Syncope ECG – The ABCs – Resident Clinical Pearl

ECG Interpretation in Syncope

Resident Clinical Pearl (RCP) – December 2018

Dr. Luke Taylor, FMEM PGY3 –  Dalhousie University, Saint John NB

Reviewed by Dr. David Lewis

 

What are you looking for on the ECG of the patient with syncope?

Quick review of frequently pimped question on shift!

Two approaches – One using systematic ECG analysis, the other a mnemonic.

ECG Analysis (1)

Standard format of rate, rhythm, axis, and segments (PR, QRS, QT, ST).

Method of calculating heart rate (2)

Rate: Simple — Is the patient going too fast or too slow? *Remember this easy way to check:
Rhythm: Look at leads II, VI and aVR for P waves.
Ask yourself:
Are they upright in II/VI and inverted in aVR?
Does a QRS follow every P and a P before every QRS?

If so likely sinus rhythm.

In the setting of syncope we are looking to see if there is any signs of heart block – a P wave not conducted to a QRS, especially being sure not to miss a Mobitz type II block.

Axis: Axis comes in to play when looking for more extensive conduction disease. Is there axis deviation along with a change in your PR and BBB indicating something like a trifasicular block?

Segments:

PR interval— is it looooong (heart block) or short (reentrant)?
Long has already been discussed in looking for signs of heart block, but a short PR may be indicative of Wolf-Parkinson-White or Lown-Ganong-Levine syndromes.

WPW – look for short PR and delta wave
LGL – short PR but no delta wave due to its conduction being very close to or even through the AV node and not through an accessory pathway.

QRS Morphology analyzing this for signs of Brugada, HOCM, WPW, ARVD, pericardial effusion, and BBB.

ECG findings of Brugada (3)

Type 1: Coved ST segment elevation with T wav inversion
Type 2: Saddleback ST segment elevation and upright T waves
Type 3: either above without the ST elevation

QT interval — is it looooong (R on T) or short (VT/VF risk)?
Long is >450 men, 470 women
Short < 330ms – tall peaked T waves no ST segment
Pearl for long – should be less than half the RR interval. —>

Normal relationship of R-R and QT interval (4)

 

ST segment — think MI or PE (rare causes of syncope but need to be considered)
MI – elevations or depressions

PE – Tachycardia, RV strain, T-wave inversion V1-V3, RBBB morphology, S1Q3T3

 

Mnemonic (5)

ABCDEFGHII

A — Aortic stenosis
Go back to patient and listen!
B — Brugada
C — Corrected QT
D — Delta wave
E — Epsilon wave as in Arrhythmogenic Right Ventricular Dysplasia (ARVD)

Epsilon: Small positive deflection (‘blip’) buried in the end of the QRS complex (6)

F — Fluid filled heart
Pericardial effusion, electrical alternans, low voltage throughout
G — Giant PE
H — Hypertrophy
LVH in someone who shouldn’t have it
I — Intervals
PR, QRS, QT
I — Ischemia

 


Looking for a Basic ECG Guide? See our Med Student Pearl Here:

Medical Student Clinical Pearl – Basic ECG Interpretation

 


 

References

  1. CanadiaEM – ECGs in Syncope https://canadiem.org/medical-concept-ecgs-in-syncope
  2. https://en.ecgpedia.org/wiki/Rate
  3. ECG Waves https://ecgwaves.com/brugada-syndrome-ecg-treatment-management
  4. https://www.healio.com/cardiology/learn-the-heart/case-questions/ecg-cases/question-3-5
  5. Hippo EM Education Shorts https://www.youtube.com/watch?v=raTTYV7_Asl
  6. https://en.ecgpedia.org/index.php?title=Arrhythmogenic_Right_Ventricular_Cardiomyopathy

 

This post was copyedited by Dr. Mandy Peach

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Resident Clinical Pearl – Epistaxis Management in the ED – 3 Step Method

Epistaxis Management

Resident Clinical Pearl (RCP) – December 2018

Luke Taylor R3 FMEM, Dalhousie University, Saint John, New Brunswick

Reviewed by Dr. Kavish Chandra

 

It’s 0300 and you are on a solo night shift when a 76 year old male with blood dripping out of both nares is brought into an examining room. It looks a little more profuse than what you saw on Stranger Things last month, but you are also wondering how to best tackle this very common emergency problem

 

History

-Laterality, duration, frequency

-Estimated blood loss, presence of any clots?

-Inciting factors such as trauma or coagulopathy

-Past medical history, especially hypertension, clotting disorder, HHT

-Medications such as anticoagulants or anti-platelets

 

Physical examination

-Have patient blow nose or use suction to clear clots

-Do not try and visualize until decongestion complete

-Visualize with nasal speculum for site of bleeding. If an anterior bleed, most commonly the bleeding site will be Little’s area (Figure 1)

-See below for management if patient’s ABCs stable. If unstable be prepared to secure airway and call for help – ENT/interventional radiology

 

Figure 1. Nasal vascular anatomy, adapted from https://www.juniordentist.com/what-is-littles-area-or-kiesselbachs-area-and-the-arteries-in-it.html.

