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References

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177

39. Schiffrin EL. Remodeling of resistance arteries in essential hypertension and effects of antihypertensive treatment. Am J Hypertens. 2004;17(12 Pt 1):1192–

200. https://doi.org/10.1016/j.amjhyper.2004.05.023. PMID: 15607629.

40. Harazny JM, Ritt M, Baleanu D, Ott C, Heckmann J, Schlaich MP, Michelson G, Schmieder RE. Increased wall:lumen ratio of retinal arterioles in male patients with a history of a cerebrovascular event. Hypertension. 2007;50(4):623–9. https://doi.

org/10.1161/HYPERTENSIONAHA.107.090779.

Epub 2007 Aug 13. PMID: 17698722.

41. Cheung CY, Biousse V, Keane PA, Schiffrin EL, Wong TY. Hypertensive eye disease. Nat Rev Dis Primers. 2022;8(1):14.

00342- 0. PMID: 35273180.

42. Wang S, Xu L, Jonas JB, Wang YS, Wang YX, You QS, Yang H, Zhou JQ. Five-year incidence of retinal microvascular abnormalities and associations with arterial hypertension: the Beijing Eye Study 2001/2006. Ophthalmology. 2012;119(12):2592–9.

https://doi.org/10.1016/j.ophtha.2012.06.031. Epub

2012 Aug 20. PMID: 22917887.

43. Wong TY, Mitchell P. Hypertensive retinopathy. N Engl J Med. 2004;351(22):2310–7. https://doi.

org/10.1056/NEJMra032865. PMID: 15564546.

44. Yatsuya H, Folsom AR, Wong TY, Klein R, Klein BE, Sharrett AR, ARIC Study Investigators. Retinal microvascular abnormalities and risk of lacunar stroke: Atherosclerosis Risk in Communities Study. Stroke. 2010;41(7):1349–55. https://doi.org/10.1161/

https://doi.org/10.1038/s41572- 022-

STROKEAHA.110.580837. Epub 2010 Jun 3. PMID:

20522816; PMCID: PMC2894269.

45. Burnasheva MA, Maltsev DS, Kulikov AN, Sherbakova KA, Barsukov AV.Association of chronic paracentral acute middle maculopathy lesions with hypertension. Ophthalmol Retina. 2020;4(5):504–9.

https://doi.org/10.1016/j.oret.2019.12.001. Epub

2019 Dec 16. PMID: 31948908.

46. Too GT, Hill JB. Hypertensive crisis during pregnancy and postpartum period. Semin Perinatol. 2013;37(4):280–7. https://doi.org/10.1053/j.sem-

peri.2013.04.007. PMID: 23916027.

47. Keith NM. Classication of hypertension and clinical differentiation of the malignant type. Am Heart J. 1927;2:597–608. https://doi.org/10.1016/

S0002- 8703(27)90207- 5.

48. Shantsila A, Lip GYH. Malignant hypertension revisited-does this still exist? Am J Hypertens. 2017;30(6):543–9. https://doi.org/10.1093/ajh/

hpx008. PMID: 28200072.

49. Hayreh SS, Servais GE, Virdi PS.Fundus lesions in malignant hypertension. VI.Hypertensive choroidopathy. Ophthalmology. 1986;93(11):1383–400. https://

doi.org/10.1016/s0161- 6420(86)33554- 1. PMID:

3808599.

50. American Diabetes Association. Standards of Medical Care in Diabetes—2022 abridged for primary care providers. Clin Diabetes. 2022;40(1):10–38. https://

doi.org/10.2337/cd22- as01. PMID: 35221470;

PMCID: PMC8865785.

Retinal Vascular Occlusions

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9.1 Introduction

Retinal vascular occlusions are often associated with life-threatening cardiovascular and cerebrovascular disorders and should initiate a search for either genetic or acquired prothrombotic factors. The incidence of retinal arterial occlusions varies from 1:100,000in the US population [1] to 1.4– 10:100,000 in the Korean population [2]. Major systemic risk factors include type 2 diabetes mellitus, smoking, arteriolosclerosis, carotid atherosclerosis, hypertension, high-serum lipid levels, high body mass index, coagulopathy, and atrial brillation [3]. See Box 9.1.

