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9 Retinal Vascular Occlusions
Fig. 9.18 Inammatory BRVO of lower temporal vein showing exuberant perivenous inammatory exudates (a).
Following treatment, the haemorrhages started resolving at 6weeks (b), 4months (c), and 9months (d)
countries, the most common cause is tubercular retinal periphlebitis, which was until
recently labelled as Eales’ disease. Peripheral
retinal veins are often affected, which may
show exuberant perivenous inammatory exudates (Fig.9.18). Tubercular retinal periphlebitis is often associated with healed or actively
inamed chorioretinal lesions. See Box 9.4.
On FFA, there is extensive capillary non-perfusion which leads to retinal neovascularization.
They may remain asymptomatic or have oaters or a diminution of vision. When presenting
late, they may have total obscuration of vision
due to vitreous haemorrhage and still later
develop tractional or combined retinal detachments. Other causes of retinal vasculitis/periphlebitis include Behcet’s disease, sarcoidosis,
Syphilis, Lyme disease, leptospira, toxoplasmosis, cat scratch disease, HSV retinitis, CMV
retinitis, leukaemias, multiple sclerosis, and
Box 9.4 Idiopathic Retinal Periphlebitis
(Eales’ Disease; Tubercular Retinal
Periphlebitis)
1 Young men>women, often systemically
asymptomatic, seen in TB-endemic
countries
2 Acute -vitritis; snowballs; vitreous
haemorrhage in quiescent stage
3 Acute -segmental periphlebitis (vessel
wall exudates, thrombosis)
4 Acute -retinal haemorrhages; macular
oedema
5 Acute/healed -perivenular chorioretinitis
lesions/scars
6 Healed stage-pipe stem sheathing in
healed stage
7 On FFA, extensive capillary non-
perfusion, neovessels on optic disc or
elsewhere on retina
8 Tractional retinal detachment (TRD) in
neglected cases
many others [79].

References
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9 Lab tests in acute stage-tuberculin skin
test; CT chest; RT-PCR from ocular uids;
exclude other causes of inammation
Healed stage—no labs
10 In acute stage standard 4-drug anti-TB
therapy for 9months with oral
corticosteroids; in healed stage-laser
photocoagulation if neovessels; pars plana
vitrectomy for vitreous haemorrhage and
TRD
References: [80–82]
References
1. Brown GC, Magargal LE, Shields JA, Goldberg RE,
Walsh PN.Retinal arterial obstruction in children and
young adults. Ophthalmology. 1981;88(1):18–25.
https://doi.org/10.1016/s0161- 6420(81)35080- 5.
PMID: 7243224.
2. Park SJ, Choi NK, Seo KH, Park KH, Woo
SJ.Nationwide incidence of clinically diagnosed central retinal artery occlusion in Korea, 2008 to 2011.
Ophthalmology. 2014;121(10):1933–8. https://doi.
org/10.1016/j.ophtha.2014.04.029. Epub 2014 Jun 7.
PMID: 24913283.
3. Flaxel CJ, Adelman RA, Bailey ST, Fawzi A, Lim
JI, Vemulakonda GA, Ying GS.Retinal and ophthalmic artery occlusions preferred practice pattern®.
Ophthalmology. 2020;127(2):259–87. https://doi.
org/10.1016/j.ophtha.2019.09.028. Epub 2019 Sep 25.
Erratum in: Ophthalmology. 2020 Sep;127(9):1280.
PMID: 31757501.
4. Scoles D, McGeehan B, VanderBeek BL.The association of stroke with central and branch retinal arterial
occlusion. Eye (Lond). 2022;36(4):835–43. https://
doi.org/10.1038/s41433- 021- 01546- 6. Epub 2021
Apr 28. PMID: 33911211; PMCID: PMC8956663.
5. Lee WA, Liao IC.Giant cell arteritis presenting as central retinal artery occlusion. QJM. 2022;115(1):32–3.
https://doi.org/10.1093/qjmed/hcab196. PMID:
34264347.
6. Guclu H, Gurlu VP, Ozal SA, Guclu O. Central
retinal artery occlusion in Takayasu’s arteritis
as the rst presentation of the disease. Case Rep
Ophthalmol Med. 2016;2016:6492513. https://doi.
org/10.1155/2016/6492513. Epub 2016 Oct 27.
PMID: 27867673; PMCID: PMC5102719.
7. Kaushik S, Gupta A, Gupta V, Jain S, Lal V. Retinal
arterial occlusion in Takayasu’s arteritis. Indian
J Ophthalmol. 2005;53(3):194–6. https://doi.
org/10.4103/0301- 4738.16680. PMID: 16137966.
8. Emad Y, Basaffar S, Ragab Y, Zeinhom F, Gheita
T. A case of polyarteritis nodosa complicated by
left central retinal artery occlusion, ischemic optic
199
neuropathy, and retinal vasculitis. Clin Rheumatol.
2007;26(5):814–6. https://doi.org/10.1007/s10067-
006- 0270- x. Epub 2006 Mar 31. PMID: 16575492.
9. Hsu CT, Kerrison JB, Miller NR, Goldberg
MF. Choroidal infarction, anterior ischemic optic
neuropathy, and central retinal artery occlusion from
polyarteritis nodosa. Retina. 2001;21(4):348–51.
https://doi.org/10.1097/00006982- 200108000- 00009.
PMID: 11508881.
