Posterior Ciliary Artery Occlusion Research Articles

Amalric triangular sign: Combined central retinal artery and posterior ciliary artery occlusion presenting with macular edema

A 55-year-old female patient presented with no light perception and features suggestive of central retinal artery occlusion (CRAO) and posterior ciliary artery occlusion. Multimodal imaging analysis revealed retinal thickening, cherry-red spot, pallid optic disc with choroidal infarction (Amalric sign), and macular edema. Carotid Doppler disclosed 70% stenosis of the right common carotid artery. Systemic investigations showed elevated erythrocyte sedimentation rate, total cholesterol, and low-density lipoprotein level. The Amalric triangular sign with CRAO may present with macular edema. Prompt cardiac and carotid evaluation with appropriate management should be done.

Pathogenesis of Terson syndrome.

The aim of this experimental study was to investigate the pathogenesis of Terson syndrome (TS), which currently is controversial. The central retinal artery (in 39 orbits), posterior ciliary arteries (in 8 orbits), and central retinal vein (CRV in 21 orbits) were occluded in rhesus monkeys by exposing them to lateral orbitotomy. Fundus examination and fluorescein fundus angiography were performed before and immediately after cutting the vessels and serially thereafter during the follow-up period. The rationale of the experimental study design is discussed. In eyes with central retinal artery occlusion, retinal hemorrhages were seen soon after the procedure in 7 eyes, and on follow-up in a total of 15 eyes. In posterior ciliary artery occlusion, retinal hemorrhages were seen soon after the procedure in one eye, and on follow-up in a total of three eyes. In eyes with CRV, all eyes had extensive scattered retinal hemorrhages. The findings of this experimental study, and my basic, experimental, and comprehensive clinical studies on CRVO, suggest the following concept of the pathogenesis of TS: Compression of the CRV plays a crucial role in the development of TS. The CRV is compressed, as it lies in the subarachnoid space of the optic nerve sheath, by raised cerebrospinal fluid pressure and/or accumulated blood. venous stasis and raised venous pressure in the retinal veins, leading to venous engorgement, rupture of the retinal capillaries. retinal hemorrhages. The clinical importance of compression of the CRV and not occlusion of CRV in TS is that optic nerve sheath decompression by opening it and releasing the blood and raised cerebrospinal fluid (CSF) pressure, would result in immediate decompressing of the CRV in the subarachnoid space and restoration of normal circulation and prevent visual loss.

Filler-induced blindness “seen” by ophthalmologists: Case presentation and treatment algorithm

Filler-induced blindness (FIB) is the most threatening complication following periocular injection. To date, no standard of care has been established. The goal of this study is to report a new case of FIB with partial visual recovery and present our personalized algorithm for treatment based on fluorescein angiography findings. Case report with 24 months follow-up and treatment algorithm. Our patient experienced complete vision loss to no light perception following forehead lipofilling. Retinal angiography identified a posterior ciliary artery occlusion. Antiplatelet medication, steroids and intraocular pressure lowering medications were administrated, followed by hyperbaric oxygen treatment (HBOT). Visual acuity improved to +0.8 logMar. The HBOT treatment was monitored by fluorescein angiogram. Based on this case and on the ophthalmic literature on retinal and ciliary artery occlusion, we established a personalized FIB protocol guided by fluorescein angiography. Although prevention remains the best treatment, all physicians should be prepared to manage FIB. Prompt management at the office guided by written protocols, as well as emergency kits, are essential. In referral centers, personalized treatment should be undertaken based on fluorescein angiography findings.

Ocular Complications Post-Cosmetic Periocular Hyaluronic Acid Injections: A Systematic Review

