01Approach to the Critical Patient/attcp71

Immediate priorities

›Carotid artery dissection recognition

›Unilateral neck, face, or periorbital pain with new neurologic or oculosympathetic symptoms

›Abrupt or subacute onset

›Pain often precedes cerebral or retinal ischemic symptoms by hours to days

›Anterior circulation deficit pattern

›Contralateral hemiparesis, hemisensory loss, or aphasia

›Amaurosis fugax or partial Horner syndrome as isolated presenting features without stroke

›Mechanical or minor trauma history

›Cervical hyperextension or rotation, sports injury, intraoral trauma, or minor blunt neck trauma

›Trivial mechanism does not exclude dissection

›Segment and hemorrhage risk triage

›Extracranial (cervical) internal carotid artery dissection

›Site of dissection in the large majority of cases, from 2 cm above the bifurcation to the skull base

›Antithrombotic therapy is the primary treatment axis

›Low subarachnoid hemorrhage risk because the segment is extradural

›Intracranial internal carotid artery dissection (petrous, cavernous, or supraclinoid segments)

›Uncommon compared with extracranial dissection

›Intradural extension carries subarachnoid hemorrhage risk and changes anticoagulation decision

›If thunderclap headache or meningismus, non-contrast CT head before any antithrombotic

›Exclude subarachnoid hemorrhage from intracranial extension or rupture

›Neurosurgery activation if hemorrhage present

›If acute anterior circulation stroke deficits, activate stroke code

›Time last known well drives thrombolysis and thrombectomy eligibility

›Cervical artery dissection is not an absolute contraindication to IV thrombolysis

›Aortic arch dissection and intracranial hemorrhage remain absolute contraindications

›Parallel processing of imaging, labs, and neurology notification

›Door-to-CT target under 25 minutes

›Door-to-needle target under 60 minutes for IV thrombolysis

›Suspected internal carotid artery terminus or M1 occlusion (dense hemiparesis, gaze deviation, aphasia or neglect)

›Neurointerventional activation before CTA confirmation if resources allow

›Tandem occlusion (cervical dissection plus intracranial embolus) requires combined endovascular strategy

Hemodynamic and monitoring targets

›Blood pressure strategy

›Permissive hypertension when no reperfusion therapy planned

›Avoid lowering BP unless over 220/120 mmHg

›Rationale is preserving flow through a stenosed or narrowed dissected segment

›Pre-thrombolysis target SBP under 185 mmHg and DBP under 110 mmHg

›Labetalol 10 to 20 mg IV over 1 to 2 minutes, may repeat once, maximum 40 mg

›Nicardipine infusion 5 mg/hour, titrate by 2.5 mg/hour every 5 to 15 minutes, maximum 15 mg/hour

›Post-thrombolysis target SBP under 180 mmHg and DBP under 105 mmHg for 24 hours

›Avoid SBP below 120 mmHg because it reduces collateral perfusion through the dissected segment

›Exceptions to standard thresholds

›Chronic hypertension shifts the autoregulation curve rightward, tolerate higher permissive values

›Concurrent tandem intracranial occlusion with poor collaterals may warrant a higher individualized permissive ceiling before recanalization

›Monitoring bundle

›Continuous cardiac monitor for arrhythmia and concomitant cardioembolic source screening

›New atrial fibrillation on telemetry changes antithrombotic strategy independent of the dissection itself

›Continuous pulse oximetry, SpO2 target 94 to 98%

›Supplemental oxygen only if SpO2 under 94%

›Avoid hyperoxia, which can promote cerebral vasoconstriction and reduce collateral flow

›Exception: chronic hypoxemia, chronic lung disease, or pulmonary hypertension tolerate a lower baseline SpO2 and should not be force-corrected to 98%

›Serial neurologic checks every 15 minutes for the first 2 hours after reperfusion therapy, then hourly

›Watch specifically for new aphasia, worsening hemiparesis, declining consciousness, or new pupillary asymmetry

›Airway and swallow monitoring

›Lower cranial nerve palsy (dysphagia, dysphonia, absent gag) predicts aspiration risk

Immediate consults and escalation triggers

›Consultation triggers

›Vascular neurology or stroke neurology at presentation

›All confirmed or suspected cervical artery dissection with neurologic or ocular ischemic symptoms

›Neurointerventional radiology

›Internal carotid terminus or M1 occlusion, tandem occlusion, or flow-limiting pseudoaneurysm

›Ophthalmology

›Amaurosis fugax or retinal artery occlusion for fundoscopic confirmation and documentation