10. Thurtell MJ, Rucker JC. Transient visual loss.
Int Ophthalmol Clin. 2009;49(3):147–66. https://
doi.org/10.1097/IIO.0b013e3181a8d41f. PMID:
19584627.
11. Mitchell P, Wang JJ, Smith W. Risk factors and signicance of nding asymptomatic retinal emboli.
Clin Exp Ophthalmol. 2000;28(1):13–7. https://
doi.org/10.1046/j.1442- 9071.2000.00218.x. PMID:
11345337.
12. Klein R, Klein BE, Jensen SC, Moss SE, Meuer
SM. Retinal emboli and stroke: the Beaver Dam
Eye Study. Arch Ophthalmol. 1999;117(8):1063–8.
https://doi.org/10.1001/archopht.117.8.1063. PMID:
10448750.
13. Tobalem S, Schutz JS, Chronopoulos A. Central
retinal artery occlusion—rethinking retinal survival
time. BMC Ophthalmol. 2018;18(1):101. https://doi.
org/10.1186/s12886- 018- 0768- 4. PMID: 29669523;
PMCID: PMC5907384.
14. Brown GC, Magargal LE. Central retinal artery
obstruction and visual acuity. Ophthalmology.
1982;89(1):14–9. https://doi.org/10.1016/s0161-
6420(82)34853- 8. PMID: 7070767.
15. Sharma S, Brown GC, Pater JL, Cruess AF. Does a
visible retinal embolus increase the likelihood of
hemodynamically signicant carotid artery stenosis in patients with acute retinal arterial occlusion?
Arch Ophthalmol. 1998;116(12):1602–6. https://doi.
org/10.1001/archopht.116.12.1602. PMID: 9869788.
16. Sharma S, Naqvi A, Sharma SM, Cruess AF,
Brown GC. Transthoracic echocardiographic ndings in patients with acute retinal arterial obstruction. A retrospective review. Retinal Emboli
of Cardiac Origin Group. Arch Ophthalmol.
1996;114(10):1189–92. https://doi.org/10.1001/archo
pht.1996.01100140389004. PMID: 8859076.
17. Hayreh SS, Zimmerman MB.Ocular arterial occlusive disorders and carotid artery disease. Ophthalmol
Retina. 2017;1(1):12–8. https://doi.org/10.1016/j.
oret.2016.08.003. PMID: 28547004; PMCID:
PMC5439962.
18. Arruga J, Sanders MD. Ophthalmologic ndings
in 70 patients with evidence of retinal embolism.
Ophthalmology. 1982;89(12):1336–47. https://
doi.org/10.1016/s0161- 6420(82)34626- 6. PMID:
7162779.
19. Ardila Jurado E, Sturm V, Brugger F, Nedeltchev K,
Arnold M, Bonati LH, Carrera E, Michel P, Cereda
CW, Bolognese M, Albert S, Medlin F, Berger C,
Schelosky L, Renaud S, Niederhauser J, Bonvin C,
Mono ML, Rodic B, Tarnutzer AA, Schwegler G,

200
https://t.me/medicina_free
9 Retinal Vascular Occlusions
Salmen S, Luft AR, Peters N, Vehoff J, Kägi G, Swiss
Stroke Registry Investigators. Central retinal artery
occlusion: current practice, awareness and prehospital
delays in Switzerland. Front Neurol. 2022;13:888456.
https://doi.org/10.3389/fneur.2022.888456. PMID:
35677327; PMCID: PMC9167925.
20. Cugati S, Varma DD, Chen CS, Lee AW.Treatment
options for central retinal artery occlusion. Curr
Treat Options Neurol. 2013;15(1):63–77. https://doi.
org/10.1007/s11940- 012- 0202- 9. PMID: 23070637;
PMCID: PMC3553407.
21. Thangamathesvaran L, Miller SC, Tsou B, Fliotsos
MJ, Yonekawa Y, Chen A, Hoskin AK, Blanch RJ,
Cavuoto K, Meeralakshmi P, Low R, Gardiner
M, Alvin Liu TY, Agrawal R, Justin GA, Woreta
FA, International Globe and Adnexal Trauma
Epidemiology Study (IGATES)(18) Group. Global
current practice patterns for the management of
central retinal artery occlusion. Ophthalmol Retina.
2022;6(5):429–31. https://doi.org/10.1016/j.
oret.2022.01.014. Epub 2022 Jan 31. PMID:
35101631.
22. Schumacher M, Schmidt D, Jurklies B, Gall C,
Wanke I, Schmoor C, Maier-Lenz H, Solymosi L,
Brueckmann H, Neubauer AS, Wolf A, Feltgen N,
EAGLE-Study Group. Central retinal artery occlusion: local intra-arterial brinolysis versus conservative treatment, a multicenter randomized trial.
Ophthalmology. 2010;117(7):1367–75.e1. https://doi.
org/10.1016/j.ophtha.2010.03.061. PMID: 20609991.
23. Mac Grory B, Schrag M, Biousse V, Furie KL,
Gerhard-Herman M, Lavin PJ, Sobrin L, Tjoumakaris
SI, Weyand CM, Yaghi S, American Heart Association
Stroke Council; Council on Arteriosclerosis,
Thrombosis and Vascular Biology; Council on
Hypertension; and Council on Peripheral Vascular
Disease. Management of central retinal artery occlusion: a scientic statement from the American Heart
Association. Stroke. 2021;52(6):e282–94. https://doi.
org/10.1161/STR.0000000000000366. Epub 2021
Mar 8. Erratum in: Stroke 2021 Jun;52(6):e309.
