CONTINUING EDUCATION CET & TRAINING 2 FREE CET POINTS OT CET content supports Giving Sight Approved for Optometrists 4 Approved for Dispensing Opticians 4 “How do I complete this exam?” Go to www.optometrytoday.tv/FAQ

the arteriolosclerotic changes result from Management & Investigation thickening of the arteriolar wall. Retinal microaneurysms occur in a wide variety of Vascular Conditions of retinal vascular diseases, including , and represent a non- Module 13 Part 6: CLINICAL OPTOMETRY specific finding. There is an association Course code: C-13921 O/D of microaneurysms, , 34 and non-perfusion of retinal capillaries in hypertension, but these types of changes are also seen in other vascular conditions such as diabetes. Indeed, there may be a crossover between clinical conditions, as chronic hypertensive changes are part of the pathogenesis of the ocular ischaemic syndrome and arterio-venous (“a/v”) nipping is frequently seen in cases of branch retinal vein occlusion (see later sections). Acute hypertension can enter an exaggerated or malignant stage 04/06/10 CET characterised by fibrinoid necrosis of the arterioles and papilloedema (Figure 2). Symptoms include , , , dimness in vision, and photopsia. Ophthalmic findings in acute malignant hypertensive Louise O’Toole MMedSci FRCSI(Ophth) MRCOphth FEBO include focal arteriolar The previous article in this series discussed the investigation and narrowing, cotton wool spots, intra- management of retinal conditions that may be seen in clinical retinal transudates, macular oedema optometric practice. The present article covers the more common and retinal haemorrhages. There are also choroidal changes seen in malignant vascular conditions of the eye that could be encountered. This article hypertension, with focal occlusion of does not, however, discuss , since this topic has the choriocapillaris leading to necrosis been comprehensively covered in previous articles in Optometry Today. and atrophy of the retinal pigment epithelium (RPE), forming Elschnig’s spots. There is vasoconstriction of the Hypertensive retinopathy and dilatation of the retinal arterioles, posterior ciliary arteries supplying the Hypertension may be classified as “nipping” of the veins by overlying head, which leads to optic either essential hypertension, or the arterioles (Figure 1), an increase in the disc oedema. In severe hypertensive less common malignant hypertension. arteriolar light reflex, tortuosity of the retinopathy there may be a macular star Essential hypertension is diagnosed retinal vessels, and loss of transparency and even exudative retinal detachments. when the average systemic blood of the intra-arterial blood column. There Pregnancy-induced hypertension 1 pressure measures >140mmHg systolic is the Scheie system of classification for affects both the retinal and choroidal or 90mmHg diastolic, on two subsequent grading fundal changes in hypertensive vasculature with clinical findings occasions. Malignant hypertension retinopathy (Table 1). In this system resembling hypertensive retinopathy. occurs when there is a rapid and severe of classification, Scheie quantifies Involvement of the occipital cortex in elevation of with a systolic the changes of hypertension and pregnancy-induced hypertension can component greater than 200 mmHg. arteriolosclerosis separately, in a five- lead to transient cortical blindness. Systemic arterial hypertension stage classification ranging from normal will affect the retinal, choroidal and to the most severe changes visible in Management of Hypertensive optic nerve head circulation. Ocular the . The arteriolar changes of Retinopathy manifestations of chronic essential hypertension have been considered to Treatment of hypertensive retinopathy is hypertension include focal constriction result primarily from vasospasm whereas aimed at bringing the underlying systemic “How do I complete this exam?” Go to www.optometrytoday.tv/FAQ