Box 9.1 Systemic Associations of Central/ Branch Retinal Artery Occlusion

1 Atherosclerosis of carotid arteries; aortic arch 2 Hypertension; diabetes mellitus;

dyslipidaemia 3 Rheumatic heart disease 4 Giant cell arteritis; polyarteritis nodosa

including its monogenic variant DADA2;

granulomatosis with polyangiitis

(Wegener’s syndrome); Takayasu’s arteritis;

Susac’s syndrome 5 Systemic lupus erythematosus;

antiphospholipid antibodies syndrome 6 Hypercoagulable state;

hyperhomocysteinemia; oral contraceptives

Reference: Recchia and Brown (2007)

There is a signicant risk for stroke immediately before or within a week to a month following retinal artery occlusion (RAO). All such patients need to be evaluated by a stroke unit [3, 4]. Rarely, giant cell arteritis, systemic vasculitis of large vessels, may rst present as an arteritic central retinal artery occlusion (CRAO) [5]. Involvement of the retinal circulation may be the rst manifestation of Takayasu’s arteritis, another large vessel systemic vasculitis that preferentially affects the arch of the aorta and its branches [6, 7]. Polyarteritis nodosa, another systemic vasculitis affecting the medium and small arteries, may rarely involve the posterior ciliary arteries and cause infarction of the choroid [8,

9]. Immune complex deposition may block periph-

eral retinal arterioles in systemic lupus erythematosus (SLE). There is an extensive and diffuse inammation of retinal vessels with Bechet’s disease. Several inammatory disorders may cause retinal vascular occlusions and are summarized in Box

9.2. In TB-endemic countries, occlusive peripheral

retinal periphlebitis is not an uncommon cause of vision loss. The vascular occlusions in the eye often lead to irreversible vision loss (arterial occlusions) and, even if reversible (non- ischaemic branch and central retinal vein occlusions), lead to high-visual morbidity. Although the branch and the central retinal artery (CRA) occlusions are less common than the branch retinal vein occlusions (BRVO) and the central retinal vein occlusion (CRVO), these portend systemic severe health issues and are discussed rst.

https://doi.org/10.1007/978-981-99-7923-3_9

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9 Retinal Vascular Occlusions

Box 9.2 Retinal Vasculopathy in Autoimmune Systemic Vasculitis, Inammatory, Infectious, and Demyelinating Diseases

Systemic disease Key systemic signs and symptoms Ocular signs Key labs Giant cell

arteritis

Takayasu’s arteritis

Poly arteritis nodosa (small- and medium-sized arteries)

Granulomatosis with polyangiitis

SLE Women >30years; malar rash;

Sarcoidosis Low-grade fever; cough;

Behcet’s disease Multiorgan thrombotic and

Toxoplasmosis Fever; lymphadenopathy;

Syphilis Primary chancre on genitalia;

Age>50years; extracranial branches of carotid; temporal headache; low-grade fever; malaise; jaw claudication; temporal artery tenderness, and occlusion

Women <40years; myalgia; low-grade fever; limb claudication; fainting spells; absent peripheral pulses; amaurosis fugax; carotid bruit; asymmetric BP in various limbs

Weight loss; myalgia; testicular pain; cardiac systolic dysfunction; peripheral gangrene; mono/ polyneuropathy; elevated diastolic BP; strokes (especially in monogenic variant DADA2)