PMID: 33677974.
24. Klein R, Klein BE, Moss SE, Meuer SM.The epidemiology of retinal vein occlusion: the Beaver Dam
Eye Study. Trans Am Ophthalmol Soc. 2000;98:133–
41; discussion 141–3. PMID: 11190017; PMCID:
PMC1298220.
25. Klein R, Moss SE, Meuer SM, Klein BE. The
15-year cumulative incidence of retinal vein occlusion: the Beaver Dam Eye Study. Arch Ophthalmol.
2008;126(4):513–8. https://doi.org/10.1001/
archopht.126.4.513. PMID: 18413521.
26. Rogers S, McIntosh RL, Cheung N, Lim L, Wang
JJ, Mitchell P, Kowalski JW, Nguyen H, Wong TY,
International Eye Disease Consortium. The prevalence of retinal vein occlusion: pooled data from population studies from the United States, Europe, Asia,
and Australia. Ophthalmology. 2010;117(2):313–9.
e1. https://doi.org/10.1016/j.ophtha.2009.07.017.
PMID: 20022117; PMCID: PMC2945292.
27. Rogers SL, McIntosh RL, Lim L, Mitchell P, Cheung
N, Kowalski JW, Nguyen HP, Wang JJ, Wong
TY. Natural history of branch retinal vein occlusion:
an evidence-based systematic review. Ophthalmology.
2010;117(6):1094–1101.e5. https://doi.org/10.1016/j.
ophtha.2010.01.058. PMID: 20430447.
28. Cugati S, Wang JJ, Knudtson MD, Rochtchina E,
Klein R, Klein BE, Wong TY, Mitchell P.Retinal vein
occlusion and vascular mortality: pooled data analysis of 2 population-based cohorts. Ophthalmology.
2007;114(3):520–4. https://doi.org/10.1016/j.
ophtha.2006.06.061. Epub 2006 Nov 30. PMID:
17141315.
29. Group. Baseline and early natural history report.
The central vein occlusion study. Arch Ophthalmol.
1993;111(8):1087–95. https://doi.org/10.1001/archo
pht.1993.01090080083022. PMID: 7688950.
30. Group. Risk factors for branch retinal vein occlusion.
The Eye Disease Case-control Study Group. Am J
Ophthalmol. 1993;116(3):286–96. PMID: 8357052.
31. Weinberg D, Dodwell DG, Fern SA.Anatomy of arteriovenous crossings in branch retinal vein occlusion.
Am J Ophthalmol. 1990;109(3):298–302. https://
doi.org/10.1016/s0002- 9394(14)74554- 4. PMID:
2309862.
32. Christoffersen NL, Larsen M.Pathophysiology and
hemodynamics of branch retinal vein occlusion.
Ophthalmology. 1999;106(11):2054–62. https://
doi.org/10.1016/S0161- 6420(99)90483- 9. PMID:
10571337.
33. Hayreh SS, Zimmerman MB. Branch retinal vein
occlusion: natural history of visual outcome.
JAMA Ophthalmol. 2014;132(1):13–22. https://doi.
org/10.1001/jamaophthalmol.2013.5515. PMID:
24158729.
34. Suzuki N, Hirano Y, Tomiyasu T, Kurobe R, Yasuda Y,
Esaki Y, Yasukawa T, Yoshida M, Ogura Y.Collateral
vessels on optical coherence tomography angiography in eyes with branch retinal vein occlusion. Br
J Ophthalmol. 2019;103(10):1373–9. https://doi.
org/10.1136/bjophthalmol- 2018- 313322. Epub 2018
Nov 22. PMID: 30467130.
35. Freund KB, Sarraf D, Leong BCS, Garrity ST,
Vupparaboina KK, Dansingani KK. Association of
optical coherence tomography angiography of collaterals in retinal vein occlusion with major venous
outow through the deep vascular complex. JAMA
Ophthalmol. 2018;136(11):1262–70. https://doi.
org/10.1001/jamaophthalmol.2018.3586. PMID:
30352115; PMCID: PMC6248171.
36. Group. Argon laser photocoagulation for macular edema in branch vein occlusion. The Branch
Vein Occlusion Study Group. Am J Ophthalmol.
1984;98(3):271–82. https://doi.org/10.1016/0002-
9394(84)90316- 7. PMID: 6383055.
37. Tomiyasu T, Hirano Y, Yoshida M, Suzuki N,
Nishiyama T, Uemura A, Yasukawa T, Ogura
Y.Microaneurysms cause refractory macular edema in
branch retinal vein occlusion. Sci Rep. 2016;6:29445.

References
https://t.me/medicina_free
201
https://doi.org/10.1038/srep29445. PMID: 27389770;
PMCID: PMC4937381.
38. An Y, Park SP, Kim YK.Aqueous humour inammatory cytokine levels and choroidal thickness in patients
with macular edema associated with branch retinal
vein occlusion. Int Ophthalmol. 2021;41(7):2433–44.
https://doi.org/10.1007/s10792- 021- 01798- x. Epub
2021 Mar 19. PMID: 33740201.
39. Schmidt-Erfurth U, Garcia-Arumi J, Gerendas
BS, Midena E, Sivaprasad S, Tadayoni R, Wolf
S, Loewenstein A. Guidelines for the management of retinal vein occlusion by the European
Society of Retina Specialists (EURETINA).