 

Management

-Get IV access, draw CBC and coagulation profile when indicated

-Treat as unstable until proven otherwise

 

Pearls

  • Apply ice to the hard palate (popsicles, ice in the mouth) to reduce nasal blood flow up to 25%
  • TXA in patients on anti-platelets (primarily aspirin) results in faster cessation of bleeding
  • Ducanto suction in future -> SALAD technique – Ducanto-bougie intubation for large bleeds
  • Only reverse anticoagulants if absolutely necessary – “local problem, local solution”

 

Three Step Approach to Epistaxis

1. Visualize and decongest

  1. Have patient blow their nose to clear all clots
  2. Visualize nasal cavity and oropharynx now and with each reassessment for source of bleeding. Don’t forget to wear mask and use a headlamp
  3. Soak cotton balls or pledgets in lidocaine with epinephrine and 500mg of tranexamic acid
  4. Pack nose with soaked cotton and replace clamp for 10 mins

2. Cauterize

  1. Remove clamp and packing
  2. Area should be well blanched and anesthetized
  3. Visualize plexus and cauterize proximal to bleeding area for 10 sec max AND never both sides of septum (higher risk of septal perforation)
  4. If successful and bleeding ceases on reassessment, apply surgicel wrapped around a small piece of surgifoam to create a “dissolvable sandwich”and discharge home

3. Tamponade

  1. Apply unilateral nasal packing (Rapid Rhino, Merocel, etc)
  2. Reassess in 10 mins, visualizing oropharynx for continued bleeding
  3. If stops, can discharge home with packing in place and follow up in ED or ENT clinic in 48hrs for removal. No antibiotics required in immunocompetent patients.
  4. If continues to bleed, move the patient to a higher acuity area and apply bilateral nasal packs

When to call ENT

If bilateral nasal packing bleeding continues, assume posterior bleed and initiate resuscitation, draw labs (CBC, coagulation profile, cross-match if not already done). Reverse known coagulopathy and consult for OR or embolization.

 

ED Rounds – Epistaxis

 

 

References:

Dr Christopher Chin and his informative talk

http://rebelem.com/topical-txa-in-epistaxis/

https://emergencymedicinecases.com/ent-emergencies/ 

https://lifeinthefastlane.com/epistaxis/

 

This post was copyedited by Kavish Chandra @kavishpchandra

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Resident Clinical Pearl – Scalp Lacerations – “You Can Leave Your HAT On!”

You can leave your “HAT” on: An approach to scalp lacerations and review of the hair apposition technique

Resident Clinical Pearl (RCP) – November 2018

Devon Webster – FMEM PGY1, Dalhousie University, Saint John, New Brunswick

Reviewed by Dr. David Lewis

 


Quick case!

Joe Cocker and Randy Newman had an altercation while debating who recorded the best version of “You can leave your hat on”. Randy won (mainly because he is still alive), but unfortunately he sustained a nasty head injury in the process. You deduce that he does not require a CT head but he’s got a 7 cm lac over his scalp. What should you do next?

 

Review of scalp anatomy:

The scalp is divided into 5 layers, which can conveniently be recalled using the mnemonic, SCALP:

  • Skin

    Ref 1

  • dense Connective tissue
  • Aponeurosis
  • Loose connective tissue
  • Periosteum

 

Recall that the dense connective tissue layer is richly vascularized. The tight adhesion of these vessels to the connective tissue inhibits effective vasoconstriction, hence the profuse bleeding often seen with scalp wounds.

The loose connective tissue layer = the DANGER ZONE when lacerated. This layer contains the emissary veins, which connect with the intracranial venous sinuses. Consequently, lacerations reaching this layer are high risk for spreading infection to the meninges

 

 

 

Examining the laceration:

Ref 2

Prior to choosing the most appropriate closure technique, the wound should be cleaned and cleared of debris and the depth of the wound should be determined.

  • Superficial wounds: generally do not gape and have not gone beyond the aponeurosis. Adherence to the aponeurosis should prevent the wound edges from separating.
  • Deep wounds: gape widely due to laceration of the aponeurosis in the coronal plane. Tension secondary to the occipitofrontalis muscles will pull the wound open in opposite directions.

 

Ref 2

(A) Scalp laceration that extends through the aponeurosis
(B) CT showing an associated skull fracture

 

Choosing a closure technique:

A. The HAT technique: Hair Apposition Technique

What it is: A fast and simple technique for superficial laceration closure whereby the physician twists hair on either side of the laceration together and seals the twist with a drop of glue for primary closure. Various advantages, as described below, including no need for follow up suture or staple removal.

When to use it: Consider using HAT for linear, superficial lacerations, <10 cm that have achieved appropriate hemostasis (assuming the patient has hair!).

The evidence for HAT: An RCT based out of Singapore, comparing suturing (n=93) to HAT (n=96) for scalp lacerations <10 cm found HAT to be equally acceptable if not superior to suturing. Patients were more satisfied (100% vs 75%), had less scarring (6.3% vs 20.4%), fewer complications (7.3% vs 21.5%), lower pain scores (2 vs 4), shorter procedure times (5 vs 15 min) and less wound breakdown (0% vs 4.3%) (Ref 4)

A follow up study by the same group assessing cost-effectiveness of HAT compared to suturing found a cost savings of $28.50 USD (95% CI $16.30 to $43.40) in favor of HAT when taking into consideration materials, staff time, need for removal appointments and treatment of complications (Ref 5)

A retrospective observational study comparing HAT (n=37) to suturing (n=48) and stapling (n=49) also found HAT to be superior to both suturing and stapling due to increased patient satisfaction at days 7 and 15, reduced pain, lower cosmetic issues and complication rates (Ref 6)

 

How to do HAT (see diagram):

  1. Choose 4-5 strands of hair in a bundle on either side of laceration
  2. Cross the strands
  3. Make a single twist to appose the wound edges
  4. Secure with a single drop of glue
  5. Advise patient that the glue will eventually come off on its on and no formal removal is required.

Cautions with HAT: avoid getting glue into the wound as it may result in wide scarring with a bald spot (Ref 3)

 

B. Wound Staples

If the HAT technique is not an option (no glue, bald, etc) and the lac is superficial (above the aponeurosis), staples are preferred over suturing due to Ref 3:

  • Rapid closure of wound edges
  • Non-circumferential wound closure avoid potential strangulation
  • No cross hatch marks
  • Less expensive

C. Wound Sutures

Sutures are appropriate for deep, gaping wounds or those requiring immediate hemostasis.

