|Year : 2022 | Volume
| Issue : 1 | Page : 235-239
Orbital cellulitis complicated by central retinal artery occlusion with sparing of cilioretinal artery: A case report and review
Gaurav Garg1, Narendra Patidar2, Vinit Dahiya2
1 Oculoplasty, Ocular Oncology and Facial Aesthetics Services, View Care, New Delhi, India
2 Department of Orbit, Oculoplasty and Ocular Oncology, Shri Sadguru Seva Sangh Trust, Chitrakoot, Madhya Pradesh, India
|Date of Submission||05-Apr-2021|
|Date of Acceptance||30-Jun-2021|
|Date of Web Publication||07-Jan-2022|
Dr. Narendra Patidar
Department of Orbit, Oculoplasty and Ocular Oncology, Sadguru Netra Chikitsalaya, Chitrakoot - 210 204, Madhya Pradesh
Source of Support: None, Conflict of Interest: None
Orbital cellulitis (OC) with an incidence of 0.1 per 100,000 is a sight and life-threatening emergency with a dreadful potential to cause orbital apex syndrome and central retinal artery occlusion (CRAO). In the era of modern antibiotics, visual loss in the case of isolated OC has significantly reduced. But in the event of the added complication of orbital apex syndrome and CRAO, the visual prognosis decreases markedly. A 24-year-old Asian Indian male presented with left eye staphylococcal OC complicated by orbital apex syndrome and CRAO with cilioretinal artery sparing following nasal folliculitis and upper lid preseptal cellulitis. He was promptly treated with culture-sensitive antibiotics, lateral canthotomy, and cantholysis. On follow-up, his vision improved from hand movements to 20/40 with the resolution of inflammation, proptosis, and ophthalmoplegia. To conclude, promptness in diagnosis, treatment, and presence of foveal-sparing CRAO may improve the prognosis of OC.
Keywords: Central retinal artery occlusion, orbital apex syndrome, orbital cellulitis, orbital cellulitis with central retinal artery occlusion, orbital cellulitis with orbital apex syndrome
|How to cite this article:|
Garg G, Patidar N, Dahiya V. Orbital cellulitis complicated by central retinal artery occlusion with sparing of cilioretinal artery: A case report and review. Indian J Ophthalmol Case Rep 2022;2:235-9
|How to cite this URL:|
Garg G, Patidar N, Dahiya V. Orbital cellulitis complicated by central retinal artery occlusion with sparing of cilioretinal artery: A case report and review. Indian J Ophthalmol Case Rep [serial online] 2022 [cited 2022 Jan 16];2:235-9. Available from: https://www.ijoreports.in/text.asp?2022/2/1/235/334974
Orbital cellulitis (OC) with an incidence of 1.6 per 100,000 and 0.1 per 100,000 in pediatric and adult age-groups, respectively, can lead to sight and life-threatening complications, necessitating a prompt diagnosis and treatment. OC manifests as proptosis (46.9%–100%), decreased vision (12.5%–37%), afferent pupillary defect (5.5%–16.7%), impaired color vision (16.7%), and limited ocular motility (39.1%–84.6%). It can progress to orbital apex syndrome (OAS) by the involvement of the optic nerve, oculomotor nerve, trochlear nerve, abducens nerve, and the ophthalmic branch of the trigeminal nerve.
OC is notorious to cause sight-threatening complications by the involvement of the vasculature of the orbit and ischemia leading from either the thrombophlebitis of the orbital veins, by compression or occlusion of the ophthalmic artery, short posterior ciliary arteries, or central retinal artery. Usually, ischemic vasculopathies are more prone to cause permanent visual loss. But with the advent of the modern antibiotic era, permanent loss of vision has significantly reduced to 20% of OC.
Central retinal artery occlusion (CRAO) has an incidence of 1 in 100,000 people with around 1 in 10,000 ophthalmological outpatient visits mostly due to embolic occlusion, whereas cilioretinal artery is found in 6.9% to 49.5% per individual and 4.0% to 32.1% per eye. CRAO is widely accepted to cause permanent visual loss, which may differ to a better outcome in the presence of foveal vascular supply preservation.
There is a paucity of literature with only eight case reports on CRAO as sequelae to OC, and with only two case reports describing OAS and CRAO. All of them had extremely poor visual outcomes posttreatment because of foveal involvement. Herein, we present a case of CRAO as a sequelae to OC with foveal sparing due to cilioretinal artery preservation with an extremely gratifying anatomical, functional, and visual outcome.
