official Dalhousie Doffing and Donning Video

 

 


Horizon – Interim Infection Prevention and Control Guidelines for the Management of Suspect COVID-19

IPC Guidance for Suspect COVID 19 ( March 15 2020) V 2.0

GNB – Chief Medical Officer – COVID-19 – PPE for IPC from March 22 – Mar 23 2020

 


Self-Presenting Patient Flow Pathway – Saint John Regional Hospital Emergency Department

 

 

 

 

 


NB Health Screening Tool and Referral forms to Surge Clinic – 20 March 2020 

Screening Tool – http://sjrhem.ca/wp-content/uploads/2020/03/COVID-19-Screening-Tool-2020-03-19-MD.pdf

Referral Form – http://sjrhem.ca/wp-content/uploads/2020/03/Example-COVID-19-Referral-Form_EN-2-1.pdf

FAX Number = 506 462-2040

 


Self-Isolation Information Leaflet for Patients

Self-Isolate and Alternative Self-Isolate Leaflet

Self Management COVID

 


SJRH Emergency Department Patient & Staff IP&C Flow Map

 

Traffic Flow

(March 13, 2020)

COVID- 19:

  • Triaged at main ED vestibule
  • Travel the patient corridor until back entrance to RAZ à into the unit
  • For external procedures travel down the public corridor following all precautions

Clean patients needing x-ray or other external sever (ambulatory or via Porter)

  • Out internal RAZ doors (11.523) and travel down the main staff corridor
  • Returning via the staff corridor and can us AMB intercom for Safety service to provide re-entry

ED Staff / physicians

  • Travel the main staff corridor and loop back into the public corridor (11.161)
  • Will use the new card access doors to gain entrance to the “anti-room”

EMS

  • Any suspect case to park at the ED main entrance and use the established path to the Covid-19 Unit via the public corridor

Inpatient and Visitor traffic

  • All this traffic will be filtered through the main entrance
  • After hours that will be monitored by Safety services

 

Control points

  • Main staff corridor
  • RAZ- back entrance (main staff entrance to Covid-19 space)
  • RAZ – emergency exit into staff corridor (access needs to be restricted)
  • New access point @ link corridor (by ED conference room)
    • Need lists for who will be provide access
  • Public hall by RAZ waiting room entrance
    • Option 1- physical barrier with wall and door (bed accessible)
    • Option 2 – staff presence

 

COVID-19 Testing – Public Health Advise and Viral Swabs 

Summary of Current Guidance :

  • Need to balance the need for detection of as many imported cases of COVID-19 as possible is critical to mitigate the spread of this virus in the community setting with the the fact that Laboratory capacity and supplies are limited provincially and nationally.
  • We need to be careful to choose wisely to maintain the integrity of our diagnostic system
  • Consider:
    • Travel history outside NB in last 14 days
    • At Least one of: Fever/Chills, Cough, Difficulty Breathing
    • Note 80% of COVID-19 cases are mild so clinical severity is not a marker of likelihood of infection
    • More severe clinical presentations (pneumonia, unusual presentation should be considered for testing regardless of travel history
  • Collect (or arrange for collection of) ONE nasopharyngeal swab for COVID-19, indicating symptom onset date, travel history including date of return, and clinical severity (if indicated)
  • 5 Hospitals across NB, only SJRH in R2
  • 5 per day of those being discharged
  • 5 per day of those being admitted
  • Use pre labeled ‘sentinel swab’
  • Fever or Cough but NO travel or contact hx

 

How to Collect NP Swab

 


COVID-19 Triage

Full process here:  COVID Full triage to mild moderate severe critical V5

 


PoCUS

Indications for PoCUS are limited in COVID-19 patients. The usual lung, cardiac and procedural guidance indications may be appropriate in assisting with resuscitation and managing complications. Specific findings in COVID include:

  • Focal B-lines and fused B-lines
  • Discontinuous, rough appearance to the pleural line, with subpleural consolidation
  • Foci of disease located predominantly in the posterior lung fields, particularly in the lower lung fields
  • Images can be viewed here

Neither PoCUS, CXR or CT are sufficiently sensitive to provide a diagnosis of COVID. The use of PoCUS should be limited to assisting with resuscitation and managing complications.

Infection Prevention and Control measures are divided into two areas

Assuming that we are in the containment phase (i.e we are successfully identifying cases of COVID at Triage) – This may change.

General Emergency Department

  • These patients have been screened as low risk for COVID-19, i.e they are presenting with an unrelated pathology.
  • Before and after using the ultrasound machine on each patient the following established protocol applies
    • Using the viru/bactericidal hydrogen peroxide wipes, thoroughly clean the:
      • Transducers and cables
      • Keyboard and cart handles
  • Only use the ultrasound machine for clinically indicated examinations (No scanning rounds or non-clinical teaching scans)
  • In the presence of blood or other bodily fluid contaminants use a transducer sheath

 

High Consequence Infection Decision Unit

  • These patients have been screened as moderate to high risk for COVID-19, i.e they are presenting with an Influenza Like Illness (ILI) and meet the case definition criteria.
  • A dedicated ultrasound machine has been located in the HCIDU
  • Before and after using the ultrasound machine on each patient the following established protocol applies
    • Using the viru/bactericidal hydrogen peroxide wipes, thoroughly clean the:
      • Transducers and cables
      • Keyboard and cart handles
  • A transducer sheath must be used on every patient.
  • During the examination, try not to directly touch the machine controls. Use a transparent polythene drape / or alternative barrier over the keyboard controls
  • After use, move the machine back to its storage area away from the patient beds.
  • Try to avoid using the machine on another patient for at least 30 minutes.

 


Case Definition – New Brunswick

based on the Canada Public Health  –  NB Interim national case definition  – March 24

Person under investigation (PUI)

A person with fever and/or cough who meets the exposure criteria and for whom a laboratory test for COVID-19 has been or is expected to be requested.

Probable

A person:

  • with fever (over 38 degrees Celsius) and/or new onset of (or exacerbation of chronic) cough
    AND
  • who meets the COVID-19 exposure criteria
    AND
  • in whom laboratory diagnosis of COVID-19 is inconclusive,negative (if specimen quality or timing is suspect), or
    positive but not confirmed by the National Microbiology Laboratory (NML)

Confirmed

A person with laboratory confirmation of infection with SARS-CoV-2 as a result of nucleic acid amplification testing (NAAT).

 

SJRHEM ADVICE – 19 March 2020

Consider any patient who presents with an Influenza Like Illness – irrespective of above case definition as being suspicious for COVID-19 and take appropriate PPE precautions.


Exposure Criteria

In the 14 days before onset of illness, a person who:

  • Traveled to an affected area i.e. anyone who travelled outside New Brunswick. OR
  • Had close contact with a person with acute respiratory illness who has been to an affected area (anyone who travelled outside NB within 14 days prior to their illness onset) OR
  • Had laboratory exposure to biological material (e.g. primary clinical specimens, virus culture isolates) known to contain COVID-19.