Upper and lower respiratory symptoms; epistaxis; nasal crusting; cough; haemoptysis; renal involvement; palpable purpura and arthralgia; myalgia

fever; fatigue; weight loss; alopecia; hypertension; renal failure; thrombosis; abdominal pain; encephalopathy

dyspnoea; fatigue; lupus pernio; Erythema nodosum; facial palsy

necrotizing vasculitis; recurrent oral and genital ulceration; pseudofolliculitis; deep vein thrombosis; recurrent diarrhoea; arthritis; encephalopathy; thromboembolism; IHD

abortion; encephalopathy in HIV+

maculopapular rash; rash in oral cavity and palm; dementia

Arteritic- AION CRAO; BRAO; OAO; CLRAO

Hypotensive retinopathy; microaneurysms; anastomotic vessels on optic disc, arteriolar dilatation; iris neovessels; low IOP; hypertensive retinopathy in type 3 (renal artery involvement); rarely BRAO

PCA occlusion HBV serology; LFT;

Necrotizing scleritis; orbital inammation and proptosis; diplopia; retinal haemorrhages; vision loss

Peripheral branch retinal arteriolar occlusion; cotton wool spots; retinal haemorrhages; retinal neovessels

Panuveitis, vitritis; nodular perivenous inltrates, arteriolar macroaneurysms; choroidal granuloma

Recurrent hypopyon; vitritis; retinitis; retinal vasculopathy-(capillaries, veins, and arteries); retinal neovessels; retinal vessel occlusion; ION

Retinochoroiditis; Kyrieleis arteritis

Vitritis; retinal vasculitis; placoid retinopathy; choroidopathy

ESR; CRP; TA ultrasonography; TA biopsy; PET-FDG axillary arteries

MR/CT angiography; CRP; ESR; PET-FDG FFA

ANCA-ve; CRP; renal functions; CT/MR arteriography to detect microaneurysms and focal narrowing of medium arteries; biopsy. ADA2 gene mutation and ADA2 levels in monogenic variant DADA2

PR3 and MPO ANCA; CRP; ESR; TLC; urine analysis; CT chest

CBC; APTT; ESR; CRP; ANA; dsDNA; RFT; urine analysis; chest X-ray; ECG; FFA

X-ray/CT chest; ACE; RFT; PFT; lysozyme; lymphocytosis Tuberculin skin test

HLA B5101; pathergy test serum homocysteine; ESR; C-reactive proteins; ASO; neopterin;

α-1trypsin; α-2 macroglobulin;

FFA Toxo serology; HIV

serology in bilateral and severe cases

TPHA; VDRL; HIV

9.1 Introduction

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Systemic disease Key systemic signs and symptoms Ocular signs Key labs Herpes simplex

virus (HSV) Varicella- Zoster

virus (VZV)

Cytomegalovirus infection (CMV)

Leptospira Rural; ooding; asymptomatic in

Dengue fever (Vector: aedes aegypti and aedes albopictus)

Chikungunya (Vector: aedes aegypti and aedes albopictus)

Rift valley fever Asymptomatic in the majority;

Lyme disease Erythema migrans; fever;

Cat scratch disease

Multiple sclerosis

Unrecognized primary disease ARN; occlusive

vasculopathy

Acute VZV infection— chickenpox in childhood; herpes zoster in adults and immunocompromised

In immunocompetentasymptomatic or fever lymphadenopathy, lymphocytosis

most; fever; respiratory failure; haemoptysis; high mortality

Fever; with retro-ocular pain; myalgia; arthralgia; rash; coagulopathy; haemorrhages of varying severity; respiratory distress; pleural effusion; hepatomegaly; second infection severe with high mortality

Fever; myalgia; rash; polyarthritis; polyarthralgia; encephalopathy; myocarditis; pericarditis; nephritis; bleeding; pneumonia

fever

arthralgia; myalgia Fever; maculopapular skin rash

lymphadenopathy Women 20–40years; temporary

loss of vision, sensory loss

Progressive outer retinal necrosis; retinal vessel sparing

Retinitis; vasculopathy CMV qPCR; CD4+

Hypopyon; panuveitis; retinal vasculopathy

Retinopathy, cotton wool spots; vasculopathy; macular oedema; foveolitis

Retinopathy, retinal haemorrhages, cotton wool spots, retinal opacication

Retinopathy; retinal vasculopathy; retinal haemorrhages; cotton wool spots

Vitritis Immunouorescence test;