Note: This report adhered to the ethical principles outlined in the Declaration of Helsinki as amended in 2013. Informed consent was obtained from the patient to publish this case report and his images.
| Case Report|| |
A 24-year-old Asian Indian man presented with a history of pain, proptosis, mechanical ptosis, and diminution of vision in the left eye for the past 2 days. This was preceded by painful swelling in the left nostril for the past 7 days. The patient was treated with injection amikacin 250 mg BD, oral cefixime 200 mg BD, oral deflazacort 6 mg OD, and eye ointment chloramphenicol, and polymyxin B combination (polymyxin B 10,000 IU, chloramphenicol 10 mg/g) by the primary physician. Following nonresolution after 2 days, he presented to us for a second opinion. There was no other significant relevant history.
On general examination, the patient was febrile and had a pustular swelling of 3 × 3 mm in the left nostril. His visual acuity was 20/20 in the right eye and hand movement close to the face in the left eye. The anterior and posterior segment of the right eye was normal. In the left eye, there was a pus point at the superomedial aspect of the left upper lid with periocular edema, erythema, tenderness, localized warmth, severe ptosis of the upper eyelid, and proptosis of 4 mm with total ophthalmoplegia. Intraocular pressure was digitally raised with significant resistance to retropulsion with an intact ophthalmic and maxillary branch of trigeminal innervation. The anterior segment of the left eye showed diffuse severe conjunctival congestion and chemosis with a relative afferent pupillary defect. The posterior segment of the left eye showed acute CRAO with cherry-red spot and superficial retinal whitening, more prominent in the perifoveal area except in the region papillomacular bundle, which was preserved and was supplied by a patent cilioretinal artery [Figure 1]a and [Figure 1]b. The ultrasound B-scan of the orbit revealed fluid in the posterior subtenon space around the optic nerve head ('T' sign) [Figure 2]c. Optical coherence tomography showed subretinal fluid at the macula with the presence of internal limiting membrane folds and retinal thickening. The computed tomography scan of orbit revealed significant proptosis with extraocular muscles thickening and adnexal inflammation. The optic nerve appears to be stretched with coning of the posterior globe, extraconal, and intraconal fat stranding [Figure 1]c, [Figure 1]d, [Figure 1]e. A diagnosis of the left eye OC with OAS and CRAO with spared cilioretinal artery with stretch optic neuropathy was made. Initially, he was started on empirical treatment with broad-spectrum antibiotics; tazobactam, piperacillin combination, metronidazole, and acetazolamide, and he underwent lateral canthotomy and cantholysis to relieve intraorbital pressure. On culture sensitivity, Staphylococcus aureus (methicillin resistant) was found, for which he was switched to intravenous injection of clindamycin 600 mg BD, linezolid 600 mg BD over the next 10 days, and intravenous dexamethasone 8 mg BD for the next 7 days and was discharged on oral clindamycin 600 mg and linezolid 300 mg 8 hourly. On 2 months follow-up, he showed complete resolution of inflammation and restoration of ocular motility with visual acuity of 20/40 [Figure 2]a, [Figure 2]b and [Figure 2]d.
|Figure 1: Left eye at initial presentation. (a) Clinical photography showing total ophthalmoplegia and proptosis. (b) Fundus photography showing central retinal artery occlusion with cilioretinal artery sparing. (c and e) Axial and coronal cuts of the computed tomography showing proptosis, infiltration of the extraocular muscles, and stretching of the optic nerve with coning of posterior globe. (d) Optical coherence tomography showing subretinal fluid and thickening of the retinal layers temporal to the fovea|
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|Figure 2: Left eye on 2 months follow-up. (a) Clinical photography showing resolution of ophthalmoplegia and proptosis. (b) Fundus photography showing resolution of central retinal artery occlusion. (c) Ultrasonography B-scan showing positive T-sign at initial presentation. (d) Optical coherence tomography showing resolution subretinal fluid and atrophy of the retinal layers temporal to the fovea|
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| Discussion|| |
OC in a severe scenario may progress to OAS, which is characterized by multiple cranial nerves (II–VI) palsies, causing ptosis, proptosis, total ophthalmoplegia, decreased visual acuity, and pain along the ophthalmic branch of the trigeminal nerve. Severe visual loss in OC can occur by the sheer mechanical pressure of the inflammation of the orbital structures, which can further complicate as raised intraocular pressure with reduced retinal circulation, a direct compressive optic neuropathy, compression of small vessels of the optic nerve leading to its ischemic neuropathy, or stretch optic neuropathy with coning of the posterior globe. Our review of the literature using PubMed and Medline revealed eight case reports [Table 1] defining OC, subperiosteal abscess, OAS, or orbital abscess with CRAO as sequelae and its poor visual outcomes.,,,,,,,,,
|Table 1: Review of cases of orbital cellulitis with central retinal artery occlusion|
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CRAO's potential to cause devastating visual loss and its management have always been a major concern for ophthalmologists. More so if it is preceded by OC, which in itself is a sight and life-threatening disease. Visual prognosis and its natural course of CRAO have always been debatable. Generally, visual acuity of counting fingers within 7 days of onset may improve by 22% in nonarteritic CRAO, by 67% in nonarteritic CRAO with cilioretinal artery sparing, and by 82% in transient nonarteritic CRAO, whereas there is no improvement seen in arteritic CRAO.
