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• W2024508247 abstract "A case of delayed postoperative visual loss due to bilateral traumatic carotid artery dissection is presented. In patients with a major craniofacial injury due to a high-speed motor vehicle accident, we suggest that carotid artery duplex ultrasonography be used in the initial evaluation for possible carotid artery dissection. Magnetic resonance imaging of the head and neck with magnetic resonance angiography should be performed subsequently if indicated. Early diagnosis and initiation of therapy can minimize complications. A case of delayed postoperative visual loss due to bilateral traumatic carotid artery dissection is presented. In patients with a major craniofacial injury due to a high-speed motor vehicle accident, we suggest that carotid artery duplex ultrasonography be used in the initial evaluation for possible carotid artery dissection. Magnetic resonance imaging of the head and neck with magnetic resonance angiography should be performed subsequently if indicated. Early diagnosis and initiation of therapy can minimize complications. Serious ocular injuries have been noted in 12.5% of orbital blow-out and 37.5% of zygomatico-orbital fractures.1Gossman MD Roberts DM Barr CC Ophthalmic aspects of orbital injury: a comprehensive diagnostic and management approach.Clin Plast Surg. 1992; 19: 71-85PubMed Google Scholar Blindness associated with orbital injuries is thought to be caused by either direct trauma to the optic nerve itself or ischemia of the optic nerve induced by pressure or hemorrhage.2Nicholson DH Guzak SW Visual loss complicating repair of orbital floor fractures.Arch Ophthalmol. 1971; 86: 369-375Crossref PubMed Scopus (107) Google Scholar3Ledcrman IR Loss of vision associated with surgical treatment of zygomatic-orbital floor fracture.Plast Reconstr Surg. 1981; 68: 94-99Crossref PubMed Scopus (42) Google Scholar The classic symptoms of retrobulbar compression are pain, ptosis, and third nerve palsy with a gradual decrease in visual acuity. Visual loss can be related to trauma to the globe, which can produce vitreous hemorrhage, retinal detachment, retinal edema, or choroidal rupture. Ischemic optic neuropathy is usually due to a disease of small optic nerve vessels. We report a case of bilateral traumatic internal carotid artery dissection with delayed visual loss due to ischemic optic neuropathy. A 43-year-old woman, who was wearing a seat belt, had a single-car high-speed motor vehicle accident in which the air bag was deployed. The patient was unconscious for an unknown period and was subsequently brought to the emergency department. Right periorbital ecchymosis and enophthalmos were noted on admission. As part of the initial evaluation, computed tomography (CT) of the head and abdomen was performed, along with the usual trauma films (radiography of the chest, cervical spine, and pelvis). The patient's injuries consisted of a mild closed head injury, an open nasal fracture, a right zygomaticoorbital fracture, a grade 1 spleen laceration, and a right clavicular fracture. Reduced visual acuity of the right eye (20/200) was thought to be due to posttraumatic optic neuropathy, and therapy with corticosteroids was initiated. The patient was admitted to the hospital, and additional work-up was performed. The facial fractures were evaluated with coronal and axial CT scans with 3-dimensional reconstruction. She had a nasal bone fracture as well as right medial and inferior orbital wall fractures with a zygomatic fracture involving the maxillary buttress and zygo-matic arch. A subcondylar fracture of the mandible on the right side was also noted. Five days after the injury, the patient's visual acuity was improving (right eye, 20/120; left eye, 20/40). Her cervical spine was clinically reexamined, and the ligamentous system was found to be uninjured. The patient was taken to the operating room 8 days after the injury for open reduction and internal fixation of her facial fractures. The facial fractures were anatomically reduced by using standard coronal, subciliary, and Caldwell-Luc incisions. Rigid fixation was obtained by using 1.5-mm titanium plates. The orbital floor and medial wall fractures were reconstructed with use of a 0.85-mm Medpore plate, which was secured with titanium screws. The lacrimal system was reconstructed by immediate dacryocystorhinostomy. The mandibular