With the global rise in the use of hyaluronic acid (HA) fillers as a minimally invasive cosmetic procedure, significant adverse effects such as vascular compromise and blindness have become common. Hence, we present the first systematic review aimed to investigate ocular complications secondary to a facial HA injection and to understand the presentation, cause, management, and outcome of these complications. The preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines were used to report this review. A systematic search was performed in July 2021 for published literature using the PubMed, MEDLINE, and Cochrane databases. The following terms were used: facial fillers, facial injections, hyaluronic acid, blindness, ophthalmoplegia, diplopia, ptosis, ophthalmic artery occlusion, posterior ciliary artery occlusion, and ocular ischemic syndrome. A total of 2496 publications were searched, and 34 articles published between January 2000 and July 2021 were included. Twenty-seven case reports and seven case series were evaluated. The nose was the most common site of injection (n = 25; 40.67%). Ocular pain was the most common initial symptom of ocular complications (n = 13, 22.41 %). The most common complication was vision loss (n = 17, 50%). The majority of patients received hyaluronidase, aspirin, and steroids. Regarding the outcome, 15 (45.45%) of the published studies showed no improvement in complications even after management. HA is gaining popularity in cosmetic applications. Post-HA ocular complications nearly always have an immediate onset. Proper knowledge of potential adverse events is crucial for clinicians to attempt to decrease complications and improve outcomes. This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266.

O31 Giant cell arteritis - a rare ocular presentation

O31 Giant cell arteritis - a rare ocular presentation

Ischemic Choroidal Diseases.

Ischemic choroidal diseases are an underdiagnosed entity. The clinical pattern varies according to the size and the localisation of the affected vascular structure. In eyes with occlusion of the long posterior ciliary arteries, characteristic triangular patches of choroidal ischemia (Amalric sign) are seen, which in the course of time merge into well-defined areas of atrophy of the retinal pigment epithelium. Above the non-perfused choroidal areas, hyperpigmented, grouped lines appear (Siegrist streaks). Circumscribed ischemia of smaller choroidal arterioles and capillary vessels appears as multifocal, yellowish lesions in the posterior fundus (Elschnig spots). Vortex vein occlusion becomes manifest as exudative haemorrhagic choroidal swelling in the periphery. Apart from arterial hypertension as a major risk factor, some immunological disorders such as giant cell arteritis and systemic lupus erythematosus and haematological pathologies also affect choroidal perfusion. Furthermore, choroidal ischemia occurs due to local inflammation, as found in eyes with acute multifocal posterior placoid pigment epitheliopathy (APMPPE). Rarely, choroidal infarction is of iatrogenic origin or drug-induced. Recent advances in imaging, such as the introduction of enhanced depth imaging optical coherence tomography (EDI-OCT) and OCT angiography (OCT-A), have improved the visualisation of the choroidal vasculature and complement the classical angiographic procedures. In patients with age-related macular degeneration (AMD) and diabetes, some changes in choroidal blood flow and vascular structure have also been noted. While in AMD the choroidal pathologies correlate with the disease progression and the functional prognosis, the pathophysiological relationship between diabetic choroidopathy and retinopathy is currently unclear. With regard to the limited therapeutic options for choroidal ischemia, optimisation of the cardiovascular risk profile and the management of accompanying ocular and systemic diseases are essential.

An Atypical Presentation of Giant Cell Arteritis with Bilateral Choroidal Ischaemia

Background: Giant cell arteritis is an immune-mediated, medium to large vessel vasculopathy affecting individuals over 50 years of age. It can cause sudden, severe and irreversible loss of vision, most commonly from an arteritic posterior ciliary artery occlusion causing anterior ischaemic optic neuropathy. The optic nerve appearance would typically be swollen and chalky white. Visual reduction secondary to choroidal ischaemia is a much less frequent presentation, the signs of which can be more subtle in appearance, making its early recognition potentially more challenging. Case Presentation: A 51-year-old male presented to eye casualty complaining of a one-week history of neck pain, intermittent headaches and jaw claudication, associated with reduced vision in his right eye. Presenting visual acuity was hand movements and 6/5 in the right and left eyes respectively. On examination, he was noted to have a right relative afferent pupillary defect, a pale macular area in the right eye with a possible cherry red spot. There was no optic disc swelling. ESR was 34 and CRP was 46 and he was wrongly diagnosed with a non-arteritic central retinal artery occlusion. He subsequently re-presented 5 weeks later with vision loss in his left eye. Best corrected visual acuity was now 6/60 and 6/12 in the right and left eyes respectively. Dilated fundoscopy showed multiple yellow-white lesions in the posterior pole of the left eye and a retinal cotton wool spot. The right optic nerve was pale, and left was normal. A fundus fluorescein angiogram showed delayed choroidal filling and the temporal artery biopsy was suggestive of GCA. He was started on 110mgs of oral prednisolone. After 4 weeks of steroids his BCVA was 6/36 and 6/6 in the right and left eyes respectively. His neck pain, headaches and jaw claudication had all resolved and his ESR and CRP had returned to normal levels. Conclusion: Our case highlights the need for increased awareness of this uncommon presentation of this potentially blinding disease, to allow prompt and appropriate treatment. Our case is unusual in that despite a delayed diagnosis of 5 weeks, visual acuity initially improved with treatment.