Close contact = A close contact is defined as a person who provided care for the patient, including healthcare workers, family members or other caregivers, or who had other similar close physical contact or who lived with or otherwise had close prolonged contact with a probable or confirmed case while the case was ill.


Affected Areas

Public Health Canada Affected Area List

UPDATEAll travel outside New Brunswick


 

 

 

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Modified Valsalva maneuver in the treatment of SVT – REVERT Trial

Falling heels over head: you make my heart skip a beat

Resident Clinical Pearl (RCP) November 2019

 

Patricia Marks – PGY1 (FRCPC) Dalhousie University, Halifax, NS

Reviewed by Dr David Lewis

 


 

Introduction:

Supraventricular tachycardias (SVT) is a common presentation to the emergency room, and most patients will require treatment with adenosine or electrical cardioversion, as vagal maneuvers are less than 20% of the time in clinical practice. Adenosine and electrical cardioversion both require additional hospital resources, and adenosine is poorly tolerated by patients.

 

The REVERT trial published in 2015 in the Lancet by Appelboam et al. proposed a modified Valsalva maneuver in the treatment of SVT.  The study was a multicentre randomized control trial in England involving 433 patients with stable SVT. According to an intention to treat analysis, the authors found a 43% success rate of conversion to sinus rhythm with the modified Valsalva maneuver compared to 17% with standard Valsalva. No significant dangerous adverse effects occurred in this study.

 


Modified Valsalva: The How-To

  1. Patient identification:

    1. Is my patient eligible for Valsalva?
      • Stable SVT
      • Age > 18 years
      • Able to perform Valsalva
      • Able to lie flat and have legs lifted
    2. Contraindications:
      • Unstable or indication for immediate cardioversion
      • Atrial fibrillation, atrial flutter, sinus tachycardia
      • Recent MI
      • Aortic stenosis
      • Glaucoma
      • Retinopathy
      • Third trimester of pregnancy
  2. Materials

      • 10cc syringe
      • Manometer (optional)
  3. Performing the modified Valsalva maneuver

    1. Position the patient in a semi-recumbent position (45º)
    2. Instruct the patient to blow into the tip of a 10cc syringe for 15 seconds. The patient should be targeting a pressure reading on the manometer of 40mmHg, or blowing hard enough to move the plunger tip*
    3. Lower the patient flat and passively raise their legs to a 45º angle for 15 seconds
    4. Return the patient to a semi-recumbent position for an additional 45 seconds
    5. Assess the rhythm
    6. Repeat x1 if unsuccessful before moving on to adenosine or electrical cardioversion (provided the patient remains stable)

*The REVERT trial used a manometer to measure 40mmHg of pressure, however Smith and Boyle have demonstrated that 40mmHg of pressure is generated when a patient is instructed to blow into a 10cc syringe until the plunger moves

Image obtained from https://www.ecgmedicaltraining.com/wp-content/uploads/2016/06/REVERT-Trial-SVT.jpg on February 21, 2020.

 


Watch the REVERT authors perform the maneuver:

 


 

Benefits of this method:

  • Easy to instruct patients; can try at home
  • Higher success rate than standard Valsalva
  • Similar ED length of stay compared to standard Valsalva
  • Less patients require adenosine or cardioversion

Additional considerations

  • No formal studies exist for pediatric patients, however a recent case report by Rayburn and Wagers did demonstrate successful conversion to sinus rhythm with this maneuver

 

Bottom Line 

In adults with stable SVT, the modified Valsalva maneuver as published in the REVERT trial achieves a high rate of conversion to sinus rhythm with a NNT of 3.8 and without significant adverse effects. In patients without contraindications, the modified Valsalva maneuver is a low-cost and easy to teach strategy that should be trialled to convert patients in SVT prior to adenosine or electrical cardioversion.

 


 

References

  • Appelboam A, Reuben A, Mann C, Gagg J, Ewings P, Barton A, Lobban T, Dayer M, Vickery J, Benger J; REVERT trial collaborators. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet. 2015 Oct 31;386(10005):1747-53. doi: 10.1016/S0140-6736(15)61485-4.
  • Rayburn D, Wagers B. Modified Valsalva Maneuver for Pediatric Supraventricular Tachycardia. Pediatr Emerg Care. 2020 Jan;36(1):e8-e9. doi: 10.1097/PEC.0000000000002023
  • Smith G, Boyle MJ. The 10 mL syringe is useful in generating the recommended standard of 40 mmHg intrathoracic pressure for the Valsalva manoeuvre. Emerg Med  Australas. 2009 Dec;21(6):449-54. doi: 10.1111/j.1742-6723.2009.01228.x
  • Smith GD, Fry MM, Taylor D, Morgans A, Cantwell K. Effectiveness of the Valsalva Manoeuvre for reversion of supraventricular tachycardia. Cochrane Database of Systematic Reviews 2015, Issue 2. Art. No.: CD009502. DOI: 10.1002/14651858.CD009502.pub3
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Introduction to Transesophageal Echo – Basic Technique

Thanks to Dr. Jennifer Cloutier, Cardiac Anesthesiologist, for delivering a great session.


This beginner guide is designed for those familiar with transthoracic echo and just starting to use TEE. ED indications and TEE utility in the emergency setting are briefly discussed at the end of this post.


Requirements

  • Sterile transducer – This requires a sterilization facility, protocol and collaboration with other departments
  • Patient preparation – In ED usually intubated, unconscious or sedated.
  • Optional – spray the transducer with topical local anesthetic

Contraindications

  • Suspected esophageal perforation, stricture or trauma
  • Varices

Insertion

  • Hold transducer control module with left hand and support against your abdomen (see pic 1)
  • Extend transducer to full length, holding end with right hand
  • Check the control wheels are functioning correctly before inserting the transducer
  • Ensure transducer head is facing upwards (use anterior length markings to maintain orientation)
  • Insert transducer on left side of tongue
  • Use bite guard – e.g cut corrugated airway tubing
  • Advance to mid esophagus
  • Look for left atrium – this is the first window

 

Orientation

The transducer can be manipulated into several orientations:

  • Rotate control module clockwise to orientate to patient right
  • Rotate control module anticlockwise to orientate to patient left
  • Rotate “Big Wheel” clockwise to antiflex and orientate anteriorly
  • Rotate “Big Wheel” anticlockwise to retroflex and orientate posteriorly
  • Rotate “Small Wheel” clockwise to flex right
  • Rotate “Small Wheel” anticlockwise to flex left
  • Advance transducer deeper into esophagus
  • Withdraw transducer less deeply in esophagus

(a) Advance, withdraw: Pushing or pulling the tip of the TEE probe; (b) turn to right, turn to left (also referred as clockwise and anticlockwise): rotating the anterior aspect of the TEE probe to the right or left of the patient; (c) anteflex, retroflex: anteflex is flexing the tip of the TEE probe anteriorly by turning the large control wheel clockwise. Retroflex is flexing the tip of the TEE probe posteriorly by turning the large wheel anticlockwise; (d) Flex to right, Flex to left: flexing the tip of the TEE probe with the small control wheel to the patient’s right or left. The probe flexion to the right and left may not be necessary and should be avoided to minimize trauma to the esophagus 

 

 

Multiplane Imaging Angle

With all modern TEE transducers the transducer beam can be rotated within the probe to generate different beam angles. This is achieved using 2 buttons on the control module, one button rotates from 0 to 180 degrees, the other button rotates it back from 180 to 0 degrees. Using the buttons in combination any desired angle between 0 and 180 degrees can be achieved.