fracture was reduced, and the patient was placed in intermaxillary fixation. The patient's early postoperative course was uneventful. Regular postoperative visual examinations by the craniofacial team revealed no subjective visual changes. On the fifth postoperative day, the patient reported decreased visual acuity in her right eye in the early morning; 4 hours later, this had progressed to no light perception. Urgent CT of the orbits revealed no bony fragments compressing the optic nerve (Figure 1). Evaluation of the right fundus revealed mild nasal swelling of the optic disc. A high-dose corticosteroid drip (5.4 mg/kg in the first 15 minutes and then 0.9 mg/kg per hour for 72 hours) was initiated. No improvement in her vision was noted after 12 hours of corticosteroid treatment (right eye, no light perception; left eye, 20/30). At that time, the craniofacial and ear, nose, and throat teams decided to proceed with endoscopic transethmoidal optic canal decompression. The high-dose corticosteroids were continued after the decompression for 48 hours, but vision in the right eye did not improve. Computed tomography demonstrated a low attenuated 2-cm lesion in the anterior limb of the left internal capsule and left caudate nucleus. The patient had no neurologic symptoms. A CT scan of the head repeated 48 hours later showed a new area of infarction, 1.5 cm in diameter, in the left frontal lobe. Additional work-up to determine the source of embolization consisted of a transthoracic echocardiogram and magnetic resonance imaging (MRI) of the head and neck with magnetic resonance angiography. Findings on the echocardiogram were unremarkable, but MRI revealed dissection of the carotid arteries bilaterally. Dissection involved the intracranial portion of both internal carotid arteries, with 50% stenosis on the right side (Figure 2). Thrombus formation was visualized in the cxtracranial part of both carotid arteries. Anticoagulant therapy was initiated immediately. Assessment by a vascular surgeon revealed that the patient was not an operative candidate for carotid artery reconstruction. The anticoagulant therapy is being continued, and MRI and duplex ultrasonography will be performed in 3 months to monitor for pseudoaneurysm formation. The patient was dismissed after the 12th day of hospitalization. She was receiving oral anticoagulation, and the international normalized ratio was 2 to 3. Optic disc atrophy was noted on a fundus examination at that time. She continued to have no light perception in her right eye. The exact incidence of extracranial carotid artery dissection after blunt trauma is unknown. It was once thought to be rare, but increased awareness and noninvasive duplex ultrasonography and MRI have demonstrated more frequent occurrence. Nonetheless, it probably remains undiagnosed in a number of patients with and without precerebral neurologic events because it can clear spontaneously.4Javid H Chawla SK Dye WS et al.Carotid body rumor: resection or reflection.Arch Surg. 1976; 111: 344-347Crossref PubMed Scopus (27) Google Scholar In 1982, Zelenock et al5Zelenock GB Kazmers A Whilehouse Jr, WM et al.Extracranial internal carotid artery dissections: noniatrogenic traumatic lesions.Arch Surg. 1982; 117: 425-432Crossref PubMed Scopus (98) Google Scholar described 2 main mechanisms of injury leading to dissection caused by blunt trauma. First is flexion of the neck with a compression injury to the internal carotid artery between the angle of the mandible and upper cervical vertebrae (C2 through C3), resulting in intimal disruption. The second mechanism is cxiension and rotation of the neck that produce a stretch injury of the internal carotid artery over the upper cervical vertebrae, resulting in intimal disruption and dissection. One of the clinical findings induced by embolization from an intimal injury of the carotid artery is an ischemic event to the eye.6Galetta SL Leahey A Nichols CW Raps EC Orbital ischemia, ophthalmoparesis, and carotid dissection.J Clin Neuroophtkalmol. 1991; 11: 284-287PubMed Google Scholar7Newman NJ Kline LB Leifer D Lessell S Ocular stroke and carotid artery dissection.Neurology. 1989; 39: 1462-1464Crossref PubMed Google Scholar In 80 consecutive patients with extracranial carotid artery dissection, Biousse et al8Biousse V D'Anglejan-Chatillon J Touboul PJ Amarenco P Bousser MG Time course of symptoms in extracranial carotid artery dissections: a series of 80 patients.Stroke. 