Clinical Observations and the Anatomical Basis of Blindness After Facial Hyaluronic Acid Injection

BackgroundBlindness or visual loss is the most serious complication resulting from facial hyaluronic acid (HA) injection. In this study, three recent clinical cases were analyzed, and the relevant anatomy of cadavers was evaluated to investigate the mechanism behind visual impairment due to HA injection.MethodsThree patients with different extents of visual loss after HA injection were studied. Ophthalmic testing and corresponding treatments were performed, and the clinical progress was observed. In addition, thirty-six fresh Asian cadaver hemifaces were anatomized to investigate the morphology of the ophthalmic artery and its branches. The minimum dose of HA for central retinal artery embolism was calculated based on the ophthalmic arterial volumes of cadavers.ResultsVisual impairment was more severe in central retinal artery occlusion and combined intraocular branch occlusion than in posterior ciliary artery occlusion. During follow-up, no improvement was observed in terms of visual impairment. Cadaver study reconfirmed that the ophthalmic artery included facial and intraocular branches. The ophthalmic arterial volumes running from the supraorbital artery and supratrochlear artery to the central retinal artery were 0.083 cm3 and 0.089 cm3, respectively.ConclusionsThe severity of blindness caused by HA injection may be associated with the occlusion site. Our clinical observations indicate that conventional treatments, such as retrobulbar hyaluronidase injection, are insufficient to relieve visual impairment. Injecting as little as 0.08 ml of HA into the facial branch is enough to cause central retinal artery embolism. Limiting the volume per injection could represent a simple prophylactic strategy.Level of Evidence VThis journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266.

Posterior Ciliary Artery Occlusion

To compare the severity of ischemic damage following posterior ciliary artery (PCA) occlusion in old, atherosclerotic, hypertensive monkeys to that in young monkeys. Experimental study. Seven eyes of normal, healthy rhesus monkeys and 8 of old, atherosclerotic, hypertensive monkeys. By lateral orbitotomy, all PCAs were cut behind the eyeball in both groups of animals. The fundus and the optic disc were evaluated by repeated ophthalmoscopy, color fundus photography and fluorescein fundus angiography, before and immediately after cutting the PCAs and serially thereafter during the follow-up period. Severity of acute ischemic damage to the choroidal, outer retinal and optic nerve head. Cutting all the PCAs resulted in the development of ischemic infarction of the choroid, retinal pigment epithelium, outer part of the retina and the optic nerve head within 24-hours, in both groups of animals. The severity of the various ischemic fundus and retinal lesions and of the optic disc during the acute phase showed no statistically significant differences between the two groups of animals. Fluorescein fundus angiography soon after cutting the PCAs showed no filling of the entire choroid and the optic disc in both groups of animals. On follow-up for up to about 3 months, in both groups, the white opacity of the infract in the fundus seen during the acute phase gradually resolved in about 2-3 weeks, leaving greyish, granular, depigmented fundus, unmasking of the large choroidal vessels and optic atrophy; fluorescein angiography revealed gradual restoration of the choroidal blood flow and unmasking of the big choroidal vessels. The study showed that the severity of ischemic damage following occlusion of all the PCAs was similar in both the young healthy and the old, atherosclerotic, hypertensive monkeys. This is in contrast to the findings of our similar study dealing with central retinal artery occlusion, where the young suffered much severe ischemic damage than the old.