›Neurosurgery

›Intracranial internal carotid dissection with subarachnoid hemorrhage

›Large hemispheric infarction with malignant edema risk

›Deterioration triggers

›Recurrent transient symptoms (amaurosis fugax, hemiparesis, aphasia) despite antithrombotic therapy

›Reimage for dissection progression, new thrombus, or pseudoaneurysm enlargement

›Consider escalation to endovascular therapy

›Progressive hemispheric signs or declining consciousness

›Internal carotid terminus occlusion or malignant middle cerebral artery syndrome concern

›Herniation risk from edema, typically peaking 2 to 5 days after a large hemispheric infarct

02History/hx77

Presentation pattern

›Pain characteristics

›Unilateral anterior neck or upper cervical pain

›Ipsilateral to the dissected artery

›Present in a majority of confirmed cases

›Facial, periorbital, or retro-orbital headache

›Dull, constant, or unfamiliar quality compared to prior headaches

›New or different headache pattern is a key clue

›Interval between pain onset and ischemic symptoms

›Hours to days in most cases

›Delayed presentation is common and increases missed-diagnosis risk

›Sentinel and warning symptoms

›Transient monocular vision loss, hemiparesis, or aphasia preceding a completed stroke

›Represents anterior circulation TIA

›Recurrence within days to weeks carries high stroke risk

›Pulsatile tinnitus

›Patient hears a bruit synchronous with the pulse

›Suggests turbulent flow through a stenosed or narrowed segment

›Thunderclap headache

›Consider intracranial internal carotid dissection with subarachnoid extension

›Non-contrast CT head before further workup

Precipitants and mechanical triggers

›Mechanical events

›Cervical spine manipulation (chiropractic or osteopathic)

›Recognized but less strongly associated precipitant than for vertebral dissection

›Extreme or sustained neck rotation or hyperextension

›Sports, motor vehicle collision with seatbelt injury, strangulation, or hanging

›Coughing, vomiting, or forceful nose-blowing reported in some cases

›Intraoral or peritonsillar trauma

›Falling with an object in the mouth (a pen, toothbrush, or stick)

›Recognized precipitant particularly in children and adolescents

›Minor cervical or blunt neck trauma

›Trivial mechanism does not exclude dissection

›Delayed symptom onset after the inciting event is common

›Spontaneous presentation

›No identifiable mechanical trigger in a substantial proportion of cases

›More often spontaneous than vertebral dissection, which is more frequently mechanically triggered

Risk factors and connective tissue disease

›Vascular substrate

›Fibromuscular dysplasia

›Recognized underlying arteriopathy in a subset of spontaneous dissections

›Migraine history

›Independently associated with cervical artery dissection risk

›Hypertension

›Associated risk factor, distinct from the acute permissive hypertension strategy used once dissection has occurred

›Heritable connective tissue disorders

›Vascular Ehlers-Danlos syndrome

›Highest dissection and arterial rupture risk of the connective tissue disorders

›Multiple or recurrent dissections raise suspicion

›Marfan syndrome

›Aortic root surveillance also indicated

›Loeys-Dietz syndrome

›Aggressive arterial tortuosity and dissection phenotype

›Family and recurrence history

›Family history of arterial dissection or unexplained young stroke

›Consider connective tissue disorder evaluation

›Prior cervical artery dissection

›Recurrence risk highest in the first weeks after the index event

Ocular, otologic, and cranial nerve symptom review

›Ocular symptom review

›Amaurosis fugax

›Transient monocular vision loss described as a curtain descending

›Retinal or ophthalmic artery embolic mechanism, since the ophthalmic artery is the first major intracranial branch of the internal carotid

›Eye or periorbital pain

›Often ipsilateral and associated with partial Horner syndrome

›Otologic symptom review

›Pulsatile tinnitus

›Unilateral hearing change (uncommon, from proximity to the skull base)

›Lower cranial nerve symptom review

›Hoarseness or voice change (vagus nerve)

›Tongue weakness or deviation, dysarthria (hypoglossal nerve)

›Most common lower cranial nerve palsy in carotid dissection, from compression at the skull base

›Shoulder droop or weakness turning the head (spinal accessory nerve)

›Dysphagia (glossopharyngeal or vagus nerve)