Ophthalmologica. 2019;242(3):123–62. https://doi.
org/10.1159/000502041. Epub 2019 Aug 14. PMID:
31412332.
40. Tan MH, McAllister IL, Gillies ME, Verma N,
Banerjee G, Smithies LA, Wong WL, Wong
TY. Randomized controlled trial of intravitreal
ranibizumab versus standard grid laser for macular
edema following branch retinal vein occlusion. Am
J Ophthalmol. 2014;157(1):237–247.e1. https://doi.
org/10.1016/j.ajo.2013.08.013. Epub 2013 Oct 7.
PMID: 24112635.
41. Shalchi Z, Mahroo O, Bunce C, Mitry D. Antivascular endothelial growth factor for macular
oedema secondary to branch retinal vein occlusion.
Cochrane Database Syst Rev. 2020;7(7):CD009510.
https://doi.org/10.1002/14651858.CD009510.pub3.
PMID: 32633861; PMCID: PMC7388176.
42. Zou W, Du Y, Ji X, Zhang J, Ding H, Chen J, Wang
T, Ji F, Huang J. Comparison of the efciency of
anti-VEGF drugs intravitreal injections treatment
with or without retinal laser photocoagulation for
macular edema secondary to retinal vein occlusion: a systematic review and meta-analysis. Front
Pharmacol. 2022;13:948852. https://doi.org/10.3389/
fphar.2022.948852. PMID: 35935843; PMCID:
PMC9355043.
43. Miao J, Yu J, Zou W, Su N, Peng Z, Wu X, Huang
J, Fang Y, Yuan S, Xie P, Huang K, Chen Q, Hu Z,
Liu Q. Deep learning models for segmenting nonperfusion area of color fundus photographs in patients
with branch retinal vein occlusion. Front Med
(Lausanne). 2022;9:794045. https://doi.org/10.3389/
fmed.2022.794045. PMID: 35847781; PMCID:
PMC9279621.
44. Hayreh SS, Zimmerman MB. Fundus changes
in branch retinal vein occlusion. Retina.
2015;35(5):1016–27. https://doi.org/10.1097/
IAE.0000000000000418. PMID: 25574785; PMCID:
PMC4408204.
45. Group. Argon laser scatter photocoagulation for
prevention of neovascularization and vitreous hemorrhage in branch vein occlusion. A randomized
clinical trial. Branch Vein Occlusion Study Group.
Arch Ophthalmol. 1986;104(1):34–41. https://doi.
org/10.1001/archopht.1986.01050130044017. PMID:
2417579.
46. Hayreh SS, Rubenstein L, Podhajsky P.Argon laser
scatter photocoagulation in treatment of branch
retinal vein occlusion. A prospective clinical trial.
Ophthalmologica. 1993;206(1):1–14. https://doi.
org/10.1159/000310354. PMID: 7506400.
47. Recchia FM, Brown GC. Systemic disorders
associated with retinal vascular occlusion. Curr
Opin Ophthalmol. 2000;11(6):462–7. https://doi.
org/10.1097/00055735- 200012000- 00013. PMID:
11141642.
48. Romiti GF, Corica B, Borgi M, Visioli G, Pacella E,
Cangemi R, Proietti M, Basili S, Raparelli V.Inherited
and acquired thrombophilia in adults with retinal
vascular occlusion: a systematic review and metaanalysis. J Thromb Haemost. 2020;18(12):3249–66.
https://doi.org/10.1111/jth.15068. Epub 2020 Oct 6.
PMID: 32805772.
49. Taylor AW, Sehu W, Williamson TH, Lee
WR. Morphometric assessment of the central retinal artery and vein in the optic nerve head. Can J
Ophthalmol. 1993;28(7):320–4. PMID: 8313218.
50. McAllister IL.Central retinal vein occlusion: a review.
Clin Exp Ophthalmol. 2012;40(1):48–58. https://doi.
org/10.1111/j.1442- 9071.2011.02713.x. Epub 2011
Dec 6. PMID: 22003973.
51. Scott IU, Campochiaro PA, Newman NJ,
Biousse V. Retinal vascular occlusions. Lancet.
2020;396(10266):1927–40. https://doi.org/10.1016/
S0140- 6736(20)31559- 2. PMID: 33308475.
52. Green WR, Chan CC, Hutchins GM, Terry JM.Central
retinal vein occlusion: a prospective histopathologic
study of 29 eyes in 28 cases. Trans Am Ophthalmol
Soc. 1981;79:371–422. PMID: 7342407; PMCID:
PMC1312193.
53. Hayreh SS, Podhajsky PA, Zimmerman MB.Natural
history of visual outcome in central retinal vein
occlusion. Ophthalmology. 2011;118(1):119–133.
e1–2. https://doi.org/10.1016/j.ophtha.2010.04.019.
Epub 2010 Aug 17. PMID: 20723991; PMCID:
PMC2989417.
54. Hayreh SS.Classication of central retinal vein occlusion. Ophthalmology. 1983;90(5):458–74. https://
doi.org/10.1016/s0161- 6420(83)34530- 9. PMID:
6877778.
55. Hayreh SS, Klugman MR, Podhajsky P, Kolder
HE.Electroretinography in central retinal vein occlusion. Correlation of electroretinographic changes
with pupillary abnormalities. Graefes Arch Clin
Exp Ophthalmol. 1989;227(6):549–61. https://doi.
org/10.1007/BF02169451. PMID: 2483144.