Clinical analysis of visual loss caused by facial cosmetic fillers injection

Objective: To investigate the risk factors, clinical manifestations, and treatment of visual loss caused by cosmetic fillers injection. Methods: It was a retrospetive case series study. Collect the clinical data of 18 cases (18 eyes) which were diagnosed as visual loss caused by facial cosmetic fillers injection in the Second Hospital of Dalian Medical University during December, 2014 to June, 2016. Summarize the general condition, medical history, clinical examination results (including visual acuity, intraocular pressure, fundus condition, etc.) and the patient's facial appearance at the time of admission. Take the examinations such as VEP, FFA, OCT, etc. Confirm the composition of the fillers according to the medical history and the product packaging. After the diagnosis, all patients were treated generally combined with intraocular pressure reduction treatment and other treatment measures. Results: All the patients were female, 24-45 years old, with average age of 33.4. The fillers were mainly consisted of hyaluronic acid or autologous fat. For 6 patients the fillers were injected in the forehead, 8 patients were in the nose, the other 4 patients were in both sites. The mean time was 31.7 hours since the onset to the acceptance of medical treatment. All the patients manifested as no light perception, injection site ischemia, different degree of ptosis and fundus examination showed artery occlusion signs. Seventeen patients were central retinal artery occlusion, one was posterior ciliary artery occlusion. After active treatment, 2 patients' visual acuity improved to light perception, one improved to hand movements, while the others had no significant improvement. Conclusions: Most patients who suffered visual loss after cosmetic injections are young or middle-aged women, with most common injection sites at nose or forehead. The visual loss is mainly caused by central retinal artery occlusion which leads to an ineffective clinical treatment. The main factors that may induce artery occlusion are: injection done by informal medical organization, use of non-standard drugs, inadequate understanding of facial anatomy of the operator, and improper injection methods.(Chin J Ophthalmol, 2017, 53: 594-598).

Polycythemia causing posterior segment vascular occlusions

A 44-year-old male patient presented with features suggestive of transient central retinal artery occlusion (CRAO) followed by permanent CRAO and lateral posterior ciliary artery occlusion. He had diagnostic features of polycythemia vera (PV). When presented for the first time, the patient had features of ocular ischemia such as ocular pain, conjunctival congestion, and retinal opacification but with normal arm-to-retina time and normal arteriovenous transit time. During the second presentation, he had ocular pain, congested conjunctiva, retinal opacification, cherry red spot with box-carrying of retinal vessels, and choroidal infarct (Amalric's sign). He had lost light perception in that eye. Patients with polycythemia are prone to multifocal vascular occlusions and this can be the presenting feature in PV. A timely diagnosis and prompt management can prevent these repeated thromboembolic occlusive episodes.

Lamina cribrosa thickness correlated with posterior scleral thickness and axial length in monkeys.

To explore associations of lamina cribrosa thickness with axial length and thickness of the posterior sclera in monkeys. Examining histological sections by light microscopy, we measured the thickness of the lamina cribrosa and posterior sclera and axial length. The study included 28 animals (28 eyes) with a mean age of 13.3±4.9years (range: 3-24years) and mean axial length of 18.9±1.4mm (range: 17-21mm) (22 eyes after experimental temporary central retinal artery occlusion; four eyes after a permanent occlusion of the posterior ciliary artery; and two eyes without any intervention). Mean thickness of the lamina cribrosa was 167±30μm (range: 115-273μm). Thinner lamina cribrosa thickness was significantly associated with longer axial length (standardized correlation coefficient beta: -0.42; p=0.026), with thinner sclera at the posterior pole (beta: 0.56; p=0.002) and with thinner sclera at the disc border (beta: 0.55; p=0.002). Lamina cribrosa thickness was not significantly related to temporary central retinal artery occlusion (p=0.14) or to permanent posterior ciliary artery occlusion (p=0.49) or age (p=0.46). As in humans, lamina cribrosa thickness in non-glaucomatous monkeys got thinner with longer axial length and with thinner posterior sclera. These data may be of interest for studies on the process of emmetropization/myopization in monkeys, and they may be of interest for the studies on the biomechanics of the optic nerve head.

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.