›Important negatives and clues

›Absence of fever or systemic infectious symptoms

›Argues against retropharyngeal or deep neck space infection mimic

›Absence of jaw claudication or scalp tenderness

›Argues against giant cell arteritis mimic in older patients

›Prior similar headache episodes

›History of migraine complicates but does not exclude diagnosis

03Physical Exam/exam44

Vital signs and vascular exam

›Blood pressure

›Bilateral arm pressures

›Asymmetry over 20 mmHg suggests concomitant subclavian or aortic arch process

›Hypertension common and often reactive

›Do not treat aggressively before thrombolysis decision is made

›Neck and vascular findings

›Cervical bruit

›Nonspecific but supportive when present, particularly a new bruit in a young patient without atherosclerotic risk factors

›Neck tenderness or fullness along the carotid course

›Nonspecific musculoskeletal overlap with carotidynia

›Carotid and peripheral pulses

›Assess for concurrent vertebral or subclavian dissection or systemic vasculopathy

Partial Horner syndrome and oculosympathetic findings

›Ipsilateral partial Horner syndrome

›Ptosis and miosis without anhidrosis

›Classic and localizing finding for carotid dissection

›Anhidrosis is absent or limited to a small medial forehead strip because facial sudomotor sympathetic fibers travel with the external carotid artery, not the internal carotid

›Distinguishing feature from a preganglionic (second-order) Horner syndrome

›A full Horner syndrome with anhidrosis of the entire face favors a lesion proximal to the carotid bifurcation, such as a Pancoast tumor or brainstem lesion

›Partial Horner syndrome sparing facial sweating localizes to a postganglionic lesion along the internal carotid

›Associated ocular findings

›Enophthalmos, upside-down ptosis of the lower lid

›Anisocoria more apparent in dim light, since the miotic pupil dilates poorly

Cerebral and lower cranial nerve findings

›Cortical and hemispheric findings

›Aphasia

›Expressive, receptive, or global, dominant hemisphere involvement

04Differential Diagnosis/ddx47

Cannot-miss diagnoses

›Internal carotid terminus or M1 middle cerebral artery occlusion

›ICD-10 I63.9

›Dense hemiparesis, aphasia or neglect, gaze deviation

›Can result from carotid dissection with distal embolization or tandem occlusion

›Subarachnoid hemorrhage

›ICD-10 I60.x

›Thunderclap headache, meningismus

›Consider intracranial internal carotid dissection as the source

›Vertebral artery dissection

›ICD-10 I77.74

›Posterior neck pain and posterior circulation deficits (vertigo, diplopia, dysarthria, ataxia)

›Differentiating clue against carotid dissection when anterior circulation signs are absent

›Giant cell arteritis

›ICD-10 M31.6

›Age over 50, jaw claudication, scalp tenderness, visual symptoms

›Elevated ESR and CRP redirect diagnosis toward vasculitis rather than dissection

›Pancoast (superior sulcus) tumor

›Full Horner syndrome with facial anhidrosis, arm pain, and hand weakness

›Preganglionic lesion, distinguishing it from the partial Horner syndrome of carotid dissection

Carotid territory stroke syndromes

›Middle cerebral artery territory infarction

›Contralateral hemiparesis and hemisensory loss, face and arm greater than leg

›Aphasia if dominant hemisphere, neglect if non-dominant

›Ophthalmic artery or central retinal artery occlusion

›Monocular vision loss, may be transient (amaurosis fugax) or permanent

›Embolic source from the dissected internal carotid

›Watershed (borderzone) infarction

05Laboratory Tests/lt22

Diagnostic and rule-out labs

›Complete blood count and coagulation panel

›Baseline before antithrombotic initiation

›Platelets under 100,000 per microliter is a caution for thrombolysis and anticoagulation

›PT/INR and aPTT for baseline coagulation status

›D-dimer

›Not validated as a rule-out test for cervical artery dissection

›Unlike aortic dissection, no established D-dimer threshold excludes carotid dissection

›A normal D-dimer must not delay imaging

›ESR and CRP

›Ordered when giant cell arteritis is a competing consideration, especially with amaurosis fugax in a patient over 50

›Marked elevation redirects workup toward vasculitis rather than dissection

›Normal inflammatory markers do not exclude dissection, since dissection itself does not typically elevate them

Pre-procedural and connective tissue labs

›Pre-thrombolysis and pre-anticoagulation labs

›Point-of-care glucose

›Hypoglycemia under 3.0 mmol/l corrected before attributing deficits to stroke

›Renal function

›Creatinine for contrast planning and DOAC dosing

›Selected connective tissue and hypercoagulability workup

›Genetic testing for vascular Ehlers-Danlos syndrome (COL3A1) when recurrent or multiple dissections

›Hypercoagulability panel in young patients with no mechanical trigger identified

›Draw before anticoagulation initiation when feasible

›Interpret with caution in the acute phase, since acute-phase reactants affect results

