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

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Lisfranc Injuries

LIsfranc…just another one of these obnoxiously named orthopedic injuries? Actually, its named after this guy: 

Jacques Lisfranc de St. Martin, who actually was a gynecologist, with a side-gig as one of Napoleons battlefield surgons. Less obnoxious now?

Why does it matter:

  • if undiagnosed, it can cause chronic instability, deformity, functional deficiency and pain
  • not common (1:55.000), but frequently missed (appr 20% of cases)
  • x-ray findings are often subtle or even absent on standard views. 

Basic anatomy:

 

  • the Lisfranc joint is a name for all the tarsometatarsal joints,
  • the joint separates the forefoot from the midfoot (there is also a hindfoot, if you’re wondering)
  • the Lisfranc ligament secures the second metatarsal to the medial cuneiform, serving as a mortise joint anchoring the entire complex and preventing medio-lateral or plantar displacement.
  • fractures and concomitant disarticulations of this joint are termed Lisfranc fracture-dislocations

How does it happen:

  • often high-energy trauma, such as MVAs, falls from height, and athletic injuries, but can be low-energy rotations, especially in elderly individuals 
  • most often axial load through hyperplantar flexed forefoot 

 

 

 

How do we diagnose it?

  • suspect for anyone with severe midfoot pain, tenderness to palpation over midfoot, unable to bear weight. If complete ligamentous tear, ecchymosis on the plantar surface for the foot can sometimes be seen
  • stress examination of the midfoot is positive
  • the “Piano Key” test: Exacerbation of pain with dorsal and plantar flexion of each digit 
  • findings may be subtle
  • regular XR for foot does not rule out Lisfranc injury, so weight bearing XR or CT is essential if strong suspicion
  • XR of foot may show obvious fracture, but other subtle findings may require bilateral weight bearing XRs. Findings include:
    • loss of the smooth alignments at the medial border of the second metatarsal with the medial cuneiform and/or the medial border of the fourth metatarsal with the cuboid
    • diastasis of the space between the bases of the 1st and 2nd metatarsals (>2mm in a normal foot, or >1mm relative to the contralateral foot)
  • CT will give diagnosis if XR is equivocal

Treatment and folllow-up

  • if strong suspicion, ortho or podiatry consult if they are in-house
  • a significantly displaced injury or dislocation (>2mm widening at the Lisfranc joint) – immediate orthopedics referral in the ED is required for urgent surgical intervention.
  • if no ortho in house, give posterior splint and strict non-weight bearing on crutches
  • ortho or podiatry f/u within a week
  • some of these patients will require operative management

Sources: Orthoinfo

CoreEM

Orthobullets

Emergency Medicine Cases

Rosens

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Hyphema

Facial Trauma: Hyphema

Hyphema
Inline image 1
Hyphema results from ocular trauma that causes bleeding into the anterior chamber. The bleeding originates from vessels in the ciliary body or iris. The blood tends to layer over time, and left undisturbed, will form a visible meniscus when the patient sits upright. Patients typically complain of pain, photophobia, and possibly blurred vision secondary to obstructing cells. Intraocular pressure should be measured because acute glaucoma may be caused by RBC clogging of the trabecular meshwork with impedance to aqueous outflow. Prevention of further hemorrhage is the principal treatment goalMost rebleeding occurs within the first 72 hours and, when present, tends to be more extensive than the initial event. Patients should be instructed to rest in the supine position with their head slightly elevated. In addition, carbonic anhydrase inhibitors should be avoided in patients with sickle cell anemia because they can cause RBCs to sickle in the anterior chamber, which can lead to increased IOP.
There are 4 grades of Hyphema. Below is an image showing the grades and 
 
Inline image 2
 
Evaluation - Best done under a slit-lamp exam. Watch the videos below for  
 
Dr. Anna Pickens has great videos on the slit-lamp exam and hyphema, please watch below: 
 
1. Slit Lamp: https://emin5.com/2016/02/07/slit-lamp-anatomy/
2. Hyphema: https://www.youtube.com/watch?v=vQG9kL7mpyA 
  • Blood in anterior chamber
    • May only see difference in color of irises if patient is supine because blood layering is gravity dependent
    • Blood in anterior chamber only visible on slit lamp is a microhyphema
  • Vision loss / Acuity changes
  • Inspect the lids, lashes, lacrimal ducts, and cornea
    • Corneal abrasions often co-exist
  • Assess direct and consensual pupillary response for the presence of a relative afferent pupillary defect
  • Assess for Ruptured Globe which is associated with high energy mechanisms (shrapnel, BB guns, paint balls, etc)
  • Check intraocular pressure after Globe Rupture is excluded
  • Inquire about bleeding diathesis, anticoagulant/NSAID/aspirin use
 
Management
 
  • Elevate head of bed and upright position to layer blood by gravity, open visual field while blood resorbs
  • Eye shield
  • Pharmacologic control of pain and emesis
  • Weigh risks and benefits of stopping NSAIDs, ASA, anticoagulants
  • If IOP elevated (>22) the treatment is similar to glaucoma management except if there is also a concern for a retrobulbar hematoma as a result of trauma. Topical and oral treatments include
    • Timolol
    • Topical α-adrenergic agonist
    • Carbonic anhydrase inhibitors
  • Consult ophtho regarding:
    • Dilation of pupil to avoid "pupillary play" -constriction and dilation movements of the iris in response to changing lighting, which can stretch the involved iris vessel causing additional bleeding
    • Use of topical α-agonists and/or acetazolamide to decrease intraocular pressure
  • Cycloplegic can be given for comfort and to decease pupillary play if globe rupture has been excluded. Options include:
    • Tropicamide (Mydriacyl)
    • Homatropine
    • Cyclopentolate (Cyclogyl, Cylate, Pentolair)
    • Scopolamine
  • Topical steroid
  • Treat any underlying coagulopathy
Disposition
  • Should be made by the ophthalmologist after examining the patient
    • Hyphemas <33% of anterior chamber are frequently managed as outpatients
  • Patients being managed as an outpatient should have ophthalmologist referral and consider outpatient screening for spontaneous hypthemas due to the association with sickle cell disease and hemophilia
  • Patients on anticoagulation or anti-platelets agents should be admitted for reversal and observation.
Discharge Instructions
  • No reading (accommodation may further stress injured blood vessels)
  • Avoid NSAIDs
  • Wear hard shield at all times
  • Return to ED if rapid increase in size of hyphema or large increase in pain
Prognosis
  • Rebleeding worsens prognosis as patients are at higher risk of permanent vision loss.
    • Occurs 3-5 days after initial incident
    • Complicates ~30% of cases
    • Populations at highest risk:
      • Sickle cell disease or sickle cell trait
      • Bleeding dyscrasia (including aspirin, NSAID, or anticoagulant use)
      • Initial intraocular pressure >22 mmHg
      • Pediatric patients
Grade Anterior Chamber Filling Normal Vision Prognosis
I <33% 90%
II 33-50% 70%
III >50% 50%
IV 100% 50%
Sources: EM in 5, Rosh Review, Wikem.
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