Neuroretinitis; multifocal retinitis; BRAO; BRVO

Peripheral retinal vasculopathy; vitritis

181

PCR; HIV; IgM; IgG FFA

HIV; IgM; IgG FFA

FFA

CBC; PCR; urine test; IgM; microscopic agglutination test

Dengue serology (DEN-1-4); ns-1 antigen RT-PCR; platelet counts; TLC; LFT; serum proteins FFA; OCT: OCTA

Chikungunya serology (IgM, IgG); RT-PCR; TLC; platelets; FFA

RT-PCR; serology; CBC; LFT

Lyme serology; PCR Bartonella serology

MRI brain; spinal cord; AQP4 antibodies; MOG antibodies

Abbreviations: ESR erythrocyte sedimenta- tion rate, CRP c-reactive proteins, TA temporal artery, RFT renal function test, PET-FDG posi- tron emission tomography-uorodeoxyglucose, MR magnetic resonance, CT computerized tomography, F FA fundus uorescein angiography, HBV hepatitis B virus, LFT liver function tests, ANCA antineutrophil cytoplasmic antibodies, DADA2 deciency of adenosine deaminase 2, ADA adenosine deaminase 2, ANCA-PR3 anti-neutrophil cytoplasmic antibody-proteinase 3, ANCA-MPO anti-neutrophil cytoplasmic antibody-myeloperoxidase, TLC total leukocyte counts, CBC complete blood counts, APTT activated partial thromboplastin time, ANA antinuclear antibody, dsDNA double-stranded DNA,

ECG electrocardiograph, PFT pulmonary function tests, ASO antistreptolysin O tires, Toxo toxoplasmosis, HIV human immunodeciency virus, TPHA treponemal haemagglutination test, VDRL venereal disease research laboratory test, PCR polymerase chain reaction, IgM immunoglobulin M, IgG immunoglobulin G, CMV cytomegalovirus, qPCR quantitative polymerase chain reaction, CD4+ clusters of differentiation 4+ cells, ACE angiotensin-converting enzyme, RT-PCR reverse transcriptase polymerase chain reaction, OCT optical coherence tomography, OCTA optical coherence tomography angiography, AQP4 aquaporin 4 antibody, MOG anti-myelin oligodendrocyte glycoprotein antibodies

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9 Retinal Vascular Occlusions

9.2 Non-arteritic Central andBranch Retinal Artery Occlusion

The most common cause of a non-arteritic central or branch retinal artery occlusion (BRAO) is emboli that arise from a thrombus developing on an ulcerated atheromatous plaque in the internal carotid artery and, depending on the size of the emboli may occlude the CRA or pass down any of the branches and usually get stuck at the bifurcation of the arterioles. The patients may report episodes of transient visual loss due to very small emboli, which may nally lodge into the peripheral retinal arterioles. A thorough retinal examination should be done to detect any visible emboli. See Box 9.3.

Asymptomatic retinal emboli may be seen in up to 1.4% of the general population [11], with the prevalence rising in people above the age of 70–75years [11, 12]. All such patients need to be thoroughly assessed for any risk factors listed above as they are at a higher risk of dying from stroke than those who do not show asymptomatic emboli. The CRA and its branches supply the inner retina up to the outer border of the inner nuclear layer. Complete occlusion of the CRA leads to an immediate loss of vision from the affected eye. Fundus examination reveals a pale opacication of the inner retina with a cherry red spot in the macula (Fig.9.1). The absence of the inner retinal elements in the fovea centralis (retinal ganglion cells, inner plexiform layer, and the