hypertension under control in cases in ischaemic whitening of the retina in of essential, malignant, or pregnancy- the territory of the obstructed artery. In induced hypertension, and therefore the acute phase, the retinal arterioles appropriate referral to the patient’s appeared thin and attenuated and may GP is required. However, patients exhibit segmentation of blood flow presenting with clear signs of malignant termed “box-carring”. The characteristic hypertension, most notably the presence finding of a CRAO is a cherry red spot at of papilloedema, should be referred to the macula. At this point the choroidal 35 the nearest hospital as an emergency. circulation is visible and contrasts against the pale white ischaemic retina. Retinal arterial occlusion Figure 1 A CRAO is an ophthalmic emergency Retinal arterial occlusions (RAO) may An arteriole crossing a vein, illustrating “a/v” and patients should receive active be divided anatomically into central nipping treatment in the acute phase. Ocular (CRAO) or branch (BRAO) forms, massage should be attempted either depending on the site of obstruction. can be maintained (Figure 3). There will digitally or using a Goldman contact A CRAO occurs when the blockage is always be a relative afferent pupillary . In rare instances, this manipulation within the optic nerve substance itself defect (APD) present in the affected eye. can dislodge an obstructing embolus. and therefore the site of obstruction is Within the first few minutes to hours Massage should increase the intraocular generally not visible on ophthalmoscopy. after the obstruction, the may pressure (IOP) for 10 to 15 seconds, BRAO occurs when the site of blockage appear relatively normal. However, the followed by a sudden release, 04/06/10 CET is distal to the laminar cribrosa of the decreased blood flow to the eye will result which can dislodge the obstruction. optic nerve, and therefore a cause in the arterial circulation of the retina Changes of may be observable. The mean age of Hypertension patients who experience retinal arterial Stage 0 Although the patient has diagnosed hypertension, there are no occlusions is approximately 60 years visible retinal vascular abnormalities at presentation. Men appear to be more Stage I Diffuse arteriolar narrowing is seen, especially in the smaller vessels. susceptible than women, with a male to Arteriolar calibre is uniform, with no focal constriction female ratio of 2:1. The cause of retinal arterial obstruction may be either due Stage II Arteriolar narrowing is more pronounced, and there can be focal to an embolus from another site or the areas of arteriolar constriction development of a thrombosis at the site Stage III Both focal and diffuse arteriolar narrowing is more obvious and of obstruction. Vasculitis may present severe, and retinal haemorrhages may be present as an arterial occlusion. Structural Stage IV Stage I, II, or III abnormalities may be present, along with retinal abnormalities of the eye such as pre- oedema, exudates, and oedema papillary arterial loops or have also been associated with CRAO. Vasospasm induced by either a Changes of migraine or cocaine use has also been Arteriolosclerosis linked to retinal arterial occlusion. Stage 0 Normal

Central Retinal Artery Occlusion (CRAO) Stage 1 There is broadening of the light reflex from the arteriole, with minimal In a CRAO, patients experience painless or no arterio-venous compression vision loss occurring over several seconds. In some instances, there may Stage 2 Light reflex changes and crossing changes are more prominent be a preceding history of . The (VA) is reduced Stage 3 The arterioles have a “copper wire” appearance and there is more to 6/120 or worse. However, if there is a arterio-venous compression patent cilio-retinal artery present, there Stage 4 The arterioles have a “silver wire” appearance, and the arterio-venous may be normal foveal perfusion with crossing changes are most severe no loss of central VA; this artery is a branch of the posterior ciliary artery and Table1 therefore macular perfusion and function The Scheie Classification of Hypertensive Retinopathy changes CONTINUING EDUCATION CET & TRAINING 2 FREE CET POINTS OT CET content supports Optometry Giving Sight Approved for Optometrists 4 Approved for Dispensing Opticians 4 “How do I complete this exam?” Go to www.optometrytoday.tv/FAQ