Suture is required for lacerations through the aponeurosis to reduce spread of infection, hematoma formation and increased scarring. Furthermore, inadequate repair of the aponeurosis may result in asymmetric contraction of the frontalis muscle (Ref 3)

 

 

Final thoughts post-closure:

  • White petroleum ointment is as effective as antibiotic ointment in post-procedural care (Ref 7). Furthermore, the next time you consider handing out bacitracin (or polysporin), recall that it was declared ‘contact allergen of the year for 2003’ by the American Contact Dermatitis Society. Bacitracin is among the top ten allergens in the US causing allergic contact dermatitis (Ref 8).
  • Wetting the wound as early as 12 hrs post-repair does not increase the risk of infection (Ref 7). Consider delaying wetting in the case of HAT.

Bottom line:

  • For superficial lacerations, <10 cm with adequate hemostatic control, the hair apposition technique is a fast, cost-effective method of wound closure with high patient satisfaction, reduced pain and lower complications compared to suturing and staples.
  • Lacerations through the aponeurosis require suturing to reduce rates of complications.
  • Consider use of petroleum jelly over antibiotic containing ointments such as polysporin.

 

Video

 


 

References:

 

1 Hunt, W. “The Scalp.” Teachmeanatomy.info. Last updated Oct 24, 2018. Accessed Nov 28, 2018. URL:  https://teachmeanatomy.info/head/areas/scalp/

2 Dickinson, E. Uptodate. Accessed Nov 28, 2018 URL: https://www.uptodate.com/contents/image?imageKey=EM%2F87633&topicKey=EM%2F16696&source=see_link

3 Hollander, J. “Assessment and management of scalp lacerations.” Uptodate. Updated Feb 23, 2018. Accessed Nov 28, 2018. URL: https://www.uptodate.com/contents/assessment-and-management-of-scalp-lacerations

4 Ong ME. “A randomized controlled trial comparing the hair apposition technique with tissue glue to standard suturing in scalp lacerations (HAT study).” Annals of Emergency Medicine. July 2002. 40:1. 19-26.

5 Ong ME. “Cost-effectiveness of hair apposition technique compared with standard suturing in scalp lacerations.” Annals of Emergency Medicine. 2005 Sept; 46(3):237-42.

6 Ozturk D. “A retrospective observational study comparing hair apposition technique, suturing and stapling for scalp lacerations.” World J Emerg Surg. 2013; 8:27.

7 Forsch, R. “Essentials of skin laceration repair.” American Family Physician.

8 Fraser, J. “Allergy to bacitracin.” Dermnet NZ. September 2015. Accessed on Nov 28, 2018 URL: https://www.dermnetnz.org/topics/allergy-to-bacitracin/

 


 Randy:

 

Joe:

 

 

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Resident Clinical Pearl: Arterial bleeding

Approach to Arterial Bleeding in the Upper Extremity

Resident Clinical Pearl (RCP) – November 2018

Tara DahnCCFP-EM PGY3, Dalhousie University, Halifax NS

Reviewed by Dr. David Lewis

This post was copyedited by Dr. Mandy Peach

You are working a shift in RAZ when a pair of paramedics wheel a man on a stretcher into one of the procedure rooms. He is sitting upright and looking around but his entire left forearm and hand are wrapped in towels, which are taped tightly down. “I don’t know what’s hurt but there was a lot of blood”, he says when questioned. He had been using a reciprocating saw in his workshop.

Vital signs: T 36.5, HR 90, BP 135/90, RR 18, O2 sats 98% on RA

You ask the nurses to find a tourniquet to put around the patients arm as you start unwrapping his giant towel mitt. You get down to the skin and find a deep 1 inch transverse laceration along the radial side of the wrist. Initially there is no active bleeding, you gingerly pock the wound and …Ooops… immediately bright red pulsatile blood starts pumping out from the distal wound edge and your scrubs will need to be change before you see the next patient.

Approach to arterial bleeding in upper extremity

Life over limb

  • Get control of the bleeding and if needed focus on other more pressing injuries. Start resuscitation if needed
  • There is no bleeding in the extremity that you can’t stop with manual compression.
  • If you can’t spare a person to compress artery then consider a tourniquet. (see Table 1 on tourniquets)
  • Avoid blindly clamping as nerves are bundled with vascular structures and can be easily damaged.

 

Determine if arterial bleeding/injury exists

Look for hard or soft signs of arterial injury (See Table 2)

If hard signs of arterial injury in major vessel the patient will need operative care. Imaging is not required unless site of bleeding is not clear (and patient is stable).
If there are soft signs of arterial injury do an Arterial Pressure Index (see Box 1) to help determine if there is an underlying arterial injury.
o If API >0.9: Patient unlikely to have an arterial injury. Observe or discharge based on nature of injury/patient.
o If API < 0.9: Possible arterial injury. Patient will need further investigation, preferably by CTA.

  • API is recommended over ABI (Ankle Brachial Index) in lower extremity injuries. ABI compares lower extremity SBP to brachial SBP. Usually patients will have more atherosclerotic disease in their lower extremities, which can falsely elevate their ABI and make it harder to detect a vascular injury. The API, on the other hand, relies on the fact that the amount of atherosclerotic disease is usually symmetric between the two upper and two lower extremities.
  • API is a very good test. An API less than 0.9 has a sensitivity and specificity of 95% and 97% for major arterial injury respectively, and the negative predictive value for an API greater than 0.9 is 99% (Levy et al., 2005).