56. Hayreh SS, Fraterrigo L, Jonas J.Central retinal vein
occlusion associated with cilioretinal artery occlusion.
Retina. 2008;28(4):581–94. https://doi.org/10.1097/
IAE.0b013e31815ec29b. PMID: 18398361.
57. McLeod D.Central retinal vein occlusion with cilioretinal infarction from branch ow exclusion and
choroidal arterial steal. Retina. 2009;29(10):1381–95.
https://doi.org/10.1097/IAE.0b013e3181b85f41.
PMID: 19898176.

202
https://t.me/medicina_free
9 Retinal Vascular Occlusions
58. Ravani R, Chawla R, Jain S, Kumar A. “Dye front
reciprocation” in combined central retinal vein
occlusion with cilioretinal artery infarction. Indian
J Ophthalmol. 2017;65(11):1211–2. https://doi.
org/10.4103/ijo.IJO_552_17. PMID: 29133654;
PMCID: PMC5700596.
59. Pichi F, Fragiotta S, Freund KB, Au A, Lembo A,
Nucci P, Sebastiani S, Gutierrez Hernandez JC,
Interlandi E, Pellegrini F, Dolz-Marco R, GallegoPinazo R, Orellana-Rios J, Adatia FA, Munro M,
Abboud EB, Ghazi N, Cunha Souza E, Amer R, Neri
P, Sarraf D. Cilioretinal artery hypoperfusion and its
association with paracentral acute middle maculopathy. Br J Ophthalmol. 2019;103(8):1137–45. https://
doi.org/10.1136/bjophthalmol- 2018- 312774. Epub
2018 Sep 26. PMID: 30257961.
60. Antaki F, Milad D, Sahyoun JY, Coussa
RG. Paracentral acute middle maculopathy in nonischaemic central retinal vein occlusion: the role of
en face optical coherence tomography. BMJ Case
Rep. 2021;14(11):e246842. https://doi.org/10.1136/
bcr- 2021- 246842. PMID: 34764101; PMCID:
PMC8587704.
61. Rahimy E, Sarraf D, Dollin ML, Pitcher JD, Ho
AC. Paracentral acute middle maculopathy in
non-ischemic central retinal vein occlusion. Am J
Ophthalmol. 2014;158(2):372–380.e1. https://doi.
org/10.1016/j.ajo.2014.04.024. Epub 2014 May 1.
PMID: 24794089.
62. Iyer PG, Swaminathan SS, Trivizki O, Shi Y, Shen
M, Kansora M, Gregori G, Rosenfeld PJ.Wideeld
en face optical coherence tomography monitoring
of the peri-venular fern-like pattern of paracentral
acute middle maculopathy. Am J Ophthalmol Case
Rep. 2021;22:101047. https://doi.org/10.1016/j.
ajoc.2021.101047. PMID: 33763621; PMCID:
PMC7973291.
63. Ferrara N. Vascular endothelial growth factor:
basic science and clinical progress. Endocr Rev.
2004;25(4):581–611. https://doi.org/10.1210/er.2003-
0027. PMID: 15294883.
64. Aiello LP, Avery RL, Arrigg PG, Keyt BA, Jampel HD,
Shah ST, Pasquale LR, Thieme H, Iwamoto MA, Park
JE, etal. Vascular endothelial growth factor in ocular
uid of patients with diabetic retinopathy and other
retinal disorders. N Engl J Med. 1994;331(22):1480–
7. https://doi.org/10.1056/NEJM199412013312203.
PMID: 7526212.
65. Funk M, Kriechbaum K, Prager F, Benesch T,
Georgopoulos M, Zlabinger GJ, Schmidt-Erfurth
U. Intraocular concentrations of growth factors and
cytokines in retinal vein occlusion and the effect of
therapy with bevacizumab. Invest Ophthalmol Vis Sci.
2009;50(3):1025–32. https://doi.org/10.1167/iovs.08-
2510. Epub 2008 Dec 5. PMID: 19060280.
66. Ehlken C, Rennel ES, Michels D, Grundel B, Pielen
A, Junker B, Stahl A, Hansen LL, Feltgen N, Agostini
HT, Martin G.Levels of VEGF but not VEGF(165b)
are increased in the vitreous of patients with retinal
vein occlusion. Am J Ophthalmol. 2011;152(2):298–
303.e1. https://doi.org/10.1016/j.ajo.2011.01.040.
Epub 2011 May 28. PMID: 21621189.
67. Ferrara N.From the discovery of vascular endothelial
growth factor to the introduction of avastin in clinical trials—an interview with Napoleone Ferrara by
Domenico Ribatti. Int J Dev Biol. 2011;55(4–5):383–
8. https://doi.org/10.1387/ijdb.103216dr. PMID:
21858763.
68. Ferrara N, Damico L, Shams N, Lowman H, Kim
R. Development of ranibizumab, an anti-vascular
endothelial growth factor antigen binding fragment, as therapy for neovascular age-related macular
degeneration. Retina. 2006;26(8):859–70. https://doi.
org/10.1097/01.iae.0000242842.14624.e7. PMID:
17031284.
69. Campochiaro PA, Haz G, Shah SM, Nguyen QD,
Ying H, Do DV, Quinlan E, Zimmer-Galler I, Haller JA,
Solomon SD, Sung JU, Hadi Y, Janjua KA, Jawed N,
Choy DF, Arron JR.Ranibizumab for macular edema
due to retinal vein occlusions: implication of VEGF
as a critical stimulator. Mol Ther. 2008;16(4):791–9.
https://doi.org/10.1038/mt.2008.10. Epub 2008 Feb 5.
