Thread by @RosenelliEM

A Teal pain in the neck:

Follow along for a short #medtweetorial on #CervicalArteryDissection

or see the full handout here emboardbombs.com/s/Cervical-Art…

from @EMBoardBombs @blakebriggsMD @IltifatMD

This review will focus on spontaneous dissections, not traumatic, as well as the pathophys, risk factors, presentation, diagnosis, and management.

Cervical artery dissections are a common cause of stroke in young(<50 years )w/ some reports of up to 20% being from dissections

Much like aortic dissections, there is some loss of structure along the wall of either the internal carotid artery or vertebral artery

This allows blood to collect within the intima.

In patients <50 years old, cervical artery dissections account for 20% of ischemic strokes.

The overall incidence is about 2.5 per 100,000 annually in the US alone, with a mean age of 45 years.

ICA dissections are 3-5x more common that VA dissections.

For comparison, subarachnoid hemorrhage has an incidence of ~7 per 100,000 worldwide.

They occur extra or intracranial.

Extracranial internal carotid dissection is more common, typically it occurs 2 cm or more distal from the carotid bifurcation near the skull base.

Vertebral artery dissection most commonly occurs at the V3 segment of the vert artery, at C1C2

The false lumen that forms will continue to dissect, or “unzip”, resulting in cerebral ischemia.

Ischemia is caused by both hypoperfusion or thromboembolism, with the latter being more important.

The compression of the expanding hematoma presses on sympathetic fibers

This can result in partial a Horner syndrome (see below), cranial neuropathies, and pain.

Very rarely these vessels dissect intracranially, rupturing to cause a SAH.

Risk Factors

Minor trauma: the key word is “mild” trauma, associated with up to 40% of cases.

This does not include motor vehicle crashes that end up at a level 1 trauma center with a cervical spine fracture.

These are usually activity-related: skating, basketball, volleyball, swimming, scuba diving, dancing, yoga, chiropractors (1 in 20,000 cervical manipulations)

Other risk factors include sexual intercourse, trampoline use, amusement park rides, vaginal delivery, etc.

With that being said, most CADs develop in the absence of any discernible mechanical event thus making it very difficult to indict a particular incident or factor

The most compelling risk factors likely have to do with an underlying connective tissue abnormality
These genetic predispositions are the usual culprits (Ehlers-Danlos, Marfan’s, PCKD, etc).

The most common of these is fibromuscular dysplasia.

Presentation: Think headache, neck pain, and potentially ischemic, neurologic symptoms.

It is important to add this pathology to your differential of patients with headache and neck pain, as headache and neck pain are the most common symptoms, ranging from 60-90%.

Headache is more common in carotid dissections, while neck pain is more common in vertebral dissection.

The headache onset is usually gradual, with <20% being a “thunderclap” onset.

Ischemia manifesting in TIA/stroke symptoms are present in about 70% of patients

Ischemic symptoms may not be present on initial presentation.

The risk is highest during the first 2 weeks of symptoms (77% present at the time of diagnosis).

On exam, look for obvious motor or sensory deficits & the more subtle nystagmus, truncal ataxia, ipsilateral Horner’s syndrome, tongue deviation, or ophthalmoplegia.

For vertebral dissections think of lateral medullary syndromes (Wallenberg Syndrome) and cerebellar infarctions.

Think amaurosis for carotid artery dissection.

As mentioned above, ipsilateral Horner syndrome is only in ~25% of cases.

Other possible symptoms include unilateral hearing loss, pulsatile tinnitus, auscultated bruit, dizziness, the “Deadly D’s”(dysarthria, diplopia, dysphagia

Diagnosis: Made by neuroimaging, MRA or CTA. Both are more or less equal in performance and sensitivity/specificity.

CTA is faster and has wider availability in most EDs. Historically, the gold standard was digital subtraction angiography, but this is rarely used today.

Treatment: As discussed above, cervical artery dissection increases the risk of thromboembolism, causing stroke.

This can be a deadly diagnosis as there is up to a 10% mortality prior to even initiating treatment.

In those patients who present with acute ischemic stroke, standard approaches to management of stroke should be followed.

Discussion of thrombolytics should take place with the code stroke team.

There is no increased harm in giving IV thrombolytic (outside of the usual harm associated with acute stroke management), but no clear benefit has been found as well (i.e. no difference in intracranial hemorrhage, mortality, or favorable outcome).

Anti-thrombotic therapy with either antiplatelet agents or anticoagulation are the preferred methods for preventing ischemic stroke and TIA complications.

They have been studied and there is no difference in their efficacy.

There is debate on the preferred antiplatelet agents: aspirin, clopidogrel, dipyridamole, or a combination of these agents.

We suggest consulting your neurologic team on this.

There is no consensus on how long patients need to be on therapy.

Some studies suggest after 3-6 months as most arterial abnormalities stabilize by then.

Repeat imaging is necessary at that time to evaluate for improvement in the dissection complications.

Endovascular/surgical repair are last resort options

Prognosis

Recurrence rate is uncertain, and hotly debated. We do know that unfavorable outcomes are more common in carotid artery dissections versus vertebral. Excellent recovery has been found in 70-85% of patients, with major disabling deficits in 10-25% and death in <10%.

It should be a “Real” and not “Teal” Pain in the neck. I’ll blame my fat fingers