Consider vessel injured

  • A good understanding of vascular anatomy is important to identify which vessel is injured. See figures 1 and 2.

Figure 1: Upper Extremity Arteries
(https://web.duke.edu/anatomy/Lab12/Lab13_preLab.html)

Figure 2: Lower Extremity Arteries
https://anatomyclass01.us/blood-vessels-lower-limb/blood-vessels-lower-limb-arteries-in-the-lower-leg-human-anatomy-lesson

Examine distal extremity well.

  • In the excitement of pulsatile bleeding it can be easy to be tempted to skip/rush this. But with bleeding controlled remember that the extremities are much less picky about blood supply than your vital organs. You can take a few minutes to examine the distal limbs neurovascular status (blood supply, sensory and motor, tendon integrity) and should as this will be important for management decisions.
  • Arterial injuries can very often be accompanied by nerve and tendon injuries. Complete a full assessment. See Figures 3 &4 for neurologic assessment of hand.
  • Most disability following arterial injuries is not due to the actual arterial injury, but due to the accompanying nerve injury (Ekim, 2009).

Figure 3: Motor examination of the hand. 1 – Median nerve. 2- Ulnar nerve. 3- Radial nerve (Thai et al., 2015)
Figure 4: Sensory innervation of the hand and nerve locations (Thai et al., 2015)

Explore wound carefully

  • It is important to explore the wound carefully to look for other structures damaged.
  • Examine tendons and muscles by putting their accompanying joints through a full ROM to see partial lacerations that may have been pulled out of sight.

Control bleeding definitively

Proximal arterial injuries (brachial artery, proximal radial/ulnar artery)

-All brachial artery injuries will require urgent repair by vascular surgeon.
-The “golden period” is 6-8 hours before ischemia-reperfusion injury will endanger the viability of the limb (Ekim, 2009). Degree of ischemia depends on whether injury is proximal or distal to the profunda brachii (Ekim, 2009)
-Larger more proximal arteries are rarely injured alone and will nearly all have nerve/tendon/muscle injuries also requiring operative repair

Forearm/hand arterial injuries
-Many arterial injuries in/near the hand will NOT require operative repair as there are very robust collaterals in the hand with dual blood supply from the radial and ulnar arteries in most people.

-Steps to management
Manual direct digital compression: 15 minutes direct pressure without interruption will often be successful on its own.

Temporary tourniquet application and wound closure with running non-absorbable suture followed by compact compressive dressing. If vessel obviously visible may try tying off but blindly clamping/tying will likely injury neighboring structures, particularly nerves.

Operative repair may be required if bleeding cannot be controlled with above measures.
Studies have shown that in the absence of acute hand ischemia, simple ligation of a lacerated radial or ulnar artery is safe and cost effective (Johnson, M. & Johansen M.F., 1993) however some surgeons may still opt to perform a primary repair.

 

Approach for our case

Life over limb

Patient was hemodynamically stable at presentation. IV access had already been obtained by the paramedics. Bleeding was controlled with direct pressure. When visualization was required at the site of the wound a tourniquet was used.

Determine if arterial bleeding
Our patient had a clear hard sign for arterial bleeding- pulsatile blood

Consider vessel injured
Our patients pulsatile bleeding was coming from the distal edge of the wound. Leading us to conclude that it was pulsing retrograde from the palmar arch (See Figure 5 for more detailed anatomy).

Examine distal extremity well
Our patient had a completely normal sensory and motor exam of his hand as well as normal tendon function. Lucky!

Explore wound carefully
A tourniquet was needed to properly visualize and explore the wound. There were no other injured structures identified.

Control the bleeding definitively
Direct pressure for 15 minutes did not stop the bleeding. The ends of the vessel were not identified on initial wound inspection. The wound was extended a short distance (~1cm) in the direction of the bleeding but still the vessel was not identified.

Plastic surgery was consulted. They extended the wound another 3 cm distally and were able to identify the artery, which had been transected longitudinally. They concluded that it was likely the radial artery just past the superficial palmar branch. The hand was well perfused and thus the artery was ligated. The wound was irrigated well, closed and the patient was discharged with a volar slab splint and follow up.

 

References:

Ekim, H. & Tuncer, M. (2009). Management of traumatic brachial artery injuries: A report on 49 patients. Ann Saudi Med. 29(2): 105-109.

Johnson, M. & Johansen, M.F. (1993). Radial or Ulnar Artery Laceration – Repair or Ligate? Arch Surg 128(9), 971-975.

Levy, B. A., Zlowodzki, M.P., Graves, M. & Cole, P.A. (2005). Screening for extremity arterial injury with the arterial pressure index. The American Journal of Emergency Medicine, 23(5), 689-695.

Thai, J.N. et al. (2015). Evidence-based Comprehensive Approach to Forearm Arterial Laceration. Western Journal of Emergency Medicine, 16(7), 1127-1134.

Life in the Fast Lane: Extremity arterial injury

Tinntinalli’s Emergency Medicine

 

This post was copyedited by Dr. Mandy Peach

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ECCU IP School 24th November – New Places Now Available!

Are you finding it difficult to get your supervised scans for CPoCUS Core IP. We are here to help!

We have just been able to open up a few spaces on the ECCU IP School 24th November in Saint John, NB.

CPoCUS IP instructors will supervise up to 90 scans in this 1-day session.

Book Here Now

ECCU IP School – Application and Payment

Staff Physicians – $850

Residents – $550

 

 

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Trauma Reflections – October 2018

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

 


Major points of interest:

 

A)  Intubated patients should not need restraints..

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.

Consider bolus of sedatives and analgesics prior to initiating infusions and prn boluses afterwards. Inadequate analgesia is often the cause of continued agitation.