06Diagnostic Tests/dt58

Scoring Systems

›NIHSS

›Quantifies anterior circulation stroke severity

›Performs better for cortical (hemispheric) deficits than for isolated Horner syndrome or amaurosis fugax without infarct

›A patient can have a disabling amaurosis fugax or TIA with an NIHSS of 0

›ABCD2 score for TIA-like presentation

›Components

›Age >= 60 years: 1 point

›Blood pressure >= 140/90 mmHg at presentation: 1 point

›Clinical features: unilateral weakness 2 points, speech disturbance without weakness 1 point, other 0 points

›Duration >= 60 minutes: 2 points, 10-59 minutes: 1 point, under 10 minutes: 0 points

›Diabetes: 1 point

›Risk stratification

›Score 0-3 (low risk): 2-day stroke risk approximately 1.0%, 90-day risk approximately 3.1%

›Score 6-7 (high risk): 2-day stroke risk approximately 8.1%, 90-day risk approximately 17.8%

›Limitation specific to dissection

›ABCD2 was derived and validated for atherosclerotic and cardioembolic TIA populations, not dissection-specific cohorts

›Vascular imaging is warranted for suspected dissection regardless of ABCD2 score

›ASPECTS

›Score 0 to 10 on non-contrast CT for middle cerebral artery territory early ischemic change

›Lower scores reflect larger established infarct and influence thrombectomy candidacy

›No validated dissection-specific pretest probability score

›Unlike the Aortic Dissection Detection Risk Score for aortic dissection, no comparably validated clinical prediction rule exists for cervical artery dissection

›Diagnosis is driven by clinical suspicion (neck or facial pain plus partial Horner syndrome, amaurosis fugax, or anterior circulation symptoms) combined with imaging rather than a scoring algorithm

MRI

›MRI and MRA neck

›Fat-saturated T1 axial sequence

›Crescent-shaped hyperintense intramural hematoma is the classic finding, eccentrically narrowing the true lumen

›Best seen in the subacute phase, roughly 3 to 7 days after onset, when hematoma is methemoglobin-rich

›Hyperacute hematoma may be isointense and easily missed

›Time-of-flight MRA

›Can show a tapered "flame sign" occlusion, intimal flap, or double lumen

›Lower sensitivity than CT angiography for distal skull base occlusion and flap detection

›MRI brain

›DWI for associated anterior circulation infarct

›Useful when CT is equivocal and time permits, but should not delay thrombectomy for a confirmed large vessel occlusion

CT

›CT angiography of the head and neck

›First-line diagnostic study

›High sensitivity for intimal flap, string sign, pseudoaneurysm, and occlusion

›Identifies the extracranial-to-skull-base extent and any tandem intracranial occlusion

›String sign

›Long-segment smooth luminal narrowing characteristic of dissection

›Pseudoaneurysm

›Focal outpouching, typically near the skull base, that requires surveillance imaging

›Non-contrast CT head

›Mandatory before any reperfusion therapy to exclude hemorrhage

›Door-to-CT target under 25 minutes

›Hyperdense MCA sign suggests a concurrent embolic large vessel occlusion

›Mandatory before antithrombotic therapy if thunderclap headache present

›Exclude subarachnoid hemorrhage from intracranial extension

Ultrasound

›Carotid duplex ultrasound

›Can identify flow abnormality in the distal common and proximal internal carotid artery

›High-resistance "thump" waveform from distal obstruction, reduced or reversed diastolic flow

›Limited sensitivity for dissection extending to the skull base

›The Doppler window cannot reliably insonate the high cervical and skull base internal carotid, where dissection frequently extends, because the vessel courses too deep beneath the mandible and mastoid process

›Cannot reliably exclude dissection alone

›A normal duplex study does not obviate CT angiography or MRA when suspicion is high

›Catheter angiography

›Historical gold standard, now reserved for equivocal noninvasive imaging or planned endovascular intervention

›Carries its own procedural stroke and access-site dissection risk

07Disposition/dispo22

Level of care

›Admission for all confirmed cervical artery dissection

›Highest stroke risk in the first 2 weeks after diagnosis

›Even isolated dissection without infarct or with isolated amaurosis fugax warrants inpatient observation in most practice

