Wellens' syndrome

Definition:

• Wellens’ syndrome is a pattern of deeply inverted or biphasic T waves in V2-3, which is highly specific for a critical stenosis of the left anterior descending artery (LAD)
• There are two patterns of T-wave abnormality in Wellens’ syndrome:
  • Type A = Biphasic, with initial positivity & terminal negativity (25% of cases)
  • Type B = Deeply and symmetrically inverted (75% of cases)

What happens exactly?

1. Sudden occlusion of the LAD, causing a transient anterior STEMI. The patient has chest pain & diaphoresis.
2. Re-perfusion of the LAD (e.g. due to spontaneous clot lysis or prehospital aspirin). The chest pain resolves. ST elevation improves and T waves become biphasic or inverted.
3. If the artery remains open, the T waves evolve over time from biphasic to deeply inverted.
4. The LAD can re-occlude at any time. If this happens, the first sign on the ECG is an apparent normalisation of the T waves (“pseudo-normalisation”). The T waves switch from biphasic/inverted to upright.
5. If the artery remains occluded, the patient now develops an evolving anterior STEMI.

Diagnostic criteria:

• Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)
• Isoelectric or minimally-elevated ST segment (< 1mm)
• No precordial Q waves
• Preserved precordial R wave progression
• Recent history of angina
• ECG pattern present in pain-free state
• Normal or slightly elevated serum cardiac markers

Why is this important?

• Myocardial infarction occurs within a mean of 6 – 8.5 days after admission
•  Myocardial infarction occurs within a mean of 21.4 days after symptoms

Management:

• Oxygen, aspirin, nitroglycerin, and heparin are the mainstay medical treatments of unstable angina, which is what Wellens’ Syndrome is, but in this specific case early cardiac revascularization is very important!
• The treatment of choice to improve both morbidity and mortality in Wellens’ Syndrome is early PCI- these patients need to go to the cath lab!
• Stress testing is contraindicated since it can induce a massive anterior myocardial infarction

Sources:

Life in the Fastlane, R.E.B.E.L EM

Tongue Lacerations

Kids are gravitationally challenged and fall all the time! This often leads to simple bumps, bruises and minor injuries. Occasionally, kids present to the ED with tongue lacerations. -       The most common location is the anterior portion of the tongue.

-       Lacerations on the lateral side of the tongue are usually associated with seizures

-       When you find one laceration, always look for another.

Management:

-       Don’t get distracted by the obvious tongue injury.

-       It’s a trauma, so assess the airway

-       The airway can be compromised by:

o   Bleeding

o   Tongue swelling

o   Retained foreign bodies:

• Fragments of teeth
• Fragments of other objects

-       To Close or Not To Close?

o   Primary repair in the ED should be considered for tongue lacerations with the following characteristics:

• Bisect the tongue extending through the free edge – creating the “snake” look
• Have large mobile flaps or U-shaped defects (>1-2cm)
• Gaping at rest
• Won’t stop bleeding

Repair:

-       You’ll need to get everything together beforehand, and consider providing sedation. Local anesthesia can be provided with 4% lidocaine gel on gauze applied for 5 minutes, 1% lidocaine injected into the tongue, or an inferior alveolar nerve block which will block the lingual nerve and the anterior 2/3 of the tongue.

-       You also need to control the tongue and keep it protruded. This can be accomplished by grabbing the tip with forceps, or by placing a large (2-0 nylon) suture through the tip.

-       Copious irrigation without drowning the patient is important.

-      Length of the procedure is an issue for younger/sedated patients, but you also want the sutures to stay in place as they can become untied due to the normal movements of the tongue. Therefore, it is important to use absorbable sutures (4-0 chromic gut) and bury the knots in the tongue itself if possible.

-       The patient should be discharged on a soft diet for 2-3 days, and encouraged to do peroxide/chlorhexidine mouth rinses after eating. Specific follow-up is only necessary for poor healing wounds, or those that lead to problems with speech or eating. Antibiotics are not necessary.

