Orbital Infarction Research Articles

Incidence of Orbital Infarction Syndrome Following Anterior Circulation Endovascular Thrombectomy

Background Orbital infarction syndrome (OIS) is a rare entity defined as acute ischemia of intraorbital structures. Its occurrence requires interruption of the rich collateral supply to the orbit from both the ophthalmic artery (OA) and branches of the external carotid artery. Three case reports have recently been published of OIS occurring after endovascular thrombectomy (EVT). The goal of this study was to determine the true incidence of post‐EVT OIS and to identify associated imaging findings on computed tomography angiography and digital subtraction angiography (DSA). Methods A retrospective cohort study was performed at our comprehensive stroke center, including all patients who underwent EVT for anterior circulation strokes in 2019 and 2020. Patient charts were reviewed up to 24 hours after EVT for the presence of acute painful vision loss, ophthalmoplegia, chemosis, and proptosis. Patients with any combination of these symptoms in the absence of a carotid‐cavernous fistula were defined as having OIS. Pre‐EVT computed tomography angiography, pre‐EVT DSA, and post‐EVT DSA images were reviewed to determine the sensitivity and specificity of absent OA opacification, nonopacified external carotid artery, and absent choroid blush (CB) for post‐EVT OIS. Patients were excluded from sensitivity and specificity analysis for each finding that was objectively impossible to assess on their images, either because it was outside the field of view or not tested during the procedure. Findings were deemed indeterminate if motion artifact or contrast timing led to uncertainty about their presence. Sensitivity and specificity calculations were performed on a worst‐case‐scenario basis, with all indeterminate findings assumed to be false positives or false negatives. Results Of 217 patients with anterior circulation EVT (male:female, 107:110; median age, 73 [21–98] years), 4 cases of OIS were discovered (male:female, 1:3; median age, 71 [66–80] years; incidence, 1.7%). The number of patients excluded from sensitivity and specificity analysis for each imaging finding was as follows: 34 for pre‐EVT CB, 45 for post‐EVT CB, 7 for pre‐EVT OA, and 19 for post‐EVT OA. CB was deemed indeterminate in 47 patients on pre‐EVT DSA and 36 patients on post‐EVT DSA. All indeterminate cases occurred in non‐OIS patients and were counted as false negatives. Absent OA opacification was 50% sensitive and 91% specific for OIS on both pre‐EVT computed tomography angiography and pre‐EVT DSA, and 0% sensitive and 97% specific on post‐EVT DSA. Absent CB was 33% sensitive and 65% specific for OIS on pre‐EVT DSA, and 100% sensitive and 73% specific on post‐EVT DSA. Conclusion Post‐EVT OIS is rare, with an incidence of 1.7%. Absent OA opacification is 91% specific for OIS on pre‐EVT computed tomography angiography and 97% specific for OIS on post‐EVT DSA. Absent post‐EVT CB is 100% sensitive for OIS, with a worst‐case scenario specificity of 73%. These findings may help alert clinicians to potential OIS cases as well as determine the underlying cause of OIS.

Orbital infarction syndrome following mechanical thrombectomy in internal carotid artery occlusion: a case report

BackgroundOrbital ischemic syndrome is a rare entity. The clinical signs typically demonstrate acute loss of visual acuity, chemosis, proptosis, ptosis, and total ophthalmoparesis. We report a case of a man who suffered an acute internal carotid artery occlusion and developed orbital ischemic syndrome after a mechanical thrombectomy.Case presentationA 57-year-old Vietnamese (Kinh ethnicity) man was brought to the emergency room with complaints of a speech disturbance, facial palsy, and severe weakness of the left arm and leg, which had started 4 hours earlier, after waking up. The National Institutes of Health Stroke Scale 12 (NIHSS 12) revealed the neurological score at admission. A head computed tomography scan showed no intracranial bleeding and an Alberta Stroke Program Early Computed Tomography Score (ASPECTS) of 8 on the right brain. Computed tomography angiography showed an occlusion of the right internal carotid artery. After that, a mechanical thrombectomy was performed, and the internal carotid artery was completely reperfused. After 10 hours, he experienced orbital pain, proptosis, ptosis, chemosis, and ophthalmoplegia of the right orbit. He also had acute loss of visual acuity, and fundoscopic examination revealed papilledema, no retinal hemorrhage, and no bruit in orbital auscultation. Intraocular pressure in the right eye was measured at 50.5 mmHg. Computed tomography angiography showed no carotid–cavernous fistula, but slight enlargement of the right medial and lateral rectus muscles. He was treated with steroids and hyperosmolar agents and recovered 7 days later, but had persistent loss of visual acuity in the right eye.ConclusionOrbital ischemic syndrome is a rare complication after mechanical thrombectomy treatment in acute ischemic stroke that can lead to loss of visual acuity.