›Stroke unit or ICU for dissection with completed infarct

›Serial neurologic checks

›Telemetry for arrhythmia and cardioembolic source detection

›Escalated level of care triggers

›Internal carotid terminus or M1 occlusion, or tandem occlusion

›Large hemispheric infarct with malignant edema risk

›Intracranial internal carotid dissection with subarachnoid hemorrhage

Transfer and discharge criteria

›Transfer indications

›No on-site neurointerventional capability with large vessel or tandem occlusion

›Drip and ship, administer IV thrombolysis if eligible before transfer

›Do not delay thrombolysis for transfer logistics

›Flow-limiting pseudoaneurysm requiring surgical or endovascular evaluation

›Vascular surgery or neurointerventional acceptance

›Discharge criteria after stabilization

›Antithrombotic regimen established and tolerated

›No recurrent transient symptoms

›Stable follow-up imaging plan in place

›Repeat CT angiography or MRA typically at 3 to 6 months to assess healing

›Neurologically stable or improving with a rehabilitation plan if deficits persist

08Treatment/t115

Antithrombotic therapy

›Extracranial (cervical) dissection without hemorrhage

›Antiplatelet therapy

›Aspirin 162 to 325 mg orally once, then 75 to 100 mg orally daily

›Anticoagulation as an alternative

›Heparin infusion without bolus if bleeding risk present, titrated to institutional aPTT target

›If no bleeding risk, bolus 60 to 80 units/kg IV followed by infusion 12 to 18 units/kg/hour

›Titrate every 6 hours to therapeutic aPTT

›Transition to warfarin, target INR 2.0 to 3.0, or a DOAC for continued anticoagulation

›Warfarin has the larger evidence base of the oral options for cervical artery dissection

›DOAC use (apixaban 5 mg orally twice daily, or rivaroxaban 20 mg orally once daily) is off-label for this indication, with evidence limited to observational and small-trial data rather than a dedicated large randomized trial

›Intracranial internal carotid dissection

›Anticoagulation is relatively contraindicated when intradural extension is present, given subarachnoid hemorrhage risk

›Antiplatelet therapy generally preferred when intracranial extension is present without hemorrhage

›Trial evidence for antiplatelet versus anticoagulation

›CADISS trial

›No significant difference in recurrent stroke between antiplatelet and anticoagulant therapy for cervical (carotid and vertebral) artery dissection

›Recurrent stroke rate was low in both arms, approximately 1 to 2% at 3 months

›TREAT-CAD trial

›Randomized non-inferiority trial of aspirin versus vitamin K antagonist for cervical artery dissection

›Did not establish non-inferiority of aspirin; numerically more ischemic events occurred in the aspirin arm, though the trial was underpowered and stopped early

›Practical synthesis

›Neither trial shows one strategy is clearly superior; choice is individualized by bleeding risk, intracranial extension, and pseudoaneurysm morphology rather than a uniform default

›Duration and choice

›Typical treatment duration 3 to 6 months pending healing on follow-up imaging

›Transition to long-term antiplatelet therapy if imaging shows healing

›Continue longer if pseudoaneurysm or persistent flow abnormality remains

›Therapy is not working

›Recurrent amaurosis fugax, hemispheric TIA, or stroke despite adequate antithrombotic therapy

›Reimage for dissection progression, new thrombus, or enlarging pseudoaneurysm

›Consider switching antiplatelet to anticoagulation or vice versa

›Consider endovascular therapy if a fixed hemodynamically significant lesion is identified

Blood pressure management

›No thrombolysis or thrombectomy planned

›Permissive hypertension, treat only if above 220/120 mmHg

›Gradual reduction of approximately 15% in the first 24 hours when treatment is required

›Pre-thrombolysis blood pressure lowering

›Target SBP under 185 mmHg and DBP under 110 mmHg before alteplase or tenecteplase administration

›Labetalol 10 to 20 mg IV over 1 to 2 minutes, may repeat once, maximum 40 mg

›Nicardipine infusion, initiate 5 mg/hour, titrate 2.5 mg/hour every 5 to 15 minutes, maximum 15 mg/hour

›Clevidipine infusion, initiate 1 to 2 mg/hour, double every 2 to 5 minutes until near goal, usual maximum 21 mg/hour

›Post-reperfusion blood pressure

›Post-thrombolysis target SBP under 180 mmHg and DBP under 105 mmHg for 24 hours

›Avoid hypotension after thrombectomy, since it reduces perfusion through a residually narrowed dissected segment

Acute ischemic stroke reperfusion therapy

›IV thrombolysis

›Alteplase 0.9 mg/kg IV, maximum 90 mg

›10% of total dose as bolus over 1 minute

›Remaining 90% as infusion over 60 minutes

›Eligible window within 4.5 hours of last known well

›Tenecteplase 0.25 mg/kg IV, maximum 25 mg, single bolus

›Reasonable alternative to alteplase

›Cervical artery dissection is not an absolute contraindication to IV thrombolysis, and IV alteplase for otherwise eligible acute ischemic stroke is a Class I recommendation (AHA/ASA) independent of dissection etiology

