COVID-19 Testing in New Brunswick

COVID Journal Club Rounds – April 2016

Dr Jo-Anne Talbott


Key Questions

  • Who should we test for COVID
  • Who can we test with the Rapid COVID test
  • What is the sensitivity and specificity of the tests
  • What are the rates of positive tests in New Brunswick
  • Will we move to testing serum for IgG, IgM

RT-PCR Test

Reverse transcription polymerase chain reaction (rRT-PCR) test

ID Microbiologists at the George Dumont used  recommended processes to develop a test for the qualitative detection of nucleic acid from SARS-CoV-2 in upper and lower respiratory specimens

Their results were validated by the National Microbiology Lab in Winnipeg, Manitoba


Rapid COVID Test

  • Xpert Xpress SARS-CoV-2 assay is performed on the GeneXpert platform
  • Rapid test used in SJRH Microbiology Lab
  • Clinically suspected COVID-19 in
    • patient currently in the ICU or being admitted to the ICU
    • pregnant patient currently in labour and being admitted
    • your clinical judgement a rapid test is required
  • Call Microbiology MD

Full Presentation

Download (PDF, 19.97MB)

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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 is updated regularly

SJRHEM COVID-19 Pages


COVID-19

New Brunswick Public Health – Link

Trauma New Brunswick Program

WorkSafe New Brunswick


Academic Activity – Dal, DMNB, Residents, News, Cancellations


Staff Wellness

 


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

COVID-19 – SOURCES OF INFORMATION

SJRHEM GRAND ROUNDS

 


SJRHEM Activity During the Pandemic


NB Health Screening Tool and Referral forms to Community Assessment Centres – 27 May 2020 

For community referral for COVID-19 screening and testing:

Referral Form – Combined Referral and Order Form

FAX Number = 506 462-2040

 


Horizon Screening Questions – May 29

Download pdf

 


Self-Isolation Information Leaflet for Patients

Self-Isolate and Alternative Self-Isolate Leaflet

Self Management COVID

 

 


 

COVID-19 Testing – Public Health Advice and Viral Swabs 

Summary of Current Guidance (May 26)

“Every New Brunswicker should remain vigilant,” said Dr. Jennifer Russell, chief medical officer of health. “Please continue to limit your close contacts to prevent the chance of spreading the virus, especially to those who are more vulnerable to complications of COVID-19. Although community transmission has not been confirmed, it is important to be aware that it remains a possibility.”

Up-to-date information about COVID-19, including the latest data on confirmed cases and laboratory testing in New Brunswick is available online.

New Brunswick is currently in Phase 3 (Yellow) of the COVID-19 recovery. Information on public health recovery phases, measures and guidelines is available online.

Dr. Jennifer Russell, chief medical officer of health, announced that testing would now be recommended for people exhibiting at least two of the following five symptoms:

  • fever above 38°C or signs of fever;
  • a new cough or worsening chronic cough;
  • sore throat;
  • runny nose;
  • headache:
  • New onset fatigue;
  • New onset muscle pain;
  • Diarrhea;
  • Loss of sense of taste or smell; and
  • In children, purple markings on fingers or toes

Those who are exhibiting at least two of these symptoms are advised to immediately self-isolate and contact 811 or their family physician for further direction. Symptoms can range from relatively mild (runny nose and sore throat) to severe such as difficulty breathing.

Summary of Current Guidance  (April 2):

The COVID-19 pandemic is rapidly evolving around the world and within Canada. At variable points in the last few weeks, many parts of Canada including Quebec have started seeing community transmission. This had led to additional concern and control measures applied to travel outside of the province. In addition, New Brunswick is now also entering the community transmission phase.

Because of these dynamics, we will be transitioning from focusing on identifying cases imported into the province as a control measure to focusing testing priorities in our province on protecting our most vulnerable populations/settings and maintaining critical health system capabilities.

Given this transition, the following are key points when clinically evaluating patients (virtually or in person) and deciding on testing:

  • Conduct a clinical assessment – clinical case definition still includes fever/history of fever and/or new onset/exacerbation of chronic cough. Other symptoms may include headache, sore throat or coryza.
    • Test those with moderate to severe symptoms (such as signs of pneumonia, dyspnea, blood O2 saturation <94%) including those who require hospitalization.
    • Recommend testing patients with risk factors such as age 60 +, hypertension, cardiovascular disease, chronic respiratory disease, diabetes, and cancer.
    • People living in crowded settings or limited capacity to self-isolate due to same

Assessment centers will be testing all referrals moving forward, and not providing secondary screening, so please ensure referrals have been clinically assessed appropriately, virtually or in person, prior to completing a referral form.

  • Test Priority groups (even with mild symptoms) – to maintain the integrity of the health care system and prevent transmission in clinical and other vulnerable group settings
    • Symptomatic health care professionals, such as physicians, nurse practitioners, nurses, pharmacists, laboratory technologists, Ambulance NB, first responders, emergency medical dispatchers, Extra Mural program
    • Staff in hospitals, nursing homes, and other institutional or group living settings with direct patient care/contact
    • Patients/residents in institutional and group living settings with vulnerable populations (including within RHA, long term care, shelters, correctional facilities, adult residential facilities)
  • Consider and inquire about exposure criteria (travel outside New Brunswick or close contact/group exposure setting (ie gathering, work setting), either within the last 14 days), but absence of such no longer excludes a patient from testing. Identification of exposure risks and clusters remains a critical public health strategy in managing COVID-19 even in the context of community transmission.
  • There are no specific directives to NOT test certain individuals or groups of individuals at this time, continue to use your professional judgement but please be aware that the situation may change quickly in the coming days to weeks, depending on capacity.
  • Full Document Here – April 2
  • 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

 


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

 


Further Reading and Viewing

 

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Acute Kidney Injury

Medical Student Clinical Pearl – January 2020

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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EM Reflections – December 2019

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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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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