A Case of Orbital Infarction Syndrome in a Patient with Hemophagocytic Lymphohistiocytosis

Purpose: To report a case of orbital infarction syndrome in a patient with hemophagocytic lymphohistiocytosis (HLH).Case summary: A 70-year-old woman with diabetes mellitus and hypertension was referred to the Department of Ophthalmology for sudden-onset left upper eyelid ptosis after being diagnosed with HLH. After 3 days, the best corrected visual acuity in the right eye was 0.8, while there was no light perception in the left eye. In the left eye, the ocular motility examination showed limitations in all fields of gaze. On fundus examination, optic disc pallor, retinal hemorrhage, and narrowed retinal arteries were observed in the left eye. Fluorescein angiography showed no blood flow in the retinal arteries and veins in the left eye. On neck computed tomography angiography, the left distal internal carotid artery was narrowed. Orbit computed tomography showed exophthalmos and extraocular muscle hypertrophy in the left eye. Orbit magnetic resonance imaging confirmed optic nerve edema, enhancement of the optic nerve sheath, and high signal intensity of the intraocular fat in the left eye. Slit-lamp examination revealed ischemia of the anterior segment and ischemic necrosis of the eyelid in the left eye. The patient was diagnosed with orbital infarction syndrome.Conclusions: Several factors may lead to ischemia of the orbital tissues in patients with HLH, including coagulopathy, an increased incidence of blood clots, and inflammation in the orbit. It is necessary to consider the possibility of orbital infarction syndrome when HLH patients present with visual loss, ocular movement limitations, and anterior segment ischemia.

Orbital infarction during drug abuse: tissues of the globe do not appear to recover function.

To describe the features of an orbital infarction syndrome arising after prolonged orbital pressure during drug-induced stupor in young people. The clinical presentation and course for drug-induced orbital infarction is described, based on a retrospective review of clinical notes and imaging. Two cases of orbital infarction syndrome, due to prolonged orbital compression caused by sleeping with pressure on the orbit during drug-induced stupor, are described. Both patients presented with very poor vision and mydriasis, marked periorbital swelling with some pain, and complete external ophthalmoplegia. Whilst the orbital changes and eye movements recovered, the affected eyes had persistent wide mydriasis, and remained blind with marked optic atrophy. With a mechanism analogous to prolonged orbital pressure due to improper head positioning during neurosurgical procedures, drug-users appear to risk developing an orbital infarction syndrome if they rest with prolonged pressure on the orbit during a drug-induced stupor.

GR.5 Incidence of orbital infarction syndrome following endovascular thrombectomy

Background: Orbital infarction syndrome (OIS) is a rare entity defined as acute ischemia of intraorbital structures. Three case reports of OIS post-endovascular thrombectomy (EVT) have recently been published, two demonstrating absent choroid blush (CB) on digital subtraction angiogram (DSA). Our goals are to determine the true incidence of OIS post-EVT and to identify imaging findings (e.g. CB) that may alert neurologists to potential cases. Methods: A retrospective cohort study including all EVT patients from Health Sciences Center (HSC), Winnipeg in 2019-20 was performed. Patient charts were reviewed to determine the incidence of OIS. Pre- and post-EVT DSA images were reviewed, and the sensitivity and specificity of absent CB for OIS was calculated. Results: Out of 248 patients, 13 were excluded for incomplete charts, and 4 cases (1.7%) of OIS were discovered. During sensitivity/specificity analysis of absent CB for OIS, 51 patients were excluded for inadequate imaging. There were 4 true positives, 0 false-negatives, 113 true-negatives, and 67 false-positives; resulting in a sensitivity of 100% and worst-case scenario specificity of 63% (assuming all 51 indeterminate cases were false positives). Conclusions: OIS is rare post-EVT with an incidence of 1.7%. Absent CB is very sensitive for diagnosing OIS with lower specificity.