treatment of this will reduce the risk of principally at arterial bifurcations has repeat vascular occlusion in the same, or been described in association with the a fellow, eye as well as preventing other disorder Idiopathic Retinal Vasculitis, associated conditions such as stroke. Aneursyms and Neuro- (IRVAN). This will involve the investigation The macroaneurysm can spontaneously and control of systemic hypertension, involute following thrombosis and diabetes and hypercholesterolaemia. fibrosis (Figure 5). Eyes with macular 36 The use of aspirin or warfarin may oedema, serous elevation of the sensory be indicated. Some patients with retina, or exudation should be treated carotid artery disease may require by gentle laser photocoagulation carotid endarterectomy. The heart to thrombose the aneurysm. may also act as an embolic source. Central retinal vein occlusion Figure 2 Branch Retinal Artery Occlusion (BRAO) (CRVO) Fundal picture in a patient with a history of A BRAO generally occurs secondary A central retinal vein occlusion (CRVO) malignant hypertension to an embolus. However, it may also occurs when there is a blockage of be secondary to inflammation or blood flow within the central retinal The use of an oxygen and carbon coagulopathies. Cholesterol emboli vein; thrombosis is thought to occur dioxide (95% O , 5% CO ) mixture originate from the ipsilateral carotid 2 2 at the lamina cribrosa. A CRVO has an

04/06/10 CET (carbogen) has been advocated by artery. They are small and refractile increased incidence with increased 2 some authors but dismissed by others. with a yellow-orange colour (Figure age and is found in association with Hyperbaric oxygen therapy has been 4). Platelet-fibrin emboli are long and diabetes mellitus and hypertension. It is shown to have some beneficial effects in white in colour. They are generally thought that these conditions promote cases of CRAO, but only if commenced associated with carotid or cardiac atherosclerosis and the thickened arterial within hours of the arterial occlusion. disease. Calcific emboli are associated wall compresses the venous wall and An increase in retinal arterial blood flow with classification of the heart valves promotes thrombosis. There may also be can be achieved by lowering IOP either or the aorta. Over 90% of BRAOs an increased risk of thrombosis in cases of physically, by performing a paracentesis, involve the temporal retinal vessels. hyperviscosity. Retinal vein thrombosis or pharmacologically, by using topical There is generally a history of acute, is a complication of polycythaemia, or systemic medication. The most unilateral, painless visual field loss multiple myeloma and leukaemia. important therapeutic intervention occurring over several seconds. As It may be precipitated by diuretics, is where the CRAO is associated with with a CRAO, there is retinal whitening dehydration, or the oral contraceptive giant cell arteritis (GCA) and high dose but usually localised to the retina pill in predisposed patients. systemic steroids must be administered surrounding the affected artery. The If the IOP is raised it increases the before the fellow eye is affected. majority of patients achieve a VA risk of venous thrombosis; it has The underlying cause of the CRAO of 6/12 or better with conservative been theorised that the increased needs to be determined and effective management but a persistent pressure bows the lamina cribrosa visual field defect may be present. posteriorly, inducing turbulence, consequent endothelial damage, and Retinal arterial thrombosis. Venous thrombosis can macroaneurysms also occur if the wall is inflamed, as Retinal arterial macroaneursyms may occurs in episodes of periphlebitis. occur as either saccular dilations or Inherent ocular predisposing factors out-pouchings from the arterioles. They include hypermetropia and congenital may be an incidental observation or else anomalies of the central retinal vein. present as a tri-laminar haemorrhage The visual loss associated with a CRVO affecting the sub-retinal, retinal and is painless and may be acute or sub-acute pre-retinal spaces. Retinal arterial in onset. The extent of retinal ischaemia Figure 3 macroaneurysms can also present determines the clinical findings. In an Central retinal artery occlusion (CRAO) with with surrounding retinal oedema. The ischaemic CRVO, the VA is generally sparing of the macula due to the cilio-retinal presence of multiple bilateral arterial 6/60 or less and there is a marked relative artery, a branch of the posterior ciliary artery aneurysmal abnormalities occurring afferent pupillary defect (RAPD). On “How do I complete this exam?” Go to www.optometrytoday.tv/FAQ

