22.4 Arterial Dissection and Carotid-Cavernous Fistula (03.I.5–6)

Blueprint items 03.I.5–6 pair two vascular complications of trauma that the noncontrast head CT can miss. Cervical arterial dissection presents as pain plus ischemia (or a painful Horner). Carotid-cavernous fistula (CCF) presents as a red, noisy, proptotic eye. Both need vascular imaging. Both punish the reflex to start a heparin drip or to pull a foreign body before you know where the internal carotid artery is.

Independent OpenExamPrep teaching for this ABIM Neurocritical Care topic uses CADISS, Barrow’s CCF types, and standard trauma-angiography practice. It is not an AHA cervical-artery-dissection guideline reprint.

Cervical internal-carotid and vertebral dissection

The cervical internal carotid artery (ICA) and vertebral artery tear when the intima splits and blood enters a false lumen. Triggers that appear on exams are blunt cervical trauma, sudden rotation or extension, coughing or vomiting, and neck manipulation including chiropractic adjustment (especially vertebral). Connective-tissue disease (vascular Ehlers–Danlos, Marfan, fibromuscular dysplasia) lowers the threshold. The mural hematoma can narrow the true lumen, throw artery-to-artery emboli, or expand into a pseudoaneurysm.

ICA dissection announces itself with ipsilateral head, face, or neck pain and a partial Horner syndrome: ptosis and miosis from interrupted oculosympathetic fibers on the ICA. Anhidrosis is often absent because sudomotor fibers travel with the external carotid artery. Hours to days later comes a retinal or hemispheric ischemic event in a young or middle-aged adult. Vertebral dissection produces occipital or cervical pain and posterior-circulation ischemia (lateral medulla, cerebellum, PCA territory) and can extend intracranially and bleed.

Imaging: CTA is the usual first test in trauma. Fat-saturated T1 MRI shows the crescent of intramural methemoglobin. Catheter angiography is reserved for uncertain anatomy, endovascular therapy, or a planned stent. Do not wait for a perfect intramural-hematoma MRI if the CTA already shows a flame-shaped occlusion or a long irregular stenosis after neck trauma.

Antithrombotic therapy versus hemorrhage

Uncomplicated extracranial dissection is treated to prevent artery-to-artery embolism. The CADISS trial (Lancet Neurology 2015; 2019 follow-up) randomized extracranial carotid or vertebral dissection to antiplatelet therapy versus anticoagulation and found no significant difference in ipsilateral stroke or death. TREAT-CAD compared aspirin with a vitamin K antagonist and did not establish aspirin as clearly non-inferior on its original composite; practice still often starts with a single antiplatelet agent when the stroke burden is small and bleeding risk is not zero.

The neuro ICU conflict is not CADISS versus TREAT-CAD. It is ischemic prevention versus traumatic hemorrhage. A patient with a cervical ICA flap plus an acute subdural hematoma, contusions, or traumatic SAH cannot safely receive a heparin infusion on the night of injury. Options: hold antithrombotics until a stability CT, use a single antiplatelet later if the extra-axial blood is small and not expanding, or stent a flow-limiting lesion if the hemisphere is dying and open surgery is not feasible. Recurrent ischemia despite medical therapy, an expanding extracranial pseudoaneurysm, or hemodynamic failure of the true lumen are the usual reasons to stent.

Intracranial dissection and blister aneurysms

Once the tear is intracranial, the wall is thinner and the presentation shifts from embolic stroke toward subarachnoid hemorrhage. Intracranial vertebral dissection is a classic cause of posterior-fossa SAH without a saccular berry aneurysm. Blister aneurysms of the supraclinoid ICA are tiny, fragile, and notorious for intraoperative rupture and early rebleeding. They are treated with reconstructive techniques (overlapping stents, flow diversion, wrapping plus bypass in selected cases) or, if the hemisphere has collateral flow, deconstructive sacrifice. They are not CADISS lesions. Anticoagulation after a blister or intracranial-dissection SAH is contraindicated until the segment is secured.

Carotid-cavernous fistula: direct versus indirect

The cavernous sinus is a venous plexus that contains the ICA and cranial nerves III, IV, V1, V2, and VI. A CCF is an abnormal shunt into that plexus.

Barrow classification:

Direct (high-flow, traumatic) CCF is the ICU lesion. The patient develops proptosis, chemosis, a pulsatile orbital bruit, diplopia, and rising intraocular pressure. Vision is the organ you can still lose after the fracture is plated. Cortical or posterior-fossa venous drainage turns a “eye problem” into an intracranial-hemorrhage problem. Indirect (dural, low-flow) fistulas present more quietly and sometimes thrombose; they still need treatment if vision is threatened or CVD is present.

Digital subtraction angiography (DSA) remains the definitive map of the rent, the steal, and the venous outlets (superior ophthalmic vein, inferior petrosal sinus, cortical veins). CTA or MRA can suggest the diagnosis when the superior ophthalmic vein is arterialized and enlarged. Treatment is endovascular closure: transarterial coils or liquid embolic across a direct rent with ICA preservation if possible; transvenous packing of the cavernous sinus for many indirect fistulas. Urgent cases are falling vision, uncontrolled intraocular pressure, and CVD. Do not temporize a direct high-flow traumatic CCF with lubricating drops and a planned “outpatient ophthalmology follow-up.”

Red flags that should force vascular imaging tonight

Worked conflicts

A 41-year-old has a rollover crash, a small traumatic SAH, and a painful Horner. CTA shows a cervical ICA dissection with 70% narrowing. Starting a heparin drip tonight treats the CADISS-style lesion and expands the SAH. The correct sequence is stability imaging, blood-pressure control that avoids both hypoperfusion and aneurysm-range spikes, and a delayed antiplatelet once the extra-axial blood is quiet — or a stent if the hemisphere infarcts on the table.

A 28-year-old with a basilar skull fracture develops a pulsatile red eye and a bruit the nurses can hear without a stethoscope. Visual acuity is falling. That is a direct high-flow CCF until DSA says otherwise. Coils or a covered reconstruction close the shunt; lubricating ointment does not.

A 55-year-old develops thunderclap headache after a trivial neck strain. CT shows prepontine SAH. CTA is “negative for berry aneurysm.” The next study is catheter angiography aimed at intracranial vertebral dissection or a blister, not a prescription for warfarin because “CADISS allows anticoagulation.”