Orbital inflammatory syndrome after mechanical thrombectomy of acute carotid occlusion

Introduction: Orbital ischemic syndrome (OIS) is a rare disorder that presents with acute loss of visual acuity, chemosis, proptosis, ptosis and ophtalmoparesis. We present a case with acute onset of orbital inflammation following mechanical thrombectomy that mimicked an OIS, except for the absence of vision loss. Case report: A 65-year-old woman presented to our emergency department after an episode of transient dysarthria and left-sided hemiparesis and paresthesia that lasted about forty minutes. Head computed tomography showed no signs of intracranial bleeding or acute ischemia. CT angiogram showed occlusion of the right ICA terminus. Mechanical thrombectomy was then performed and the clot was removed with combined technique. Eight hours later, she developed orbital pain, ptosis, chemosis and complete ophthalmoplegia of the right eye. She had no diplopia, visual acuity and funduscopic examination were normal and there was no audible bruit in the orbit. Brain MRI performed showed hyperintensity of orbital fat along with hyperintensity and enlargement of all the extraocular There were no signs of orbital infarction and the optic nerve was structurally normal. Time of flight magnetic resonance angiography revealed reduced calibre of the distal portion of ICA, with associated contrast enhancement on vessel wall imaging. She was started on intravenous dexamethasone with full recovery two days later. Discussion: We present the case of an orbital inflammatory syndrome after mechanical thrombectomy. The mechanical stress exerted by endovascular devices has been associated with endothelial damage that correlates with vessel wall thickening and contrast enhancement in high resolution MRI studies. The temporal correlation with mechanical thrombectomy, the absence of vision loss or orbital infarction and the good clinical response to steroids support the hypothesis of an internal carotid artery wall inflammation due to endovascular manipulation of the stent retriever to be responsible for this acute orbital syndrome. This case highlights the need for close postprocedural monitoring after MT and the consideration of orbital inflammation secondary to endovascular devices in the differential diagnosis of an acute orbital syndrome. Further studies are needed to understand the long-term consequences of arterial wall lesions associated with these devices.

Orbital Infarction Syndrome as a Rare Complication After Mechanical Thrombectomy in Ischemic Stroke.

Orbital Infarction Syndrome as a Rare Complication After Mechanical Thrombectomy in Ischemic Stroke.

Orbital Infarction Syndrome after Thrombectomy for Internal Carotid Artery Occlusion

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33. A case of ocular ischaemic syndrome caused by severe giant cell arteritis