›Aortic arch dissection and intracranial hemorrhage remain absolute contraindications

›Theoretical risk of extending the dissection or expanding a periarterial hematoma exists but has not been shown to outweigh reperfusion benefit in cohort data

›Post-thrombolysis monitoring

›Neurologic checks every 15 minutes for 2 hours, then hourly for 22 hours

›No antiplatelet or anticoagulant for 24 hours after thrombolysis

›Repeat non-contrast CT head at 24 hours before initiating antithrombotics

›Mechanical thrombectomy

›Confirmed internal carotid terminus, M1, or tandem occlusion within standard or extended window

›Door-to-groin puncture target under 90 minutes for direct arrivals

›Tandem occlusion strategy

›Combined cervical carotid stenting or angioplasty with intracranial thrombectomy in the same session, per local neurointerventional protocol

›Antiplatelet requirements for acute cervical stenting must be balanced against thrombolysis-related bleeding risk

Interventional and surgical options

›Endovascular stenting

›Flow-limiting stenosis or enlarging pseudoaneurysm refractory to medical therapy

›Dual antiplatelet therapy required after stent placement

›Aspirin 81 mg plus clopidogrel 75 mg daily, typically for 1 to 3 months, then single agent long-term

›Carotid endarterectomy is not the standard treatment for dissection

›Reserved for rare cases of persistent flow-limiting lesion or pseudoaneurysm unsuitable for endovascular repair

›Most extracranial dissections heal with medical therapy alone, unlike atherosclerotic carotid stenosis where endarterectomy is first-line

›Acute surgery on a friable dissected wall carries elevated technical risk

Malignant cerebral edema management

›Large hemispheric (malignant middle cerebral artery) infarction

›Edema typically peaks 2 to 5 days after infarct onset

›Declining level of consciousness or pupillary change triggers emergent reimaging

›Osmotherapy

›Mannitol 0.5 to 1 g/kg IV over 20 minutes, may repeat every 4 to 6 hours

›Maintain serum osmolality under 320 mOsm/l

›Monitor serum sodium and obtain ECG surveillance for hypernatremia-associated QTc prolongation and arrhythmia during repeated dosing

›Hypertonic saline 23.4% 30 to 60 mL via central line for refractory intracranial pressure

›Monitor serum sodium at least every 6 hours during active titration

›Decompressive hemicraniectomy

›Pooled trial data (DECIMAL, DESTINY, HAMLET) support benefit in selected patients under 60 years old treated within 48 hours of malignant MCA territory infarction

›Neurosurgical consultation early, before clinical herniation, given the narrow decision window

Iatrogenic harms and interventions to avoid

›Intubation

›Neck hyperextension during laryngoscopy can mechanically extend a dissection

›In-line neutral positioning and video laryngoscopy preferred

›Lower cranial nerve dysfunction (absent gag, dysphonia, dysphagia) is an indication for airway protection

›Anticipate a difficult or bulbar-compromised airway; avoid induction-related hypotension, which reduces perfusion through the narrowed dissected segment

›Sedation

›Can mask evolving neurologic exam needed for serial stroke monitoring

›Propofol-associated hypotension reduces cerebral perfusion pressure through the stenosed vessel

›Fluid loading

›Maintain euvolemia with isotonic fluids

›Avoid hypotonic fluids, which worsen cerebral edema

›Avoid hypovolemia, which compounds hypoperfusion in a permissive-hypertension strategy

›Oxygen

›Supplemental oxygen only if SpO2 under 94%

›Hyperoxia is not beneficial and may promote vasoconstriction, reducing collateral flow

›Vasopressors

›Not routine, but appropriate if permissive hypertension is undermined by iatrogenic hypotension (for example, sedation or overcorrection with antihypertensives)

›Goal is restoring perfusion pressure through the dissected segment, not a fixed pressor protocol

›Mechanical circulatory support

›Intra-aortic balloon pump and other mechanical circulatory support are not indicated

›Carotid artery dissection is a cervical arterial process, not a cardiac output problem

›Anticoagulation

›Contraindicated in intracranial internal carotid dissection with subarachnoid hemorrhage

›Relatively contraindicated with a large completed infarct due to hemorrhagic transformation risk

›Acceptable in extracranial dissection without hemorrhage, with outcomes similar to antiplatelet therapy