PMID: 18362932.
70. Kida T, Flammer J, Konieczka K, Ikeda T. Retinal
venous pressure is decreased after anti-VEGF therapy in patients with retinal vein occlusion-related
macular edema. Graefes Arch Clin Exp Ophthalmol.
2021;259(7):1853–8. https://doi.org/10.1007/s00417-
020- 05068- x. Epub 2021 Jan 15. PMID: 33447857;
PMCID: PMC8277612.
71. Gale R, Gill C, Pikoula M, Lee AY, Hanson RLW,
Denaxas S, Egan C, Tufail A, Taylor P, UK EMR
Database Users Group. Multicentre study of 4626
patients assesses the effectiveness, safety and burden of two categories of treatments for central retinal
vein occlusion: intravitreal anti-vascular endothelial
growth factor injections and intravitreal Ozurdex
injections. Br J Ophthalmol. 2021;105(11):1571–6.
https://doi.org/10.1136/bjophthalmol- 2020- 317306.
Epub 2020 Sep 22. PMID: 32962992; PMCID:
PMC8140590.
72. Qian T, Zhao M, Xu X. Comparison between antiVEGF therapy and corticosteroid or laser therapy for
macular oedema secondary to retinal vein occlusion:
a meta-analysis. J Clin Pharm Ther. 2017;42(5):519–
29. https://doi.org/10.1111/jcpt.12551. Epub 2017
Jun 22. PMID: 28639290.
73. Nanji K, Khan M, Khalid MF, Xie JS, Sarohia GS,
Phillips M, Thabane L, Garg SJ, Kaiser P, Sivaprasad S,
Wykoff CC, Chaudhary V.Treat-and-extend regimens
of anti-vascular endothelial growth factor therapy for
retinal vein occlusions: a systematic review and metaanalysis. Acta Ophthalmol. 2022;100(6):e1199–208.
https://doi.org/10.1111/aos.15068. Epub 2021 Nov
29. PMID: 34845830.
74. Scott IU, VanVeldhuisen PC, Oden NL, Ip MS, Blodi
BA, SCORE2 Investigator Group. Month 60 outcomes after treatment initiation with anti-vascular
endothelial growth factor therapy for macular edema
due to central retinal or hemiretinal vein occlusion.

References
https://t.me/medicina_free
203
Am J Ophthalmol. 2022;240:330–41. https://doi.
org/10.1016/j.ajo.2022.04.001. Epub 2022 Apr 21.
PMID: 35461831.
75. Spooner KL, Fraser-Bell S, Hong T, Wong JG, Chang
AA. Long-term outcomes of anti-VEGF treatment of
retinal vein occlusion. Eye (Lond). 2022;36(6):1194–
201. https://doi.org/10.1038/s41433- 021- 01620- z. Epub
2021 Jun 11. PMID: 34117379; PMCID: PMC9151794.
76. Hayreh SS.Photocoagulation for retinal vein occlusion. Prog Retin Eye Res. 2021;85:100964. https://
doi.org/10.1016/j.preteyeres.2021.100964. Epub
2021 Mar 11. PMID: 33713810.
77. Brown DM, Wykoff CC, Wong TP, Mariani AF, Croft
DE, Schuetzle KL, RAVE Study Group. Ranibizumab in preproliferative (ischemic) central retinal
vein occlusion: the rubeosis anti-VEGF (RAVE) trial.
Retina. 2014;34(9):1728–35. https://doi.org/10.1097/
IAE.0000000000000191. PMID: 24914476.
78. Khayat M, Williams M, Lois N. Ischemic retinal
vein occlusion: characterizing the more severe spectrum of retinal vein occlusion. Surv Ophthalmol.
2018;63(6):816–50. https://doi.org/10.1016/j.sur-
vophthal.2018.04.005. Epub 2018 Apr 27. PMID:
29705175.
79. Abu El-Asrar AM, Herbort CP, Tabbara KF. Differential diagnosis of retinal vasculitis. Middle East
Afr J Ophthalmol. 2009;16(4):202–18. https://doi.
org/10.4103/0974- 9233.58423. PMID: 20404987;
PMCID: PMC2855661.
80. Bansal R, Moharana B, Katoch D, Gupta V, Dogra
MR, Gupta A.Outcome of pars plana vitrectomy in
patients with retinal detachments secondary to retinal
vasculitis. Indian J Ophthalmol. 2020;68(9):1905–
11. https://doi.org/10.4103/ijo.IJO_551_20. PMID:
32823412; PMCID: PMC7690542.
81. Gupta A, Gupta V, Arora S, Dogra MR, Bambery P. PCR-positive tubercular retinal vasculitis: clinical characteristics and management.
Retina. 2001;21(5):435–44. https://doi.
org/10.1097/00006982- 200110000- 00004. PMID:
11642371.
82. Gupta A, Bansal R, Gupta V, Sharma A, Bambery
P. Ocular signs predictive of tubercular uveitis. Am
J Ophthalmol. 2010;149(4):562–70. https://doi.
org/10.1016/j.ajo.2009.11.020. Epub 2010 Feb 10.
PMID: 20149341.