Watch this short video showing a tongue laceration repair in a child under procedural sedation:

https://www.youtube.com/watch?v=6sbIrVIDzZk

Sources:

Pediatric EM morsels

PEMblog briefs

Blunt Cerebrovascular Injury

What is it:

• carotid and vertebral artery (together under the name cerebral vasculature) blunt injuries, which can cause neurologic problems, i.e. strokes
• rare but potentially devastating events. In the past, blunt carotid injury was associated with mortality rates ranging from 23 to 28 percent, with 48 to 58 percent of survivors suffering permanent severe neurologic deficits
• blunt injury to the carotid or vertebral arteries is usually the result of a significant force that twists or stretches the vessel, or impinges the vessel against the underlying bone, often for only a brief period of time. The carotid or vertebral artery may also be lacerated by bone that has fractured.
• multiple different mechanisms of injury is described, most commonly in significant trauma and involving hyperextension and contralateral roation, but lesser trauma has also been known to cause BCVIs (chiropractic manipulation, head-banging, coughing, shaving vomiting etc.
• regardless of mechanism, the the pathologic insult in most cases is an intimal tear. The exposed subendothelial collagen promotes platelet aggregation and thrombus formation, which may occlude the vessel altogether or embolize to the cerebral circulation.
• the tear may remain static, it may dissect, or form a pseudoaneurysm or free rupture.
• often associated with cervical spine injuries or thoracic injuries

Presentation:

• vary depending on the vessel affected, site of injury, injury grade and any pre-existing cerebrovascular disease
• approximately 80 percent of patients with blunt cerebrovascular injury have no obvious neurologic manifestations at presentation, often a latent period between the time of injury and the appearance of clinical manifestations, often >12h after event, most occur between 12-75h after event
• if symptoms, it looks like stroke

Screening:

• much debated
• it is unclear whether aggressive screening leads to improved outcomes

Indications for imaging:

• unexplained neurologic symptoms
• in asymptomatic patients with any of the risk factors
  • arterial hemorrhage from the neck, mouth, nose, or ear
  • cervical hematoma
  • cervical bruit in a patient younger than 50 years of age
  • focal or lateralizing neurologic deficit
  • presence of major thoracic trauma has been recommended as a screening criterion by a number of groups
  • mechanism compatible with severe cervical hyperextension/rotation or hyperflexion
  • severe facial trauma  and basilar skull fracture
  • closed head injury consistent with diffuse axonal injury with Glasgow Coma Score <6
  • cervical vertebral body or transverse foramen fracture, subluxation, or ligamentous injury at any level, or any fracture at the level of C1-C3
  • near-hanging resulting in cerebral anoxia
  • clothesline-type injury or seat belt abrasion associated with significant cervical pain, swelling or AMS

Different types of imaging:

• CT angio is imaging of choice
• cerebral digital subtraction arteriography (DSA) remains the gold standard for the diagnosis of blunt cerebrovascular injury, and may be necessary when the suspicion remains high in spite of other imaging, or when findings on other imaging are equivocal
• duplex ultrasound not supported for screening

Degrees of injury

• I: Intimal irregularity or dissection with <25 percent luminal narrowing
• II: dissection or intramural hematomas with ≥25 percent luminal narrowing, intraluminal clot, or a visible intimal flap
• III: pseudoaneurysm or hemodynamically insignificant arteriovenous fistula
• IV: complete arterial thrombosis
• V: transection
• for carotid lesions, stroke rates increase with increasing injury grade
• stroke incidence and neurologic outcomes are independent of blunt vertebral injury grade

Treatment:

• no controlled trials are available to help guide management
• most injuries (>99%) are not surgical, and antithrombotic therapy is the mainstay (heparin, warfarin, or antiplatelet therapy) but the optimal regimen is not known with respect to agent, duration of treatment, or end-point of therapy

Prognosis and follow-up:

• no good long-term outcome data exists comparing BCVIs to other stroke patients
• repeat imaging 7-10 days after injury or with any change in neurologic status
• if complete healing on repeat imaging, antithrombotic therapy can be discontinued
• if lesion remains, continue antithrombotic treatment but again, no known optimal duration or
• drug has been identified. Repeat imaging after 3 months is recommended.

Sources:

EAST Trauma Guidelines

Radiopedia

ATLS Guidelines