Acute retinal necrosis natural history, complications and prognosis
Acute retinal necrosis Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Acute retinal necrosis natural history, complications and prognosis On the Web |
American Roentgen Ray Society Images of Acute retinal necrosis natural history, complications and prognosis |
FDA on Acute retinal necrosis natural history, complications and prognosis |
CDC on Acute retinal necrosis natural history, complications and prognosis |
Acute retinal necrosis natural history, complications and prognosis in the news |
Blogs on Acute retinal necrosis natural history, complications and prognosis |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.
Overview
Symptoms of acute retinal necrosis (ARN) develop rapidly upon the onset of pathogenic infection. The natural progression of ARN depends on whether a case is mild or fulminant. Mild cases of ARN presents with white-yellow necrotic lesions that do not coalesce or lead to retinal detachment; the disease is self-limited. Fulminant cases of ARN will lead to progressive necrosis of retinal tissue, causing pigmentation scarring, vitreous debris, and retinal detachment. Without treatment, ARN will usually progress to bilateral acute retinal necrosis (BARN) within weeks to a few months. Complications resulting from acute retinal necrosis occur due to retinal tissue damage and subsequent infection from the causative pathogen. Without treatment, the prognosis for acute retinal necrosis (ARN) varies. Mild ARN is usually self-limited and will resolve itself without treatment; risk of permanent vision loss is very low. Fulminant ARN will usually progress to complications such as progressive outer retinal necrosis, and therefore carries a worse prognosis. With treatment, the prognosis for ARN is good if the appropriate therapy is administered in the early stages and sustained until symptoms resolve.
Natural History
Symptoms of acute retinal necrosis (ARN) develop rapidly from inflammatory response to the onset of pathogenic infection.[1]
- Initial signs and symptoms include conjunctivitis, vision loss, photophobia, and eye pain and pressure.
The natural progression of ARN depends on whether the case is mild or fulminant.
- Mild cases of ARN presents with white-yellow necrotic lesions that do not coalesce or lead to retinal detachment; the disease is self-limited.[2]
- Fulminant cases of ARN will lead to progressive necrosis of retinal tissue, causing pigmentation scarring, vitreous debris, and retinal detachment. Fulminant ARN has a much greater chance of blindness in the affected eye.
Without treatment, ARN will usually progress to bilateral acute retinal necrosis (BARN) within weeks to a few months.[3]
- There have been exceptions in which the disease spread from the affected to the previously unaffected eye up to 17 years after the initial diagnosis of ARN, due to reactivation of latent viral infection.[4]
Complications
Complications resulting from acute retinal necrosis occur due to retinal tissue damage and subsequent infection from the causative pathogen, including the following:[1][5]
- Retinal detachment
- Neurological conditions (e.g., encephalitis, meningitis)[6]
- Optic neuropathy
- Occlusive retinal vasculopathy
- Proliferative vitreoretinopathy[7]
- Macular pucker[8]
- Vitreous hemorrhage
- Neovascularization[9]
- Phthisis bulbi[9]
Prognosis
Without treatment, the prognosis for acute retinal necrosis (ARN) varies:[1]
- Mild ARN: Usually self-limited and will resolve itself without treatment; risk of permanent vision loss is very low.
- Fulminant ARN: Will usually progress to complications such as progressive outer retinal necrosis and has a worse prognosis.
- Retinal detachment will usually occur without treatment, leading to permanent vision loss.
- Spread of infection through the anterior chamber to the brain has a particularly poor prognosis if encephalitis or meningitis develops.
With treatment, the prognosis for ARN is good if the therapy is administered in the early stages and sustained until symptoms resolve.
- Uncommonly, prognosis can worsen if the patient is immunocompromised and experiences a subsequent infection due to vulnerability from prolonged topical corticosteroid use.
References
- ↑ 1.0 1.1 1.2 Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D (2014). "Clinical manifestation of self-limiting acute retinal necrosis". Med. Sci. Monit. 20: 2088–96. doi:10.12659/MSM.890469. PMC 4226315. PMID 25356955.
- ↑ Matsuo T, Nakayama T, Koyama T, Koyama M, Matsuo N (1988). "A proposed mild type of acute retinal necrosis syndrome". Am. J. Ophthalmol. 105 (6): 579–83. PMID 2837090.
- ↑ Gartry DS, Spalton DJ, Tilzey A, Hykin PG (1991). "Acute retinal necrosis syndrome". Br J Ophthalmol. 75 (5): 292–7. PMC 1042358. PMID 1645179.
- ↑ Okunuki Y, Usui Y, Kezuka T, Takeuchi M, Goto H (2011). "Four cases of bilateral acute retinal necrosis with a long interval after the initial onset". Br J Ophthalmol. 95 (9): 1251–4. doi:10.1136/bjo.2010.191288. PMID 21242577.
- ↑ Flaxel CJ, Yeh S, Lauer AK (2013). "Combination systemic and intravitreal antiviral therapy in the management of acute retinal necrosis syndrome (an American Ophthalmological Society thesis)". Trans Am Ophthalmol Soc. 111: 133–44. PMC 3868412. PMID 24385671.
- ↑ Liang ZG, Liu ZL, Sun XW, Tao ML, Yu GP (2015). "Viral encephalitis complicated by acute retinal necrosis syndrome: A case report". Exp Ther Med. 10 (2): 465–467. doi:10.3892/etm.2015.2557. PMC 4509005. PMID 26622338.
- ↑ Vukojević N, Popovic Suić S, Sikić J, Katusić D, Curković T, Sarić B, Jukić T (2006). "[Acute retinal necrosis]". Acta Med Croatica. 60 (2): 145–8. PMID 16848208.
- ↑ McDonald HR, Lewis H, Kreiger AE, Sidikaro Y, Heckenlively J (1991). "Surgical management of retinal detachment associated with the acute retinal necrosis syndrome". Br J Ophthalmol. 75 (8): 455–8. PMC 1042429. PMID 1873262.
- ↑ 9.0 9.1 Lau CH, Missotten T, Salzmann J, Lightman SL (2007). "Acute retinal necrosis features, management, and outcomes". Ophthalmology. 114 (4): 756–62. doi:10.1016/j.ophtha.2006.08.037. PMID 17184841.