IntroductionThis case describes a very aggressive form of giant cell arteritis (GCA) complicated by ocular ischaemic syndrome (OIS), complete bilateral visual loss and bilateral scalp muscle necrosis, despite treatment with high dose intravenous steroids. OIS, defined as ischaemia of all intraorbital and intraocular structures, is rare, estimated at 7.5 cases per million. This case also highlights the use of PET CT in management of complex cases of GCA.Case descriptionA 79-year-old lady presented with sudden onset pain above her right eye. A month earlier she had undergone curative surgery for infiltrating adenocarcinoma of the colon. 6 months earlier she had complained of bilateral shoulder pain. A month earlier she had developed pain on chewing and was unable to fully open her mouth. The next day she was reviewed in the eye hospital due to 24hrs of intermittent blurred vision. CT head was normal. Fundoscopy was normal and she was diagnosed with ocular migraine. Later that evening she lost vision in the right eye. Bloods showed CRP 58 and ESR 43. She was given 5 days of IV methylprednisolone (5x1g). Despite this she developed a right 6th nerve palsy. 2 days later her left eye developed visual loss, complete ptosis and loss of eye movements in all directions. MRI head with gadolinium showed temporoparietal juxtacortical diffuse white matter signal abnormalities.She underwent extensive investigation. ANCA was negative, lumbar puncture normal and temporal artery biopsy showed extensive fibrinoid necrosis of the vessel wall, with possible granulomata but no eosinophilia. Oral cyclophosphamide (2mg/kg) was started. 5 days later she developed severe bi-temporal pain and a rash which progressed to severe scalp necrosis. There were no vesicles to suggest shingles. Ten days later she suffered an upper gastro-intestinal bleed requiring a 4 unit transfusion. Gastroscopy showed mild gastritis. After this, cyclophosphamide was withheld, following discharge on steroids alone. Bilateral scalp necrosis remained a problem, complicated by pseudomonas infections. When a decreased left radial pulse was noted a PET CT was arranged. This showed active extensive vasculitis of the aorta. At this point methotrexate 15mg per week was added. The scalp lesions rapidly healed and the radial pulse returned to normal. The CRP has remained consistently below 5. DiscussionAn antiplatelet agent, clopidogrel was started due to the ischaemic cerebral findings on MRI, but it probably contributed, along with steroids, to her upper GI bleed. Antiplatelet therapy is no longer recommended routinely in the management of GCA. However in this case the diagnosis was still uncertain. None of us had ever seen orbital infarction syndrome as a complication of GCA. Perhaps a PET CT earlier on in the course of this lady’s disease would have made us more secure in the diagnosis. It could be argued that given the severity of her disease, methotrexate or even tocilizumab should have been commenced earlier. In fact, cyclophosphamide was used initially as it wasn’t clear if this was a medium vessel vasculitis. This was withheld when she had a large upper GI bleed (Hb dropped to 76). Once recovering, her CRP was down to 10. By this time the temporal artery biopsy was available, the ANCA was negative and GCA was felt to be the most likely diagnosis. It was also felt that given the bilateral visual loss, the most feared complication of GCA had already occurred so what was there to gain by using such strong immunosuppression? Hence cyclophosphamide was discontinued, and she was discharged on steroids alone. The addition of methotrexate had an impressive effect in terms of healing her weeping, secondarily infected scalp necrosis. Methotrexate was added in light of the PET CT which showed active large vessel vasculitis. The scalp necrosis, on reflection was due to an ongoing vasculitis that was being undertreated.There were missed opportunities for starting steroids earlier in the course of the disease: polymyalgic symptoms 6 months earlier, jaw claudication a month earlier. However it remains uncertain whether or not earlier treatment would have altered the course of this aggressive, severe disease. Key learning pointsScalp necrosis, which very easily can be mistaken for shingles or infections complicating steroid treatment, can be a feature of GCA. Orbital infarction syndrome can be a feature of GCA. Early PET CT might have clarified the diagnosis. Methotrexate should probably have been started once the limited response to IV steroids was apparent. Antiplatelet agents are no longer recommended in the updated BSR guidelines for managing GCA.Conflicts of interestThe authors have declared no conflicts of interest.

Orbital Compression Syndrome in a Child with Sickle Cell Anaemia: A Case Report And Review of Literature

Vaso-occlusive crises in sickle cell disease commonly involve bone marrow of the long bones and vertebrae. Involvement of bones with less marrow space, including the bones of the orbit, is reported rarely in the literature. The present case is a six year old boy, a known case of sickle cell disease, who presented with acute onset right upper and lower eyelid swelling, restriction of extraocular movement and pain. USG orbit showed a retro-orbital haemorrhage compressing on the orbit, probably due to orbital bone infarction. The child was managed successfully with red blood cell transfusion and intravenous antibiotics, without steroids and surgical intervention. This report highlights the importance of maintaining a high index of suspicion in patients with known sickle cell disease presenting with pain, orbital swelling and restriction of ocular movement. Timely red blood cell transfusion only may be sufficient for uneventful recovery, without steroids or surgical intervention. Expedient diagnosis of orbital compression syndrome in children with sickle cell disease is crucial because this is a potentially sight-threatening entity.