 

B)   But what about this guy with the BP of low / really low?

Consider “vitamin K” – ketamine – can augment BP in patients who are not catecholamine depleted.

 

C)  Trauma patients you know will require consultants

When services are known to be required for patients prior to arrival (intubated, critical ortho injuries, penetrating trauma, transfers etc.) call a level A activation – consultants should meet patient with you. Give the consultants notice when patient is 15 minutes out.

Required consultants need to attend to critically injured in a timely fashion. Escalate to department head or chief of staff if there is unreasonable delay.

View the SJRHEM Trauma Page for list of definitions including Trauma Team, Activation Levels etc

 

E) Managing the pediatric airway – adrenalizing for all involved

Pediatric trauma is the pinnacle of a HALF (high acuity, low frequency) event. Team approach is key. Get out the Broselow tape.

Bradycardia with intubation attempts is not infrequent in youngest patients. Consider atropine as pre-med if  < 1 year of age or < 5 years of age and using succinylcholine.

 

F) MTP

Do not forget platelets and plasma if onto 4th unit of PRBCs – 4:1:1 ratio.

 

G)  Where is this patient being admitted?

Not to the hospitalist service, that is where!

Patients with significant injuries, but not needing immediate surgical intervention, should be admitted/observed in ICE x 24 hrs. Department head and/or chief of staff are available to assist if needed.

 

H)  Chest tube types and sizes

Pigtail catheters for traumatic pneumothorax are effective, less painful and are gaining favour as an alternative to traditional chest tubes. As for sizes, there is likely little benefit for 36F over 32 F catheters – probably time to retire these monsters from the chest tube cart.

I)     Why do bedside U/S if patient about to go to CT?

Chest scan might prompt chest tube placement prior to CT if pneumothorax is identified. Although identifying blood in the abdomen prior to CT may not change your management – it may prompt an earlier call to general surgery.

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Resident Clinical Pearl – The Acute Scrotum

What to do when the balls are in your court:

An Approach to the Acute Scrotum

Resident Clinical Pearl (RCP) – October 2018

Devin Magennis – Family Medicine, PGY2, Dalhousie University, Charlottetown PEI

Reviewed by Dr. David Lewis

 

The acute scrotum is a syndrome characterized by intense, new onset scrotal pain which can be accompanied by other symptoms such as inflammation, abdominal pain, or fever3. The incidence of acute scrotal pain is highest under the age of 153, yet it can occur at any age.  To successfully diagnosis and manage the patient with an acute scrotum it is useful to formulate a differential diagnosis using the I VINDICATE mnemonic.

Table 1- Differential diagnosis for scrotal pain organized using I VINDICATE format. The diagnoses in bold are or have the potential to be life-threatening or testicle threatening. The diagnose in Italics are common.

 

 

Review of Clinically Relevant Anatomy:

It is important to remember that during development the testicles originate in the posterior abdominal wall before migrating down into the scrotum4. Consequently, testicular pathology can present not just as scrotal pain but also as: flank pain, abdominal pain or inguinal pain2.

Once in the scrotum, the testicle sits in a vertical lie. The anterior portion of the testicle adheres to the scrotal wall via the tunica vaginalis. The tunica vaginalis is double-layered. Between these layers is a potential space for fluid to collect. Along the postero-lateral aspect of the testicle is the epididymis. It originates at the postero-superior pole, runs along the lateral aspect of the testicle down to the inferior pole4

 

Figure 1- Anatomy of the testicle. Right side of photo is anterior, left side is posterior

 

When trying to localize a patient’s symptoms it helps to divide the genital tract into segments: lower segment and the upper segment. The lower genital tract consists of the urethra. While the upper genital tract consists of the testicles, epididymis and prostate.

 

 

Testicular torsion

In a patient presenting with an acute scrotum the most important diagnosis to consider is testicular torsion1-5. Classic teaching states testicular torsion occurs in the perinatal period and during puberty. and Reported will be: sudden onset of severe unilateral testicular pain within 12 hours of presentation1. Patients will typically have had similar previous episodes, feel nauseated, may have vomited and occasionally have a history of trauma1. On inspection there will be scrotal erythema; a swollen, high-riding testicle with a horizontal lie. On palpation of the testicle it would be found to be exquisitely tender and the cremasteric reflex would be absent.

Unfortunately, testicular torsion usually does not present as described above2.  In one case series 1 in 5 patients diagnosed with testicular torsion had only abdominal pain and no scrotal pain2. While in another case series 7% of patients diagnosed with testicular torsion presented with complaints of dysuria and/or urinary frequency. Furthermore, other acute scrotal conditions have considerable overlap with the classic description of torsion2. Both epididymitis and torsion of the testicular appendage can present with sudden onset of pain2. Patients with any scrotal condition can have an absent cremasteric reflex as it is absent in 30% of the population and just to make matters more confusing, multiple case series report patients with testicular torsion still having an intact cremasteric reflex1.