of retinal vein occlusions: the identification of modifiable risk factors and their medical management, and the recognition and management of sight-threatening complications. Patients presenting with a retinal vein occlusion should have a medical screen to detect hypertension, diabetes, and/or 37 hyperlipidemia. Retinal vein occlusions are associated with an increase in vascular causes of death. Treatment of hypertension reduces the severity of its Figure 4 Figure 5 complications, and additional therapy of Embolus in a retinal arteriole. This patient Spontaneous involution of macroaneursyms aspirin in well-controlled hypertensive requires a full cardiovascular assessment as they following thrombosis. There are multiple retinal subjects given as a prevention therapy are at a high risk of developing a stroke exudates and tri-laminar haemorrhages. reduces cardiovascular event rate. Cholesterol-lowering statins reduce examination of the posterior pole there CRVO. The supero-temporal vein is cardiovascular morbidity and mortality. are marked haemorrhages in the four most commonly affected (Figure 7). A In patients presenting with a retinal quadrants, associated with disc swelling BRVO occurs most commonly in the vein occlusion under the age of 50 04/06/10 CET and venous tortuosity (Figure 6). Cotton seventh decade of life. A BRVO typically years, a full thrombophilia screen wool spots may also be a feature. Close occurs at an arterio-venous crossing site. should be included in their medical follow-up is required as these patients Histological studies have demonstrated workup. In females, the contraceptive run the risk of developing retinal and that as the branch retinal artery and pill is the most common underlying iridal neovascularisation ( rubeosis) vein converge on each other, there is association, and is contraindicated in consequent to the retinal ischaemia. fusion of the adventitia - the outermost patients with retinal vein occlusion. Non-ischaemic CRVOs are more common components of their walls. The adjacent There is no proven early treatment and typically the presenting VA is better artery is usually narrowed and sclerotic, that will alter the visual prognosis than 6/60 and the RAPD is not marked. the obstructed branch vein dilated. in established CRVO. The main It is important to note that as many as Typical features include oedema, and management problem is to differentiate 20% of those classified as non-ischaemic scattered superficial and deep retinal ischaemic from non-ischaemic sub- on presentation can subsequently haemorrhages over a triangular retinal types. An ischaemic CRVO may develop convert to the ischaemic subtype. Visual sector whose apex is located to the neovascularisation and if this occurs, pan- outcomes are dependent of the degree occlusion site. The obstructed vein is retinal photocoagulation is indicated. and persistence of macular oedema. characteristically dilated and tortuous Macular laser photocoagulation in distal to the occlusion. Retinal oedema isolation has been shown not to be of Branch Vein Occlusion in the involved area is usually present. use in treating chronic macular oedema A branch retinal vein occlusion (BRVO) The involved retina demonstrates in CRVO. Several clinical trials are is three times more common than a variable degrees of scattered superficial in progress looking at the long-term and deep retinal haemorrhages, which respect the horizontal midline. Weeks to months after the onset of BRVO, collateral vessel formation can be observed characteristically located at the edge of the involved area. Collaterals are usually small tortuous venous channels that cross the horizontal raphe mostly temporal to the fovea and drain into the venous circulation of the uninvolved quadrant.

Figure 6 Management of Retinal Vein Occlusions Figure 7 Central Retinal Vein Occlusion (CRVO) There are two aims in the management Branch Retinal Vein Occlusion (BRVO) CONTINUING EDUCATION CET & TRAINING 2 FREE CET POINTS OT CET content supports Optometry Giving Sight Approved for Optometrists 4 Approved for Dispensing Opticians 4 “How do I complete this exam?” Go to www.optometrytoday.tv/FAQ