At 0 degrees the transducer beam is transverse (orientated Left screen – Right patient)

At 90 degrees the transducer beam is longitudinal

At 180 degrees the transducer beam is transverse (orientated Left screen – Left patient)

 

Multiplane Imaging angle is depicted on the monitor using a pictogram dial.

In this example the TEE probe is located in the Mid Esophageal location. View A – the multiplane imaging angle is 10 degrees and a 4 chamber view is generated. View B – the multiplane imaging angle is 90 degrees and a 2 chamber view is generated.

 

 


 

Useful video tutorial explaining orientation

 

 


 

Core Views

For the beginner, standard views can be achieved by using a guide that shows the location of the transducer (e.g Mid Esophageal, Trans-Gastric along with the optimal multiplane angle (see below).

Clearly every patient will have slightly different anatomy and cardiac axis, so these guides are just a starting point. Fine tuning of all the above will be required.

The Consensus Statement of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists provides an excellent outline of the basic perioperative TEE examination. Although this examination is likely to be much more comprehensive than what is needed in the Emergency Department (e.g during a code or peri arrest), it provides a useful guide to practicing all the important views that may be required in most situations.

 


 

This short video tutorial provides a useful outline of core views

 


ME 4 Chamber View


 

Indications

  • Cardiac Arrest – continuous echo evaluation of cardiac contractility, without impacting chest compression
  • Peri Arrest – assists with diagnosis and fluid resuscitation,
  • Undifferentiated Hypotension – assists with diagnosis and fluid resuscitation

US Probe: Transesophageal Echocardiography in Cardiac Arrest

The post above and the article below provide a more detailed discussion on the use of TEE in cardiac arrest.

New Concepts of Ultrasound in the Emergency Department: Focused Cardiac Ultrasound in Cardiac Arrest

 

 


References

Reeves ST, Finley AC, Skubas NJ, et al. Basic perioperative transesophageal echocardiography examination: a consensus statement of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists. J Am Soc Echocardiogr. 2013;26(5):443–456. doi:10.1016/j.echo.2013.02.015

Arntfield, Robert et al. Focused Transesophageal Echocardiography by Emergency Physicians is Feasible and Clinically Influential: Observational Results from a Novel Ultrasound Program. Journal of Emergency Medicine, Volume 50, Issue 2, 286 – 294

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Acute Kidney Injury

Medical Student Clinical Pearl – January 2019

Carine Nzirorera

 

Faculty of Medicine
Dalhousie University
CC3
Class of 2021

Carine Nzirorera- ResearchGate

 

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual


 

Acute kidney injury (AKI) is defined as an abrupt decrease in kidney function and is classified based on changes in serum creatinine level, reduction of urine output, and need for renal replacement therapy [1]. The Kidney Disease: Improving Global Outcomes (KDIGO) is the most preferred definition and staging system. According to KDIGO guidelines AKI is define as an 1) increase in serum creatinine by ≥0.3 mg/dL (≥26.5 µmol/L) within 48 hours, or 2) an increase in serum creatinine ≥ 1.5 fold from baseline within 7 days, or 3) urine output <0.5 mL/kg/hour for 6 hours [2].

KDIGO staging criteria [2]

Stage 1 an increase of serum creatinine level of 1.5 to 1.9 times baseline, OR increase in serum creatinine by ≥0.3mg/dL (≥26.5 µmol/L) OR a urine output less than 0.5 mL/kg/hour for 6 to 12 hours.

Stage 2 an increase of serum creatinine level of 2 to 2.9 times baseline OR a urine output less than 0.5 mL/kg/hour for more than 12 hours.

Stage 3 an increase of serum creatinine level of greater than 3 times baseline OR increase in serum creatinine to ≥4.0 mg/dL (≥353.6 µmol/L), OR a urine output less than 0.3 mL/kg/hour for ≥24 hours OR anuria output ≥12 hours OR initiation of renal replacement therapy such as dialysis.


 

Case Presentation

69y male with a history of kidney stones had experienced 1 week of hematuria, 1 month of bilateral flank pain and unintentional 20 lbs weight loss over 2 months. Patient was scheduled for a CT scan of his urinary tract and was urgently sent to emergency department after his creatinine levels were found to be severely elevated (2300 µmol/L).

Patient had a 20 year history of kidney stones and previous abdominal CT scans showed small stones in both kidneys =/< 2mm. Patient was afebrile, had no dysuria or increased frequency but complained of difficulty initiating urination and noticed a reduction of the stream even when his bladder felt full. Patient noted no vomiting, diarrhea or decrease in fluid and food intake. Patient had a positive family history of bladder cancer and was a smoker for 30+ years.


 

Etiology

Causes of acute kidney injury are organized based on located of the insult (Table 1) [1]. Causes related to decrease in renal perfusion are classified as prerenal injury. Decrease renal perfusion is seen in sepsis due to decreased arterial pressure from systemic vasodilation; intravascular volume depletion from vomiting, diarrhea or overuse of diuretics can also reduce circulation to the kidneys [1]. Lastly drugs like nonsteroidal anti-inflammatory drugs (NSAIDs) and angiotensin-converting enzyme (ACE) inhibitor can lower intraglomerular pressure causing reduced glomerular filtration rate. NSAIDs and calcineurin inhibitors constrict afferent (or preglomerular) arterioles while ACE inhibitors and angiotensin receptor blockers dilate efferent (or postglomerular) arterioles [3].

Direct renal damage to glomeruli, tubules, interstitium or vasculature are classified as Renal injury. Nephritides can be caused by infection (viral, bacterial, and fungal), medication (antibiotics, antivirals, protein pump inhibitors) toxins (ethylene glycol, aminoglycoside, rhabdomyolysis) or are secondary to conditions like hypertension, prolonged hypotension, lupus, diabetes mellitus and vasculitis.

Impaired drainage of urine distal to the kidneys due to obstruction of the urinary tract is classified as Postrenal cause of acute kidney injury.  Common causes of obstruction are kidney stones, injury, prostate, cervical or bladder cancer.