Iatrogenic Occlusion of the Ophthalmic Artery After Cosmetic Facial Filler Injections

Iatrogenic occlusion of the ophthalmic artery and its branches is a rare but devastating complication of cosmetic facial filler injections. To investigate clinical and angiographic features of iatrogenic occlusion of the ophthalmic artery and its branches caused by cosmetic facial filler injections. Data from 44 patients with occlusion of the ophthalmic artery and its branches after cosmetic facial filler injections were obtained retrospectively from a national survey completed by members of the Korean Retina Society from 27 retinal centers. Clinical features were compared between patients grouped by angiographic findings and injected filler material. Visual prognosis and its relationship to angiographic findings and injected filler material. Ophthalmic artery occlusion was classified into 6 types according to angiographic findings. Twenty-eight patients had diffuse retinal and choroidal artery occlusions (ophthalmic artery occlusion, generalized posterior ciliary artery occlusion, and central retinal artery occlusion). Sixteen patients had localized occlusions (localized posterior ciliary artery occlusion, branch retinal artery occlusion, and posterior ischemic optic neuropathy). Patients with diffuse occlusions showed worse initial and final visual acuity and less visual gain compared with those having localized occlusions. Patients receiving autologous fat injections (n = 22) had diffuse ophthalmic artery occlusions, worse visual prognosis, and a higher incidence of combined brain infarction compared with patients having hyaluronic acid injections (n = 13). Clinical features of iatrogenic occlusion of the ophthalmic artery and its branches following cosmetic facial filler injections were diverse according to the location and extent of obstruction and the injected filler material. Autologous fat injections were associated with a worse visual prognosis and a higher incidence of combined cerebral infarction. Extreme caution and care should be taken during these injections, and physicians should be aware of a diverse spectrum of complications following cosmetic facial filler injections.

A Case of Incomplete Central Retinal Artery Occlusion Associated with Short Posterior Ciliary Artery Occlusion

To our knowledge, incomplete central retinal artery occlusion associated with short posterior ciliary artery occlusion is extremely rare. Herein, we describe a case of a 62-year-old man who was referred to our hospital with of transient blindness in his right eye. At initial examination, the patient's best-corrected visual acuity was 18/20 in the right eye. Fundus examination showed multiple soft exudates around the optic disc and mild macular retinal edema in his right eye; however, a cherry red spot on the macula was not detected. Fluorescein angiography revealed delayed dye inflow into the nasal choroidal hemisphere that is supplied by the short posterior ciliary artery. The following day, the patient's visual acuity improved to 20/20. Soft exudates around the optic disc increased during observation and gradually disappeared. His hemodynamic parameters revealed subclavian steal syndrome as examined by cervical ultrasonography and digital subtraction angiography. We speculate that his transient blindness was due to ophthalmic artery spasms. In this particular case, spasms of the ophthalmic artery and occlusion of the short posterior ciliary artery occurred simultaneously. As the short posterior ciliary artery branches from the ophthalmic artery, the anatomical location of the lesion might be near the branching of both arteries.

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Munier, Francis L MD*; Beck-Popovic, Maja MD†; Balmer, Aubin MD*; Gaillard, Marie-Claire MD*; Bovey, Etienne MD*; Binaghi, Stefano MD‡ Author Information