Box 9.3 Common Causes of Retinal Emboli

1 Atheromatous internal carotid artery; aortic

arch; common carotid artery; ophthalmic artery atherosclerosis

2 Valvular heart disease; mitral valve

prolapse atrial myxoma; atrial brillation

3 Dissection of the aorta; ventral septal defect

may allow thromboembolism from deep vein thrombosis

4 Talc emboli in drug addicts; triamcinolone

acetonide /methylprednisolone injection for lid or nasal haemangiomas

Reference: [10]

inner nuclear layer) ensures that there is no retinal opacication in the centre of the fovea and no obscuration of the choroidal circulation and hence the cherry red spot. The possibility of an ophthalmic artery occlusion should be seriously considered in the absence of the cherry red spot. In acute CRAO, the retinal arterioles may show ‘Box-carring’. The fundus uorescein angiography (FFA), if done early enough after the onset of CRAO, may show a leading edge of the dye in the retinal arterioles due to the slow lling of the arterioles (Fig.9.1). In patients who have intermittent CRAO, there may be patchy opacication of the retina. In the event of BRAO, there is sectoral opacication of the retina and loss of vision in the corresponding visual eld (Fig.9.1). If the affected arterioles are the blood supply to the fovea, there may be a complete loss of central vision. The cilioretinal artery, a branch of the posterior ciliary artery, is present in nearly one third of people and may save the central vision in these fortunate patients. On the contrary, an embolus in the cilioretinal artery may lead to central vision loss. Although the experimental studies show a retina survival time of 90–240min, the survival time of the brain tissue is only 12–15min. Beyond this time, there will likely be a complete infarction of the retinal ganglion cells as well [13]. However, complete cessation of the blood ow in the CRA is uncommon, which may prolong the retina’s survival time. The emboli may be visible in about 20% of the patients with CRAO, and these patients carry the worst visual outcome (Fig.9.2) [14]. However, irrespective of the visibility of the embolus, all patients with either CRAO or BRAO should undergo evaluation of the internal carotid artery (ICA) for haemodynamically unstable carotid artery stenosis (>60% stenosis) [15] and transthoracic echocardiography to rule out a cardiac source of emboli [16]. Echocardiography can reveal the source of emboli in nearly 60% of patients with CRAO and 50% with BRAO [17]. The Doppler scan/catheter angiography of the carotid artery revealed signicant stenosis (>50%) in nearly 30% of both the CRAO and the BRAO eyes on the same side as the occlusion [17]. Simultaneous embolization in both eyes is uncommon [14]. At least three

9.2 Non-arteritic Central andBranch Retinal Artery Occlusion

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Fig. 9.1 Central retinal artery occlusion (CRAO) is seen as a diffuse pale opacication of the inner retina of the entire fundus with a cherry red spot (blue arrow) in the macula (a). Branch retinal artery occlusion (BRAO) is

Fig. 9.2 Multiple emboli (black arrows) seen as shiny refractile cholesterol emboli embedded at the bifurcation of arterioles in a patient with BRAO

seen as a partial pale opacication (black arrows) of the retina (b). Fundus uorescein angiography shows a leading edge of the dye in the retinal arteries (red arrows) due to the slow lling of the arteries (c)

types of retinal emboli can be recognized. The commonest type of emboli (~70%) are shiny refractile cholesterol emboli that are seen embedded at the bifurcation of arterioles (Fig.9.2) and arise from ICA atherosclerosis. These are often multiple, and this author has seen a shower of these refractile emboli that shoot down the arterioles to be caught at the bifurcation of the peripheral arterioles. The next common is platelet-brin emboli which arise from the ulcerated atheromatous plaque in the ICA or the heart valves. These are dull white, rather soft, and take an elongated shape in alignment with the course of the obstructed arteriole and often cause only transient arterial occlusion (Fig.9.3). The largest of the emboli is a chalky white irregular-shaped calcic embolus that is stuck in the CRA just before its division and arises from calcied mitral valves

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9 Retinal Vascular Occlusions

Fig. 9.3 A 44-year-old man presented with blurring of vision in the left eye. There was an opacication of the retina (black arrows) just below and temporal to the optic disc margin (a). FFA showed delayed perfusion (blue

[10, 18]. Patients who develop CRAO need an emergency evaluation by the hospital stroke team for possible thrombolytic therapy. Unfortunately, due to widespread ignorance about CRAO, there are signicantly more delays in symptoms-todoor time for CRAO patients than those with stroke. Compared to stroke patients, less than half (~15%) get the intravenous thrombolytic therapy of CRAO [19].