Retinal telangiectasias (a) (b) The retinal telangiectasias comprise a group of rare idiopathic retinal vascular anomalies characterised by dilatation and tortuosity of retinal vessels, formation of multiple aneurysms, leakage and lipid exudation in the macula, and 38 rarely combined with vascular changes in the retinal periphery. Idiopathic juxtafoveolar retinal telangiectasis (IRT) must be differentiated from other systemic and ocular diseases associated Figure 8 with telangiectasias like diabetic Right and left eye idiopathic juxtafoveolar retinal telangiectasias (IJRT) retinopathy, retinal vascular occlusions, Eale’s disease, retinopathy of prematurity, or . There is an outcome of intra-vitreal agents such as and occurs when there is severe and association with parafoveal telangiectasia ranibizumab (Lucentis), bevacizumab chronic arterial hypoperfusion. This and abnormal glucose tolerance tests. (Avastin) or steroids used either in condition is more common in men isolation or in combination for the compared to women by a ratio of 2:1, Idiopathic juxtafoveolar retinal 04/06/10 CET treatment of macular oedema in CRVO. reflecting the higher incidence of telangiectasia (IJRT) Approximately 50% of untreated atherosclerotic cardiovascular disease IJRT encompasses a group of disorders eyes with BRVO retain a VA of 6/12 in men. It tends to be a condition of characterised by retinal telangiectasias, or better whilst 25% will have a VA of elderly people and may be associated superficial retinal crystalline deposits, <6/60. Randomised clinical studies in with a dull ache. Typically, a 90% or right-angle venules and intra-retinal the laser treatment of macular oedema greater stenosis of the ipsilateral carotid pigment plaques (Figure 8). It is capable have demonstrated that a grid pattern arterial system is present in eyes with of causing visual loss in otherwise healthy of photocoagulation in the distribution the . Flow patients, although there is an association of leaking capillaries is beneficial but abnormalities within the vessel are seen between IJRT and glucose intolerance. it is recommended only after a period when the stenosis reaches 70%, and of three to six months following the it has been demonstrated that a 90% initial event and following absorption carotid stenosis reduces the ipsilateral Coats Disease of the majority of the haemorrhage central retinal artery perfusion pressure Coats disease is characterised and if VA is 6/12 or less.3 Intravitreal by about 50%. The obstruction can be by telangiectatic retinal vascular triamcinolone acetonide (IVTA) has present within the common carotid abnormalities in association with lipid been shown to be effective in improving or internal carotid artery. A carotid exudation. The majority of cases are vision and reducing macular oedema endarterectomy is indicated when diagnosed before the age of 20 years, with secondary to BRVO. The complications there is less than 100% stenosis. the peak incidence at the end of the first include formation and In the ocular ischaemic syndrome decade. It may present with increased IOP. The long-term safety central vision tends to be reduced. On or . It is invariably unilateral and efficacy of IVTA is currently being examination of the anterior segment and more common in males compared investigated in a multi-centre clinical there may be neovascularisation of the to females. Complications include trial known as the Standard Care iris. Posterior segment examination secondary cataract, , , Versus Corticosteroid for Retinal Vein reveals retinal arterial narrowing and secondary , Occlusion Study (SCORE).4 Secondary straightening, dilated and beaded and (atrophy of non- neovascularisation can also complicate retinal veins, retinal haemorrhages and functional eye). Treatment is either with a BRVO, and if this occurs then microaneurysms. Neovascularization laser photocoagulation or cryotherapy to sector argon laser photocoagulation is a complication of chronic retinal the peripheral vascular abnormalities. to the ischaemic area is indicated. ischaemia. Because of the poor arterial perfusion, minor pressure to the Sickle Cell Disease Ocular Ischaemic Syndrome will cause the retinal arterioles to Sickle cell haemoglobinopathies all The ocular ischaemic syndrome has also visibly pulsate. This is a very sensitive share the common feature of an abnormal been termed “slow flow retinopathy” and useful clinical observation. globin chain, which leads to sickling “How do I complete this exam?” Go to www.optometrytoday.tv/FAQ