Orbital Infarction due to Sickle Cell Disease without Orbital Pain.

Sickle cell disease is a hemoglobinopathy that results in paroxysmal arteriolar occlusion and tissue infarction that can manifest in a plurality of tissues. Rarely, these infarcted crises manifest in the bony orbit. Orbital infarction usually presents with acute onset of periorbital tenderness, swelling, erythema, and pain. Soft tissue swelling can result in proptosis and attenuation of extraocular movements. Expedient diagnosis of sickle cell orbital infarction is crucial because this is a potentially sight-threatening entity. Diagnosis can be delayed since the presentation has physical and radiographic findings mimicking various infectious and traumatic processes. We describe a patient who presented with sickle cell orbital crisis without pain. This case highlights the importance of maintaining a high index of suspicion in patients with known sickle cell disease or of African descent born outside the United States in a region where screening for hemoglobinopathy is not routine, even when the presentation is not classic.

Orbital infarction syndrome after multiple percutaneous sclerotherapy sessions for facial low-flow vascular malformation: A case report and literature review

Vision loss following sclerotherapy for facial vascular malformations (VMs) is a rare but detrimental complication. Here, we report a case of an 11-year-old boy with acute onset blepharoptosis, ophthalmoplegia, and blindness in his right eye after the 14th sclerotherapy session (percutaneous intralesional injection of sodium tetradecyl sulfate) for a right facial low-flow VM without orbital involvement. Computed tomography angiography revealed no contrast enhancement in the right ophthalmic artery, superior ophthalmic vein, or extraocular muscles. He presented with the hallmarks of orbital infarction syndrome: Clear signs of anterior and posterior segment ischemia and disrupted arterial flow to the extraocular muscles. His blepharoptosis and eye movement improved 4 months later; however, he remained blind, and phthisis bulbi developed eventually. Thus, sclerotherapy for facial VM—even without orbital involvement—may result in severe ocular and orbital complications.

Transient Sixth Nerve Palsy and Mydriasis following a Temporal Sculptra Aesthetic (Poly-(L)-Lactic Acid) Injection: A Case Report and Literature Review

Introduction: Intraocular side effects of Sculptra Aesthetic (poly-(L)-lactic acid) (PLLA) (Dermik, Bridgewater, NJ, a subsidiary of Aventis Pharmaceuticals International Inc), dermal filler have been rare. The authors seek to describe the first case of a transient sixth nerve palsy and mydriasis secondary to extraorbital PLLA filler injection and to present hypotheses explaining the complications. Materials and Methods: A case report is presented that details a complication suffered by 1 patient during a temporal PLLA injection. A thorough review of the literature was performed. The literature was evaluated with respect to the number of patients, complications, and outcomes secondary to PLLA injections. Results: In the literature, there were 3 reported cases of ocular symptoms following a PLLA injection. The findings ranged from posterior ciliary artery occlusion to orbital infarction and blindness. In our case, we propose that the PLLA accessed the orbit by leakage through the temporal orbit due to the mechanism of injection combined with an increased porosity secondary to osteopenia. Conclusions: A large majority of the patients who seek a cosmetic result that can be gained by fillers are postmenopausal women. This population is characteristically affected by osteopenia and osteoporosis. For patients similar to ours, with osteopenia or osteoporosis, extra care must be taken when injecting the temporal area secondary to its various areas of susceptibility caused by decreased density. Because of the increased use of PLLA as a dermal filler, it would be prudent to include an eye exam as part of the pretreatment and posttreatment care plan.

Radiological findings of orbital infarction syndrome following intracranial aneurysm surgery

Orbital infarction syndrome is a rare disorder resulting from cclusion of the ophthalmic artery and its branches. Zimmerman t al. first reported six patients with proptosis, opthalmoplegia nd blindness immediately after intracranial aneurysm surgery as rbital infarction syndrome [1]. To present, only ten cases (3 litertures) of orbital infarction syndrome after intracranial aneurysm urgery have been reported [1–3]. However two of three literaures were described by ophthalmologists. Neurosurgeons should ay attention to this rare but devastating complication. In order to ssist the early diagnosis of this complication, we report upon two ases of orbital infarction syndrome after intracranial aneurysm urgery.