Some conservative measures commonly used include ocular massage as the most typical strategy, followed by paracentesis, timolol, hyperventilation, oxygen therapy, acetazolamide infusion, and pentoxifylline. However, none of the strategies, including the thrombolytic therapy, if applied after 6h of the acute onset, seems to effectively change the course of the arterial

arrows) of this area (b). Late frames revealed a localized hyperuorescence of the wall of one of the small arterioles (red arrow) feeding the macula (c). Note the shape of the embolus characteristic of a soft brin-platelet embolus

occlusion [20, 21]. In a controlled multicentric trial, there was no outcome difference between the conservative treatment and intra-arterial thrombolytic therapy in acute CRAO presenting up to 20h of onset. Visual acuity improved in nearly 60% of the eyes in both groups. More than one third of the patients in the intra-arterial therapy had signicant adverse events, including cerebral and cerebellar haemorrhages [22]. Based on the opinion of the experts and a review of the current literature, the American Heart Association has recommended that patients with CRAO be evaluated by a stroke unit and consider the use of an intravenous tissue plasminogen activator within 4.5 h of the onset of symptoms as it seems to be an effective strategy. However, a need is felt for conducting con-

9.3 Branch Retinal Vein Occlusion

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trolled trials [23]. Currently, a few placebo-controlled multicentric trials are evaluating this strategy.

9.3 Branch Retinal Vein

Occlusion

9.3.1 Epidemiology ofBranch

Retinal Vein Occlusion (BRVO)

Next to diabetic retinopathy, branch retinal vein occlusion (BRVO) is the second most common retinal vascular disease. In a population-based study (the Beaver dam eye study), the prevalence and 5-year incidence of BRVO were 0.6% each [24]. When the same population was revisited, the 15-year incidence of BRVO was 1.8%. Retinal vascular occlusions (RVO) accounted for 12% of the causes of severe vision loss (<20/200) over 15years in this population [25]. In pooled data from different regions of the world, the estimated prevalence of BRVO in persons above the age of 30years was seen to vary with ethnicity, from 2.82 in Whites to 3.53 in Black, 4.96 in Asians, and 5.98 per 1000 population in the Hispanic population. It is estimated that nearly 14 million people worldwide suffer from BRVO [26, 27]. Patients between the ages of 43–69years who develop retinal vein occlusions (BRVO and CRVO) have a twofold increased risk of dying from cardiovascular diseases. In contrast, men at any age have a similar twofold, although the nonsignicant risk of dying from cerebrovascular disorders [28].

9.3.2 Risk Factors forBRVO

The signicant risk factors for developing BRVO include increasing age, hypertension, history of cardiovascular disease, smoking, low HDL levels, high BMI at the age of 20, and focal arteriolar narrowing [24, 29, 30]. It was recommended to diagnose and treat hypertension, stop smoking, reduce weight, increase physical activity, and take measures to increase HDL levels.

9.3.3 Pathogenesis ofBRVO

The upper temporal quadrant of the retina is the most common site for the occlusion of the branch retinal veins, followed by the lower temporal and least common in the nasal quadrant as there are far more AV crossings in the upper temporal retina compared to the lower temporal and the nasal retina. The eyes that develop BRVO have signicantly more AV crossing than those that do not develop BRVO.In eyes with BRVO, the retinal arterioles cross anterior to the retinal vein (AV crossing) in nearly 98% at the occlusion site compared to 67% in normal persons [31]. Notably, the retinal arterioles share a common adventitial sheath with the retinal vein. There is progressive hardening of the arterioles due to broplasia in the tunica media and intimal thickening due to arteriolosclerosis, aggravated by hypertension in ageing persons [32]. It leads to progressive nicking at the AV crossing site (Gunn sign and Salus sign). It is believed that endothelial injury caused by turbulence of the blood ow proximal to the site of the AV nicking leads to venous thrombosis [32]. Depending upon whether the occlusion is complete or incomplete, the eye may have an ischaemic (non-perfused) or a non-ischaemic (perfused) type of vein occlusion.