Previously 70% of community acquired cases of acute kidney injury are classified as prerenal causes [4], a more recent study found 55% of community acquired acute kidney injury were renal disease, 35% pre-renal disease and 10% were postrenal [5].

 


 

Clinical Presentation, History and Physical Exam

Clinical presentation of acute kidney injury varies with severity and varies with prerenal, renal and postrenal causes (Table 2). Patients with mild to moderate acute kidney injury are usually asymptomatic and identifiable by laboratory testing. Severe cases would present with vomiting, confusion, fatigue, anorexia, nausea, weight gain or edema [6]. Decline in mental status, asterixis or neurologic symptoms can be indicative of uremic encephalopathy, anemia or bleeding caused by uremic platelet dysfunction [1].

History and physical exam should determine cause of the kidney injury. Screening questions should be used to determine renal perfusion, any potential source of renal injury and any symptoms suggestive of obstructive uropathy (Table 2). Decreased renal perfusion can be assumed from a history of gastrointestinal illness, poor oral intake, use of diuretics, NSAIDs or ACE inhibitors [1,7]. Past medical history of diabetes mellitus, cardiac or liver disease can also indicate reduced renal perfusion [1,7]. Source of renal injury can be screen by assessing current medication for recent antibiotics, antiviral and protein pump inhibitors use, inquiring about past medical history of systemic illnesses such as lupus, viral, bacterial, or fungal infection or symptoms of infection such as rash, arthralgias, fatigue, and hematuria [1,7]. Postrenal cause can be determined from a history of gross hematuria, difficulty urinating, urgency or hesitancy to urinate or a history of kidney stones or bladder, prostate or cervical cancer [1,7].

 


 

Case continued

Blood work

  • CBC: elevated leukocytes (13.5) decreased erythrocytes (3.32), decreased hemoglobin (97), decreased Hematocrit (0.304) normal MCV
  • INR (1.2) APTT (44.3)
  • Liver function test were normal
  • Creatinine (2300)
  • Venous blood gas: decreased pH (7.17), decreased bicarbonate (13), pCO2 (36) and lactate (1.9 )
  • Electrolytes: elevated potassium (7.9), decreased sodium (131), decreased chloride (93), elevated glucose (10.7)

Figure 1. ECG of patient showing Sinus Rhythm and peaked T waves in V2, V3, and V4, an early manifestation of hyperkalemia. Other manifestations (not demonstrated here) include prolonged PR segment, loss of P wave, bizarre QRS complexes and sine wave.

 

PoCUS Imaging

Figure 2. Ultrasound imaging showing moderate hydronephrosis, areas of anechoic fluid indicated by red arrows.

CT Imaging

Figure 3. A) Pelvic CT showing bladder with diffuse wall thickening with a posterior globular neoplasm. B) Pelvic CT showing bladder with calculi within the neoplasm. C) Abdominal CT showing moderate bilateral hydronephrosis.

 

Diagnosis

It was determined that the cause of the acute kidney injury was diffuse thickening of the bladder wall causing obstruction of the ureterovesical junctions (Figure 3A and B). This resulted in bilateral moderate hydronephrosis (Figure 2 and 3C). Additionally, previous CBC reports showed the patient had chronic anemia likely from an underlying chronic kidney disease. This affected EPO production and resulted in decreased erythrocytes production from bone marrow.  With reduce erythrocytes, hemoglobin and hematocrit levels were also decreased. The acute kidney injury resulted in elevated creatinine level, leading to hyperkalemia and metabolic acidosis.

Management

Patient was admitted and fluid resuscitated. To correct his hyperkalemia patient was given 5 to 10 units of regular insulin and dextrose 50% intravenously to shift potassium out of circulation and into the cells. Calcium gluconate (10 mL of 10% solution infused over 5 mins) was given to reduce risk of arrhythmias.

To treat his bilateral hydronephrosis patient was sent to interventional radiology for placement of percutaneous nephrostomy tube. Follow up surgery will be needed to clear the ureters and biopsy of the bladder will be needed to determine treatment for the growth.  Depending on the remaining kidney function after treatment of the acute kidney injury the patient may require dialysis.


 

References

  1. Rahman, Mahboob, Fariha Shad, and Michael C. Smith. “Acute kidney injury: a guide to diagnosis and management.” American family physician 86.7 (2012): 631-639.
  2. KDIGO Clinical Practice Guideline for Acute Kidney Injury, Kidney Int Suppl. 2012;2(Suppl 1):8
  3. Erdbruegger Uta, Okausa Mark. “Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury in adults”. Uptodate (2019)
  4. Kaufman J, Dhakal M, Patel B, Hamburger R. Community-acquired acute renal failure. American Journal of Kidney Disease 2 (1991): 191–198.
  5. Obialo CI, Okonofua EC, Tayade AS, Riley LJ. Epidemiology of de novo acute renal failure in hospitalized African Americans: Comparing community‐acquired vs hospital‐acquired disease. Archives of Internal Medicine 160.9 (2000): 1309– 13.
  6. Meyer TW, Hostetter TH. Uremia. New England Journal of Medicine 357.13 (2007): 1316–1325.
  7. Mesropian, Paul Der, et al. “Community‐acquired acute kidney injury: A challenge and opportunity for primary care in kidney health.” Nephrology 21.9 (2016): 729-735.

 

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PoCUS in Pericardial Effusion

Medical Student Clinical Pearl – October 2019

 

Alex Pupek

Faculty of Medicine
Dalhousie University
CC4
Class of 2020

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual


Case

A 70F with a history of bladder CA, HTN and 4.9cm AAA presented to the Emergency Department (ED) and was Triaged as Level 3 with a chief complaint of generalized weakness. Initial assessment was significant for hypotension and low-grade fever with dysuria elicited on history; she was started on Ceftriaxone with a working diagnosis of urosepsis. Bloodwork and imaging studies were sent to rule out other potential sources of infection.

She had a mild leukocytosis of 12.4, pH of 7.23 and a lactate of 5.0. Point-of-care urinalysis was unremarkable. The chest x-ray revealed an enlarged cardiothoracic ratio of 0.62 compared to 0.46 ten months previously, concerning for a pericardial effusion.

Upon reassessment, the patient appeared unwell with slight mottling to the skin, cool extremities and tenuous blood pressure; point of care ultrasound revealed a large pericardial effusion.  Interventional cardiology was paged; the patient was moved to the trauma area and an emergent pericardiocentesis was performed: 360cc of bloody fluid was removed. The pericardial drain was left in situ.

Post-procedure bloodwork included a troponin of 216 and CK of 204. The patient was admitted to the Cardiac Care Unit and discharged within a week’s time.

 


Pericardial Effusions and The Role of Point-of-Care Ultrasound (POCUS)

The normal pericardial sac contains up to 50 mL of plasma ultrafiltrate [1]. Any disease affecting the pericardium can contribute to the accumulation of fluid beyond 50mL, termed a pericardial effusion. The most commonly identified causes of pericardial effusions include malignancy and infection (Table 1).