of erythrocytes and obstruction of are found at the interface between vascular tumour of the (Figure the microcirculation. Sickle vaso- perfused and non-perfused peripheral 9a). There are two distinct subtypes – occlusive events are insidious and retina, growing toward the ischaemic the diffuse and the circumscribed. The affect virtually every vascular bed in pre-equatorial retina. Sea fans may have median age of onset of ocular symptoms the eye. There are various subtypes of multiple feeding arterioles and draining in patients with the diffuse type is 8 sickle cell disease; the “SS disease” is venules, probably due to their origin from years of age, contrasting with the age associated with more severe systemic multiple buds of angiogenesis that break of 39 years for the circumscribed type. disease, whist the “SC disease” tends through the internal limiting membrane In the well-circumscribed type of 39 to cause more advanced ocular disease. of retina and grow along the surface of choroidal haemangioma, there is a A salmon patch haemorrhage is the retina at the vitreo-retinal interface. well-defined orange red dome-shaped observed in sickle cell disease and Neovascularisation can result in vitreous mass visible. Most tumours are 3-9mm appears as an oval-shaped area of intra- haemorrhage or retinal detachment and in diameter and are typically located retinal or pre-retinal blood, believed to so photocoagulation is indicated when in the posterior pole. If external occur secondary to an obstructed retinal signs of proliferative retinopathy appear. pressure is placed on the globe, it arteriole, which subsequently ruptures. may cause blanching of the tumour. After re-absorption of the salmon patch Radiation Retinopathy The diffuse choroidal haemangioma haemorrhage, the retina may appear Radiation retinopathy can be a is seen in Sturge-Weber syndrome. It is entirely normal, without any evidence complication of either localised found in 40% to 55% of Sturge-Weber of residual blood. In the location of the irradiation (brachytherapy) or external patients and is bilateral in 23.5% of haemorrhage, however, there may also beam irradiation (teletherapy). these patients. The haemangioma is 04/06/10 CET be a faint indentation or depression Brachytherapy is used when radioactive usually ipsilateral to the port wine representing thinning of the inner retina. plaques are placed on the to stain; however, variants have also been This appears on ophthalmoscopy as a irradiate choroidal tumours. Indications reported. Typically, it appears as a diffuse, dimple. Black sunburst lesions have for external beam radiation include the reddish-orange thickening of the choroid also been associated with intra-retinal treatment of structures adjacent to the eye that may cause the fundus to appear haemorrhages; these are flat, round to – tumours of the or nasopharynx. darker than the fundus of the fellow oval, black patches about 0.5–2mm in Radiation retinopathy tends to occur eye. The description, “tomato ketchup” size. Venous tortuosity is an early sign of 12 to 18 months following exposure fundus, is characteristically applied ophthalmic sickle cell disease and “silver to radiation. Retinal changes include to the diffuse choroidal haemangioma. wiring” of the arterioles is also a feature. cotton wool spots, retinal haemorrhages Presenting symptoms include vision Sickle cell disease can also cause and hard exudates. Ischaemic retinal loss, foveal distortion or hypermetropia proliferative retinopathy. Peripheral necrosis can involve both the central and from choroidal thickening. Patients retinal neovascularisation often assumes peripheral retina. Neovascularisation with port wine stains may present a frond-like configuration, resembling the may be a complication of this asymptomatically when undergoing marine invertebrate Gorgonia flabellum condition, which is then treated screenings with dilated fundus (sea fan), but intra-retinal microvascular by argon laser photocoagulation. examinations. Vision loss in affected abnormalities (IRMA) can also be found at patients is secondary to exudative retinal sites of active angiogenesis. The majority Choroidal Haemangioma detachment, cystoid degeneration or of the neovascular sea fan formations A choroidal haemangioma is a benign photoreceptor loss of overlying retina, or fibrous metaplasia of the overlying RPE. (a) (b) Exudative retinal detachment may be seen in up to 50% of patients with Sturge- Weber syndrome and diffuse choroidal haemangioma. Choroidal haemangiomas show a very good treatment response to photodynamic therapy (PDT) (Figure 9b).