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andInammation
10
10.1 Anatomical Considerations
Anatomically, the eye is divided into an anterior
chamber (AC), a posterior chamber (PC), and a
posterior segment consisting of the vitreous cavity, retina, and choroid. The cornea, iris, and anterior part of the ciliary body enclose the AC.The
PC is bound anteriorly by the iris, laterally by the
pars ciliaris, and posteriorly by the crystalline
lens and the zonular bres. The AC and PC are
lled with a transparent uid, the aqueous
humour, which is continuously secreted by the
ciliary epithelium into the PC, and a pressure gradient its movement through the pupil into the AC
and exits the eye through trabecular meshwork in
the angle of the anterior chamber. The cornea is
lined with a single layer of hexagonal cells, the
endothelial cells arranged in a honeycomb pattern. Like the brain and testes, the eye is an
immune-privileged site. The privilege is maintained via an outer retinal barrier by the retinal
pigment epithelium cells between the choroid
and the retina, the pigmented epithelial cells that
line the iris and ciliary body, and a blood-retinal
barrier by the tight endothelial cell junctions in
the retinal vessels.
One of the major strategies to maintain the
eye’s immune privilege is the phenomenon of
anterior chamber-associated immune deviation
(ACAID). The ocular barriers allow only the
exchange of oxygen, uid, and micronutrients
within the eye. These barriers also ensure that no
noxious agents or cellular elements can enter the
retina, vitreous cavity, AC, or PC under normal
circumstances. The neurosensory retina consists
of three post-mitotic retinal cell layers, namely
the photoreceptors (rods and cones, rst neuron),
bipolar cells (second neuron), and retinal ganglion cells (third neuron) and their connecting
bres, the outer and the inner plexiform layers.
Muller cells, the macroglia, extend through the
entire thickness of the retina. Their footplates
form the inner limiting membrane, and their processes contact the photoreceptors at the junction
of the inner and outer segments to form an external limiting membrane.
Along with the microglia, the resident macrophages, Muller cell processes form very intimate
contact with photoreceptors, bipolar cells, horizontal cells, amacrine cells, ganglion cells, and
the retinal capillary endothelial cells and form a
neurovascular complex that controls the retinal
microenvironment and homeostasis. The microglia are found in the retina’s inner and outer plexiform layers in their inactivated state. Once
activated by any insult, they become activated
macrophages, move through the retina, and produce cytokines. Notably, there are no progenitor
cells in the retina; once the cells die or undergo
apoptosis, there is no replacement.
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
A. Gupta et al., Ophthalmic Signs in Practice of Medicine,
https://doi.org/10.1007/978-981-99-7923-3_10
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10.2 Mediators ofInammation
A revolution in cell biology was heralded by the
discovery of interferons by Issacs and
Lindenmann in 1957 [1]. These molecules
blocked and interfered with the replication of
viruses. It was followed by the discovery of
interleukins (ILs) and a host of similar molecules
called cytokines that were abbreviated IL. As
more of these were discovered, they were
sequentially numbered as IL-1 and onwards [2].
Cytokines are short-lived cell surface proteins
that cannot enter the cells but dictate the activation of a host of intracellular signalling pathways
involved in normal physiological and pathological pathways. The cells interact with each other
via cytokines. The cytokines control the behaviour of cells, including their activation,
differentiation, and proliferation, and even
decide if the cells should die or produce more
cytokines. Cytokines are further subdivided into
interferons (prevent viral replication), interleukins (the largest cytokine family for cell-to-cell
talking), chemokines (proteins that control trafcking and migration of cells), and tumour
necrosis factor-α (TNF-α, a cytokine produced
by macrophages, lymphocytes, granulocytes
responsible for acute inammation, cell death,
and apoptosis).
The macrophages and B lymphocytes produce
IL-1, a pro-inammatory cytokine that activates
the T-helper cells. The IL-2, also a proinammatory cytokine, activates Th-1 helper
cells and furthers the proliferation of T cells. IL-6
helps differentiate B lymphocytes into plasma
cells and produce antibodies, hence a critical
player in inammation. There is a lot of redundancy and pleiotropy in the functioning of the
cytokines. More than one cell type can produce
multiple cytokines, which can interact with several different cells. [3].
Briey, IL-1 is produced by macrophages and
B cells, stimulates T-helper cells, and plays a role
in inammation; IL-2 is produced by the Th1
cells and causes proliferation and differentiation
of T cells; IL-6 is produced by a variety of cells
such as B cells, Th2 cells, macrophages, and
endothelial cells and helps in differentiation of B
cells into plasma cells and antibody production.
It is a key regulator of inammation; IL-17 is
secreted by the Th17 cells. TNF-α, an acute phase
reactant, is produced by macrophages, monocytes, lymphocytes, and granulocytes and is
responsible for acute inammation [3].
In their functions, the cytokines are either proinammatory or anti-inammatory, e.g. in acute
inammation, IL-1 and TNF-α act together to
worsen the inammatory response. Once the
infection is controlled, these stop expressing
themselves, and the inammation dies. The IL-10
and TGF-β are anti-inammatory and get upregulated in the ocular uids once the inammation is
controlled. In people predisposed to autoimmune
disorders, the genes expressing the proinammatory cytokines never shut down entirely,
thus perpetuating the autoimmune inammatory
response [4]. Among the cytokines detected in
the intraocular uids and serum of patients with
endogenous uveitis include TNF-α, IL-1β, IL-6,
IL-10, and IL-17 [5–7]. Developing antibodies to
block these cytokines has revolutionized the
treatment of systemic autoimmune disorders,
including endogenous uveitis [8], and will be discussed in a later section.