1995; 26: 235-239Crossref PubMed Scopus (317) Google Scholar found that retinal infarciion occurred in 42 and was the initial event in 9. They also found that complete stroke usually occurs within a few days after onset of the initial symptoms. In 1998, Biousse et al9Biousse V Schaison M Touboul PJ D'Anglejan-Chatillon J Bousser MG Ischemie optic neuropathy associated with internal carotid artery dissection.Arch Neurol. 1998; 55: 715-719Crossref PubMed Scopus (67) Google Scholar described 4 patients with ischemic optic neuropathy in 110 consecutive patients with carotid ariery dissection. They found that none of these patients had central retinal artery occlusion, ischemic ocular syndrome, or cerebral infarciion. Based on those findings, they believe that the mechanism of ischemic optic neuropathy in that setting is a rapid reduction in blood flow due to a sudden decrease in the caliber of the internal carotid artery. No signs of occlusion of the retinal artery or its branches were found in our patient, as described in a patient with blunt injury to the common carotid artery.10Godfrey DG Biousse V Newman NJ Delayed branch retinal artery occlusion following presumed blunt common carotid dissection [letter].Arch OphthalmoL. 1998; 116: 1120-1121PubMed Google Scholar In our patient, intraoperativc findings during optic nerve decompression were not indicative of compression since perineural perfusion appeared to be intact. Use of oxygen-free radical scavengers, as suggested by experimental data,11Babovic S Im MJ Angel MF Manson PN Role of reactive oxygen species in optic nerve compression injury: a preliminary study.Ann Plast Surg. 1998; 40: 156-159Crossref PubMed Scopus (4) Google Scholar was not warranted because of the delayed onset of optic nerve ischemia after trauma and surgery.12McDonough RL Forteza AM Flynn Jr, HW Internal carotid artery dissection causing a branch retinal artery occlusion in a young adult.Am J OphthalmoL. 1998; 125: 706-708Abstract Full Text Full Text PDF PubMed Scopus (24) Google Scholar We believe that, in our patient, ischemic optic neuropathy was caused by a rapid decrease in blood flow. In addition, CT demonstrated cerebral infarction without a distinct neurologic deficit. Delayed neurologic symptoms after a head injury were described in 1891.13von Bollinger O Ueber traumatische spat-Apoplexie: ein Beitrag zur Lehre von der Himerschhutterung.in: Internationale Beiträge zur wissenschaftlichen Medizin: festschrift, Rudolf Virchow gewidmet zur Vollendung seines 70. Vol 2. Hirchwald, Berlin, Germany1891: 459-470Google Scholar The investigator described 5 patients and postulated a theory of delayed stroke, with deaths occurring 18 to 52 days after closed head injury. Another intriguing fact is that our patient had no complaints of ocular pain, and she did not have Homer syndrome, typically seen in patients with acute optic nerve ischemia caused by retrobulbar compression. The facial trauma with swelling may have masked ptosis, but her pupils remained symmetric on routine neurologic examinations. The bilateral carotid artery dissection may have also masked pupillary changes. In a recent review of blindness after major facial injuries in patients at the Maryland Shock Trauma Center, the total incidence of blindness was 0.242%.14Girotto JA Gamble WB Robertson B et al.Blindness after reduction of facial fractures.Plast Reconstr Surg. 1998; 102: 1821-1834Crossref PubMed Scopus (100) Google Scholar The investigators explored the cause in great detail. Of 27 patients, visual loss in 5 was attributed to an unspecified mechanism of increased orbital pressure. Is it possible that carotid artery dissection had a role in any of these cases? Our patient's craniofacial trauma and ensuing carotid artery dissection suggest that high-speed motor vehicle accidents may injure the carotid artery, with devastating consequences. We recommend that, in addition to a multispecialty trauma team evaluation, patients involved in high-speed motor vehicle accidents who experience severe craniofacial injury undergo duplex ultrasonography of the carotid arteries as a screening examination to rule out carotid artery dissection." @default.
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• W2024508247 title "Traumatic Carotid Artery Dissection Causing Blindness" @default.
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