Community EM

Thumb’s Up for Diagnosing and Managing UCL Injuries

Case

32 year old right handed man presents with right thumb pain after a mechanical fall from standing onto steps.  While falling, his outstretched thumb caught on a step.  He denies other injury.  On exam, he has pain and swelling at the thumb MCP joint.  There is a palpable lump on the ulnar side of the base of his thumb.  He has full ROM and intact strength in the affected digit.

What are the next steps in this patient’s management?

Epidemiology

  • Most commonly occur in athletes when a force causes thumb abduction
  • Skiing accidents in which the thumb is abutted against a fixed pole are the prototypical injury
  • More common in males with a ratio of 3:2
  • Complete ulnar collateral ligament tears can occur by non-sport related falls, motor vehicle crashes in which the hands are on the steering wheel, or bicycle injuries from handlebars

UCL anatomy

  • Runs from middle of metacarpal head to the volar aspect of the proximal phalanx
  • Provides structural strength to the thumb
  • Resists valgus load to thumb

Mechanism of Injury

  • Hyper-extension or abduction of the thumb causes the UCL to avulse from the proximal    phalanx
  • Acute injuries result in a complete or partial tear of the ligament
  • Avulsion fractures of proximal phalanx may or may not be present

Clinical Presentation

  • Acute injuries present with pain and swelling of the base of the thumb
  • Chronic injuries, also known as Gamekeeper’s thumb, present with loss of strength of the   thumb and deformity

Traditionally, this injury was originally described in people who manually and repetitively sacrificed small game by breaking the animal’s neck.

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Exam

  • Cornerstone of diagnosis
  • Goal of exam is to evaluate joint stability
  • Valgus stress of the MCP joint reveals increased laxity
  • Test in both neutral position and with MCP joint fully flexed.  Fully flexing the joint isolates the UCL from the volar plate, which can provide additional stability
  • Angulation of >35 degrees, or a difference of >15 degrees between hands signifies a        positive test.
  • In partial tears, the loss of a distinct endpoint while stressing may be noted

Stener lesion

Occurs when the proximal end of the completely torn ligament is pulled from its normal location deep to the abductor aponeurosis and then fails to reduce itself properly, remaining superficial to the aponeurosis   

  • Present in up to 50% of complete UCL tears.
  • Exam may note a palpable lump
  • Surgical intervention is required
  • Stressing the MCP has NOT been shown to cause a Stener lesion where one did not already exist.
  • Pinch grip may be reduced in both acute and chronic injuries

ED Evaluation

  • Plain films to evaluate for avulsion fracture of proximal phalanx
  • Stener lesion will not be evident of plain films
  • Ultrasound has not been fully validated in diagnosis UCL tears
  • MRI is not cost effective in the ED, but may be obtained in follow-up in consultation with a hand surgeon

ED Management

  • Thumb spica is hallmark of ED management, allowing for immobilization of thumb MCP joint
  • If joint deemed unstable, follow-up within 1 week to a hand surgeon is advised to allow for surgical planning.  A delay in surgery can cause contracture of the UCL and increases  likelihood of chronic instability
  • For stable injuries, non-urgent follow-up within 4 weeks is recommended.

Faculty Reviewer: Dr. Kristina McAteer

References

  • Germano, T.  Falls on the Out-Stretched Hand and Other Traumatic Injuries of the Hand and Wrist: Part II.  Emergency Medicine Reports:  The Practical Journal for Emergency Physicians.  Volume 28, Number 18.  August 20, 2007.
  • Gammons, M et al.  Ulnar collateral ligament injury (gamekeeper's or skier's thumb).  Retrieved from UpToDate.com.  Accessed 4/21/2018.
  • Richard, JR.  Gamekeeper’s Thumb:  Ulnar Collateral Ligament Injury.  Am Fam Physician.  19

 

Community Case: Not Your Average Fainting Spell

A 36-year-old woman came into the ED by EMS with multiple ‘fainting spells’ throughout the day (her family thought it was because her blood sugar was low at 83 when they checked at home and treated with glucagon and candy).  I was handed this EKG by the receiving nurse:

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I walk into the Trauma Room to find a woman who is awake, alert, diaphoretic, and talking. I get handed this next EKG:

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Moments later the patient becomes suddenly unresponsive and this is what we see:

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Torsades de Pointes (TdP) = Polymorphic V Tach (PVT) + Long QT

So then what did we do?