Hayreh has identified the following factors that play a crucial role in determining the visual prognosis. The same factors can be defined as the reason for successful visual outcomes in the present case also: (A) Duration of acute retinal ischemia: In the present case, we do not know exactly when CRAO developed. But it lasted more than the cutoff of 4 hours from onset. (B) Type of CRAO: Present case was a nonarteritic CRAO with cilioretinal artery sparing. (C) Cause of CRAO: Either by direct compression or occlusion of the central retinal artery. (D) Site of occlusion: Exact identification of the site of occlusion is difficult in the absence of angiography. Being the narrowest point of the lumen, the lamina cribrosa is the most probable site of occlusion. (E) Residual retinal circulation: Presence and area supplied by cilioretinal artery had the major impact on visual outcome.
| Conclusion|| |
Herein, we report an extremely successful anatomical, functional, and visual outcome in a case of rapidly progressive methicillin-resistant staphylococcal OC in a healthy middle-aged male resulting in the rare complication of OAS and CRAO with cilioretinal artery sparing. To conclude, OC warrants a prompt diagnosis and immediate management with a thorough fundoscopy, and the presence of foveal sparing central retinal artery occlusion may improve the visual prognosis in the case of CRAO.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Tsirouki T, Dastiridou AI, Flores NI, Cerpa JC, Moschos MM, Brazitikos P, et al
. Orbital cellulitis. Surv Ophthalmol 2018;63:534-53.
Anjum S, Temkar S, Chawla R, Garg G. Occurrence of hemi-central retinal artery occlusion following embolization in a case of recurrent juvenile nasopharyngeal angiofibroma. Ophthalmic Surg Lasers Imaging Retina 2019;50:385-7.
Schneider M, Molnar A, Angeli O, Szabo D, Bernath F, Hajdu D, et al
. Prevalence of Cilioretinal Arteries: A systematic review and a prospective cross-sectional observational study. Acta Ophthalmol 2021;99:e310-8.
Hayreh SS. Central retinal artery occlusion. Indian J Ophthalmol 2018;66:1684.
] [Full text]
Okamoto Y, Hiraoka T, Okamoto F, Oshika T. A case of subperiosteal abscess of the orbit with central retinal artery occlusion. Eur J Ophthalmol 2009;19:288-91.
Luo QL, Orcutt JC, Seifter LS. Orbital mucormycosis with retinal and ciliary artery occlusions. Br J Ophthalmol 1989;73:680-3.
Bhola RM, Dhingra S, McCormick AG, Chan TK. Central retinal artery occlusion following staphylococcal orbital cellulitis. Eye 2003;17:109-11.
Song Y-M, Shin SY. Bilateral ophthalmic artery occlusion in rhino-orbito-cerebral mucormycosis. Korean J Ophthalmol KJO 2008;22:66-9.
Coşkun M, Ilhan Ö, Keskin U, Ayintap E, Tuzcu E, Semiz H, et al
. Central retinal artery occlusion secondary to orbital cellulitis and abscess following dacryocystitis. Eur J Ophthalmol 2011;21:649-52.
Proctor CM, Magrath GN, de Castro LEF, Johnson JH, Teed RG. Orbital cellulitis complicated by central retinal artery occlusion. Ophthal Plast Reconstr Surg 2013;29:e59-61.
Chakraborti C, Barua N, Chishti R, Kumar S. Orbital apex syndrome with central retinal artery occlusion following tooth extraction. Off Sci J Delhi Ophthalmol Soc 2016;27:118-20.
Keorochana N, Vongkulsiri S, Choontanom R. Combined central retinal vein, central retinal artery and cilioretinal artery occlusion with ischemic macular hole secondary to severe orbital cellulitis after black fly bite. Int Med Case Rep J 2019;12:125-34.
Subramaniam S, Tet CM, Hitam WHW, Hussein A, Khan SA, Pal HK, et al
. Orbital apex syndrome after tooth extraction in an immunocompromised patient. Int J Ophthalmol 2011;4:112-4.
Baig R, Khan QA, Sadiq MA, Awan S, Ahmad K. A case of orbital apex syndrome in a patient with malignant otitis externa. JPMA J Pak Med Assoc 2013;63:271-3.
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