 

Approach

What to ask the patient with an acute scrotum:

  • Characterize the pain
  • Location: testes, epididymis (postero-lateral aspect of testicle), upper pole of testes
  • Onset: sudden vs gradual
  • Frequency of pain
  • Radiation
  • Intensity
  • Duration
  • Events associated: trauma; dysuria, urethral discharge and urinary frequency; sexual history
  • Constitutional symptoms
  • Medical history: GU abnormalities, Recurrent UTIs, Diabetes, Alcoholism, Steroid use
  • Recent Catheterization or instrumentation of urinary tract
 

 

Physical exam for the acute scrotum

1)      Inspection:

  • Symmetry and size of testicles
  • skin erythema
  • blue dot at upper pole of testicle
  • Unilateral vein engorgement

2)      Palpation:

  • Determine site of maximal tenderness and check for masses
    • Testes
    • Epididymis
    • Upper pole of testes
    • Inguinal canal
    • McBurney’s point, Cost-vertebral angle or another abdominal or flank location

3)      Ultrasound to rule-out AAA in patients over 50

 

Management

 

The Bottom Line

  1. Testicular torsion is the one diagnosis that must be made quickly and accurately to avoid the loss of a testicle.1
  2. The classic teaching that testicular torsion can be diagnosed on history and physical exam alone is a myth. If you suspect torsion get an ultrasound and consult urology.2
  3. Torsion becomes exceedingly rare over the age of 25; however it is still possible.1
  4. Abdominal aortic aneurysm, appendicitis, nephrolithiasis and other causes of abdominal and flank pain can present as scrotal pain. Testicular torsion can present as abdominal or flank pain.2

 

References:

  1. Jefferies MT, Cox AC, Gupta A, Proctor A. The management of acute testicular pain in children and adolescents. BMJ. 2015;350:h1563. doi: 10.1136/bmj.h1563 [doi].
  2. Mellick LB. Torsion of the testicle: It is time to stop tossing the dice. Pediatr Emerg Care. 2012;28(1):80-86. doi: 10.1097/PEC.0b013e31823f5ed9 [doi].
  3. Lorenzo L, Rogel R, Sanchez-Gonzalez JV, et al. Evaluation of adult acute scrotum in the emergency room: Clinical characteristics, diagnosis, management, and costs. Urology. 2016;94:36-41. doi: 10.1016/j.urology.2016.05.018 [doi].
  4. Drake R, Vogl AW, Mitchell AWM. Gray’s anatomy for students. Saint Louis: Elsevier; 2014. Accessed 8/11/2018 11:47:58 AM.
  5. Rottenstreich M, Glick Y, Gofrit ON. The clinical findings in young adults with acute scrotal pain. Am J Emerg Med. 2016;34(10):1931-1933. doi: S0735-6757(16)30284-4 [pii].

 

 

This post was copyedited by Dr. Mandy Peach

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Medical Student Clinical Pearl – Basic ECG Interpretation

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

Medical Student Clinical Pearl – October 2018

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

Reviewed and Edited by Dr. David Lewis


Physiology

Electrical Events and Corresponding Waves and Lines on a Standard ECG

Basic Interpretation

Common Arrhythmias

Summary

Suggested Resources

References


Physiology

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

 

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


Electrical Events and Corresponding Waves and Lines on a Standard ECG

P Wave

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

PR Interval

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

PR Segment

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

QRS Complex

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

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

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

ST Segment

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

T Wave

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

QT Interval

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


 

Basic Interpretation

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

 

A. Determine Rate:

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

Thaler 2015

 

B. Intervals:

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

Normal Interval Lengths5:

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

 

 

 

 

 

 

 

C. Rhythm5:

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

 

D. Axis

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

 


 

Common Arrhythmias1

1. Sinus Tachycardia

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

 

2. Sinus Bradycardia

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

 

3. Paroxysmal Supraventricular Tachycardia

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

 

4. Atrial Flutter

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

 

 

5. Atrial Fibrillation

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

 

6. Premature Ventricular Contractions

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

 

 

7. Ventricular Tachycardia

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

 

8. Ventricular Fibrillation

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

 


 

Summary

 


 

 


 

Suggested Resources

Teaching Medicine – Rhythm Strip Interpretation Practice

ECG Guide Mobile Smartphone App

  • Available through itunes app store

The Only EKG Book You’ll Ever Need

  • PDF available online through Dalhousie Library

 

References

  1. Thaler, M. S. (2015). The Only EKG Book You’ll Ever Need (9th ed.). Lippincott, Williams & Wilkins.
  2. Andrade, J. (2013). ECG Guide [Mobile application software]. Retrieved from http://itunes.apple.com
  3. Dubin, D. (2000). Rapid interpretation of EKG’s: An interactive course (6th ed.). Tampa, Fla.: Cover Pub.
  4. McKinley, M. P., OLoughlin, V. D., Harris, R. T., & Pennefather-O’Brien, E. E. (2015). Human anatomy (4th ed.). New York, NY: McGraw-Hill Education.
  5. Khan, M. (2008). Rapid ECG interpretation (3rd ed., Contemporary cardiology (Totowa, N.J). Totowa, N.J.: Human Press.
  6. Thomas, V. (n.d.). Premature Ventricular Contractions Treatment Cape Town. Retrieved from https://cardiorhythm.co.za/premature-ventricular-contractions/
  7. https://inside.fammed.wisc.edu/medstudent/pcc/ecg/axis.html
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EM Reflections – October 2018

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

Edited by Dr David Lewis 

 


 

Top tips from this month’s rounds:

 

Trauma – Secondary Survey

DNAR Considerations 

ED Neonatal Equipment

 


Trauma – Secondary Survey

The secondary survey is performed once the primary survey and resuscitation has been completed.

The secondary survey does not begin until the primary survey (ABCDEs) is completed, resuscitative efforts are underway, and the normalization of vital functions has been demonstrated. When additional personnel are available, part of the secondary survey may be conducted while the other personnel attend to the primary survey. In this setting the conduction of the secondary survey should not interfere with the primary survey, which takes first priority. ATLS 9e

This means that on occasions trauma patients may be transferred to the OR or ICU before the secondary survey has been completed. The secondary survey is a thorough head to toe examination including where indicated adjunct investigations e.g limb radiographs. This assessment must be carefully performed and documented. It should not be rushed.

If there is not enough time to complete a thorough secondary survey (e.g patient transferred to OR during primary survey) then this should be communicated to the surgeon or other responsible physician (e.g ICU) and the documentation should reflect this.