Optic Nerve Ischaemia Optic nerve ischaemia most frequently occurs at the optic nerve head, where Figure 9(a) and (b) structural crowding of nerve fibres and (a) Choroidal haemangioma, and (b) choroidal haemangioma after treatment with PDT reduction of the vascular supply may 04/06/10 CET 40 POINTS2 FREECET Approved Approvedfor Optometrists for Dispensing Opticians there is a risk of visual loss in the the in loss as visual of emergency risk a ophthalmic is there an granulomatosis. is Wegener’s It association as conditions inflammatory in such other reported with but been (GCA) Arteritis has Cell Giant with loss. visual progressive develop patients of number small A reduced. normal slightly or is patients of third one in VA The altitudinal. typically is defect field visual associated The insult. become vascular the after may weeks six as pallor early as evident disc optic resolves then and oedema disc or The hyperaemic pale. segmental, or diffuse be may NAAION in oedema disc optic The cup. physiological absent or small a has and diameter in small is typically eye onset. contralateral the in after disc optic years The five fifth by a patients to up of in occur to involvement estimated is eye Fellow or static progressive. be may loss visual initial of course The awakening. upon noticed disease. early vascular of systemic risk from increased death an at not are NAAION with those occlusion, arterial factor. In contrast to patients with retinal risk associated an be may hypotension nocturnal Periodic disc. the and of swelling ischaemia inadequate produces which oxygenation at point a reaches eventually head, nerve the at structures supporting and fibres nerve of structural crowding by exacerbated circulation, is It thought that years. insufficiency in 50 of of the optic age disc neuropathy the over patients optic acute common neuropathy. optic ischaemic posterior visible disc oedema, this has been termed intra-orbital portion of the nerve, with no the affects ischaemia nerve optic when frequently Less (NAAION). non-arteritic optic categorised as either arteritic (AAION) or ischaemic is AION Generally (AION). anterior neuropathy syndrome termed such is common most The oedema. disc optic produce and degree to a critical perfusion to impair combine AAION is most commonly associated associated commonly most is AAION first often is impairment Visual most the is 10) (Figure NAAION CET 4 & TRAINING EDUCATION EDUCATION CONTINUING diagnosis. It should be noted that the the that noted be should histological It a diagnosis. provides biopsy raised artery a and C-Reactive Protein (ESR) (CRP). A temporal Rate Sedimentation include Erythrocyte laboratory investigations Confirmatory emergency. an as hospital nearest the to referred be haemorrhages. associated be may there and white, chalky and swollen appear will disc optic the RAPD, a be will there reduced, profoundly be will vision AAION. The with arteries, present will ciliary patient the posterior GCA the If condition. affects treatable a is it as cause, underlying the as out ruled GCA have must people elderly in disturbance neurological Any palsy. nerve the cranial be termed or fugax may amaurosis of is cause underlying GCA this claudication. eating; to jaw leading when muscles pain masseter the of areas. temporal ischaemia the experience also may Patients or to localised occipital be frontal, to tends which headache, associated an be hair. may There their brushing when tenderness scalp notice may Patients nodular. and enlarged feels artery superficial the and tenderness temporal of superficial complain will the patient If the involved, is artery temporal loss. weight malaise and general of history antecedent an be may There life. of decades eighth and renal failure. infarctions myocardial aneurysms, aortic as systemic such associations as well as eye, contralateral (NAAION) anteriorNon-arteritic ischaemicopticneuropathy Figure 10 If If GCA is suspected, the patient should and seventh the in presents GCA OT CET content supports Optometry Giving Sight 4 “How do I complete this exam?” oslain t dtc reactivation. detect to regular have consultations and years to months for to remain on immunosuppressive therapy need will patient The steroids. systemic GCA. out rule not does biopsy negative a that so pattern lesion” “skip or diffuse arteritic process affects the artery in a non- particularly in the area of Ocular Ocular of several for field the in articles written area has and the Therapeutics, in Clinical particularly in London, University, MSc City at the Optometry on teaching involved in been Institute has She Dublin Technology of the in optometrists undergraduate to lecturer a also is She Dublin. consultant Street, Eccles Hospital, Mater Private a the in is ophthalmologist medical FEBO MRCOphth Louise O’Toole MMed Sci, FRCSI(Ophth) A iya.k o cl 00 00 8352. 