 

Table 1 – UpToDate, 2019 – Diagnosis and Treatment of Pericardial Effusions


 

Evaluation of the pericardium with point-of-care ultrasound includes one of four standard views: parasternal long axis, parasternal short axis, subxiphoid and apical (Figure 1). A pericardial effusion appears as an anechoic stripe or accumulation surrounding the heart. Larger effusions may completely surround the heart while smaller fluid collections form only a thin stripe layering out posteriorly with gravity. Seen most commonly post-cardiac surgery, pericardial effusions may be loculated and compress only a portion of the heart. [1,2] (Table 2)

Figure 1[1]


Table 2 [2]


 

Both the pericardial fat pad and pleural effusions can be mistaken for pericardial effusions. The parasternal long-axis view is most helpful to accurately define the effusion with the descending aorta, posterior to the mitral valve and left atrium, serving as a landmark: the posterior pericardial reflection is located anterior to this structure. Fluid anterior to the posterior pericardial wall is pericardial, whereas a pleural effusion will lie posterior. The pericardial fat pad is an isolated dark area with bright speckles, located anteriorly; unlike fluid, it is not gravity dependent. Rather than competing with the cardiac chambers for space within the pericardial sac, the fat pad moves synchronously with the myocardium throughout the cardiac cycle. [1,2] (Figure 2)

Figure 2[1]


A pericardial effusion discovered on POCUS in the ED may be mistaken for tamponade, leading to inappropriate and invasive management in the form of pericardiocentesis.[2]

Patient tolerance of pericardial effusions depends on the rate by which they accumulate. As little as 150-200 mL of rapidly accumulating effusion can cause tamponade whereas much larger amounts of slowly accumulating fluid can be well tolerated. Pericardial effusions formed gradually are accommodated by adaptations in pericardial compliance. A tamponade physiology is reached once the intrapericardial pressure overcomes the pericardial stretch limit.[2] (Figure 3)

Figure 3[2]


The core echocardiographic findings of pericardial tamponade consist of:

  • a pericardial effusion
  • diastolic right ventricular collapse (high specificity)
  • systolic right atrial collapse (earliest sign)
  • a plethoric inferior vena cava with minimal respiratory variation (high sensitivity)
  • exaggerated respiratory cycle changes in mitral and tricuspid valve in-flow velocities as a surrogate for pulsus paradoxus

In the unstable patient with clinical and echocardiographic findings of tamponade, an emergent pericardiocentesis is indicated.[2]

A retrospective cohort study of non-trauma emergency department patients with large pericardial effusions or tamponade, ultimately undergoing pericardiocentesis, found that effusions identified by POCUS in the ED rather than incidentally or by other means saw a decreased time to drainage procedures, (11.3 vs 70.2 hours, p=0.055).[3]

Point of care ultrasound is a valuable tool during the initial evaluation of the undifferentiated hypotensive emergency department patient but should be interpreted judiciously and within clinical context to avoid unnecessary emergency procedures.


Additional Images

From GrepMed


 

echocardiogram-pericardial-tamponade-alternans-effusion

 


References

  1. Goodman, A., Perera, P., Mailhot, T., & Mandavia, D. (2012). The role of bedside ultrasound in the diagnosis of pericardial effusion and cardiac tamponade. Journal of emergencies, trauma, and shock, 5(1), 72.
  2. Alerhand, S., & Carter, J. M. (2019). What echocardiographic findings suggest a pericardial effusion is causing tamponade?. The American journal of emergency medicine, 37(2), 321-326.
  3. Alpert, E. A., Amit, U., Guranda, L., Mahagna, R., Grossman, S. A., & Bentancur, A. (2017). Emergency department point-of-care ultrasonography improves time to pericardiocentesis for clinically significant effusions. Clinical and experimental emergency medicine, 4(3), 128.

 

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Hemiplegic Migraine

Medical Student Clinical Pearl – January 2020

Alyssa BeLong, B.Sc.(Hon)

Dalhousie Medicine New Brunswick

M.D. Candidate, Class of 2021

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual


Case Presentation

A 45-year-old female presented with sudden-onset left-sided vision loss, right arm paralysis and auditory changes 24 hours ago. She subsequently developed a throbbing pain (6/10) behind her left eye which radiated over her scalp, with a sensation of water dripping down the back of her neck. Her symptoms resolved within 30 minutes except for ongoing headache and photophobia.


Differential Diagnosis

A variety of conditions may present with transient unilateral weakness or hemiplegia: (4)

  • Hemiplegic Migraine
  • Transient Ischemic Attack (TIA): Typically present with sudden onset of all symptoms rather than progression from one to another. A TIA is also less likely to present with headache, nausea, photophobia, phonophobia.
  • Brain Tumor: Typically present as progressive rather than transient neurologic symptoms.
  • Epilepsy with Post-Ictal Paralysis: Would expect paroxysmal symptoms at time of onset or change in level of consciousness as well as post-ictal confusion. Duration of symptoms also makes this unlikely.
  • Stroke-like Migraine Attacks After Radiation Therapy (SMART)
  • Other possible but rare/unlikely diagnoses include headache and neurologic deficits with cerebrospinal fluid lymphocytosis (HaNDL), CNS infection, Sturge-Weber syndrome as well as certain inherited disorders and metabolic disturbances.

Case Continued – History and Physical Exam

Clarification of visual field disturbance revealed a left homonymous hemianopia rather than loss of vision in the left eye. There was no change in speech or facial droop. There were no precipitating events and there were no alleviating or aggravating factors. The patient noted herself to be particularly stressed lately. She was otherwise healthy with a past medical history of migraines without aura many years prior. Family history was negative for thromboembolic events, she was not taking any medications and had no history of smoking or substance use.

On physical exam, the patient appeared well with all vital signs within normal limits. Cranial nerve exam was unremarkable apart from ongoing photophobia in her left eye. There was normal motor, strength, sensation, tone and reflexes bilaterally. There was no evidence of gait disturbance or dysdiadochokinesia.


Migraine Overview

Migraines typically present as severe episodic headaches often accompanied by photophobia, phonophobia and/or nausea, however presence of an aura can yield a variety of presentations. Migraines are currently thought to be neurologic in origin, although the exact pathophysiology remains unknown (2). Migraines were previously thought to be due to vascular changes, with vasodilation causing headache and vasoconstriction causing aura, however this theory is no longer viable (2).

Migraines affect 17% of women and 6% of men, with an overall prevalence of 12% (2). Migraines typically flow through four phases (2):

  1. Prodrome: Change in affect or vegetative symptoms 24-48hrs prior to onset of headache.
  2. Aura: Focal neurologic symptoms, including visual, sensory, language or motor disturbance.
  3. Headache: Often unilateral but can be bilateral, typically throbbing or pulsatile in quality, frequently accompanied by photophobia, phonophobia, nausea or vomiting.
  4. Postdrome: Sudden movement may trigger transient pain in location of the resolved headache.