*   Gave Magnesium 2 mg IV bolus x 2 immediately

*   iSTAT showed K 2.6 so started aggressive repletion, placed central venous access to increase rate of safe repletion

*   Started Magnesium drip, gave magnesium bolus PRN anytime there were prolonged runs of TdP

*   Gave lidocaine bolus 100 mg (dose can range from 0.5 to 0.75 mg.kg up to 1 to 1.5mg/kg)

*   Shocked patient three times (during prolonged runs of TdP associated with unresponsiveness):

 Blue arrow indicates defibrillation; return of NSR afterward

Blue arrow indicates defibrillation; return of NSR afterward

*   Gave isoproterenol after confirming no history LQTS or prior prolonged QTc on prior EKGs (initial dose 0.05 to 0.1 mcg/kg/min in children and 2 mcg/min in adults)

*   She was transferred to the cardiology service in good condition, awake and alert

Torsades de Pointes ECG Pearls:

·      Long QT + PVT with characteristic morphology that seems to twist around isoelectric line

·      QT interval is inversely proportional to heart rate (HR)

o   The QT shortens at faster HR

o   The QT lengthens at shorter HR

o   There are formulas to calculate the QT interval (https://lifeinthefastlane.com/ecg-library/basics/qt_interval/)

·      TdP with HR >220 more likely to degenerate into VF

·      Bigeminy in a patient with known LQTS may herald imminent TdP:

 This was the prehospital EKG

This was the prehospital EKG

Presence of abnormal giant T-U waves may also precede TdP.

Pathophysiology of TdP:

·      A prolonged QT reflects prolonged myocyte repolarization due to ion channel malfunction

·      This prolonged repolarization period also gives rise to early-after-depolarizations (EADs)

·      EADs may manifest on ECG as tall u waves; if these reach threshold amplitude, they may manifest as PVCs

·      TdP is initiated when a PVC occurs during a preceding T wave, known as ‘R-on-T’ phenomena

·      The onset of TdP is often preceded by a sequence of short-long-short PR intervals, so called ‘pause-dependent’ TdP with longer pauses associated with faster runs of VT

Clinical Significance:

·      TdP is often short lived and self-terminating, however can be associated with hemodynamic instability and ultimately may degenerate into ventricular fibrillation

·      If it does not spontaneously convert and the patient is unstable, it will need defibrillation

·      QT prolongation may be acquired and occur secondary to multiple drug effects, electrolyte abnormalities, medical conditions, or congenital long-QT syndrome (LQTS)

·      Recognizing the cause of TdP (acquired vs. congenital) allows initiation of specific treatment strategies

*   Defibrillation if unstable

*   Give magnesium (Mg 2-4 grams IV push followed by Mg drip of 3-10 mg/minute)

*   Removal of offending agent in acquired long QT

*   Correct any electrolyte abnormalities (especially hypoMg, hypoK, hypoCa)

*   Correct contributing factors such as respiratory alkalosis (which can worsen hypoK, etc)

*   Remove any offending agents (such as certain anti-arrhythmics, antibiotics, anti-emetics, psychotropics, or methadone)

*   Lidocaine may help because it can suppress PVCs, and therefore stop the R-on-T phenomena

*   Overdrive Pacing (usually at a rate of 100 bpm due to heart rate dependent effects of QT)