10.3 Retinal andChoroidal
Infections
andInammations:
Denition
As dened by the Standardization of Uveitis
Nomenclature (SUN) working group, the term
posterior uveitis includes all intraocular infections and inammations wherein the primary
anatomical site, as determined by clinical examination, is either in the retina, in the choroid, or
both [9]. It includes all cases of focal, multifocal,
diffuse choroiditis, chorioretinitis, retinochoroiditis, retinitis, and neuroretinitis. Some of the
inammatory disorders that may involve the
anterior chamber and vitreous, besides the retina
and choroid, dened as panuveitis, will also be
discussed in this chapter.

10.5 Dierentiating Retinitis fromChoroiditis
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10.4 Introduction
While nearly 40–50% of the uveitis entities
remain uncharacterized even today, physicians
must differentiate infectious uveitis from the
more commonly occurring and perhaps bettercharacterized immune-mediated non-infectious
uveitis. Diagnosis of non-infectious uveitis is
denitive due to well-characterized ocular phenotypes often associated with systemic autoinammatory/autoimmune disorders. However,
frequent recurrences of inammation in these
patients pose a major management challenge as
they often require long-term anti-inammatory
and/or immunosuppressive therapy. However, a
large majority of infectious organisms that manage to break the blood-ocular barrier to set up
infection/uveitis in the eye, although they can be
controlled with highly effective antibiotics and
other chemotherapeutic agents, the tendency for
these organisms to sequestrate/hibernate or
assume latency in the ocular tissues often results
in recurrences. The subject of intensive studies is
what triggers these organisms’ latency and reactivation to cause recurrent inammation. Detecting
organisms responsible for infectious uveitis has
also remained a major challenge. Moreover, their
phenotypic expression largely depends upon the
host’s immune status, the organism’s infectious
dose, and the possibility of multiple simultaneous infections, especially in patients with
HIV.Their diagnosis often requires invasive procedures for obtaining ocular uid samples to
reach a denitive diagnosis.
10.5 Dierentiating Retinitis
fromChoroiditis
It is critical to differentiate retinitis from choroiditis clinically. In general, retinitis is infectious
in origin and needs specic antimicrobial therapy. An exception to this statement includes
Behcet’s autoinammatory multiorgan disease
and immune-mediated retinitis caused by vectorborne viral fevers. Infectious retinitis includes
toxoplasma gondii, the herpes viruses, syphilis,
and other spirochetes like Borrelia burgdorferi
(Lyme) and nematodes. The use of corticosteroids in patients with infectious retinitis can be
disastrous for the eye. Most of the inammations
in the choroid are primarily immune-mediated
(except for cases of the infectious endogenous
endophthalmitis) and require corticosteroids for
initial control of inammation and long-term
steroid-sparing therapy with immunosuppressive
agents. As the focus of infection is set up in the
retina, many inammatory cells, cytokines, and
protein-rich exudates are released into the vitreous gel. These accumulate and cause media haze
with a spillover into the AC.The inammatory
response is generally dictated by the patient’s
immune status, being robust in patients with a
normal immune system and muted in immunocompromised patients. The inammatory exudates in the vitreous cavity are far more in
patients with retinitis than in choroiditis, and
thus, media haze is more in the former than the
latter. The retinal vessels coursing through a retinitis lesion are generally obscured in the retinitis
lesion but run a normal course over a choroiditis
lesion (Fig. 10.1a, b). On FFA, the retinitis
lesions show initial hypouorescence, staining
of the retinal vessel walls running through the
lesion, and in the late frames, intense hyperuorescence of the retinal lesion with indistinct borders (Fig.10.1c, e).
However, on FFA, the choroiditis lesions show
discrete areas of initial hypouorescence and late
hyperuorescence (Fig.10.1d, f), which is much
less exuberant than the retinitis lesions. In general, the retinal vessels overlying a choroiditis
lesion remain normal. Choroiditis lesions are
more often associated with exudative subretinal
uid than retinitis lesions (Fig.10.2). Often, the
inammatory lesion in retinitis extends into the
choroid, e.g. toxoplasma retinochoroiditis, and a
choroiditis lesion may extend into the retina
when labelled as chorioretinitis (Figs.10.1b, d, f
and 10.2b). If the retinitis lesions remain conned to the retina, it may result in only minimum
pigmentary changes upon healing, whereas the
choroiditis lesions heal with heavily pigmented
scars (Fig. 10.3). Structural optical coherence

208
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10 Retinal andChoroidal Infections andInammation
a
b
e
f
Fig. 10.1 Retinal vessels over a retinitis lesion (a) are
generally obscured, while they run a normal course over a
choroidal lesion (b). On FFA, the retinitis lesions show
staining of the retinal vessel walls running through the
lesion (c), while the choroidal lesion shows initial hypouorescence (d). In the late frames of FFA, extensive
hyperuorescence of the retinal lesion with indistinct borders (e) is seen, and the choroidal lesion shows hyperuo-
rescence not as intense as retinitis with dye pooling in the
area of exudation (f). Note that the example in (b, d, and
f) represents a case of chorioretinitis. The intense staining
in (f) is due to retinal inammation. (a, c, and e reproduced with permission from EyeNet Magazine, Gupta
AK, et al., Infectious uveitis-New challenges emerge.
September 2014)
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