040 0207 call or city.ac.uk) (m.hennelly@ emailing by Hennelly L Vision Michelle Dr Binocular further contact please For information and (September 2010). 14-16 2010) (November Disease 7 5- Eye 2010), Segment Posterior 20-22nd 2010), 18-20 (July Glaucoma (June Independent (apply web-based), Prescribing Therapeutics – anytime include: of University Principles City courses at MSc running Optometry. Masters Clinical achieve full a in to to through points readers CET allowing forces joined have OT and UNIVERSITY CITY M RVO_Guidelines_Feb_2009.pdf publications/published-guidelines/ http://www.rcophth.ac.uk/docs/ 2009 February Guidelines Vein Interim Retinal (RVO) Occlusion Ophthalmologists of College Royal S ‘references’ See www.optometry.co.uk andsearch R uggested reading uggested eferences bout the the bout Treatment of GCA is with high dose dose high with is GCA of Treatment S c in Clinical Clinical in c Go to www.optometrytoday.tv/FAQ A uthor Optometry Today. Today. Optometry O ptometry “How do I complete this exam?” Go to www.optometrytoday.tv/FAQ questions Module exams thisdate after –answers publishedonwww.optometry.co.uk to willbe themodule PLEASE NOTE d) Like a CRVO it presents with tortuosity ofthevenules itpresents withtortuosity aCRVO d) Like canhave rubeosisasafeaturec) It pulsations isassociated withretinal arterial b) It isassociated withipsilateral carotida) It stenosis syndrome isF 6. Which ofthefollowing statements ischaemic theocular about may leadto neovascularisation d) It involving hasretinal haemorrhages thefourc) It quadrantsofthefundus isassociated withdiscswelling/oedema b) It itisischaemic, therea) If willbenoRAPD occlusion isF 5. Which ofthefollowing statements acentral about retinal vein d) They canchronically leak c) They may spontaneouslyrupture b) They are treated by pan-retinal photocoagulation a) They are more patients commoninhypertensive macroaneursyms isF 4. Which ofthefollowing statements retinal about arterial d) Anti-VEGF agents c) Useofcarbogen b) Physical lowering ofintraocularpressure massage a) Ocular EXCEPT 3. A d) They are notassociated withGiantCell Arteritis c) Vasculitis occlusion cancauseanarterial b) to anembolus They may occursecondary tend toa) Men bemore frequently affected compared to women F 2. Which ofthefollowing statements occlusions retinalis about arterial d) Opticdiscoedemaisunilateral are afeature haemorrhages c) Retinal b) may assumea The arterioles “copper wire” appearance a) may assumea The arterioles “silver wire” appearance F 1. Which ofthefollowing statements hypertensive about retinopathy is ALSE? ALSE? ll ofthefollowing are treatments for acentral occlusion retinal artery : T here isonlyonecorrect answer. A ALSE? ALSE? ALSE? isnowll CET F REE . Enter online. Pleasecomplete onlineby midnight onJuly72010- You unableto willbe submit d) It responds well tod) It steroids causesintracranialaneurysms c) It may causetemporal tenderness b) It may present withjawa) It claudication is F 12. Which ofthefollowing statements Giant about Cell A d) There to thefellow isnorisk eye c) There isaRAPD b) The discis swollen andpale artery occurswhenthere ciliary isocclusionoftheposterior a) It neuropathy isF 11. Which ofthefollowing statementsischaemicoptic arteritic about hasanassociated visualfielddefect d) It isassociated withposturalhypotensionc) It presents withdiscswelling/oedema b) It istreated withhighdosesystemica) It steroids isF 10. Which ofthefollowing statementsischaemic non-arteritic about d) They may present before adolescence c) They causeanaxialmyopia b) They canbeeffectively treated withPDT a) Diffusehaemangiomas are a feature oftheSturge Weber syndrome is F 9. Which ofthefollowing statements choroidal about haemangiomas exudates d) Starburst fans c) Sea b) Salmonpatches a) Elschnig spots 8. Features cell ofsickle retinopathy includeallofthefollowing EXC EPT may causeanexudative retinald) It detachment ismore commoninmalesthanfemalesc) It bilateral istypically b) It differential isanimportant for leukocoria a) It 7. Which ofthefollowing statements Coats about diseaseisF ALSE? ALSE? Course code: C-13921O/D ALSE? ALSE? rteritis rteritis ALSE? : 41 04/06/10 CET