*   Only in acquired long QT: beta-adrenergic stimulation with isoproterenol

*   Only in LQTS: give beta-blockade (start with esmolol, then propranolol if not effective)

*   Patients with LQTS may require permanent pacing and ICD

*   Amiodarone may be harmful because it lengthens the QT interval and can possibly cause PVCs (although amiodarone has never been specifically shown to cause Torsades)

ACC/AHA/ESC Guidelines:

The 2006 American College of Cardiology/American Heart Association/European Society of Cardiology (ACC/AHA/ESC) guidelines for the management of ventricular arrhythmias and the prevention of SCD addressed the management of TdP in the setting of acquired LQTS:

*   Intravenous magnesium

*   Temporary pacing

*   Isoproterenol

References:

· Up To Date: https://www.uptodate.com/contents/acquired-long-qt-syndrome?source=search_result&search=torsades%20de%20pointes&selectedTitle=1~150

· Life In the Fast Lane: https://lifeinthefastlane.com/ecg-library/basics/qt_interval/

· HQMedEd:   http://hqmeded-ecg.blogspot.com/2013/10/polymorphic-ventricular-tachycardia.html

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

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Faculty Reviewer: Dr. Kristina McAteer

Tales From the Community: A Bike Wipeout

 

A 35 year old male is biking when he crosses are area of sand on the road. The bike fishtails and he falls onto his left shoulder. He was helmeted and denies head trauma, neck pain, or LOC. The patient is holding his left arm close to his side and across his chest. On physical exam there is a prominent acromion and coracoid anteriorly.

 

What Injury does this mechanism and presentation correlate with?

Posterior Shoulder Dislocation

 

Incidence:

Posterior Shoulder dislocations account for only 2-4% of all shoulder dislocations. Most commonly they are associated with or caused by seizure, electrical shock, FOOSH or a direct blow to the shoulder, as occurred in this patient. Given the atypical presentation, they are missed in up to 50% of cases on initial presentation.

 

Presentation:

On presentation the patient will usually presents with the arm adducted and internally rotated. More so than in an anterior shoulder dislocation, movement, especially abduction or external rotation is very painful. A prominent acromion and coracoid are palpable, with the humeral head displaced posteriorly.

 

Radiographs:

The deformity can be very subtle on the Anterior/Posterior view and most reliably visualized on the Axillary or Transscapular Y views. On the anterior/posterior view classically shows a “light bulb sign”.  This occurs when the humeral head is forced into internal rotation as it dislocates posteriorly, giving it the appearance of a light bulb.

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Another characterstic sign on radiograph after a posterior shoulder dislocation is the “Trough Sign”. This may be present when the dislocation results in a Reverse Hill-Sachs deformity. Radiographs will show a loss of overlap of the humeral head and glenoid fossa.

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Reduction:

In general, Traction - CounterTraction is the most efficacious means to reduce this dislocation. In addition to the traction, gentle pressure to the humeral head in the posterior and lateral directions can be helpful to disengage the humeral head from the posterior glenoid. In our case above, gentle pressure to the humeral head quickly disengaged the humerus from the glenoid and under procedural sedation the patients shoulder was reduced on first attempt.


Disposition:

Similar to anterior dislocations after a posterior shoulder dislocation is reduced, the patient is placed in a sling and swath and discharged with orthopedic follow-up and instructions for non-weight bearing and to keep the shoulder in the sling at all times.


Complications:

The “Reverse Hill-Sachs” lesion mentioned above is one of the complications of a posterior shoulder dislocation. This “lesion” is an osteochondral impression fracture in the anteromedial portion of the humeral headand is known by many names: enoche fracture, McLaughin lesion or reverse Hill-Sachs lesion. In posterior dislocations the shoulder rotates internally causing a anteromedial fracture while in an anterior shoulder dislocation which can lead to a Hill-Sachs deformity which is in the posteriorlateral humeral head.

Reviewed by: Dr Kristina McAteer