We would recommend that all trauma patients admitted to the ICU undergo a repeat secondary survey assessment as part of the standard admission process. In some systems this is referred to as a Tertiary survey.

This systematic review reports a reduction missed injury rate when a tertiary survey is used as part of a trauma system.

Trauma.org article on tertiary survey


DNAR Considerations 

The CMPA provides excellent guidance for clinicians considering Do Not Attempt Resuscitation orders. CMPA Website

CMPA – Key Concepts for End of Life Issues

  • The best interests of the patient are paramount.

  • The capable patient has the right to consent to or refuse medical treatment, including life-sustaining treatment.

  • Thoughtful and timely advance care planning, discussion, and documentation of a patient’s wishes and healthcare goals can help avoid misunderstandings.

  • Physicians should be familiar with any relevant laws and regulatory authority (College) policies concerning end-of-life care, and the withholding or withdrawing of life-sustaining treatment, and medical assistance in dying.

  • When considering placing a do-not-resuscitate order in the medical record, or acting upon a do-not-resuscitate order, consent from the patient or substitute decision-maker is advisable. It may also be helpful and appropriate to consult with physician colleagues and the patient’s family to determine support for the order.

  • Decisions about withholding or withdrawing life-sustaining treatment that is considered futile or not medically indicated should be discussed with the patient, or the substitute decision-maker on behalf of an incapable patient. When consensus is not achieved despite discussions with the substitute decision-maker, the family, and others such as ethics consultants, patient advocates, and spiritual advisors, it may be necessary to make an application to the court (or an administrative body) or seek intervention from the local public guardian’s office.

  • Physicians considering a request for medical assistance in dying should be familiar with the eligibility criteria set out in the Criminal Codewith applicable provincial legislation, and with applicable regulatory authority (College) guidelines.

  • Physicians should be familiar with the role of advance directives (including living wills).

  • End-of-life decisions should be carefully documented in the patient’s medical record.

Horizon Health, NB uses these accepted Canadian DNAR definitions:

 


 

ED Neonatal Equipment

Perinatal Services BC, Canada have published an excellent document – Standards for Neonatal Resuscitation

It includes this Appendix for suggested Radiant Warmer Equipment checklist:

 

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ED Rounds – Competency By Design

ED Rounds – September 2018

Dr. Jo-Ann Talbot

 


 


Competency-based medical education (CBME) is an outcomes-based approach to the design, implementation, assessment, and evaluation of a medical education program using an organizing framework of competencies.

Competence by Design (CBD) is the Royal College’s version of CBME. It is a transformational change initiative designed to enhance CBME in residency training and specialty practice in Canada.

The first stage in residency is known as Transition to discipline. It emphasizes the orientation and assessment of new trainees. Foundations of discipline, the second stage, covers broad-based competencies that every trainee must acquire before moving on to the third stage, which is known as Core of discipline. The third stage covers more advanced, discipline-specific competencies. As part of CBD, the Royal College is also exploring moving the Royal College exam to the end of this stage.5 The fourth and final stage of residency education is known as Transition to practice. During this stage the trainee demonstrates readiness for autonomous practice

RCPSC 2016


 

Dr. Talbot’s Presentation

Competence by Design – Are You Ready?

Competency by Design Are You Ready? Dr. Jo-Ann Talbot – 2018

Click link above to view


Further Reading

CBD Cheatsheet

Download (PDF, 128KB)


Emergency Medicine – Entrustable Professional Activities 

Download (PDF, 71KB)


 

Entrustable Professional Activity Guide: Emergency Medicine

EPA-guide-emergency-medicine RCPSC 2018

Click link above to view


 

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EM Reflections – September 2018

Thanks to Dr. Joanna Middleton for leading the discussions this month

Edited by Dr David Lewis 

 

 


 

Top tips from this month’s rounds:

 

Pediatric Head Injury

Clonazepam Toxicity

Pediatric(< 3 months)Fever

Wide Complex Tachycardia

 


Pediatric Head Injury

  • What are the criteria for CT Head?

In a recent Lancet article (2017),  PECARN, CATCH and CHALICE were compared.

The highest point validation sensitivities were shown for PECARN in children younger than 2 years (100·0%, 95% CI 90·7–100·0; 38 patients identified of 38 with outcome [38/38]) and PECARN in children 2 years and older (99·0%, 94·4–100·0; 97/98)

  • How do I use PECARN?


 

A useful review by EM Cases can be accessed here. In an update to this review they have noted recent new evidence that isolated vomiting without any other positive rule predictors may warrant observation only:

Update 2018:  A secondary analysis of the Australasian Paediatric Head Injury Rule Study demonstrated head injury with isolated vomiting (i.e. vomiting without any of clinical decision rule predictors) was uncommonly associated with TBI on CT, or the presence of clinically important TBI.  This study suggests a strategy of observation without head CT may be appropriate management.  Abstract

Vomiting alone should not instigate CT.  Risk goes up with any other Head Injury symptoms (Headache etc). These children should be observed until they are able to tolerate oral intake and the treating clinician feels comfortable that the patient is stable without additional symptoms of head injury.

This article discusses linear skull fractures. It reminds us to always consider Non-Accidental Injury in all cases of pediatric head injury, especially in the pre-mobile age group.

PoCUS may have a role to play in fine tuning risk stratification and a recent study (2018) has further evaluated diagnostic accuracy:

We enrolled a convenience sample of 115 of 151 (76.1%) eligible patients. Of the 115 enrolled, 88 (76.5%) had skull fractures. POCUS had a sensitivity of 80 of 88 (90.9%; 95% CI 82.9-96.0) and a specificity of 23 of 27 (85.2%; 95% CI 66.3-95.8) for identifying skull fractures.