While many types of migraines exist, 75% of migraines do not have an aura (2). Some patients also experience aura without headache. Factors thought to be involved in precipitation of migraine include stress, menstruation, fasting, weather, nitrates, wine and visual triggers (2, 3).  

Hemiplegic Migraine

  1. At least two attacks fulfilling criteria B and C
  2. Aura consisting of both of the following:
    1. Fully reversible motor weakness
    2. Fully reversible visual, sensory and/or speech/language symptoms
  3. At least two of the following four characteristics:
    1. At least one aura symptom spreads gradually over ≥5 minutes, and/or two or more symptoms occur in succession
    2. Each individual non-motor aura symptom lasts 5 to 60 minutes, and motor symptoms last <72 hours
    3. At least one aura symptom is unilateral
    4. The aura is accompanied, or followed within 60 minutes, by headache
  4. Not better accounted for by another ICHD-3 diagnosis, and transient ischemic attack and stroke have been excluded

Familial hemiplegic migraine requires one first or second degree relative to meet the above criteria for hemiplegic migraine. Sporadic hemiplegic migraine encompasses those who do not meet familial criteria. (4, 5).

  1.  

Treatment

Treatment of acute migraine in the emergency department follows similar principles to abortive management in an outpatient setting (6):

Abortive Agents

  • Triptans
    • Sumatriptan 6mg SC
  • Antiemetics / Dopamine Receptor Blockers
    • Metoclopramide 10mg IV, Prochlorperazine 10mg IV or Chlorpromazine 0.1mg/kg IV up to 25mg IV)
    • Diphenhydramine: given with parenteral antiemetics to prevent akathisia or dystonia. 12.5-25mg IV (q1h up to two doses)
  • Dihydroergotamine 1mg IV + Metoclopramide 10mg IV can be given if Metoclopramide monotherapy is ineffective.
  • Dexamethasone 10-25mg IV (or IM): Recommended in conjunction with the above treatments to lower risk of early headache recurrence.

In general, hemiplegic migraines can be treated the same as typical migraine with aura (4). Triptans and ergotamine are currently contraindicated due to their effect on vasoconstriction and theoretical risk of ischemic events, although this recommendation may change with evolving theory of migraine pathophysiology (4, 7).

Opioids are not recommended as first-line therapy and should not be routinely used in the acute management of migraine (6, 8).  


Case Continued – Treatment

The following medications were given in the emergency department:

  1. 10mg Metoclopramide IV
  2. 1mg Benztropine IV (for prevention of dystonia)
  3. 10mg Dexamethasone IV

Case Conclusion

The patient’s headache resolved with IV medications. She was advised to take it easy and consider scaling back on her shifts at work – a significant source of her stress. The patient was very pleased with her treatment and was discharged home.


Sources

  1. Donnelly K (2011). Homonymous Hemianopsia. In: Kreutzer J.S., DeLuca J., Caplan B. (eds) Encyclopedia of Clinical Neuropsychology. Springer, New York, NY. DOI: https://doi.org/10.1007/978-0-387-79948-3_739
  2. Cutrer F. Pathophysiology, clinical manifestations, and diagnosis of migraine in adults. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on December 23rd, 2019.)
  3. Martin VT, Behbehani MM (2001). Toward a rational understanding of migraine trigger factors. Medical Clinics of North America 85(4):911.
  4. Robertson C. Hemiplegic Migraine. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on December 23rd, 2019.)
  5. Headache Classification Committee of the International Headache Society (IHS) (2013). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia 33(9):629-808. DOI: 10.1177/0333102413485658
  6. Smith J. Acute Treatment of Migraine in Adults. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on December 23rd, 2019.)
  7. Russell MB, Ducros A (2011). Sporadic and familial hemiplegic migraine: pathophysiological mechanisms, clinical characteristics, diagnosis, and management. Lancet Neurology 10(5):457-70. DOI: 10.1016/S1474-4422(11)70048-5
  8. Friedman BW, West J, Vinson DR, Minen MT, Restivo A, Gallagher EJ (2015). Current management of migraine in US emergency departments: an analysis of the National Hospital Ambulatory Medical Care Survey. Cephalalgia 35(4):301.
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EM Reflections – January 2020

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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Trauma Reflections – December 2019

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, Trauma Codes were called 80% of time.

If a Trauma Code was called, trauma note use increased to 90% and time to disposition to an ICE setting was significantly decreased.

Please review the attached updated SIMPLIFIED activation criteria.

 

B) End of year AWARDS –  the “Crashys”

  1. ‘Crashy’ for the Busiest TTL of the Year with 17 cases …

P “I don’t see weak and dizzy patients” P

 

  1. ‘Crashy’ for the Most Trauma Intubations of the Year with 7 …

C “If he’s not move’n, I’m a tube’n” A

 

  1. ‘Crashy’ for the Most Trauma Chest Tubes of the Year with 3 …

T “Fetch me my scalpel” W

 

        Congratulations to all   (Sorry, there is no monetary gift associated with these awards!)     

 

C) Head injury, combative and on methadone – this should be easy..

Not really. Post-intubation sedation and analgesia can be challenging. Key is to avoid starting medications that could potentially drop blood pressure at very high infusion rates, but we need sedation and analgesia promptly. Under-dosing analgesic is often the reason adequate sedation is a struggle. Bolus, then increase infusion. Repeat.

 

D) End-tidal CO2 is an important vital sign

Especially in intubated patients.

 

E) Pediatric head injury transfer for imaging

Reassessing these patients on arrival, prior to CT, may influence management.

If there has been worsening in clinical condition, neurosurgery can be pre-alerted.

If there has been complete resolution of symptoms, CT scan may be deemed unnecessary.

 

F) “Clearing C-spine” can’t be done remotely..

CT C-spine is not 100% sensitive for ruling out injury. If radiologist reports there is no significant abnormality seen, it is a CLINICIAN”S responsibility to examine the neck before removing c-collar. If there is discrepancy (elevated pain, tenderness or neurologic symptoms/signs) or inability to cooperate with exam, leave the collar in place.

Make it known c-spine has not been cleared.

 

G) 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.

 

H) ‘Shock’ dosing of sedatives

Hypotension is not good for damaged neurons.

Shocked patients should have 1/2 dose of induction agents during RSI.