Hemi-central retinal artery occlusion in young adults

Dear Editor, We thank Chopdar[1] for the interest in our article,[2] and concur with the author about our finding of early branching of the central retinal artery (CRA) prior to its entry through the lamina cribrosa. We used the term ‘Hemi-central retinal artery occlusion’ to describe a clinical entity. This early branching pattern of CRA has been documented on Doppler imaging [Fig. 7] for the first time in our report.[2] This provides evidence for an embryological basis of the unusual branching pattern of CRA. The author states, “In Case 1, [Fig. 1] shows associated choroidal infarct of the upper half of the fundus.” We agree that choroidal infarction may be seen concomitantly along with central retinal artery occlusion (CRAO) but we did not encounter such lesions in our case, as is also evident from Fig. 3. Choroidal ischemic lesions as seen in malignant hypertension consist of retinal pigment epithelial lesions (secondary to choroidal infarction), serous retinal detachment and in some eyes, white lines due to choroidal sclerosis.[3] Our patients lacked any of these lesions. Fundus fluorescein angiography (FFA) findings of choroidal ischemia may range from delayed filling of choroidal circulation to near-total lack of choroidal perfusion in infarction. A spectrum of choroidal perfusion defects have been reported to exist with CRAO.[4] Amalric described it earlier[5] and similar findings (Amalric sign) have also been reported by others in cases with CRAO and lateral posterior ciliary artery occlusion. The author further states that, “Fig. 2 shows that the upper artery is a cilioretinal artery whereas the lower one is the true central retinal artery.” Figs 2, 9, 14 and 18 depict separate evolution of central retinal hemi-trunks from the optic disc cup and not at the margin of the optic disc.[2] This has been corroborated with Doppler imaging that shows branching from CRA and not from choroidal circulation. Cilioretinal arteries have been shown histologically to originate from short posterior ciliary arteries and, in rare instances, directly from choroidal vessels.[6] First described by Muller in 1856,[6] they appear ophthalmoscopically to emerge from the optic disc or disc margin separately from CRA or its branches.[7] They make a characteristic bend as they leave the disc margin and are recognizable on fundoscopy. It has also been recognized, however, that ophthalmoscopic examination is not a true guide to the presence or absence of a cilioretinal artery.[4] Hence, it is difficult to say just from Fig. 2 of Case 1 that the upper artery is a cilioretinal artery. The author further states that, “FFA in Fig. 3 shows that the upper artery is brighter than the lower indicating that this is an earlier branch”. FFA in our cases shows that the upper artery is brighter than the lower but this does not necessarily mean that it is a cilioretinal artery. However, carotid Doppler study in all cases showed bifurcation of CRA into two hemi-trunks just behind the lamina cribrosa, ruling out the possibility that the upper artery is an earlier branch. We rather postulate that the affected branch being possibly less tortuous in its course shows earlier filling than the other. Finally, the author states that, “Cases 2, 3, and 4 are identical to Case 1 and all of them are associated with choroidal and retinal ischemia”. This aspect has already been dealt with as above.

Amalric sign and central retinal artery with lateral posterior ciliary artery occlusion

Amalric sign and central retinal artery with lateral posterior ciliary artery occlusion

Central Retinal and Posterior Ciliary Artery Occlusion After Intralesional Injection of Sclerosant to Glabellar Subcutaneous Hemangioma

The aim of this study is to describe vision loss caused by central retinal artery and posterior ciliary artery occlusion as a consequence of sclerotherapy with a polidocanol injection to a glabellar hemangioma. An 18-year-old man underwent direct injection with a 23-gauge needle of 1 mL of a polidocanol-carbon dioxide emulsion into the glabellar subcutaneous hemangioma under ultrasound visualization of the needle tip by radiologists. He developed lid swelling the next day, and 3 days later at referral, the visual acuity in the left eye was no light perception. Funduscopy revealed central retinal artery occlusion and fluorescein angiography disclosed no perfusion at all in the left fundus, indicating concurrent posterior ciliary artery occlusion. The patient also showed mydriasis, blepharoptosis, and total external ophthalmoplegia on the left side. Magnetic resonance imaging demonstrated the swollen medial rectus muscle. In a month, blepharoptosis and ophthalmoplegia resolved but the visual acuity remained no light perception. Sclerosing therapy for facial hemangioma may develop a severe complication such as permanent visual loss.

An occult case of giant cell arteritis presenting with combined anterior ischemic optic neuropathy and cilioretinal artery occlusion

A 61-year-old female presented with a moderate decrease in vision in the left eye. The patient denied any other ocular or systemic symptoms related to giant cell arteritis. Visual acuity was 20/50 in the left eye with a 2+ relative afferent pupillary defect and markedly abnormal color vision. Dilated fundus examination and flourescein angiography revealed optic disc edema as well as a cilioretinal artery occlusion. Erythrocyte sedimentation rate was only slightly elevated. Subsequent biopsy of the superficial temporal artery confirmed the diagnosis of giant cell arteritis. Cilioretinal arteries are anatomical variants derived from the short posterior ciliary arteries. Arteritic anterior ischemic optic neuropathy typically results from thrombotic occlusion of the short posterior ciliary arteries. Consequently, arteritic occlusion of the short posterior ciliary arteries can result in concomitant occlusion of the cilioretinal artery. This case highlights the situation where clinical symptoms were not suspicious for giant cell arteritis but the presence of an anterior ischemic optic neuropathy and a cilioretinal artery occlusion was virtually pathognomonic for giant cell arteritis.