9.3.4 Clinical Presentations ofBRVO

The patients may complain of acute loss of vision in the corresponding eld of vision, blurring of vision or even remain asymptomatic depending upon the anatomical site of the occlusion and involvement of the macula. There are at least four anatomical sites where BRVO may occur. The commonest is a major vein occlusion near the optic disc either at the rst or the second AV crossing in the upper temporal quadrant or a little less common in the lower temporal quadrant (Fig.9.4). The next common is a macular vein occlusion which occurs when a small venous tributary draining the macula gets blocked (Fig.9.5). The least common is the peripheral and the nasal sites. The BRVO in the nasal retinal and

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Fig. 9.4 Branch retinal vein occlusion (BRVO) in the upper temporal quadrant (a) or lower temporal quadrant (b) as the commonest sites

9 Retinal Vascular Occlusions

Fig. 9.5 Macular retinal vein occlusion occurs when a small venous tributary draining the macula gets blocked

the peripheral retina often remain asymptomatic as the macula is not affected and is detected either by chance on routine examination or much later if the

patient develops either a new BRVO or develops vitreous haemorrhage from neovascular complications that arise typically several months after the acute episode. Acute retinal vein occlusions are characterized by dilatation and tortuosity of the obstructed vein and ame-shaped and dot and blot retinal haemorrhages in the drainage area of the

Fig. 9.6 Macular retinal vein occlusion (a) with cystoid macular oedema as seen on OCT (b)

blocked vein. The major and macular vein occlusions often accompany macular oedema (Fig.9.6). There may be cotton wool spots due to occlusion of the precapillary arterioles supplying blood in the territory of the obstructed retinal vein and are suggestive of the ischaemic type of BRVO.At presentation, nearly one fourth of the patients with major

vein occlusion and a little less than 50% of the macular vein occlusion eyes may have visual acuity of 20/30 or better [33]. Within 6weeks to 6months, the retinal capillaries develop collateral channels across the horizontal raphe and start draining the blood/uid via the venous channels in the opposite

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a b

187

Fig. 9.7 A case of upper temporal BRVO (a) at 6months follow-up, showing the formation of collaterals (red arrows) as seen on OCT angiography (b). Areas of capil-

quadrant [32]. These collateral channels help drain the leaky uid and help reduce the tissue pressure in the extravascular space, thereby helping resolve the macular oedema. Retinal haemorrhages may prevent visualization of the collateral channels in the acute phase. Recently using optical coherence tomography angiography (OCTA), more than 80% of the eyes were shown to have developed collaterals in the macula (Fig.9.7). However, some of these collaterals also developed microaneurysms responsible for macular oedema’s persistence [34]. Further, it has been shown that these collaterals develop in the deep vascular plexus rather than the supercial plexus [35].

9.3.5 Role ofFundus Fluorescein

Angiography

Extensive retinal haemorrhages in the acute phase of BRVO show blocked uorescence on fundus uorescein angiography (FFA). However, the staining of the vessel walls of the obstructed vein and its tributaries, uid in the extravascular spaces in the affected sector of the retina, and cystoid macular oedema can still be appreciated. There are three main causes of diminution of vision in the acute stage of BRVO—the retinal haemorrhage in the foveal centre blocking the

lary non-perfusion are seen as non-perfused areas (blue arrows) on OCT angiography (b)

Fig. 9.8 Fundus uorescein angiography in a case of BRVO showing areas of capillary non-perfusion (blue arrows)

transmission of light, ischaemia or macular oedema. Since the absorption of haemorrhages may take up to 3months for spontaneous resolution, FFA in the acute stage does not help determine the cause of the diminution of vision. However, when most of the haemorrhages have resolved, FFA helps to determine whether it is a perfused or a non-perfused (ischaemic) BRVO (Figs. 9.8 and 9.9), perfusion/non-perfusion of

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