RSI Drugs

ADULT Rapid Sequence Intubation and Post-Intubation Analgesia and Sedation for Major Trauma Patients – NB Trauma

 

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Tardive Dyskinesia in an Emergency Setting

Medical Student Clinical Pearl – October 2019

Faith Moore

Faculty of Medicine
Dalhousie University
CC3
Class of 2021

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual



Case

A 48-year-old female was brought to the emergency department by EMS after developing dystonia that morning, a couple hours earlier, following a restless night. The dystonia had begun affecting her arms, torso and buccal region, but eventually moved to also involve her legs. She had a history of recurrent tardive dyskinesia for the past 20 years since taking stelazine and developing tardive dystonia. She was switched to olanzopine after developing dystonia and stayed on it until two months ago. Her citalopram and clozapam dosing had been increased two weeks ago, and she had also started Gingko biloba extract two weeks ago. She had started Nuplazid 3 days ago.

Upon exam she was diaphoretic with no other abnormal findings other than dystonia affecting the entire body.


Tardive Dyskinesia

Pathophysiology

    • Tardive dyskinesia is a hyperkinetic movement disorder that is associated with the use of dopamine receptor-blocking medications.1 The exact mechanism is under debate, but the main hypotheses include an exaggerated response by dopamine receptors due to a chronic dopamine blockade, oxidative stress, gamma-aminobutyric acid (GABA) depletion, cholinergic deficiency, altered synaptic plasticity, neurotoxicity and defective neuroadaptive signaling. 2 The most accepted theory of the mechanism is that the chronic dopamine blockade caused by the dopamine receptor-blocking medications results in a hypersensitivity of the receptors, specifically at the basal ganglia. 1
    • The medications that are known to have the possibility to cause tardive dyskinesia include antipsychotic drugs, anticholinergic agents (ex. Procyclidine), antidepressants, antiemetics (ex. Metoclopramide), anticonvulsants, antihistamines, decongestants (ex. pseudoephedrine and phenylephrine), antimalarials, antiparkinson agents, anxiolytics, biogenic amines, mood stabilizers and stimulants.1

Who is most at risk?

    • The medications that are the most common culprits are first- and second-generation antipsychotics and metoclopramide. The incidence of tardive dyskinesia from chronic first-generation antipsychotic exposure is 5-6% 3, and is 4% for second generation antipsychotics 4. There is no prospective research on chronic metoclopramide use and the risk for tardive dyskinesia at this point and time5, but a study in the UK in 1985 showed 1 case of tardive dyskinesia for every 35 000 prescriptions6.
      • Most prominent risk factors
        • Old age5
        • Chronic exposure5
        • Patients who develop extrapyramidal symptoms while on antipsychotic drugs.7

Signs and Symptoms

      • Repetitive involuntary body movements that may involve the face, tongue, eyes, arms, torso and legs

Diagnosis

    • The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) classifies tardive dyskinesia as “involuntary movements (lasting at least a few weeks) generally of the tongue, lower face and jaw, and extremities (but sometimes involving the pharyngeal, diaphragmatic, or trunk muscles), developing in association with the use of a neuroleptic medication for at least a few months” and that persists for at least one month after the medication is stopped.8

Differential Diagnosis

    • Acute dyskinesia
    • Akathisia
    • Parkinsonism and tremor
    • Perioral tremor
    • Stereotypies and mannerisms
    • Spontaneous or idiopathic dyskinesias
    • Isolated dystonia
    • Primary movement disorders
    • Chorea from systemic causes 9

Key Questions for History and Physical

    • Are the movements voluntary?
    • Is there an accompanied feeling of restlessness?
      • If yes, might point towards akathisia.
    • When did these movements began?
    • What is the body distribution of the involuntary movements?
    • Are there any extrapyramidal signs and symptoms?
    • Are there any associated features?
    • Have there been any drug changes in the past few months?

 

Management in the Emergency Department

    • First line treatment of tardive dyskinesia generally begins with discontinuation of the offending drug. In the emergency department this should be done after consulting with the treating physician. These patients are often being treated for psychiatric disorder and the treatment of the psychiatric disorder must be balanced with the risk of tardive dyskinesia. It may be appropriate to switch from a first generation antipsychotic medication to a second generation antipsychotic generation medication.
    • If the symptoms of tardive dyskinesia need to be treated, like in our case with this patient, there are various drugs that can be tried.
    • Tetrabenazine is considered first line.10
      • Suggested doses of 12.5-25 mg starting daily dose with a 25-200 mg/day dose range.10
    • Other treatment options
      • Dextromethorphan11
        • In a recent case study patients took under 1mg/kg, not exceeding 42 mg/day.11
        • This was recommended by a local neurologist here at the Saint John Regional Hospital.
      • Valbenazine 12
        • Suggested dose of 40 mg UID, increasing to 80 mg UID after one week.12
      • Amantadine10
        • Suggested dose of 100 mg starting daily dose with a dose range of 100-300 mg/day 10
      • Benzodiazepines12
        • Clonazepam initiated at 0.5 mg and titrated by 0.5 mg increments every 5 days to response up to a maximum dose of 3-4 mg/day. 12
      • Diphenhydramine suggested dose of 25-50 mg IV13
      • Botulinum toxin injections12
    • Commonly used treatments lacking evidence of efficacy
      • Benztropine10

Drug Starting Dose Recommendations Dose Range
1st Line
Tetrabenazine 12.5-25 mg UID 25-200 mg UID
Other options
Dextromethorphan Under 1 mg/kg Not exceeding 42 mg UID
Valbenazine 40 mg UID Increase to 80 mg after 1 week
Amantadine 100 mg UID 100-300 mg UID
Clonazepam 0.5 mg 0.5-4.0 mg UID
Diphenhydramine 25 mg IV 25-50 mg IV
Botulinum toxin injection local injection to treat specific painful dystonia resistant to systemic therapy

 


Case Continued

The patient was given 2mg of Benztropine IV with no effect. Twenty minutes later he was then given 1mg of Ativan SL with no effect. Thirty minutes later the patient was given 150 mg Benadryl IV, and some improvement was then witnessed, the patient was allowed to sleep and was discharged approximately 5 hours after his arrival with no symptoms.