  • If I don’t perform a CT, then how long should a child with a head injury be observed?

There is no definite evidence-based answer to this question. However this study suggest that 6 hrs is probably safe.

Key Points

  1. Always use a clinical decision rule to determine whether a child with head injury requires CT, Observation or can be safely discharged
  2. When using a decision rule utilize a ‘shared decision-making’ philosophy – i.e involve the parents/carers
  3. A period of observation can reduce the number of CTs performed.
  4. If observation is recommended, then allow 6hrs.
  5. Always consider non-accidental injury during your assessment of pediatric head injury.

 

 


 

Clonazepam Toxicity

  • Overdosage of clonazepam may produce somnolence, confusion, ataxia, diminished reflexes, or coma
  • Clonazepam is extensively metabolized in the liver to several metabolites
  • Clonazepam is rapidly and well absorbed from the GI tract
  • Peak blood concentrations are reached in 2 -4 hours
  • Elimination half-life … 18.7 to 39 hr

Full ToxNet entry

Treatment

Treatment is entirely supportive with IV access and fluids and maintenance of the airway and ventilation if required

Oral activated charcoal is of little value in pure benzodiazepine poisoning. It may be given to patients who have recently ingested benzodiazepines with other drugs that may benefit from decontamination

Flumazenil is rarely indicated except for iatrogenic oversedation or respiratory depression. In addition, flumazenil may cause withdrawal states and result in seizures, adrenergic stimulation, or autonomic instability in patients chronically taking benzodiazepine, or in those with ventricular dysrhythmias and seizures who are concomitantly using cocaine or tricyclic antidepressants.

Dispostion

All patients with intentional ingestion or significant ataxia, drowsiness, or respiratory depression should be observed.

Patients with severe symptoms (ie, coma, respiratory failure, or hypotension unresponsive to IV fluids) should be consulted to ICU.

Given the prolonged half-life patients strongly consider admitting patients who present with significant drowsiness or are known to have taken a large overdose.

Patients with a significant sedative drug overdose should be advised not to drive until potential interference with psychomotor performance has resolved. For significant benzodiazepine overdose, this is at least 24 hours after discharge.

Key Points

  1. Clonazepam overdose is treated with supportive measures.
  2. Clonazepam has a very long half-life. For significant drowsiness, admission should be considered to avoid potentially very long ED observation periods.

 


Pediatric (< 3 months) Fever

The management of fever in infants less than 1 month is relatively straightforward. Guidelines are generally consistent (Merck,

  • Full blood lab work-up (CBC, CRP, Cultures)
  • Urine culture
  • CXR
  • RSV, Flu nasal swabs
  • LP
  • Empiric IV Antibiotics (e.g Ampicillin 50mg/kg and Cefotaxime 50mg/kg)
  • Consult Pediatrics and Admit

Emergency Medicine Cases article can be viewed here – Episode 48 – Pediatric Fever Without A Source

*********

For infants older than 30 days and younger than 3 months the guidelines are variable:

ALiEM: Paucis Verbis: Fever without a source (29 days-3 months old)

NICE Guidelines (UK):  Fever in under 5s: assessment and initial management

MD Calc – Step-by-Step Approach Calculator 

Suggested Emergency Department Approach

  • If Sick-Appearing treat as <3 months (see above)
  • If Well- Appearing (age normal vitals):
    • Full blood lab work-up (CBC, CRP, Cultures)
    • Urine culture
    • Consider CXR
    • Consult Pediatrics (Depending on results of above will either need admission +/- antibiotics or 24hr follow-up)

Yukon Guidelines


 

Wide Complex Tachycardia

Differential Diagnosis (note: repetition is deliberate!)

  • Ventricular Tachycardia
  • Ventricular Tachycardia
  • Ventricular Tachycardia
  • SVT with aberrant conduction – lots of causes
    • Pre-existing/rate-related BBB
    • Ventricular pre-excitation (AVNRT/AVRT)
    • Dysfunction of IV conduction system (toxic, metabolic, infectious, drug related etc) – hyper K, sodium channel blockers

No ‘rule’ is specific enough to correctly identify, so treat like VT

Treatment 

  • Unstable?
    • ANY sign of end-organ dysfunction – hypotension, altered LOC, CHF/SOB, CP, diaphoretic etc
    • SHOCK
  • Stable?
    • Shock or medical management
    • Amiodarone vs procainamide, ?adenosine (see below)

Adenosine/vagal – consider in patients where uncertain of diagnosis, unlikely to be VT, no hx of CAD, young, hx of SVT

Adenosine with WPW – ContraIndicated – may induce AV block and accelerate conduction of atrial fibrillatory impulses through the bypass tract, which can lead to very rapid ventricular arrhythmias that degenerate to VF.

“Avoidance of IV beta blockers, calcium channel blockers and digoxin due to the potential for hemodynamic deterioration in patients with stable WCT, potentially resulting in hypotension, VF and cardiac arrest”. (Uptodate)

Verapamil and diltiazem are calcium channel blockers (CCBs) that should be avoided in WCTs, as cardiac arrests from hemodynamic collapse have been reported following their administration.  Not only do these agents cause negative inotropy and at times profound vasodilation, but they may also allow WCTs to degenerate into VFIB

Caveat – RRWCT (Regular Really Wide Complex Tachy)

  • One situation where you may not want to assume VT….
  • What question should you ask?
    • What is the K,
    • what is the OD?
  • Really, really wide complex tachycardia – >200 mseconds – consider tox or metabolic – try bicarb or calcium – if it narrows – not VTach.
  • Avoid procainamide and amiodarone in these patients.

 

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