Bilateral orbital infarction and retinal detachment in a previously undiagnosed sickle cell hemoglobinopathy African child

Bone infarction involving the orbit in sickle cell disease is not common. Bilateral orbital infarction in a previously undiagnosed sickle cell hemoglobinopathy has not been previously reported. In this report, we present a case of an 11-year-old previously undiagnosed sickle cell disease Nigerian girl with severe acute bilateral orbital infarction and retinal detachment to highlight that hemoglobinopathy induced orbital infarction should be considered in African children with acute onset proptosis with or without previous history of sickle cell hemoglobinopathy.

Orbital Infarction Syndrome After Transcanalicular Dacryocystorhinostomy With Diode Laser

Orbital infarction syndrome is a rare but devastating disorder resulting in sudden visual loss. A patient with orbital infarction syndrome due to orbital cellulitis after transcanalicular dacryocystorhinostomy with diode laser is described. A 55-year-old woman presented 3 days after transcanalicular dacryocystorhinostomy. Initial examination revealed significant eyelid swelling, marked proptosis, total ophthalmoplegia, and no light perception in the right eye. Fundus examination revealed ophthalmic artery occlusion. The clinical findings of the patient were consistent with orbital infarction syndrome. Clinical findings improved with antibiotic therapy, but visual acuity did not change.

Severe Visual Loss and Orbital Infarction Following Periorbital Aesthetic Poly-(L)-Lactic Acid (PLLA) Injection

Visual loss following esthetic treatment of the face is a rare but devastating iatrogenic complication. The authors report a case of a 43-year-old man with blindness and ophthalmoplegia of the left eye following a treatment of the left periorbital region with the subcutaneous filler poly-(L)-lactic acid. The patient's symptoms began immediately following one of the tunneled injections. On presentation, the patient had clear signs of ocular and orbital ischemia. Angiography and further history suggested an embolic orbital infarction as the mechanism of injury. The increased usage of subcutaneous fillers for facial rejuvenation had introduced a small but proven risk of embolization of these viscous materials to the eye and orbit.

Crise vaso-occlusive orbitaire chez un enfant drépanocytaire

Vaso-occlusive crises are the most common complication of sickle cell disease. Orbital bone infarction is an unusual manifestation of sickling disorders. It is suspected in patients with acute painful periorbital swelling. Orbital compression syndrome with possible optic nerve injury is a rare but serious complication; therefore, this diagnosis should be considered. Orbital infarction can be difficult to distinguish from osteomyelitis or skin infections. Imaging can be helpful in differentiating infection from infarction. We report a case of orbital bone infarction in a 14-year-old boy with sickle cell disease. Under medical treatment, the clinical course resolved with no sequelae.

Bilateral Orbital Bone Infarction in Sickle-Cell Disease

This is a case of a 2-year-old boy with sickle cell disease who presented with bilateral eyelid swelling, limited extraocular motility, and lateral subperiosteal fluid collection associated with bilateral lateral orbital wall infarctions on MRI. The patient was managed medically with intravenous fluids, analgesics, broad-spectrum antibiotics, systemic steroids, and clinically improved. Patients with sickle cell disease are susceptible to infarction of the orbital bones during vaso-occlusive crises. Orbital wall infarction can lead to acute proptosis and restricted extraocular motility. Orbital wall infarction should be considered in sickle cell patients with orbital diseases so that appropriate treatment can be instituted promptly to prevent the serious sequelae of orbital compression syndrome.

Hématome sous-périosté orbitaire chez un enfant drépano-thalassémique

Sickle cell anemia is the most common hemoglobinopathy worldwide; its musculoskeletal complications consist more often of medullary infarctions involving long bones. Orbital infarction is uncommon. We report on a case of orbital subperiosteal hematoma in a 9-year-old male with a medical history of sickle cell thalassemia.