External Resources

Treatment strategies for dystonia

Diagnosis & Treatment of Dystonia


References

  1. Cornett EM, Novitch M, Kaye AD, Kata V, Kaye AM. Medication-Induced Tardive Dyskinesia: A Review and Update.Ochsner J. 2017 Summer;17(2):162-174. Review. PubMed PMID: 28638290; PubMed Central PMCID: PMC5472076.
  2. Kulkarni SK, Naidu PS. Pathophysiology and drug therapy of tardive dyskinesia: current concepts and future perspectives.Drugs Today (Barc). 2003 Jan;39(1):19-49. Review. PubMed PMID: 12669107.
  3. Glazer WM.Review of incidence studies of tardive dyskinesia associated with typical antipsychotics. J Clin Psychiatry. 2000;61 Suppl 4:15-20.  PubMed PMID: 10739326.
  4. Correll CU, Schenk EM.Tardive dyskinesia and new antipsychotics. Curr Opin Psychiatry. 2008 Mar;21(2):151-6. doi: 10.1097/YCO.0b013e3282f53132.  PubMed PMID: 18332662.
  5. Rao AS, Camilleri M.Review article: metoclopramide and tardive dyskinesia.Aliment Pharmacol Ther. 2010 Jan;31(1):11-9. doi: 10.1111/j.1365-2036.2009.04189.x.  PubMed PMID: 19886950.
  6. Bateman DN, Rawlins MD, Simpson JM.Extrapyramidal reactions with metoclopramide. Br Med J (Clin Res Ed). 1985 Oct 5;291(6500):930-2. doi: 10.1136/bmj.291.6500.930. PubMed PMID: 3929968; PubMed Central PMCID: PMC1417247
  7. Novick D, Haro JM, Bertsch J, Haddad PM.Incidence of extrapyramidal symptoms and tardive dyskinesia in schizophrenia: thirty-six-month results from the European schizophrenia outpatient health outcomes study. J Clin Psychopharmacol. 2010 Oct;30(5):531-40. doi: 10.1097/JCP.0b013e3181f14098. PubMed PMID: 20814320.
  1. American Psychiatric Association, Medication-induced movement disorders and other adverse effects of medication, Diagnostic and Statistical Manual of Mental Disorders, fifth edition, American Psychiatric Association, 2013.
  2. Tarsy D, Deik A. Tardive dyskinesia: Etiology, risk factors, clinical features, and diagnosis. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on September 9, 2019.)
  1. DynaMed [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No.T113751, Tardive Dyskinesia; [updated 2018 Nov 30, cited September 9, 2019]. Available from https://www.dynamed.com/topics/dmp~AN~T113751. Registration and login required.
  1. Kim J. (2014). Dextromethorphan for Tardive Dyskinesia. International Neuropsychiatric Disease Journal. 2. 136-140. 10.9734/INDJ/2014/7970.
  2. Tarsy D, Deik A. Tardive dyskinesia: Prevention, prognosis, and treatment. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on September 9, 2019.)
  1. Buttaravoli P, Leffler SM. Chapter 1 – dystonic drug reaction. 2012:1-3. doi:https://doi.org/10.1016/B978-0-323-07909-9.00001-5 “.
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Pediatric Hip PoCUS

Pediatric Hip PoCUS

PoCUS Pearl

Dr. Sultan Ali Alrobaian

Dalhousie EM PoCUS Fellowship

Saint John, NB

@AlrobaianSultan

 

Reviewed and Edited by Dr. David Lewis


 

Case:

A 5 year old healthy boy, came to ED with history of limping since waking that morning. He had worsening right hip discomfort. No history of trauma. He had history of cold symptoms for the last 3 days associated with documented low grade fever.

On physical examination, he looked uncomfortable and unwell looking, he had temperature of 38.1 C, HR 130, BP 110/70, RR 20 and O2 saturation of 98% on RA. He was non-weight-bearing with decreased ROM of right hip because of pain.

Pelvis x-ray was unremarkable, he had WBC of 14.4 x 103  and CRP of 40 .

PoCUS of the right hip was performed.


 

Pediatric Hip Ultrasound

Ultrasonography is an excellent modality to evaluate pathologies in both the intra-articular and extra-articular soft tissues including muscles, tendons, and bursae. PoCUS to detect hip effusion can serve as an adjunct to the history and physical examination in case with hip pain.  It is easily accessible, no radiation exposure and low cost.

Technique:

The child should be in supine position. Expose the hip with drapes for patient comfort. If the patient will tolerate it, position the leg in slight abduction and external rotation. A high frequency linear probe is the preferred transducer to scan the relatively superficial pediatric hip, use the curvilinear probe if increased depth is required.

With the patient lying supine, identify the greater trochanter on the symptomatic hip of the patient. Place the linear probe in the sagittal oblique plane parallel to the long axis of the femoral neck (with the indicator toward the patient’s head).

If the femoral neck cannot easily be found, it can be approached using the proximal femur. Place the probe transversely across the upper thigh. Identify the cortex of the proximal femur and then move the probe proximally until the femoral neck appears medially, then slightly rotate the probe and move medially to align in the long axis of the femoral neck.

Assistance is often required from a parent who may be asked to provide reassurance, apply the gel and help with positioning.

Both symptomatic and asymptomatic hips should be examined.

Negative hip ultrasound in a limping child should prompt examination of the knee and ankle joint (for effusion) and the tibia (for toddler’s fracture)

Hip X-ray should be performed to rule out other causes (depending on age – e.g. Perthes, Osteomyelitis, SCFE, Tumour). Limb X-ray should be performed if history of trauma or NAI.

 

Anatomy of the Pediatric Hip:

The ED Physician should readily identify the sonographic landmarks of the pediatric hip. These landmarks include the femoral head, epiphysis and neck, acetabulum, joint capsule and iliopsoas muscle and tendon.

 

A normal joint may have a small anechoic stripe (normal hypoechoic joint cartilage) between cortex and capsule. This will measure less than 2mm and be symmetrical between hips.

 

Ultrasound Findings:

Measure the maximal distance between the anterior surface of the femoral neck and the posterior surface of the iliopsoas muscle. An effusion will result in a larger anechoic stripe (>2mm) that takes on a lenticular shape as the capsule distends. Asymmetry between hips is confirmatory. Synovial thickening may also be visualized.

FH- Femoral Head, S- Synovium, E – Effusion, FN – Femoral Neck

Criteria for a pediatric hip effusion is:

  • A capsular-synovial thickness of 5 mm measured at the concavity of the femoral neck, from the anterior surface of the femoral neck to the posterior surface of the iliopsoas muscle
  • OR a 2-mm difference compared to the asymptomatic contralateral hip

Right hip effusion, normal left hip, arrow heads – joint capsule, IP – iliopsoas


Interpretation

PoCUS has high sensitivity and specificity for pediatric hip effusion.

  • —
  • Sensitivity of 90%
  • Specificity of 100%
  • Positive predictive value of 100%
  • Negative predictive value of 92%

 

PoCUS cannot determine the cause of an effusion. It cannot differentiate between transient synovitis and septic arthritis. Diagnosis will be determined by combining history, pre-test probability, examination, inflammatory markers and PoCUS findings. If in doubt, septic arthritis is the primary differential diagnosis until proven otherwise.

Several clinical prediction algorithms have been proposed. This post from pedemmorsels.com outlines these nicely:

 

Septic Arthritis

 

 


 

Back to our case:

Ultrasonography cannot definitively distinguish between septic arthritis and transient synovitis, the ED physician’s concern for septic arthritis should be based on history, clinical suspicion and available laboratory findings.

The patient was diagnosed as case of septic arthritis. The patient received intravenous antibiotics empirically. Pediatric orthopedic consultation was obtained, and ED arthrocentesis was deferred as the patient was immediately taken to the operating room for hip joint aspiration and irrigation, confirming the diagnosis.


 

References

 

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