›Fibrinolysis

›Not an absolute contraindication for cervical artery dissection causing acute ischemic stroke

›Remains absolutely contraindicated if aortic arch dissection or intracranial hemorrhage is present

›Analgesia

›IV opioids for severe neck or facial pain, fentanyl 25 to 50 mcg IV titrated, or morphine 2 to 4 mg IV titrated

›Acetaminophen 650 to 1000 mg orally or IV every 4 to 6 hours, maximum 4000 mg per 24 hours, as a non-sedating first-line option

›Use opioids cautiously once anticoagulation is initiated, since oversedation can mask a change in neurologic exam

›NSAIDs used with caution once an antithrombotic plan is set, given additive bleeding risk with anticoagulation

09Special Populations/sp55

Pregnancy

›Epidemiology and risk in pregnancy

›Cervical artery dissection is uncommon in pregnancy but reported in the peripartum period

›Valsalva during labor is a proposed mechanical contributor

›Imaging in pregnancy

›MRI and MRA without contrast preferred

›CT angiography with abdominal shielding when benefit outweighs radiation risk

›Antithrombotic therapy in pregnancy

›LMWH (enoxaparin) preferred anticoagulant, 1 mg/kg subcutaneously twice daily, safe in pregnancy

›Warfarin contraindicated, teratogenic and associated with fetal hemorrhage

›DOACs contraindicated in pregnancy

›Aspirin 81 to 162 mg daily acceptable in the second and third trimester

›Thrombolysis in pregnancy

›Alteplase is not an absolute contraindication

›Placental bleeding is the main theoretical concern

›Multidisciplinary decision with maternal-fetal medicine

›Blood pressure management in pregnancy

›Avoid ACE inhibitors and ARBs, teratogenic

›Labetalol 10 to 20 mg IV bolus and hydralazine 5 to 10 mg IV bolus preferred antihypertensives

Geriatric

›Presentation differences

›Atypical or minimized neck and facial pain reporting is common

›Dissection is a less common stroke cause in this age group than large-artery atherosclerosis or cardioembolism, but still occurs, often superimposed on an atherosclerotic vessel

›Thrombolysis and anticoagulation considerations

›No upper age limit for IV alteplase or tenecteplase

›Higher rate of symptomatic intracranial hemorrhage over age 80, approximately 7 to 9% versus 5 to 6% overall

›Renal function affects DOAC dosing

›Dabigatran requires creatinine clearance above 30 mL/min

10Background/b47

Epidemiology

›Incidence

›Carotid artery dissection incidence approximately 1.7 to 3 per 100,000 per year

›Accounts for roughly 65 to 75% of cervical (carotid plus vertebral) artery dissections, more common than vertebral dissection

›Accounts for approximately 2% of all ischemic strokes overall

›Accounts for up to approximately 20% of ischemic strokes in patients under age 45

›Demographics

›Mean age of onset in the mid-40s, younger than typical atherosclerotic stroke

›No strong sex predominance established for carotid dissection specifically

›Multiplicity and recurrence

›Multiple or bilateral cervical artery dissection in roughly 10 to 16% of cases

›Recurrent dissection risk approximately 1% per year after the index event

›Higher recurrence risk with an underlying connective tissue disorder or strong family history

›Outcomes

›Overall mortality is low, generally under 5%

›Higher mortality with bilateral involvement, tandem intracranial occlusion, or large hemispheric infarct

›Most patients with extracranial dissection and appropriate antithrombotic therapy have a favorable long-term vascular outcome

Pathophysiology

›Anatomic segments

›Cervical (extracranial) internal carotid artery, from approximately 2 cm above the bifurcation to the skull base

›Site of dissection in the large majority of carotid dissections

›Petrous, cavernous, and supraclinoid (intracranial) segments

›Uncommon site of dissection; the cavernous and intradural segments lack a robust external elastic lamina

›Intradural extension carries disproportionate subarachnoid hemorrhage risk

›Mechanism of dissection

›Intimal tear allows blood to enter the arterial wall

›Intramural hematoma narrows or occludes the true lumen

›Subintimal hematoma causes stenosis or occlusion; subadventitial hematoma can form a pseudoaneurysm or, intracranially, rupture into the subarachnoid space

›Ischemic mechanism is predominantly artery-to-artery embolism from thrombus at the dissection site

›Hemodynamic (low-flow, watershed) mechanism also contributes when stenosis is severe and collaterals are poor

›Underlying arteriopathy

›Fibromuscular dysplasia and connective tissue disorders weaken the arterial wall

›A mechanical trigger unmasks an underlying structural vulnerability in many spontaneous cases

›Basis of the partial Horner syndrome

›Postganglionic sympathetic fibers to the pupil and eyelid travel with the internal carotid artery

›Sudomotor fibers to facial sweat glands diverge earlier and travel with the external carotid artery, sparing facial sweating when the lesion is at the internal carotid

Therapeutic Considerations

›Antithrombotic evidence base

›CADISS trial demonstrated no significant difference in recurrent stroke between antiplatelet and anticoagulant therapy for cervical artery dissection

›Overall recurrent stroke rate was low in both treatment arms

›TREAT-CAD trial did not establish non-inferiority of aspirin to vitamin K antagonist therapy, a signal (not proof, given underpowering) that anticoagulation may not be inferior for some patients

›Choice between antiplatelet and anticoagulation is individualized based on hemorrhage risk, intracranial extension, and pseudoaneurysm morphology rather than a uniform default

›Reperfusion therapy evidence

›Cervical artery dissection causing acute ischemic stroke is treated according to standard thrombolysis and thrombectomy criteria

›Dissection-related stroke is not systematically excluded from thrombolysis trials or registries

›Healing and imaging follow-up

›Most extracranial dissections show partial or complete luminal recovery on follow-up imaging within 3 to 6 months

›Persistent occlusion or pseudoaneurysm may warrant longer antithrombotic duration or endovascular referral

›Activity modification

›Avoid high-risk neck manipulation and extreme rotational or hyperextension activities until healing is confirmed

11Patient Discharge Instructions/pdi26

copy discharge instructions

›What happened to you

›A tear formed in the wall of an artery in your neck that supplies blood to part of your brain and eye

›This can cause a blood clot to form or reduce blood flow to the brain or eye

›Most of these arteries heal over the following 3 to 6 months with treatment

›Your medications

›Take your blood thinner or aspirin exactly as prescribed every day

›Do not stop your blood thinner or aspirin without talking to your doctor first

›Do not start any new over-the-counter medication, supplement, or herbal remedy without checking first, since some increase bleeding risk

›Activity guidance

›Avoid chiropractic neck manipulation and cervical spine adjustment until your doctor clears you

›Avoid extreme or forceful neck rotation and hyperextension, including certain yoga poses and contact sports

›Avoid heavy lifting and straining

›Light to moderate walking is encouraged

›Follow-up appointments

›Vascular neurology or stroke clinic within 1 to 2 weeks of discharge

›Repeat CT angiography or MRA at 3 to 6 months to check healing

›Ophthalmology follow-up if amaurosis fugax or vision changes occurred

›Primary care within 2 to 4 weeks

›Return to the emergency department immediately if you develop

›New or worsening neck, face, or headache pain

›New vision loss in one eye, even if brief

›New weakness, numbness, or drooping on one side of the face or body

›New difficulty speaking, understanding speech, or swallowing

›A new drooping eyelid or unequal pupil size

›Sudden severe headache unlike any you have had before

›Any sign of unusual bleeding or bruising if you are taking a blood thinner

12References/r19

Guidelines and key sources

›AHA/ASA scientific statement on the diagnosis and management of cervical artery dissection

›American Heart Association / American Stroke Association, Stroke, 2024

›European Stroke Organisation guideline on the diagnosis and management of cervical artery dissection

›Debette S, et al. European Stroke Organisation, 2021

›AHA/ASA guideline for early management of patients with acute ischemic stroke

›Powers WJ, et al. Stroke, 2019 update

›Established IV thrombolysis and thrombectomy eligibility criteria applied to dissection-related stroke

›AHA/ASA guideline for prevention of stroke in patients with stroke and TIA

›Kleindorfer DO, et al. Stroke, 2021

›Antithrombotic regimen selection is individualized for cervical artery dissection rather than protocolized

Landmark trials

›CADISS trial (Cervical Artery Dissection in Stroke Study)

›CADISS trial investigators, Lancet Neurology, 2015

›Randomized antiplatelet versus anticoagulant therapy, no significant difference in recurrent stroke at 3 months

›TREAT-CAD trial

›Engelter ST, et al. Lancet Neurology, 2021

›Randomized non-inferiority trial of aspirin versus vitamin K antagonist for cervical artery dissection; non-inferiority of aspirin not established

›Pooled analysis of decompressive hemicraniectomy trials (DECIMAL, DESTINY, HAMLET)

›Vahedi K, et al. Lancet Neurology, 2007

›Early decompressive hemicraniectomy improved survival and functional outcome in malignant MCA infarction in patients under 60

Evidence & Review

Evidence & Review